CVJA Volume 28 Issue 4 by Clinics Cardive Publishing

JULY/AUGUST 2017 VOL 28 NO 4

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CardioVascular Journal of Africa (official journal for PASCAR)

• Changing spectrum of rheumatic mitral regurgitation in Soweto • Pulmonary embolism in HIV-positive patients in Cape Town • Nuclear cardiology practices and radiation exposure in Africa • Risk factors for cardiovascular disease in Cameroonians • Streptococcal pharyngitis and rheumatic heart disease in Zambia • Acute rheumatic fever and rheumatic heart disease in Port Elizabeth • Primary care in prevention, treatment and control of cardiovascular disease • PASCAR roadmap for 25% hypertension control in Africa by 2025

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PUBLISHED ONLINE: • Aorta–right atrial tunnel with windsock aneurysm: diagnosis and treatment

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the affordable5 endurance ACE-inhibitor For further product information contact PHARMA DYNAMICS P O Box 30958 Tokai Cape Town 7966 Tel 021 707 7000 Fax 021 701 5898 Email info@pharmadynamics.co.za CUSTOMER CARE LINE 0860 PHARMA (742 762) www.pharmadynamics.co.za PEARINDA 4 and 8. Each tablet contains 4, 8 mg perindopril tert-butylamine respectively. S3 A41/7.1.3/0649, 0650. NAM NS2 10/7.1.3/0476, 0477. For full prescribing information, refer to the package insert approved by the Medicines Control Council, April 2009. PEARINDA PLUS 4. Each tablet contains 4 mg perindopril tert-butylamine and 1,25 mg indapamide. S3 A41/7.1.3/0633. NAM NS2 10/7.1.3/0611. For full prescribing information, refer to the package insert approved by the Medicines Control Council, April 2010. 1) The EUROPA study Investigators. “Efficacy of perindopril in reduction of cardiovascular events among patients with stable coronary artery disease: randomized, double-blind, placebo-controlled, multicentre trial (the EUROPA study)”. The Lancet 2003;362:782-788. 2) The PREAMI study Investigators. “Effects of angiotensin-converting enzyme inhibition with perindopril on left ventricular remodelling and clinical outcome. Results of the randomized perindopril and remodelling in elderly with acute myocardial infarction (PREAMI) study”. Arch Intern Med 2006;166:659-666. 3) PROGRESS Collaborative Group. “Randomised trial of a perindopril-based blood-pressure-lowering regimen among 6105 individuals with previous stroke or transient ischaemic attack”. The Lancet 2001;358:1033-41. 4) Guerin AP, et al. “Impact of Aortic Stiffness Attenuation on Survival of Patients in End-Stage Renal Failure”. Circulation 2001;103;987-992. 5) Database of Medicine Prices (14 March 2017). Department of Health website. http://www.mpr.gov.za - Accessed on 30 March 2017. PAG398/04/2017.

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ISSN 1995-1892 (print) ISSN 1680-0745 (online)

Vol 28, No 4, JULY/AUGUST 2017

CONTENTS

Cardiovascular Journal of Africa 207

www.cvja.co.za

FROM THE EDITOR’S DESK P Commerford

CARDIOVASCULAR TOPICS 208

Endomyocardial fibrosis in Sudan: clinical and echocardiographic features SI Khalil • S Khalil • S El Tigani • HA Saad

215

The changing spectrum of rheumatic mitral regurgitation in Soweto, South Africa R Meel • F Peters • E Libhaber • MR Essop

221

The prevalence and radiological findings of pulmonary embolism in HIV-positive patients referred for computed tomography pulmonary angiography in the Western Cape of South Africa R Ramlakhan • S Andronikou • A Rajkumar

229

Nuclear cardiology practices and radiation exposure in Africa: results from the IAEA Nuclear Cardiology Protocols Study (INCAPS) SE Bouyoucef • M Mercuri • TNB Pascual • AH Allam • M Vangu • JV Vitola • N Better • G Karthikeyan • JJ Mahmarian • MM Rehani • R Kashyap • M Dondi • D Paez • AJ Einstein • for the INCAPS investigators group

235

Pilot study of risk factors associated with cardiovascular disease in northern and southern Cameroonians JD Chiadak • J Perret • HM Womeni • JR Kuiaté • P Cullus • C Senterre • C Delporte

242

A programme to increase appropriate usage of benzathine penicillin for management of streptococcal pharyngitis and rheumatic heart disease in Zambia A Long • J Chipili • E Machila • S Schwaninger • J Spector • B Tadmor • M Fishman • BM Mayosi • J Musuku

248

Clinical presentation and outcomes of patients with acute rheumatic fever and rheumatic heart disease seen at a tertiary hospital setting in Port Elizabeth, South Africa ZM Makrexeni • L Pepeta

INDEXED AT SCISEARCH (SCI), PUBMED, PUBMED CENTRAL AND SABINET

Editors

SUBJECT Editors

Editorial Board

Editor-in-Chief (South Africa) Prof Pat Commerford

Nuclear Medicine and Imaging DR MM SATHEKGE

prof PA Brink Experimental & Laboratory Cardiology

PROF A LOCHNER Biochemistry/Laboratory Science

PROF R DELPORT Chemical Pathology

PROF BM MAYOSI Chronic Rheumatic Heart Disease

Assistant Editor Prof JAMES KER (JUN) Regional Editor DR A Dzudie Regional Editor (Kenya) Dr F Bukachi Regional Editor (South Africa) PROF R DELPORT

Heart Failure Dr g visagie Paediatric dr s brown Paediatric Surgery Dr Darshan Reddy Renal Hypertension dr brian rayner Surgical dr f aziz Adult Surgery dr j rossouw Epidemiology and Preventionist dr ap kengne Pregnancy-associated Heart Disease Prof K Sliwa-hahnle

PROF MR ESSOP Haemodynamics, Heart Failure DR MT MPE Cardiomyopathy & Valvular Heart Disease DR OB FAMILONI Clinical Cardiology DR V GRIGOROV Invasive Cardiology & Heart Failure

International Advisory Board PROF DAVID CELEMAJER Australia (Clinical Cardiology) PROF KEITH COPELIN FERDINAND USA (General Cardiology) DR SAMUEL KINGUE Cameroon (General Cardiology)

PROF DP NAIDOO Echocardiography

DR GEORGE A MENSAH USA (General Cardiology)

PROF B RAYNER Hypertension/Society

PROF WILLIAM NELSON USA (Electrocardiology)

PROF MM SATHEKGE Nuclear Medicine/Society PROF J KER (SEN) Hypertension, Cardiomyopathy, PROF YK SEEDAT Cardiovascular Physiology Diabetes & Hypertension

DR ULRICH VON OPPEL Wales (Cardiovascular Surgery)

DR J LAWRENSON Paediatric Heart Disease

PROF ERNST VON SCHWARZ USA (Interventional Cardiology)

PROF H DU T THERON Invasive Cardiology

PROF PETER SCHWARTZ Italy (Dysrhythmias)

REVIEW ARTICLE 251

Primary care in the prevention, treatment and control of cardiovascular disease in sub-Saharan Africa DB Ojji • K Lamont • OI Ojji • N Egenti • K Sliwa

257

Reviewing the causes of electrocardiographic pauses C Viljoen • R Smith • A Chin

262

Roadmap to achieve 25% hypertension control in Africa by 2025 A Dzudie • B Rayner • D Ojji • AE Schutte • M Twagirumukiza • A Damasceno • SA Ba • A Kane • E Kramoh • JBA Kacou • B Onwubere • R Cornick • K Sliwa • B Anisiuba • AO Mocumbi • E Ogola • M Awad • G Nel • H Otieno • AI Toure • S Kingue • AP Kengne • P Perel • A Adler • N Poulter • B Mayosi • on behalf of the PASCAR task force on hypertension

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Illuminating the pathway for the next generation of cardiovascular medicine practitioners and researchers: Highlights of the Joint PASCAR–SCC clinical symposium on hypertension and heart failure, Cameroon MH Abanda • A Dzudie • B Hamadou • Y Monkam • H Luma • MS Douala • L Nganhyim • BS Dzekem • TN Nana • AO Mocumbi • S Stewart • K Sliwa • EB Priso

PUBLISHED ONLINE (Available on www.cvja.co.za and in PubMed)

An unusual case of aorta–right atrial tunnel with windsock aneurysm: imaging, diagnosis and treatment SAM Khan • L Scholtz • FA Snyders • J de Villiers

Management of a complicated redo giant dissecting aortic aneurysm I Kara • A Erkin • HI Erkengel • K Asil

Left ventricular haematoma mimicking lateral wall myocardial infarction secondary to percutaneous coronary intervention O Senarslan • NB Tamci • UH Kantarci • M Eyuboglu • DA Senarslan

Vol 28, No 4, JULY/AUGUST 2017

CONTENTS

ECG SERIES

PASCAR ROADMAP ON HYPERTENSION

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GAUTENG CONTRIBUTOR PETER WAGENAAR Cell 082 413 9954 e-mail: skylark65@myconnection.co.za The Cardiovascular Journal of Africa, incorporating the Cardiovascular Journal of South Africa, is published 10 times a year, the publication date being the third week of the designated month. Copyright: Clinics Cardive Publishing (Pty) Ltd.

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From the Editor’s Desk Call me old fashioned if you wish, but I remain saddened by the apparent erosion of clinical skills in cardiology and the determined rush to involve ever more-sophisticated imaging modalities prior to simple clinical evaluation, examination of a chest radiograph and an ECG. The ECG remains one of the oldest ways of evaluating the heart; it is cheap and non-invasive and when interpreted correctly, can contribute an enormous amount of information. In this issue of the journal, Viljoen and colleagues (page 257) provide an example of the utility of the simple resting 12-lead ECG in explaining the patient’s symptoms and prompting appropriate treatment. If this ECG abnormality had been recognised at primary or secondary level, the patient could have been referred promptly. Instead, he joined the queue for unnecessary echocardiography. This will, I hope, be the first in an ECG series, of which each will consist of a brief clinical vignette, an ECG and an explanation linking the clinical features to the ECG. It is a particular pleasure to write this piece to introduce the articles in this issue. All of them emanate from Africa and all address common and important diseases of Africa. On page 262, Dzudie and his colleagues from PASCAR outline a roadmap for hypertension in Africa. The intention is to develop practical guidelines on how to implement strategies that translate existing knowledge into effective action and improve detection, treatment and control of hypertension in sub-Saharan Africa by the year 2025. Given the importance of hypertension to cardiovascular disease in Africa, successful adoption of such a roadmap should make a major contribution to health on the continent. Rheumatic heart disease remains a problem in Africa. Given the scarcity of surgical facilities, prevention and secondary prophylaxis remain at the heart of attempts to control the condition, and Long and colleagues (page 242) describe an initiative in Zambia, consisting of an educational and accessto-medicine programme aimed at increasing appropriate use of benzathine penicillin for the prevention and management of rheumatic heart disease. They describe well-established barriers to correct care, including the concerns of healthcare workers. Gratifyingly, they are able to show a measure of success, as indicated by increased use of benzathine penicillin. A programme such as that described by Long will only succeed on a large scale if it is incorporated into an effective primary care network such as that envisaged for Africa by Ojji and co-authors (page 251). Such a programme requires effective political will and has substantial financial implications but remains essential. Continuing the theme of rheumatic heart disease, in a retrospective record review, Makrexeni and colleagues describe the spectrum of rheumatic heart disease at a paediatric cardiology tertiary care service in Port Elizabeth, South Africa (page 248). Sadly, the majority presented with established structural heart disease and a minority with acute rheumatic fever, which would allow institution of effective prophylaxis. Such retrospective

Professor PJ Commerford

series are often criticised but they do serve the important role of reminding us of the reality of our day-to-day practice. Meel and co-authors (page 215), using echocardiographic evaluation of a contemporary cohort of patients with rheumatic mitral regurgitation, describe similar changes to the presentation at another institution, with few patients having acute rheumatic fever, most being older and characterised by more co-morbidities and thickened and calcified valves. Endomyocardial fibrosis remains a rare and poorly understood condition with striking geographic variability in its distribution. Khalil and co-authors present an analysis of their echocardiographic experience (page 208) and provide echocardiographic images, which should be helpful to all performing imaging in this condition. It is a great privilege to be able to publish in this journal the work of African authors reporting their experiences with important diseases of Africa. Pat Commerford Editor-in-Chief

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Cardiovascular Topics Endomyocardial fibrosis in Sudan: clinical and echocardiographic features Siddiq Ibrahim Khalil, Suha Khalil, Salma El Tigani, Hanan A Saad

Abstract Objective: Endomyocardial fibrosis (EMF) is a rare disease and is often an underdiagnosed and forgotten cardiomyopathy. The objective of this study was to document the current frequency of EMF in Sudan by defining and selecting cases from patients attending the echocardiography laboratory. Additionally we aimed to create an EMF registry for Sudan. Methods: The study started in January 2007 and is on-going. All the patients attending our echocardiography clinics in four different hospitals in Khartoum, Sudan, were included. Transthoracic echocardiography was used as the main diagnostic and selection tool. The diagnosis of EMF was based on predefined criteria and definitions, and was further supported by additional clinical, ECG, laboratory and chest X-ray findings. Results: Out of 4 332 cases studied, 23 (0.5%) were found to have features of EMF. Females constituted 52% and the age range was 24 to 67 years. All patients presented with dyspnoea grades III–IV. Advanced heart failure with gross fluid overload was seen in 54% of cases and ascites was seen in 30%. EMF was biventricular in 53%, left ventricular in 29% and right ventricular in 18% of cases. Apical and ventricular wall fibrosis was found in all cases, followed by atrial enlargement, atrioventricular valve incompetence, ventricular cavity obliteration, restrictive flow pattern and pericardial effusion. Additional echocardiographic features are defined and discussed. Conclusion: Although a rare disease, cases of EMF can be identified in Sudan if a high index of suspicion is observed. New echocardiographic features of ventricular wall layering, endocardial fibrous shelf and endomyocardiopericarial fibrosis were identified and are discussed.

Department of Medicine, University of Medical Sciences and Technology, Khartoum, Sudan Siddiq Ibrahim Khalil, MD, FRCP, FESC, FACC, psiddiq@gmail. com

The Heart Clinic, Khartoum, Sudan Suha Khalil, MB BS, MRCGP

Amal National Hospital, Khartoum, Sudan Salma El Tigani, MB BS, MRCP

Academy Teaching Hospital, Khartoum, Sudan Hanan A Saad, MD

Keywords: endomyocardial fibrosis in Sudan, apical fibrosis, ventricular cavity obliteration, endocardial fibrous shelf, endomyocardiopericarial fibrosis Submitted 23/5/16, accepted 2/8/16 Cardiovasc J Afr 2017; 28: 208–214

www.cvja.co.za

DOI: 10.5830/CVJA-2016-079

Endomyocardial fibrosis (EMF) is a form of cardiomyopathy characterised by fibrosis and thickening that distinctly involves the ventricular apex and walls. It is one of the common causes of restrictive cardiomyopathy and is frequently underdiagnosed and occasionally mislabelled as rheumatic valvular disease or hypertrophic cardiomyopathy. EMF was described by Loffler in 1936 in a patient with associated eosinophilia,1 and in Africa in 1946 by Bedford and Konstam,2 but its clinicopathological features were first recognised by Davies in Uganda in 1948.3 Although sporadic cases with similar clinical and pathological features have since been reported from other parts of the world, the majority of reported cases have come from West and Central Africa. In Uganda, it accounted for 25% of cases reported for echocardiography, and for 20% in a random population sample in Mozambique.4,5 EMF has also been reported from other subtropical countries such as Egypt6 and Nigeria, and some sub-Saharan countries,7,8 Brazil, and Kerala in India,9,10 It is exceedingly rare in Europe and North America; however a few cases have been reported in China11 and Japan.12 The aetiology of EMF is unknown, however on an epidemiological basis, it behaves like a vector-transmitted disease. In addition to geography, several factors have been associated with the pathogenesis of EMF in Africa, including ethnicity, poverty, diet, age and gender, infection and eosinophilia.3 There is now evidence that the initial heart lesion in EMF may be associated with abnormalities of the eosinophils, although eosinophilia is common in many tropical regions where EMF does not appear to be prevalent. This suggests that other factors, possibly immunological in nature, are also necessary to determine the prevalence of the disease in a particular location.3,6 There is agreement among researchers that African endomyocardial fibrosis is a distinct entity and, despite the similarity in pathological features with Loffler’s endocarditis and the cardiac lesions seen in eosinophilic leukaemia or reactive eosinophilia, there is no hard evidence to suggest that African endomyocardial fibrosis is a variant of Loffler’s disease.13-15

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Despite the lack of evidence to pinpoint the aetiology of EMF, some progress has been made in the diagnosis as well as in medical and surgical treatment. In earlier reports, the diagnosis of EMF was based on post mortem findings and clinical correlations but presently echocardiography is the standard diagnostic tool. Recently, cardiac magnetic resonance imaging (CMR) emerged as an additional tool to define the primary and secondary structural and functional abnormalities of EMF. CMR with gadolinium enhancement seems ideally suited to diagnose this condition and monitor response to medical and/ or surgical therapy.16 Medical treatment of EMF entails reduction of fluid overload with diuretics and preload with nitrates. Rate and rhythm control may help in patients presenting with tachyarrhythmias, including atrial fibrillation. Surgical treatment of EMF was practiced for many years and consisted of removal of fibrosis from both ventricles, and atrioventricular valve replacement. Mitral or tricuspid annuloplasty has had only limited success.17 In Sudan, EMF was first described by O’Brien in 1954 and later by El Hassan, who had carried out post mortem studies in 133 cases of cardiovascular deaths. Among these, six out of 13 cases of cardiomyopathy had EMF affecting both left and right ventricles, with fibrosis that involved the endocardium and subendocardial tissues and covering the apex, papillary muscles and posterior ventricular wall, leading to atrioventricular valve dysfunction.18,19 The objective of our study was to document the current frequency of EMF in Sudan by identifying and selecting cases from patients attending our echocardiography clinics in four different hospitals, and creating an EMF registry. However during the process of acquisition and analysis of images, it emerged that there were new echocardiographic features that had not been reported before. These findings are presented and discussed below.

Methods This study is a prospective, descriptive study, which started in January 2007 and is on-going. Patients attending our echocardiography sessions at Amal National Hospital from 2007 to 2009, and the Academy Teaching and Yastabshiroun Hospitals from 2010 to 2011 were included; however the majority of the selected patients were enrolled from the Heart Clinic in Khartoum, Sudan. Permission for the study was obtained from the ethics committees in the four centres and informed verbal consent was obtained from each patient. Transthoracic echocardiography using Mylab30 (Esaote, Italy) was performed by SIK on all selected patients, using the American Society of Echocardiography (ASE) standards.20 Additional information was obtained from the Echo Manual by Oh, Seward and Tajik.21 The following standard echocardiographic views were used: parasternal long-axis (PLAX), short-axis (SAX), M-mode, apical two-, four- and five-chamber views (AP2, AP4, AP5) and the apical long-axis view (APLX). Additionally, a modified APLX view, obtained by angulating the probe medially and rotating counter-clockwise to focus on the recess between the posterior papillary muscle and the posterior mitral valve leaflet was used. The diagnosis of EMF was made on cases that fulfilled the following echocardiographic features and definitions:

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• Generalised endomyocardial thickening and fibrosis of the apex, ventricular walls and papillary muscles, and atrioventricular (AV) valve incompetence. • Obliteration of the ventricular cavity by fibrous tissue, defined as left ventricular (LV) diastolic volume less than 40 ml, measured by the modified Simpson’s rule in AP4 view and right ventricular (RV) size less than 20 mm, measured by the mid-RV diameter in the AP4 view. • Left atrial (LA) volume was measured with the biplane method of disks (modified Simpson’s rule) from AP4 and AP2 views at ventricular end-diastole. Huge left atrium was defined as atrial volume of more than 70 ml. • Right atrium (RA) was quantified from the apical four-chamber view. The minor-axis diameter was measured according to ASE recommendations.19 Right atrial dilatation was assumed when the mid-axis diameter was more than 5.0 cm. Diagnosis was made from a detailed initial examination and ascertained by two review examinations, carried out during the first four weeks after the case was identified. Additional information was derived from targeted history, clinical examination, 12-lead electrocardiogram (ECG), chest X-ray and complete blood count, including total blood count, differential white cell count and absolute eosinophilia (> 600 cells/μl).

Results Out of 4 332 cases studied, 23 (0.5%) were found to have features of EMF. Of these 23 cases identified, two were from Amal Hospital, two from Yastabshiroun Hospital, five from Academy Teaching Hospital and 14 cases were from the Heart Clinic in Khartoum. Females constituted 52% and the age range was 24 to 67 years. All patients presented with dyspnoea grades III–IV, and advanced heart failure with gross fluid overload was seen in 54% of cases and ascites was seen in 30%. ECG findings were non-specific; sinus tachycardia was found in 22% of patients, atrial abnormality in 43%, first-degree heart block in 39% and atrial fibrillation in 13% of patients. Chest X-ray findings were also non-specific and showed cardiomegaly in 92% of patients. Haematological findings included absolute eosinophilia in three patients and five cases had iron deficiency. EMF was biventricular in 53%, left ventricular in 29% and right ventricular in 18% of cases. Echocardiographic features of EMF are summarised in Table 1. Table 1. Frequencies of echocardiographic features of EMF (n = 23) Echocardiographic features Apical fibrosis Ventricular wall fibrosis Atrial enlargement Atrioventricular valve regurgitation Ventricular cavity obliteration Pericardial effusion Endocardium fibrous shelf formation Restrictive flow pattern Ascites Thrombus formation

Percentage of patients 100 100 100 100 91 87 82 76 30 6

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Echocardiographic images of EMF were divided into the following subgroups: images of basic echocardiographic features (covered in Figs 1â&#x20AC;&#x201C;3), images of additional A

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echocardiographic details (shown in Fig. 4) and images of new echocardiographic features (shown and described in Figs 5 and 6). B

Fig. 1. B asic echocardiographic features of left ventricular EMF. A and B, apical four-chamber view. The huge left atrium with apical and LV wall fibrosis, obliterated LV and mitral regurgitation (MR) (B), are the characteristic features of left ventricular EMF.

Fig. 2. B asic echocardiographic features of advanced left ventricular EMF. Images from a 42-year-old female who presented with intractable heart failure. A is a subcostal view showing the typically huge left atrium occupying half the cardiac size. B is an AP four-chamber view showing apical fibrosis extending to the septum and ventricular walls, leading to severe obliteration of the left ventricular cavity.

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CARDIOVASCULAR JOURNAL OF AFRICA â&#x20AC;˘ Volume 28, No 4, July/August 2017

Discussion This descriptive study that discusses the clinical and echocardiographic features of EMF in Sudan is not intended to redefine the pathognomonic echocardiographic features of the A

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disease, which have been well described in previous works.3,4,6,22 The main objective was to determine the current frequency of EMF in Sudan, as the last report on the disease dates back more than 40 years. B

Fig. 3. R ight ventricular (RV) and biventricular EMF. A (AP4) showing EMF of the RV; note the apical fibrosis engulfing the moderator band, fibrosis of the anterior interventricular septum, dilated RA and obliterated RV. B (AP5) shows biventricular EMF. A

Fig. 4. L ayering. A is a short-axis view of a patient with advanced EMF showing layering of the thickened endocardium with the myocardium and pericardium. The posterior mitral valve leaflet (MV) is seen tethered to the endocardium. B is M-mode showing the distinct layers of the posterior wall with thickened endocardium and myocardium. A thickened pericardium with effusions can be seen peripherally.

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The method we used was to identify and select cases of EMF from patients attending our echocardiography laboratory using predefined features and definitions. All images relate to advanced forms of EMF, which were available in the hospital setting. We did not see mild or early forms of the disease and speculate that population-based studies are more appropriate for reporting these types of EMF.4 As we recognised only 23 cases of EMF during the course of eight years, we infer that the disease is rare in Sudan and that

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only isolated cases are prevalent. Consequently, a study of this nature will help improve the awareness of physicians to diagnose this disease. The basic diagnostic echocardiographic features are shown in Figs 1 to 3. The images of apical and ventricular wall fibrosis together with huge atria should alert the investigator to the possibility of EMF. The presence of moderate-to-severe atrioventricular valve regurgitation and obliterated ventricles should provide further confirmation of the diagnosis (Fig. 1A, Fig. 2B, C).

Fig. 5. E ndocardial fibrous shelf. A is PLAX, B is AP4, and C and D are modified APLX views from three different patients (B and D from same patient), with left ventricular EMF showing thickened endocardium spreading over the recess between the posterior papillary muscle and the posterior mitral valve leaflet, engulfing the leaflet and forming an immobile endocardial fibrous shelf (S). The anterior mitral valve leaflet although moderately thickened, moves freely, while the whole mitral structure appears reduced to a single leaflet valve.

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These findings conform to features described in previous works.4,6,23 Right ventricular EMF echocardiographic features included fibrosis of the apex, right ventricular free wall and anterior interventricular septum with obliteration of the ventricular cavity and dilated right atrium (Fig. 3A). The pericardium was also found to be affected and looked fibrosed and thickened, with mild-to-moderate effusion in the majority of cases (87%). Severe effusion (32 mm) was noted in one case, without evidence of cardiac tamponade, possibly due to the chronicity of the disease. As a result of fibrosis, the three layers forming the heart wall were identified as separate layers, especially in the posterior ventricular wall. This feature resulted in a form of ‘layering’ and is shown in Fig. 3 in both the short-axis (3A) and M-mode views (3B). Layering can be seen on all left ventricular walls, specifically the lateral and posterior walls. Although the thick fibrosis of the three separate layers was recognised in post mortem findings reported by Davies,24 echocardiographic images of layering have not been reported before.

New echocardiographic features Endocardial fibrous shelf: in countries where EMF is prevalent, the rates of rheumatic heart disease are also high and diagnostic difficulties arise in differentiating patients with mitral stenosis from those with EMF. A new echocardiographic feature, the

Fig. 6. E ndomyocardiopericardial fibrosis (EMPF). A shortaxis view from a patient with advanced EMF and intractable heart failure. The endocardium looks dense and bright with the myocardium clearly seen underneath it. The striking finding is the appearance of densely fibrosed and calcified pericardium with effusion forming an endomyocardiopericarial fibrosis. Note the presence of pericardial effusion and the posterior papillary muscle being engulfed by the thickened endocardium.

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endocardial fibrous shelf (EFS) seen in Fig. 5A–D provides useful diagnostic help. These echocardiographic images correlate well with a previously recognised pathological finding first described by Davies in 1955. He reported that the posterior mitral cusp was completely immobilised by adherence to the endocardium of the posterior wall of the ventricle, and the end result was a fibrous surface running straight down from the atrium to the ventricle where the cusp had become embedded.22 Davies further added that in other cases, the remains of the cusp projected as a short, thick shelf. This finding is shown echocardiographically by an immobile posterior mitral leaflet tethered to the endocardium and appearing like a solid shelf. The anterior mitral valve leaflet, although moderately thick, moves freely, while the whole mitral structure becomes reduced to a single leaflet valve. The echocardiographic endocardial fibrous shelf can be visualised in the modified APLX in all cases of left ventricular and biventricular EMF and provides a mark for differentiation between EMF of the left ventricle and rheumatic mitral stenosis, where the leaflets and subvalvular structure are fibrosed and may be calcified but the posterior LV wall remains free. Endomyocardiopericardial fibrosis: in three cases of advanced EMF, a dense fibrous pericardium and pericardial calcification were seen (Fig. 6). This entity behaved clinically like constrictive pericarditis, as the three patients presented with tachycardia, ascites and gross oedema of the ankles. We opted to give this type of EMF, in which the pericardium played a significant pathological and clinical role, the name endomyocardiopericardial fibrosis (EMPF), and considered it a cause of pericardial constriction. Although EMF is among the common causes of restrictive cardiomyopathy, its role in pericardial constriction has not been described before. Despite the fact that an endomyocardial biopsy from patients with both tuberculous constrictive pericarditis and endomyocardial fibrosis revealed similar histopathological changes of endocardial thickening and focal myofibrosis, evidence to support pericardial constriction in EMF could not be confirmed.25 The echocardiographic and clinical presentation of patients with EMPF lends support to pericardial constriction in association with EMF. The differentiation of EMF from hypertrophic cardiomyopathy (HCM), especially the apical type, can be difficult. However our observations are consistent with the view of Fawzy, Ziady and Halilm in that with EMF, apical obliteration appears during both systole and diastole, in contrast to HCM where it occurs only in systole.26 One additional observation is the characteristically huge left atrium (91 mm in one case), which could not be seen, even in cases of severe mitral stenosis. Among the explanations offered were the obliteration of the ventricular cavity, and hence the increase in filling pressure, together with the additional volume load due to mitral regurgitation. This study has provided high-definition images of the main diagnostic features of EMF. Images of layering provide additional identification of this multi-layer disease. This study has described and shown images of a new echocardiographic feature: the endocardial fibrous shelf, which offers an additional feature for left ventricular EMF. We also report a new entity, EMPF, a form of advanced EMF that clinically behaved like constrictive pericarditis.

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One limitation of the study is that the new echocardiographic features reported in this study, namely endocardial fibrous shelf and endomyocardiopericarial fibrosis, were collected from a largely descriptive and small study, This needs further verification, which can only be achieved in a large study.

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endomyocardial fibrosis in Bahia, Brazil. Am Heart J 1971; 81: 7–19. 10. Vijayaraghavan G, Sivasankaran S. Tropical endomyocardial fibrosis in India: A vanishing disease. Indian J Med Res 2012; 136: 729–738. 11. Yin R. Endomyocardial fibrosis in China. Chin Med Sci J 2000; 15: 55–60. 12. Niino T, Shiono M, et al. A case of left ventricular endomyocardial

Conclusion This study confirmed that isolated cases of EMF are still seen in Sudan. The main features of EMF were apical and ventricular wall fibrosis, atrial enlargement and obliterated ventricles. New details on endomyocardial pericardial layering and images of endocardial fibrous shelf are described. A new echocardiographic entity, EMPF, an advanced form of EMF that behaves like constrictive pericarditis, was identified. Diagnosis of EMF needed a high index of suspicion to differentiate it from other conditions discussed in this article.

fibrosis. Ann Thorac Cardiovasc Surg 2002; 8: 173–176. 13. Patel AK, D’Arbela PG, Somers K. Endomyocardial fibrosis and eosinophilia. Br Heart J 1977; 39: 238–241. 14. Oakley CM, Olsen EGJ. Eosinphilia and heart disease. Br Heart J 1977; 39: 233–237. 15. Andy JJ, Bishara FF, Soyinka OO. Relation of severe eosinophilia and microfilariasis to chronic African endomyocardial fibrosis. Br Heart J 1981; 45: 672–680. 16. Smedema JP, Stephan K, Winckels G, et al. Tropical endomyocardial fibrosis (Davies’ disease): case report demonstrating the role of magnetic resonance imaging. Int J Cardiovasc Imag 2004; 20: 517–522. 17. Oliveira SA, Barreto AC, Mady C. Surgical treatment of EMF, a new approach. J Am Coll Cardiol 1990; 16: 1246–1251.

As the time course of the study may suggest, many doctors, nurses and medical records staff have provided assistance during the preparation, collection

18. O’Brien W. Endocardial fibrosis in the Sudan. Br Med J 1954; 2: 899–903.

and recording of this work. We are grateful for their help and support. We thank Dr Sally Khalil for copy editing the manuscript.

19. El Hassan AM, Wasfi AI. Cardiovascular disease in Khartoum: Post-

References

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mortem and clinical evidence. Trop Geogr Med 1972; 24: 118–123.

Lofler W. Endocarditis parietalis fibroplastica mit Bluteosinophilie:

by Echocardiography in Adults: An Update from the American Society

ein eingenartiges Krankheitsbild. Schweizer medizin Wochensch 1936;

of Echocardiography and the European Association of Cardiovascular

17: 817. 2.

Bedford DE, Konstam GLS. Heart failure of unknown aetiology in Africans. Br Heart J 1946; 8: 236.

Davies JNP. Endomyocardial fibrosis in Africans. East Afr Med J 1948; 25: 10–17.

Sliwa K, Damasceno A, Mayosi BM. Epidemiology and etiology of cardiomyopathy in Africa. Circulation 2005; 112(23): 3577–3583.

Mocumbi AO, Ferreira MB, Sidi D, Yacoub MH. A population study of endomyocardial fibrosis in a rural area of Mozambique. N Engl J Med 2008; 359: 43–49.

Rashwan MA, Ayman M, Ashour S, Hassanin MM, Ziena AA. Endomyocardial fibrosis in Egypt. Br Heart J 1995; 73(3): 284–289.

Mocumbi AOH, Falase AO. Recent advances in the epidemiology, diagnosis and treatment of endomyocardial fibrosis in Africa. Heart 2013;

Imaging. J Am Soc Echocardiogr 2015; 28: 1–39. 21. Jae K Oh, Seward JB, Tajik AJ. No Normal heart chamber measurement by two-dimensional echocardiography. In: The Echo Manual. Philadelpia: Lippincott Williams & Wilkins, 1999. 22. Aquataella H, Shiller N, Puigbo JJ, Gomez-Mancebo, Suarez C, Aquatella G. Value of two-dimensional echocardiography in endomyocardial disease with and without eosinophilia: a clinical and pathologic study. Circulation 1983; 67: 1219–1226. 23. Hassan WM, Fawzy ME. Pitfalls in diagnosis and clinical, echocardiographic and hemodynamic findings in endomyocardial fibrosis. Chest 2005; 128; 3985–3992. 24. Davies JNP, Ball JD. The pathology of endomyocardial fibrosis in Uganda. Br Heart J 1955; 17: 337–359. 25. Dave T, Narula JP, Chopra P. Myocardial and endocardial involvement

99: 1481–1487.

in tuberculous constrictive pericarditis: difficulty in biopsy distinction

Damasceno A, Mayosi BM, et al. The Sub-Saharan Africa Survey

from endomyocardial fibrosis as a cause of restrictive heart disease. Int

of Heart Failure (THESUS-HF). Arch Intern Med 2012; 172(18): 1386–1394. 9.

Lang RM, Luigi P. Badano LP, Mor-Avi V, Afilalo J, Armstrong A, Ernande L, et al. Recommendations for Cardiac Chamber Quantification

Guimarães AC, Esteves JP, Filho AS, Macedo V. Clinical aspects of

J Cardiol 1990; 28: 245–251. 26. Fawzy ME, Ziady G, Halim NM, et al. Endomyocardial fibrosis: report of eight cases. J Am Coll Cardiol 1985; 5: 983–988.

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The changing spectrum of rheumatic mitral regurgitation in Soweto, South Africa Ruchika Meel, Ferande Peters, Elena Libhaber, Mohammed Rafique Essop

Abstract Objectives: To determine the clinical and echocardiographic characteristics of contemporary patients with rheumatic mitral regurgitation (MR) at Chris Hani Baragwanath Academic Hospital. Methods: This prospective, cross-sectional study included 84 patients with isolated moderate or severe rheumatic MR who underwent clinical and echocardiographic assessment. Results: Mean age of the patients was 44 ± 15.3 years (84% females). Acute rheumatic fever was rare. Hypertension and HIV were present in 52 and 26%, respectively. Echocardiography showed leaflet thickening and calcification, restricted motion and subvalvular disease in 41, 25 and 34%, respectively. Carpentier IIIa leaflet dysfunction occurred in 80% of patients and leaflet prolapse was seen in only 20%. These findings contrast with the previous literature, where patients were younger, they had rheumatic carditis and there were no co-morbidities. Leaflets were pliable, isolated leaflet prolapse was common and commissural fusion was absent. Conclusion: Contemporary patients with rheumatic MR were older, fewer had rheumatic fever and there were more co-morbidities. Echocardiographic features had evolved to greater leaflet thickening, calcification and reduced motion with minimal prolapse. These findings may have important implications for surgical management of this disease. Keywords: rheumatic mitral regurgitation, echocardiography Submitted 4/6/16, accepted 15/9/17 Cardiovasc J Afr 2017; 28: 215–220

www.cvja.co.za

DOI: 10.5830/CVJA-2016-086

The epidemiology of mitral regurgitation (MR) shows striking regional variation.1,2 In developed countries, degenerative disease is the major cause of MR and when surgery is indicated, repair of the valve is the preferred therapy.2 In geographically lowand middle-income areas, MR is still predominantly due to rheumatic disease, and when severe, mitral valve replacement is often required.1

Department of Cardiology Chris Hani Baragwanath Academic Hospital, University of the Witwatersrand, Johannesburg, South Africa Ruchika Meel, MB ChB, MMed, Cert Card (SA), PhD, ruchikameel@gmail.com Ferande Peters, MB BCh, FCP, Cert Card (SA), FACC Elena Libhaber, MSc, PhD Mohammed Rafique Essop, MB BCh, FCP, FRCP, FACC

While the demographic profile and echocardiographic features of degenerative MR have been well documented, there remains uncertainty regarding rheumatic MR, ranging from diagnostic echocardiographic criteria to optimal management.1-3 This difficulty is compounded by several factors, including the declining incidence of acute rheumatic fever (ARF), the rising incidence of co-morbidities such as human immunodeficiency virus (HIV) infection, and chronic diseases of lifestyle associated with increasing urbanisation.4,5 In a landmark study of 700 patients with rheumatic valvular disease from this institution, published approximately 30 years ago, Marcus et al. provided detailed echocardiographic and surgical data.6 The demographic profile and echocardiographic features of patients with rheumatic MR within that cohort were characterised by a disease afflicting predominantly young individuals with a high burden of concomitant acute rheumatic carditis. We therefore chose to examine our contemporary patient population with severe rheumatic MR, specifically to detect the changing demographic and echocardiographic profile in a hospital serving the large community of Soweto in South Africa.

Methods We conducted a prospective cross-sectional study at the Chris Hani Baragwanath Academic Hospital (CHBAH). Patients were enrolled between January and October 2014 from the valvular heart disease clinic. This study forms part of an ongoing study of rheumatic mitral regurgitation. The study was approved by the University of the Witwatersrand Ethics Committee (M140114). All patients were screened and patients deemed to have moderate or severe rheumatic MR were referred for possible inclusion in the study. A total of 91 patients with presumed rheumatic MR underwent clinical evaluation, resting electrocardiogram and detailed echocardiographic assessment according to a predetermined protocol. The inclusion criteria were patients aged 14 years or older with echocardiographic features of moderate or severe rheumatic MR. Patients were excluded if they had significant aortic valve disease, concurrent mitral stenosis (MS) with a valve area of less than 2.0 cm2 (as assessed by planimetry), documented ischaemic heart disease, pre-existing non-valvular cardiomyopathy, prior cardiac surgery, congenital or pericardial disease, pregnancy, severe systemic disorders such as renal failure, uncontrolled hypertension (systolic blood pressure > 140 mmHg and diastolic blood pressure > 90 mmHg) on medication, or severe anaemia (haemoglobin < 10 g/dl). Seven patients were excluded due to the following: anaemia, renal dysfunction, mild MR, and MR of non-rheumatic aetiology. The final sample included 84 patients. After obtaining voluntary consent, all patients underwent a detailed clinical evaluation and 12-lead electrocardiogram,

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followed by transthoracic echocardiography. The assessment of previous heart failure (HF) was made based on a combination of the patient’s prior history, as well as available clinical records. Acute or recurrent rheumatic carditis was diagnosed using the modified Jones and World Health Organisation criteria.7,8 The HIV status was available on all patients from prior medical records. Transthoracic echocardiography was performed on all patients in the left lateral position using a S5-1 transducer on a Philips iE33 system (Amsterdam, the Netherlands). Images were obtained according to a standardised protocol. Data were transferred and analysed offline using the Xcelera workstation (Philips). All linear chamber measurements were performed according to the American Society of Echocardiography (ASE) chamber guidelines.9 Left atrial (LA) volume was measured using the biplane area length method (apical four- and two-chamber for LA) and was indexed to body surface area (BSA).9 Left ventricular (LV) end-diastolic volume (EDV), end-systolic volume (ESV) and ejection fraction (EF) were assessed using the Simpsons method.9 LV mass was calculated according to ASE recommendations and was indexed to BSA.9 LV diastolic function measurements were performed in accordance with the ASE guidelines on diastolic function and included pulse-wave Doppler at the mitral tips and tissue Doppler of both medial and lateral mitral annuli.10 Measurements relating to the right ventricle (RV) were based on the ASE guidelines for the RV.11 MR severity was assessed using qualitative, semi-quantitative and quantitative methods as per European Association of Echocardiography valvular regurgitation guidelines.12 In equivocal cases, the echocardiographic data were integrated with the clinical evaluation by an experienced cardiologist to distinguish moderate from severe MR. MR was considered of rheumatic aetiology when the morphology of the valve satisfied the proposed World Heart Federation (WHF) criteria for the diagnosis of chronic rheumatic heart disease (RHD).13 The Carpentier classification was used to assess leaflet motion.14 The extent of morphological abnormality of the valve was determined using the Wilkins score.15 The Wilkins score was used to characterise the mitral valve due to the absence of an alternate scoring system. Although it was originally designed for prediction of success for balloon mitral valvotomy in mitral stenosis (MS), its systematic classification of structural changes to the mitral valve was considered useful to characterise the morphology of chronic rheumatic valve disease and therefore was used in this study. The Wilkins score is divided into four components: (1) leaflet thickening, (2) leaflet mobility, (3) leaflet calcification, and (4) subvalvular apparatus involvement. The individual components are then graded from 0 (absent) to 4 (severe), depending on the extent of involvement, ranging from none to severe.15

Statistical analysis Statistical analysis was performed with Statistica version 12.5 series 0414 for Windows. Continuous variables are expressed as mean ± SD or median (IQR). The Student’s t-test or Mann– Whitney U-test was used to compare continuous variables. Categorical variables were evaluated by the chi-squared and Fishers exact test when necessary. A p-value of < 0.05 was recognised as statistically significant.

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Results The baseline characteristics of the study patients are listed in Table 1. All patients were black South Africans, predominantly from Soweto. MR was moderate in 59 (68%) and severe in 25 (32%) patients. The mean age of patients was 44 ± 15.3 years with 84% females. Two-thirds of patients were in New York Heart Association (NYHA) II or III, with 26% having been hospitalised for heart failure (HF) in the preceding year. Only one patient presented with features of acute rheumatic carditis two years prior to this study. No patients had recurrent rheumatic carditis despite only 6% being on penicillin for secondary prophylaxis for ARF. Four (5%) patients were in atrial fibrillation (AF).

Table 1. Baseline clinical and echocardiographic characteristics* Characteristics

Number = 84

Clinical Age (years) Females (%) Systolic blood pressure (mmHg)

44 ± 15.3 84 124.1 ± 11.4

Diastolic blood pressure (mmHg)

77.2 ± 8.8

Heart rate (beats/min)

78.2 ± 12.7

Body mass index (kg/m2)

27.1 ± 6.1

Body surface area (m2) NYHA functional class (I/II/III/IV) (%) Hypertension

1.7 ± 0.2 34/42/24/0 52

Diabetes mellitus type 2

Human immunodeficiency virus

Medication (%) Highly active antiretroviral therapy

Diuretics

Spironolactone

Angiotensin converting enzyme inhibitor

Beta-receptor antagonists

Calcium channel antagonists

Aspirin

Warfarin

Digoxin

Amiodarone

Left ventricle Left ventricular end-diastolic diameter (mm)

55.3 ± 9.5

Left ventricular end-systolic diameter (mm)

41.4 ± 10.3

Interventricular septal diameter (mm) Posterior wall diameter (mm) End-diastolic volume indexed (ml/m2)†

8.9 ± 3.5 8.6 ± 1.6 93.8 ± 31.4

End-systolic volume indexed (ml/m2)†

39.7 ± 22.3

Left ventricular mass (g)

175.7 ± 64.2

Left ventricular mass indexed (g/m2)†

77.9 ± 22.5

Left ventricular ejection fraction (%)

58.8 ± 12.8

Average E/E′ (cm/s) Deceleration time (cm/s)

18 ± 10.0 214.2 ± 63.3

E′ (cm/s)

8.6 ± 3.3

E/A ratio

1.5 ± 0.7

Left atrium Left atrial volume indexed (ml/m2)†

69.5 ± 50.7

Right ventricle Right ventricle S′ (cm/s)

12.8 ± 11.0

Pulmonary artery systolic blood pressure (mmHg)

36.2 ± 18.9

Tricuspid regurgitation (none/mild/moderate or severe) (%)

36/33/31

*Data are presented as mean ± SD or %. †Values are indexed to body surface area. NYHA: New York Heart Association.

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Leaflet thickness 14% Subvalvular apparatus 34% Leaflet mobility 25%

Leaflet calcification 27%

Fig. 1. D istribution of abnormality according to the components comprising the Wilkins score.

Hypertension was the most important co-morbidity, present in 52% of patients. Concomitant HIV infection occurred in 26% of patients and 19% were on highly active antiretroviral therapy. The majority of patients (85%) were on varying combinations of medical therapy for either hypertension or HF and AF, with only 15% not on any drug therapy. None of the eight patients who underwent coronary angiography during their surgical work-up had occlusive coronary artery disease. The mean LVEF was 58 ± 12.7% with 43% of patients having a LVEF < 60%. The EDV and ESV were 93.8 ± 31.4 and 39.7 ± 22.3 ml/m2, respectively. Pulmonary hypertension was present in 38 (45%) subjects with no patients having contributing pulmonary abnormality. Concomitant organic rheumatic tricuspid valve (TV) disease was present in 29% of patients, with the mean tricuspid annulus diameter 38 ± 7.2 mm. Tricuspid regurgitation (TR) was present in 64% of patients with moderate or severe TR present in 31% of cases (Table 1).

100 90

Percentage

217

The mean mitral annulus diameter was 43 ± 8.5 mm, with 71 (84.5%) patients having an annulus diameter greater than 35 mm. A Wilkins score of 4–8 and 8–12 was present in 26 and 74% of patients with chronic rheumatic MR, respectively. Subvalvular apparatus thickening contributed the most to the total score (34.4%), followed by leaflet calcification (27%) (Fig. 1). Fig. 2 depicts the overall distribution of subjects in each component of the Wilkins score. Chordae were not elongated and echocardiographic features suggestive of calcification within the leaflets were found in all subjects. Significant commissural fusion was present in 30% of cases. Eighty per cent of cases were classified as having restrictive Carpentier type IIIa leaflet dysfunction, while the remaining 20% of patients had a mixed lesion that was a combination of type 2 (excessive leaflet motion) and type IIIa dysfunction. All patients had a greater degree of restriction of the posterior mitral leaflet (PML), except in three cases where the anterior mitral leaflet (AML) was restricted to a greater degree than the PML. A posteriorly directed eccentric MR jet was present in 96% of cases, except for the three subjects who had an anteriorly directed jet secondary to posterior mitral leaflet prolapse (Fig. 3). A comparison between the clinical characteristics and mitral valve morphology of our cohort with those of Marcus et al. is depicted in Table 2. Patients younger and older than 30 years of age were compared (Table 3). Twenty-six per cent of patients were younger than 30 years of age. There was no significant difference in the proportion of individuals with moderate or severe MR (p > 0.05). The remodelling parameters of the LV, LVEF and LA volume were similar in both groups (p > 0.05). Older patients were more likely to have co-morbidities, including hypertension (69 vs 9%, p < 0.01) and HIV (32 vs 9%, p = 0.03), and a greater degree of impairment of early diastolic relaxation (E′ = 11.4 ± 3.3 vs 7.6 ± 2.3, p < 0.01). Comparative analysis of the morphology of the mitral valve revealed no significant differences in overall Wilkins score between the two groups (8.31 ± 1.2 vs 8.1 ± 1.0, p = 0.33). No statistically significant difference was noted in the degree of calcification of the leaflets, mobility, subvalvular apparatus thickening and commissural abnormality (p > 0.05). Compared to normotensive patients with MR, patients with hypertension were older (51.7 ± 11.1 vs 35.1 ± 14.2 years, p <

70 60 50 40 30 20 10 0 Mobility

Subvalvular Leaflet Leaflet apparatus thickening calcification thickening Category

Score 1

Score 2

Score 3

Score 4

Fig. 2. D istribution of patients according to each component of the Wilkins score.

Fig. 3. Parasternal long-axis view showing an eccentric mitral regurgitation jet due to restricted anterior and posterior leaflet motion.

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0.0001), and the majority were in NYHA functional class II or III (71 vs 44%, p = 0.03) with a greater prevalence of moderate MR, accompanied by a greater degree of impairment of early relaxation in diastole (Table 4). Normotensive MR patients had a greater prevalence of dilatation of the left ventricle and severe MR with larger left atrial volume (Table 4). There were no significant differences with regard to the morphology of the mitral valve apparatus or Carpentier classification of leaflet dysfunction between the two groups (p > 0.05). A greater proportion of patients with HIV had severe MR compared to HIV-negative patients (50 vs 23%, p = 0.015). However no significant differences were observed in the echocardiographic parameters relating to dilatation of the LV, LVEF, LV diastolic function or LA volumes (p > 0.05). Similarly no significant differences were noted in any morphological parameters or Wilkins score between the two groups (8.4 ± 1.2 vs 8.0 ± 0.9, p = 0.14). All HIV-positive patients had type IIIa (restrictive) leaflet dysfunction, compared to HIV-negative individuals, of whom 15% had mixed lesions (p = 0.05). Concomitant organic morphological TV disease was more common in HIV-positive than in HIV-negative patients (50 vs 21%, p = 0.02). A similar degree of TR (p > 0.05) was present in both groups. There was no difference in the pulmonary artery systolic pressure between the HIV-positive and HIV-negative groups (37.2 ± 15.4 vs 35.2 ± 18.7 mmHg, p = 0.64). The degree of RV dilatation (33.5 ± 9.0 vs 31.4 ± 5.8 mm, p = 0.22) and RV function (11.9 ± 2.9 vs 13.4 ± 13.2 cm/s, p = 0.61) were not statistically different between the HIV-positive and -negative groups.

The pertinent findings in this contemporary cohort of patients with moderate or severe rheumatic MR include: (1) a significant increase in the mean age of the patients compared to previous studies; (2) infrequent occurrence of ARF; (3) a high incidence of co-morbid disease, including hypertension and HIV; and (4) advanced morphological changes in the mitral valve, including leaflets and subvalvular apparatus on echocardiography. Table 2. Comparison of the study by Marcus et al.6 with the current cohort of patients with isolated rheumatic mitral regurgitation Marcus et al.6 (n = 219)

Meel et al. (n = 84)

p-value

Age (years)

19 ± 11

44 ± 15.3

< 0.001

Females (%)

Not specified

Black Africans

III (100)

III (24)

Acute rheumatic fever (%)

1.2

< 0.001

Co-morbidities (%)

< 0.001

84.5

Clinical

Race NYHA functional class (%)

Variables

Age < 30 years Age > 30 years (n = 22) (n = 62)

p-value

Clinical Systolic blood pressure

121.9 ± 11.2

124.9 ± 11.3

Diastolic blood pressure

77.8 ± 6.83

76.6 ± 9.6

0.60

Body mass index (kg/m2)

23.84 ± 4.78

28.2 ± 6.23

0.19

Body surface area (m2)

1.62 ± 0.16

1.72 ± 0.18

0.04

14/8

21/41

0.01

18/4 (81/19)

53/9 (85/15)

0.68

Moderate mitral regurgitation (%)

13 (59)

46 (74)

Severe mitral regurgitation (%)

9 (41)

16 (26)

0.18

LV end-diastolic diameter (mm)

53.7 ± 9.06

55.7 ±9.7

< 0.0001

LV end-systolic diameter (mm)

38.7 ± 9.31

42.3 ± 10.5

0.15

9.8 ± 5.9

8.6 ± 2.3

0.21

NYHA functional class (I/II and III) Gender (F/M) (%)

0.29

Echocardiographic

Interventricular septum diameter (mm) Posterior wall diameter (mm) LV EDV indexed (ml/m2)†

7.9 ± 1.1

8.9 ± 1.6

0.01

90.8 ± 22.9

94.8 ± 33.9

0.61

LV ESV indexed (ml/m2)†

35.5 ± 16.9

42.4 ± 24.7

0.23

LV mass indexed (g/m2)†

102.2 ± 44.2

105.7 ± 38.5

0.72

Relative wall thickness

0.30 ± 0.1

0.33 ± 0.1

0.24

LV ejection fraction (%)

61.4 ± 12.7

57.1 ± 12.7

0.26

Ejection fraction ≥ 60%

Ejection fraction < 60%

0.006

Average E′ (cm/s)

11.4 ± 3.3

7.6 ± 2.3

< 0.01

E/E′ lateral (cm/s)

13.2 ± 8.2

17.2 ± 9.3

0.04

E/A ratio

1.7 ± 0.34

1.4 ± 0.7

0.05

S′ lateral (cm/s)

8.9 ± 3.3

6.63 ± 1.7

< 0.0001

Left atrial volume indexed (ml/m2)†* 45 (37.1–148.5) 53 (41.2–74.5)

0.53

Data are presented as mean ± SD. LV: left ventricle, NYHA: New York Heart Association; EDV: end-diastolic volume; ESV: end-systolic volume. *Median (interquartile range) or percentage. †Values are indexed to body surface area.

Discussion

Variables

Table 3. Clinical and echocardiographic characteristics according to age

0.001

Mitral valve morphology (%) Dilated annulus

0.001

Leaflet thickness and pliability < 0.001

Thin, pliable

Thickened, non-pliable

0.0049

Leaflet prolapse

< 0.001

Leaflet calcification (rigid)

< 0.001

Elongated chordae

< 0.001

Ruptured chordae

< 0.001

Commissural fusion

< 0.001

NYHA: New York Heart Association.

These findings are in marked contrast to the detailed evaluation published by Marcus et al. from the same hospital but almost three decades earlier.6 In that study, from the total cohort of 737 patients, 219 had pure MR, 275 pure mitral stenosis and 220 mixed lesions. Furthermore, in the Marcus study, patients with pure MR had thin leaflets, elongated chordae, a dilated annulus and anterior leaflet prolapse; findings that were corroborated at the time of surgery.6 Pure MR was largely a function of active rheumatic carditis and age; most were younger than 20 years with clinical carditis documented in 14% and surgical features of acute rheumatic carditis in 47% of the entire MR cohort.6 In contradistinction, we found only one patient with active carditis. The mean age of our cohort was 44 ± 15.3 years and echocardiography revealed no leaflet prolapse, and instead, marked leaflet thickening, calcification and retraction, accompanied not infrequently by abnormality of the chordal structures. These features are compatible with the proposal that Marcus and ourselves have advanced, where fulminant carditis is thought to lead on to pure severe MR, and milder or recurrent carditis to progress to pure mitral stenosis or mixed mitral valve disease.1,4,6 Rheumatic MR of patients in the current era results in the predominance of Carpentier type IIIa leaflet dysfunction with Wilkins scores that are similar to patients with MS. We postulate that less fusion of the commissures, a predominance of posterior leaflet thickening and immobility, accompanied by subvalvular abnormality, predispose patients to develop predominantly

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Table 4. Clinical and echocardiographic features according to the presence or absence of hypertension* Hypertension (n = 45)

Normotension (n = 39)

p-value

Age (years)

51.7 ± 11.1

35.1 ± 14.2

< 0.0001

Female (%)

0.62

Systolic blood pressure (mmHg)

127.9 ± 8.4

119.5 ± 12.8

Diastolic blood pressure (mmHg)

79.2 ± 8.5

74.2 ± 8.8

0.01

Body mass index (kg/m2)

28.6 ± 6.1

25.0 ± 5.8

0.01

Body surface area (m2)

1.7 ± 0.2

0.21

29/71

56/44

0.03

LV end-diastolic diameter (mm)

52.4 ± 8.4

58.3 ± 9.8

0.004

LV end-systolic diameter (mm)

39.7 ± 9.5

43.2 ± 10.9

0.12

Interventricular septal diameter (mm)

9.0 ± 2.3

8.9 ± 4.6

0.97

Posterior wall diameter (mm)

9.1 ± 1.6

8.1 ± 1.3

87.7 ± 29.9

100.9 ± 32.0

0.05 0.046

Variables Clinical parameters

NYHA functional class (I/II and III)

0.0008

Left ventricle

End-diastolic volume indexed (mls/m2)†

35.9 ± 17.7

46.1 ± 27.4

100.1 ± 39.4

110.4 ± 40.2

0.4 ± 0.1

0.3 ± 0.1

LV ejection fraction (%)

58.4 ± 12.6

58.1 ± 13.1

Ejection fraction ≥ 60%

End-systolic volume indexed (mls/m2)† LV mass indexed (g/m2)† Relative wall thickness

Ejection fraction < 60%

0.0009

0.24 0.0001 0.91

19.2 ± 10.9

17.7 ± 8.9

E′ (cm/s)

7.4 ± 2.5

9.9 ± 3.4

0.006

E/A ratio

1.3 ± 0.6

1.6 ± 0.6

0.008

57.6 ± 24.1

83.37 ± 67.7

0.42

Right ventricle S′ (cm/s)

14.6 ± 15.6

11.2 ± 2.5

0.18

Pulmonary artery systolic pressure (mmHg)

33.7 ± 19.2

37.9 ± 16.1

0.28

Tricuspid regurgitation (none/mild/ moderate to severe) (%)

38/36/26

33/31/36

0.46

Average E/E′ (cm/s)

0.61

Left atrium Left atrial volume indexed (ml/m2)† Right ventricle

Mitral regurgitation severity Moderate mitral regurgitation (%)

Severe mitral regurgitation (%)

0.009

*Data are presented as mean ± SD or %. †Values are indexed to body surface area. LV: left ventricle; NYHA: New York Heart Association.

regurgitant lesions. The reason why some patients develop pure MS is unknown.4 Differences in the interaction of host immunity, initial or recurrent streptococcal infections and chronic exposure of the valve leaflets to abnormalities of haemodynamic flow may account for these difference in morphology and dictate which lesion may predominate. The current data confirm that there has been a dramatic decline in the incidence of rheumatic carditis in the population of Soweto, although the reasons for this are not entirely clear. The striking trend toward a substantial decline in ARF has also been documented in the paediatric section of Baragwanath Hospital, with a reduction from 64 cases per year in 1993 to three per year in 2010.16 This decline was attributed to improved socioeconomic status and better access to healthcare.16 Thirty years ago McClaren et al. (by auscultation alone) reported a RHD incidence of 6.9/1 000 among school children in Soweto.16 Recently, Engel et al. (by echocardiography) reported a RHD incidence of 20.2/1 000 cases among scholars in the Bonteheuwel and Langa communities of Cape Town, with the prevalence being higher in poorer communities.17 Data from other areas of the country are scarce; the REMEDY study did

219

not report on the incidence or prevalence of RHD. However, 25.8% (863/3343) of participants were from upper middleincome countries (South Africa and Namibia).18 Concomitant with the decline in rheumatic fever, diseases associated with a Western lifestyle and urbanisation have emerged. A considerable number of patients with rheumatic MR currently have co-morbidities of hypertension (52%) and HIV (26%). These findings differ considerably from previous studies conducted in our institution. These co-morbidities mandate a careful assessment of the patient’s clinical presentation, since symptoms may not be solely attributed to MR; elevated blood pressure could overestimate the echocardiographic severity of MR and left ventricular dysfunction may be attributed to concomitant HIV infection rather than volume overload. The morphological abnormalities of the mitral apparatus (thickened and shortened subvalvular apparatus) and the nature of leaflet dysfunction (Carpentier IIIa) described in the current population has diagnostic implications. MR jets that are eccentric may require careful off-axis imaging to accurately delineate the full extent of the colour jet. Furthermore, an integrated evaluation of MR severity is mandatory due to the limitations of quantitative Doppler in some instances of eccentric jets. Our findings also have important therapeutic implications in terms of surgery for rheumatic mitral regurgitation. Mitral valve repair has several advantages compared to replacement, including lower peri-operative mortality rate, better preservation of postoperative left ventricular function, no need for anticoagulant therapy, and a safer pregnancy.19 In younger patients, absence of advanced subvalvular and valvular thickening, calcification and restriction of motion make it likely that a variety of repair techniques would be successful. In the older, contemporary population that we have described, the need for valve repair is less pressing compared to younger patients and the probability of surgical failure higher, given the presence of extensive subvalvular and valvular disruption. An important observation was the high frequency of concurrent TV leaflet abnormality and tricuspid annular dilatation. These abnormalities were not reported by Marcus et al.6 and no data on surgical repair were given. Our findings suggest that once rheumatic MR is identified, careful assessment of the morphology and function of TV is mandatory when selecting patients who will undergo mitral valve surgery. This strategy may reduce the likelihood of the late consequences of unrepaired TR in rheumatic patients, which has been previously highlighted.20 Late TR causes increased morbidity and mortality rates despite the presence of successful mitral valve surgery, and in addition, a second operation to correct the residual TR carries increased mortality rates.20 There are several limitations to this study. The initial diagnosis of HF was made outside of our clinic with no uniform criteria applied. None of the patients had surgery, so that surgical confirmation of the echocardiographic abnormality was not possible. Finally, the population studied may not truly reflect the nature of the disease in younger rural populations where a greater prevalence of acute rheumatic carditis may be found.

Conclusion The modern cohort of patients with rheumatic MR was older, had less acute rheumatic fever and greater associated co-morbidities.

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The echocardiographic features had evolved to greater leaflet thickening, calcification and reduced motion with very little prolapse. These findings may have significant implications for the current management of rheumatic mitral valve disease and contribute to better understanding of the evolution from acute to chronic rheumatic heart disease.

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10. Nagueh SF, Appleton CP, Gillebert TC, et al. Recommendations for the evaluation of left ventricular diastolic function by echocardiography. Eur J Echocardiogr 2009; 10: 165–193. [PMID: 19270053]. 11. Rudski LG, Lai WW, Afilalo J, et al. Guidelines for the echocardiographic assessment of the right heart in adults: a report from the American Society of Echocardiography endorsed by the European Association of Echocardiography, a registered branch of the European

R Meel was the recipient of the Carnegie PhD Fellowship award (Carnegie

Society of Cardiology, and the Canadian Society of Echocardiography.

Corporation grant no. b8749.r01).

J Am Soc Echocardiogr 2010; 23: 685–713. [http://.dx.doi: 10.1016/j. echo.2010.05.010].

References 1.

regurgitation. Part 2: mitral and tricuspid regurgitation (native valve

disease. Epidemiology, management, and prevention in Africa.

disease). Eur J Echocardiogr 2010; 11: 307–332. doi: 10.1093/ejechocard/

Enriquez-Sarano M, Akins C W, Vahanian A. Mitral regurgitation.

echocardiographic diagnosis of rheumatic heart disease – an evidence-

Adams A, Rosenhek R. Degenerative mitral valve regurgitation: best

based guideline. Nat Rev Cardiol 2012; 28: 297–309. [http://.dx.doi: 14. Chauvaud S, Fuzellier J, Berrebi A, et al. Long-term (29 years)

chronic rheumatic heart disease. Circulation 2014; 130: 2181–2188.

results of reconstructive surgery in rheumatic mitral valve insufficiency. 15. Wilkins GT, Weyman AE, Abascal VM, et al. Percutaneous balloon

failure in the heart of Soweto study cohort: emerging challenges for

dilatation of the mitral valve: an analysis of echocardiographic variables

urban African communities. Circulation 2008; 118: 2360–2367. [PMID:

related to outcome and the mechanism of dilatation. Br Heart J 1988; 16. Cilliers A. Rheumatic fever and rheumatic heart disease in Gauteng on

matic mitral valve disease in a developing country. Correlations among

the decline: Experience at Chris Hani Baragwanath Academic Hospital,

clinical presentation, surgical pathologic findings, and hemodynamic

Johannesburg, South Africa. S Afr Med J 2014; 104: 632–634. [http://. 17. Engel ME, Haileamlak A, Zühlke L, et al. Prevalence of rheu-

rheumatic fever, endocarditis and Kawasaki disease of the Council

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criteria, 1992 update. J Am Med Assoc 1992; 268: 2069–2073. [PMID:

heartjnl-2015-307444]. 18. Zühlke L, Engel ME, Karthikeyan G, et al. Characteristics, complica-

1404745].

tions, and gaps in evidence-based interventions in rheumatic heart

World Health Organisation. Rheumatic fever and rheumatic heart

disease: the Global Rheumatic Heart Disease Registry (the REMEDY

disease. World Health Org Tech Rep Ser 2001; 923: 1–122. [PMID:

study). Eur Heart J 2015; 36: 1115–1122. [http://.dx. doi: 10.1093/

15382606]. 9.

dx.doi: 10.7196/samj.8318].

Dajani A, Ayoub E, Bierman F, et al. Special writing committee on

Association. Guidelines for the diagnosis of rheumatic fever, Jones

60: 299–308. [PMID: 3190958].

Marcus RH, Sareli P, Pocock WA, et al. The spectrum of severe rheu-

sequelae. Ann of Inter Med 1994; 120: 177–183. [PMID: 8043061]. 7.

Circulation 2001; 104(12 Suppl 1): I12–5. [PMID: 11568022].

Stewart S, Wilkinson D, Hansen C, et al. Predominance of heart

19029467]. 6.

10.1038/nrcardio.2012.7].

Essop MR, Peters F. Contemporary issues in rheumatic fever and [PMID: 25602946].

jeq031. 13. Reményi B, Wilson N, Steer A, et al. World Heart Federation criteria for

Lancet 2009; 373: 1382–1394. [PMID: 19356795]. practice revolution. Eur Heart J 2010; 31: 1958–1967. [PMID: 20624767]. 4.

Echocardiography recommendations for the assessment of valvular

Essop MR, Nkomo V. Rheumatic and non-rheumatic valvular heart Circulation 2005; 112: 3584–3591. [PMID: 16330700].

12. Lancellotti P, Moura L, Pierard LA, et al. European Association of

eurheartj/ehu449].

Lang RM, Badano LP, Mor-Avi V, et al. Recommendations for cardiac

19. Choudhary S, Talwar S, Dubey B, et al. Mitral valve repair in a predom-

chamber quantification by echocardiography in adults: an update

inantly rheumatic population: long-term results. Tex Heart Inst J 2001;

from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. Eur Heart J Cardiovasc Imag 2015; 16: 233–270. [doi: 10.1093/ehjci/jev014].

28: 8–15. [PMCID: PMC101122]. 20. Antunes M, Barlow JB. Management of tricuspid valve regurgitation. Heart 2007; 93: 271–276. [PMID: 17228081].

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Abstract Aim: To provide imaging data and report associations between human immunodeficiency virus (HIV), tuberculosis (TB) and pulmonary embolism (PE) in a South African population that underwent computed tomography pulmonary angiography (CTPA) for suspected PE. Methods: A validated Qanadli severity scoring system for PE was used for 164 CTPA scans, and parenchymal, pleural and cardiovascular complications were reported. Serological confirmation of HIV testing and microbiological confirmation of TB were recorded. Results: Prevalence of PE in the CTPA population was 26% (95% CI: 19.67–33.65%). HIV-positive prevalence in patients with PE was 67% (95% CI: 48.17–82.04%), however it was not statistically significantly different when compared with the patients without PE (p = 1). HIV-positive patients had more extensive partial thrombus in the right middle lobe (p = 0.045), but no other differences when compared with HIV-negative patients. TB prevalence in patients with PE was 57% (95% CI: 34.49–76.81%). This was statistically significantly different when compared with the patients without PE (p = 0.073 at the 10% level). Prevalence of TB co-morbidity in the HIV-positive group with proven PE was 71% (95% CI: 41.90– 91.61%), however there was no statistically significant difference in comparison with the HIV-negative patients with TB and PE (p= 0.305). Conclusion: The high number of patients presenting for CTPA who were HIV infected (and also infected with TB) highlights that PE evaluation should include severity/extent of the disease, as these patients may have more severe disease in specific lung lobes. The use of a validated scoring system, such as the Qanadli score, when reporting PE may have a profound effect on patient risk stratification, management

Department of Radiology, Groote Schuur Hospital and University of Cape Town, South Africa Raksha Ramlakhan, BMedSc (UDW), MB BCh (Wits), docrakshar@gmail.com

Department of Paediatric Radiology, University of Bristol and the Bristol Royal Hospital for Children, Bristol, United Kingdom and Department of Radiology, University of Cape Town, South Africa Savvas Andronikou, MB BCh (Wits), FCRad (Diag) (SA), FRCR (Lond), PhD (UCT), PhD (Wits)

Department of Radiology, Mitchell’s Plain Hospital, Mitchells Plain, Cape Town, South Africa Ashmitha Rajkumar, MB ChB (UCT), FCRad (D) SA

and prognosis and would also provide a system for collecting larger volumes of data for analysis. Keywords: pulmonary embolism, computed tomography pulmonary angiography (CTPA), HIV, Western Cape Submitted 5/6/16, accepted 21/9/16 Published online 15/2/17 Cardiovasc J Afr 2017; 28: 221–228

www.cvja.co.za

DOI: 10.5830/CVJA-2016-083

Pulmonary embolism (PE) is a life-threatening condition if not diagnosed early. The overall mortality rate in untreated patients is 30%, with approximately 10% of patients dying within one hour of the event.1 Haemodynamically unstable patients have the highest mortality rate, which can be as high as 58%.1 In the United States, PE is the third leading cause of death, accounting for 100 000 to 300 000 estimated deaths per year.2 In Europe, an estimated 370 000 PE-related deaths occur annually.3 In Africa, PE has been reported in 3.8% of autopsied patients in Nigeria.4 Ogengo et al. described a PE incidence rate of 0.032% over a five-year period in black Africans at a tertiary hospital in Kenya.5 A study undertaken at a universityaffiliated hospital in Cameroon reported a 32.4% incidence of PE in patients with clinical suspicion of PE, using computed tomography pulmonary angiography (CTPA).6 In an autopsy series conducted in an adult population in Cape Town between 2001 and 2005, pulmonary thromboembolism was found to be the third most common cause of natural death in females.7 The true prevalence of PE in South Africa however, remains largely unknown. Human immunodeficiency virus (HIV) is a hypercoagulable state that predisposes patients to a two- to 10-fold increased risk of venous thromboembolic events, such as pulmonary emboli, in comparison with the general population.8 Venous thromboembolic disease (VTE) in association with HIV has been reported in the literature since 1980.9 In 2011, a systematic review by Bibas et al. looked at 13 main studies on VTE, from 1991 to 2007, which reported on the occurrence of VTE among HIV-infected patients, with a frequency ranging from 0.19 to 7.63% per year.8 In Africa, HIV in association with PE was reported as a co-morbidity occurring in 10.9% of hospitalised black Kenyan patients.5 The prevalence of HIV in association with PE in South Africa is not known. The work undertaken on VTE in TB-infected patients in Africa is limited. A Kenyan study by Ogengo et al. reported that TB was present as a co-morbid condition in 12.5% of hospitalised

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black African patients with PE.5 There are no studies evaluating the incidence/prevalence of TB in HIV-infected patients with PE. Correct diagnosis and prompt therapy can significantly lower mortality rates of PE to between 2.5 and 8%.1 Diagnostic imaging of patients with clinical suspicion of PE is primarily through CTPA, which is currently the gold standard for the diagnosis of pulmonary emboli, as per the European Society of Cardiology (ESC) guidelines on the management of acute pulmonary embolism.10 In reporting of PE, the presence and location of the clot, with a rough visual estimate of the extent of the clot is usually described but the magnitude can be calculated at CT by applying a dedicated CT score.11 The Qanadli score is an objective and reproducible CT quantification of the severity of PE, based on the location of the embolus and the degree of obstruction.12 The severity of PE has an impact on management and prognosis, and is determined by a number of factors, including volume of the embolus, underlying cardiorespiratory function and the degree of obstruction. Cardiac CT measurements such as ratio of right-to-left ventricular (RV:LV) diameter have shown good correlation with severity of PE. The ratio of RV:LV diameter is an indicator of right ventricular strain/dysfunction.11 The ratio of the diameter of the main pulmonary artery and the aorta (PA:AO) has also been shown to correlate with severity of acute PE by predicting pulmonary hypertension.13 The prevalence and severity of PE in South African patients undergoing CTPA requires investigation, particularly with regard to HIV status and TB co-infection. The aim was to compare HIV-infected and uninfected patients, regarding the presence, distribution and extent of pulmonary emboli as found on CTPA, and to compare findings of HIV-infected and uninfected patients, with regard to the presence of parenchymal, pleural and cardiovascular complications as well as TB co-infection.

Methods This retrospective, descriptive study was undertaken at GF Jooste Hospital, a public-sector regional hospital in Mannenberg, Western Cape, South Africa. The Human Research Ethics Committee of the Faculty of Health Sciences, University of Cape Town (HREC REF: 361/2013) and the Provincial Ethics Research Committee (RP 112/2013) provided ethical clearance. CTPA scans spanning a two-year period from January 2011 to December 2012 from the Department of Radiology at the GF Jooste Hospital CT scan database and CT request forms were used for the radiological interpretation. The National Health Laboratory Service database and patient folders were accessed for the relevant laboratory results. The inclusion criteria were patients referred for CTPA with clinical suspicion of pulmonary embolus. The exclusion criteria were patients with scans with no request form, non-retrievable patient folders, absent clinical history regarding suspicion of PE, and CT studies not performed as CTPA protocols. The CTPA scans, as per standard protocol, were performed on a six-slice Philips Brilliance CT scanner (Cleveland, Ohio, USA) at GF Jooste Hospital. Approximately 90 ml of 370 mg/ml Omnipaque contrast was used, via an antecubital vein, at a rate of 3.5–4.0 ml per second via an 18–20-G cannula, using an automated power injector (Covidien Injection system, Cincinnati, Ohio, USA).

DICOM CT data were viewed on a Siemens Syngo CT workstation (Siemens Healthcare, Siemens Erlangen, Germany), in the Radiology Department at Mitchell’s Plain Hospital, using the Somaris/5 Syngo CT 2012E software with MPR capabilities (Siemens Healthcare, Siemens Erlangen, Germany). A consultant radiologist with more than five years’ experience performed the reading of the CT scans according to a prescribed data-collection sheet, using a previously externally validated Qanadli severity scoring system.12 Severity of the Qanadli score was defined as a score > 40%. The Qanadli score or CT obstruction index, is reached by regarding the arterial tree of each lung as having 10 segmental arteries (three to the upper lobes, two to the middle lobe and lingula, and five to the lower lobes) (Fig. 1). Embolus in a segmental artery = 1 point; embolus in the most proximal arterial level = a value equal to the number of segmental arteries arising distally. Weighting factor (for residual perfusion) = the degree of vascular obstruction (no thrombus = 0; partially occlusive thrombus =1; total occlusion = 2). The maximal CT obstruction index = 40 for each patient (10 × maximum weighting of 2 = 20 for each side). [Isolated sub-segmental embolus is considered equal to a partially occluded segmental artery (value of 1)]. The percentage of vascular obstruction is calculated by dividing the patient score by the maximal total score and by multiplying the result by 100. Therefore, the CT obstruction index can be expressed as: Σ (n × d)

;   _______ 40 × 100

where Σ = sum, n = value of the proximal thrombus in the pulmonary arterial tree equal to the number of segmental branches arising distally (minimum 1; maximum 20), d = degree of obstruction (minimum 0; maximum 2). An example of how the score is calculated from the images is provided in Fig. 2. Cardiovascular complications were recorded. The heart was evaluated for obvious right ventricular enlargement based on RV:LV diameter ratio > 1. Pulmonary artery enlargement was evaluated by recording the diameter of the main pulmonary artery, as well as the pulmonary artery:aorta (PA:AO) ratio (abnormal ratio > 1). Parenchymal complications were recorded according to accepted radiological principles: atelectasis, consolidation, wedge-shaped pleural-based density and groundglass opacity. The presence of pleural effusions was recorded as right, left or bilateral. Additional or alternative findings

1 1

3 10

2 1

1 1

Fig. 1. Schematic representation of the arterial tree of the lung and the Qanadli score.

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were detailed. These were described as either intra- or extrapulmonary findings. The CT features of TB, when present, were documented. Scan limitations were recorded as either of ‘diagnostic quality’, ‘suboptimal but readable’, or ‘suboptimal and not reliable’. Lastly, additional information was collected from the laboratory, patient notes and request forms and these included: CD4 count*, viral load*, microbiological diagnosis of tuberculosis (sputum, lymph-node histology, pleural fluid analysis)*, and highly active anti-retroviral therapy (HAART) commencement date and drug regimen. *Only results from the NHLS database within six months of the CTPA scan having been performed were recorded.

Statistical analysis Data were analysed with the aid of statisticians using the following software tools and packages: Stata MP data analysis and statistical software (versions 11 and 13) provided by StataCorp LP, Texas, USA; IBM SPSS Statistics (version 22, 64-bit edition, IBM Corporation), USA; R (version 3.1.3, 64-bit version, the R Foundation for Statistical Computing); and GNU project free software with worldwide contributors. Frequencies and percentages were recorded for the presence of all findings. The descriptive data such as the distribution and extent of PE (according to the lobar arterial anatomy of the lung) were reproduced in the form of frequency tables. Qanadli scores were reported as percentages (derived from the degree of occlusion as per the segmental and lobar arterial anatomy of the lung).

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Fishers exact test of association was used to compare the differences in severity of PE between the HIV-positive and -negative groups. Comparison was made between HIV-positive/ HIV-negative, PE-absent/PE-present, and TB-absent/TB-present groups, by producing contingency tables of counts and using the Chi-squared test/Fishers exact tests of association. The analysis included only TB results that were available within six months of the scan being performed. The Mann–Whitney U-test was used to test for a difference in the distribution of the cardiovascular parameters by HIV status.

Results There were 164 patients; 115 (70.1%) females and 49 (29.9%) males (age range 21–87 years, mean 45) (Fig. 3) in the study made up of 49% HIV-infected patients, 23% uninfected and 27% patients whose HIV status was unknown (Table 1). The frequency/prevalence of pulmonary embolism in the sample was 43 out of a total of 164 patients (26%; 95% CI: 19.67–33.65%). HIV positivity in our CTPA population for suspected PE was 68% (Table 2). The prevalence of HIV in patients with proven PE was 67% (95% CI: 48.17–82.04%, p = 1.000) (Table 2). Only 76 of the total sample of 164 patients had a microbiologically confirmed TB result. The prevalence of TB in those who underwent TB testing was 40% (95% CI: 28.44– 51.35%) (Table 3). The prevalence of TB in the PE-positive group was 57% (95% CI: 34.49–76.81%) while the prevalence of TB in the PE-negative group was 32% (95% CI: 19.92–46.32%) (Table 3). The Fisher’s exact test showed a statistically significant association between PE and TB status (p = 0.073) at the 10% level. Only 19 patients of the sample of 33 patients with HIV testing and proven PE had a microbiologically confirmed TB result (Table 4). The prevalence of TB in the HIV-positive patients with PE was 71% (95% CI: 41.90–91.61%) while the prevalence of TB

Total scans included for review 267

Excluded due to lack of clinical information or different imaging performed 7

Excluded due to no request form or no folder retrievable 92

168

Fig. 2. E xample of calculation of the Qanadli obstruction index from CTPA. Axial CT scan shows a proximal completely occlusive thrombus (long arrow) in the right main pulmonary artery, and partial thrombus in the left main pulmonary artery (short arrow). The Qanadli score index would therefore be [(10 × 2) + (10 × 1) = 30/40] = 75%.

1 Repeat scan during the collection period

3 Scans could not be accessed for image interpretation due to inability to open the files

Final sample size = 164

Fig. 3. Flow chart showing the final sample size after exclusion criteria were applied.

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Table 1. Distribution of patients according to HIV status and confirmation of status (n = 164 patients) HIV positive

HIV negative

Table 3. Cross-tabulation demonstrating the presence of TB according to presence of PE (n = 76)

HIV status unknown

TB microbiology

Information provided on request form

Information retrieved from folders

Based on a negative rapid-strip bedside test

Based on a formal Elisa test

Based on information from request form, NHLS and folder

Based on information from request form and NHLS. No folder retrievable

Pulmonary embolism

Present

81 (49.4%)

38 (23.2%)

Positive

Negative

Total

Absent

45 (27.4%)

Total = 164 (100%); subtotal of patients tested for HIV = 119 (72.6%).

Count

% within PE

67.9

32.1

Count

% within PE

43.5

56.5

Count

% within PE

60.5

39.5

100.0 23 100.0

Total Table 2. Cross-tabulation showing the frequency of HIV in those with and without pulmonary embolism (n = 119)

*Only TB results within six months of the scan being performed were considered.

HIV Pulmonary embolism

Positive

Negative

Total

Absent Count

% within PE

68.6

31.4

Table 4. Cross-tabulation demonstrating the presence of TB according to HIV status in patients with proven PE (n = 19)

86 100.0

TB microbiology

Present Count

% within PE

66.7

33.3

76* 100.0

HIV status

33 100.0

Count

119

68.1

31.9

100.0

Negative

Total

HIV positive Count

Total % within PE

Positive 4

% within PE

28.6

71.4

100.0

HIV negative Count % within PE

60.0

40.0

100.0

Total

in the HIV-negative patients with PE was 40% (95% CI: 5.27– 86.34%) (Table 4). The Fisher’s exact test showed no statistical difference between the HIV-positive and -negative groups with PE, for the prevalence of TB (p = 0.305). The prevalence of PE, according to the lobar arterial anatomy of the lung, is summarised in Table 5. Fisher’s exact test showed no significant difference between the prevalence of PE and HIV positivity in a particular lobe of the lung (Table 5). The extent of PE in terms of the degree of occlusion according to the lobar arterial anatomy of the lung in both HIV-positive and -negative patients is summarised in Table 6. The degree of obstruction as per the Qanadli score derivation was described as either a partial clot or a complete clot. If thrombus was absent, it was described as no clot (Fig. 4). Fisher’s exact test demonstrated statistically significant differences in the severity of PE between the HIV-positive and -negative groups in the right middle lobe. Here the HIV-positive group demonstrated more extensive PE (p = 0.045) with regard to partially occlusive thrombus at the proximal arterial level (origin of the segmental arteries). Comparison of the severity of the Qanadli score between HIV-positive and -negative groups is summarised in Table 7. Fisher’s exact test demonstrated no statistically significant differences in the severity of the Qanadli score between the HIV-positive and -negative groups (p = 0.465). The comparison of frequency of parenchymal and pleural complications in both HIV-positive and -negative groups with

Count

% within PE

36.8

63.2

100.0

Table 6. Extent of PE (with percentages in brackets) according to degree of occlusion by lobar arterial anatomy (n = 33) HIV status Lobes of the lung

Category

RUL

No clot, n (%) Partial clot, n (%) Clot, n (%)

RML

No clot, n (%)

RLL

6 (54.55)

9 (40.91)

5 (45.45)

1 (4.55)

0 (0) 9 (81.82)

8 (36.36)

0 (0)

Clot, n (%)

1 (4.55)

2 (18.18)

No clot, n (%)

7 (31.82)

7 (63.64)

10 (45.45)

1 (9.09)

5 (22.73)

3 (27.27)

No clot, n (%)

11 (50)

Partial clot, n (%) Clot, n (%) No clot, n (%)

LLL

12 (54.55)

Partial clot, n (%)

Clot, n (%)

Lingula

HIV negative (n = 11)

13 (59.09)

Partial clot, n (%) LUL

HIV positive (n = 22)

8 (72.73)

9 (40.91)

3 (27.27)

2 (9.09)

0 (0)

11 (50)

6 (54.55)

Partial clot, n (%)

6 (27.27)

5 (45.45)

Clot, n (%)

5 (22.73)

0 (0)

No clot, n (%)

8 (36.36)

3 (27.27)

13 (59.09)

8 (72.73)

Partial clot, n (%) Clot, n (%)

1 (4.55)

p-value 1

0.045

0.089

0.412

0.218

0.802

0 (0)

RUL, right upper lobe; RML, right middle lobe; RLL, right lower lobe; LUL, left upper lobe; LLL, left lower lobe.

Table 5. Prevalence of pulmonary embolism according to lobar arterial anatomy of the lung in both HIV-positive and -negative patients (n = 33). Lobes of the lung HIV status HIV positive, n (%) HIV negative, n (%) Total, n (%) p-value

RUL

RML

RLL

LUL

Lingula

LLL

Total

11 (50)

18 (81.8)

13 (59.1)

11 (50)

19 (86.4)

22 (100)

10 (90.9)

11 (100)

29 (87.9)

33 (100)

6 (54.6)

4 (36.4)

7 (63.6)

4 (36.36)

17 (51.52)

15 (45.5)

25 (75.8)

17 (51.52)

0.712

0.391

0.282

RUL, right upper lobe; RML, right middle lobe; RLL, right lower lobe; LUL, left upper lobe; LLL, left lower lobe.

6 (54.55) 17 (51.5) 1

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Fig. 4. T he CTPA appearances, showing the different degrees of obstruction in the lobar and segmental arteries, are depicted in the series of images. (A) Axial CT scan showing partially occlusive thrombi (short arrows) in the right and left lower lobe basal segmental arteries. (B) Axial CT scan showing partially occlusive thrombus (long arrow) in the right lower lobe artery. (C) Axial CT scan showing totally occlusive thrombus (long arrow) in the right lower lobe artery.

identified PE is presented in Table 8. Fisher’s exact test showed no significant association between HIV status of the patient and the presence of each of the complications. Comparisons between HIV-positive and -negative groups with regard to Qanadli scores, and RV:LV and PA:AO ratios are demonstrated in Figs 5–7. The Mann–Whitney U-test demonstrated no significant differences between HIV-positive and -negative categories for any of the above variables (p = 0.440, p = 0.611 and p = 0.191, respectively) in patients with PE.

a two-year period.6 Our CTPA prevalence of PE is comparable at 26%. CTPA is a high-dose and costly study but can be performed at most regional, some district and all tertiary institutions in South Africa. Approximately 10 CT scans per month performed at our study hospital were CTPAs, yet only a quarter of patients imaged had positive findings of PE. 100

Discussion Prevalence of PE in a CTPA population Previously published studies have reported the general prevalence of PE in hospital populations. In our study, we differ in that we report the prevalence of PE in a population of patients who underwent CTPA for suspected PE. Similar studies evaluating the presence of PE in a CTPA population are sparse. A study in Cameroon (Africa), undertaken at a university-affiliated hospital, demonstrated a CTPA incidence of PE of 32.4% over

Qanadli score

Table 7. Comparison of the severity of the Qanadli score between HIV-positive and -negative patients (n = 33)

Qanadli score HIV status

< 40%

≥ 40%

10 (45.45)

12 (54.55)

22 (100)

HIV negative, n (%)

7 (63.64)

4 (36.36)

11 (100)

17 (51.52)

16 (48.48)

33 (100)

HIV negative

HIV status

Total

HIV positive, n (%) Total, n (%)

HIV positive

Fig. 5. Differences between HIV positive and negative according to Qanadli scores (p = 0.440).

Table 8. Comparison of frequency (with percentages in brackets) of parenchymal and pleural complications present in HIV-positive and -negative patients with pulmonary embolism (n = 33). Complications Wedge-shaped pleuralbased density

Ground-glass opacity

Pleural effusion

None*

9 (40.91)

10 (45.45)

2 (9.09)

22 (100)

0 (0)

11 (100)

2 (6.06)

33 (100)

HIV status

Atelectasis

Consolidation

HIV positive, n (%)

10 (45.45)

15 (68.18)

4 (18.18)

7 (63.64)

5 (45.45)

1 (9.09)

7 (63.64)

4 (36.36)

17 (51.52)

20 (60.61)

5 (15.15)

16 (48.48)

14 (42.42)

HIV negative, n (%) Total, n (%) p-value

0.465

0.270

Subjects who reported none of the named complications

0.643

0.282

0.719

0.542

Total

2.00

1.50

1.00

21 61

1.00

80 *

103

0.50

0.00

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PA/AO ratio

VI/LV ratio

226

HIV positive

HIV status

HIV negative

0.00

HIV positive

HIV status

HIV negative

Fig. 6. D ifferences between HIV positive and negative according to RV:LV ratios (p = 0.611).

Fig. 7. Differences between HIV positive and negative according to PA:AO ratios (p = 0.191).

The high HIV burden in South Africa and the known prothrombotic nature of HIV has sensitised clinicians to investigate HIV-infected patients with respiratory symptoms for PE. The non-specific signs of PE, as well as the added TB disease burden often confounds the clinical scenario in these patients and probably results in more patients being imaged. As the prevalence of HIV increases globally, the trend towards increased CTPA imaging may result in higher incidence rates of PE. This is yet to be proven by new studies undertaken in this decade.

Forty per cent of patients undergoing CTPA, who were tested for TB, had microbiological confirmation of TB. We found a statistically significant association (at the 10% level) between TB positivity and PE. Additional randomised studies are however required to confirm a positive association between PE and TB, as we evaluated only patients with an available TB laboratory result.

Prevalence of HIV in patients with PE Major studies published to date have evaluated the relationship between VTE and HIV by determining the frequency of PE in HIV-positive hospital populations. Our study differs in that it examined a population of patients with suspected PE who had CTPA, and then determined the HIV prevalence in the whole group as well as in those with proven PE. More than two-thirds (68%) of the population undergoing CTPA who were tested for HIV was shown to be infected. This is the first study, performed at a local South African hospital, to report on the prevalence of HIV in patients referred for CTPA with confirmed PE (67%). This increased prevalence reflects the population demographics of this hospital, which is known to have the highest HIV burden locally in the Cape metropolitan area,14 and is therefore also reflective of the high clinical index of suspicion of PE in HIV-positive patients presenting to this hospital. No statistical significance was found in the prevalence of HIV in patients with and without proven PE. This can be explained by our small sample size, as there were insufficient data to suggest a statistically significant association. The known association, however, has already been proven by larger studies conducted worldwide.

Pulmonary embolism and TB Published studies evaluating the relationship between PE and TB are limited and report the prevalence of VTE in TB populations. Our study differs in that it determined the TB prevalence in patients who underwent CTPA for suspected PE, and those with proven PE.

Pulmonary embolism and the influence of TB in HIV We further evaluated the HIV-positive group with confirmed PE on CTPA to determine the prevalence of TB co-morbidity. We found an overall 71% prevalence of TB in HIV-positive patients with proven PE. No statistically significant difference however was found in the prevalence of TB co-morbidity between HIV-positive and -negative groups with identified PE. This prevalence was much higher than the 47% rate of TB infection in HIV-positive patients who developed DVT during their hospital admissions, reported previously by Govender et al., in South Africa.15 There is no agreement in the literature as yet as to whether antiretroviral therapy has a progressive or additive effect in promoting VTE. Some studies have implicated protease inhibitors in VTE, while other studies showed no association.8,16 Only 50% of our patients who were HIV infected and had PE were on HAART regimens at any time during or prior to the study. These numbers did not allow for evaluation of the effects of HAART on severity and extent of PE. Further studies are required to examine the effects of HAART regimens on VTE severity.

Distribution and severity of PE No studies in the literature have compared detailed imaging data with regard to CTPA findings between HIV-positive and -negative patients. We demonstrated that in HIV-positive patients, thrombi were most frequently found in the right (82%) and left lower lobes (86%) of the lung. In the HIV-negative patients, the most commonly affected lobe of the lung was the left lower lobe (91%). No statistical difference was, however, demonstrated in the prevalence of PE between the HIV-infected and uninfected groups performed per lobe of the lung. In evaluating the degree of occlusion in the different lobar arteries/most proximal segments giving origin to the distal segmental arteries of the lung, we found more extensive PE

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(partially occlusive thrombus) in the right middle lobe of the lung (p = 0.045). We have no specific reasons to account for this difference. In our study, the severity of PE was quantified using the Qanadli score and two cardiovascular parameters, namely the ratios of RV:LV diameter and PA:AO, all of which can be used to indicate right ventricular dysfunction. Right ventricular dilatation is important in the risk stratification of patients, especially in the suspected high-risk PE patient. The presence of right ventricular overload guides the clinician to immediate PE-specific treatment, such as thrombolysis, surgical embolectomy or catheter-directed treatment where available.10 In addition, right ventricular dysfunction is used to identify patients with a high likelihood of fatal pulmonary embolism.10 In the study by Qanadli et al. in 2001, a CT obstruction of 40% and greater predicted and identified more than 90% of their patients with right ventricular dilatation.12 The degree of obstruction in their study was considered the most important factor in determining right ventricular response to PE. In our study we found no statistically significant differences between HIV-positive and -negative groups in terms of severity of the Qanadli score or with regard to the RV:LV and PA:AO ratios. The most common CTPA-detectable parenchymal and pleural complications reported in association with PE are as follows: atelectasis in from 5517 to 71%18 of patients,consolidation in 39%,17 wedge-shaped opacity in 31%,17 ground-glass opacity 43%,17 and pleural effusion in more than 50% of patients.18 In comparison, our data showed a higher frequency of consolidation, atelectasis and ground-glass opacification (atelectasis 52%, consolidation 61%, wedge-shaped opacity 15%, ground-glass opacity 48% and pleural effusion 42%). In the HIV-infected patients, the frequency of consolidation (68%), wedge-shaped opacity (18%), and pleural effusion (45%) was higher when compared with HIV-uninfected patients but there were no statistically significant associations between HIV status of the patient and the presence of any of the complications.

Africa, as this information is extremely limited. The high number of patients presenting for CTPA who were HIV infected (and also infected with TB) highlights that PE evaluation should include severity/extent of the disease, as these patients may have more severe disease in specific lobes. The use of a validated scoring system such as the Qanadli score when reporting PE may have a profound effect on patient risk stratification, management, and prognosis and would also provide a system for collecting larger volumes of data for analysis. Larger, local studies should be performed prospectively to evaluate associations between PE, TB and HIV The authors acknowledge the contributions of the Statistical Consulting Service (SCS), Department of Statistical Sciences, University of Cape Town (consultants: Reshma Kassanjee and Katya Mauff).

References 1.

The data were collected from patients attending a regional hospital in the Western Cape, which has a high incidence of both TB and HIV.14 The sample was dominated by HIV-infected patients (68% in the proportion tested). A large number of patients were excluded (103) because of missing information, and a further 45 patients could not be considered for comparing HIV-infected and uninfected patients because testing had not been done. This resulted in a sample size that was statistically small and may have accounted for the low/poor correlations of prevalence across the various groups of TB and HIV-infected and non-infected patients. In addition, the reading of the scans by a single radiologist is a limitation, and did not allow for evaluation of inter-observer error in this study. The shortage of radiologist consultants at the public institutions and the workload on the existing consultants restricts the availability of senior staff for research purposes.

Worsley DF, Alavi A. Radionuclide imaging of acute pulmonary embolism. Semin Nuclear Med 2003; 33(4): 259–278.

Laack TA, Goyal DG. Pulmonary embolism: an unsuspected killer. Emerg Med Clin Nth Am 2004; 22(4): 961–983.

Tapson VF. Advances in the diagnosis and treatment of acute pulmonary embolism. F1000 Med Rep 2012; 4: 9.

Awotedu AA, Igbokwe EO, Akang EE, Aghadiuno PO. Pulmonary embolism in Ibadan, Nigeria: five years autopsy report. Central Afr J Med 1992; 38(11): 432–435.

Ogeng’o JA, Obimbo MM, Olabu BO, Gatonga PM, Ong’era D. Pulmonary thromboembolism in an East African tertiary referral hospital. J Thromb Thrombol 2011; 32(3): 386–391.

Tambe J, Moifo B, Fongang E, Guegang E, Juimo AG. Acute pulmonary embolism in the era of multi-detector CT: a reality in sub-Saharan Africa. BMC Med Imag 2012; 12: 31.

Tiemensma M, Burger EH. Sudden and unexpected deaths in an adult population, Cape Town, South Africa, 2001–2005. Sth Afr Med J 2012; 102(2): 90–94.

Limitations

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Bibas M, Biava G, Antinori A. HIV-associated venous thromboembolism. Med J Hematol Infect Dis 2011; 3(1): e2011030.

Eyal A, Veller M. HIV and venous thrombotic events. Sth Afr J Surg 2007; 45: 54–56.

10. Konstantinides SV. 2014 ESC guidelines on the diagnosis and management of acute pulmonary embolism. Eur Heart J 2014; 35(45): 3145–3146. 11. Ghaye B, Ghuysen A, Bruyere PJ, D’Orio V, Dondelinger RF. Can CT pulmonary angiography allow assessment of severity and prognosis in patients presenting with pulmonary embolism? What the radiologist needs to know. Radiographics 2006; 26(1): 23–40. 12. Qanadli SD, El Hajjam M, Vieillard-Baron A, Joseph T, Mesurolle B, Oliva VL, et al. New CT index to quantify arterial obstruction in pulmonary embolism: comparison with angiographic index and echocardiography. Am J Roentgenol 2001; 176(6): 1415–1420. 13. Ng CS, Wells AU, Padley SP. A CT sign of chronic pulmonary arterial hypertension: the ratio of main pulmonary artery to aortic diameter. J Thorac Imag 1999; 14(4): 270–278. 14. GF Jooste Hospital 2013 [Available from: http://www.medimmune. co.za.

Conclusion This study provides a foundation for additional studies to be performed regarding thromboembolism in HIV, particularly in

15. Govender I, Mabuza HL, Ogunbanjo GA. The characteristics of HIV and AIDS patients with deep vein thrombosis at Dr George Mukhari Academic Hospital. Afr J Prim Health Care Fam Med 2015; 7(1): 1–3. 16. Crum-Cianflone NF, Weekes J, Bavaro M. Review: thromboses among

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HIV-infected patients during the highly active antiretroviral therapy era. AIDS Patient Care STDs 2008; 22(10): 771–778.

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189–196. 18. Shah AA, Davis SD, Gamsu G, Intriere L. Parenchymal and pleural

17. Karabulut N, Kiroglu Y. Relationship of parenchymal and pleural abnormalities with acute pulmonary embolism: CT findings in patients

findings in patients with and patients without acute pulmonary embolism detected at spiral CT. Radiology 1999; 211(1): 147–153.

with and without embolism. Diagn Interv Radiol (Ank) 2008; 14(4):

CSI AFRICA 2017 CATHETER INTERVENTIONS IN CONGENITAL, STRUCTURAL AND VALVAR HEART DISEASE DECEMBER 1 – 2, 2017 | NAIROBI | KENYA

SAVE THE DATE CSI Africa 2017 will take place on December 1 – 2, 2017 in Nairobi, Kenya. Please join us for an overview of catheter interventions in congenital, structural and valvar heart disease in children and adults. CSI Africa will provide a forum for physicians from Central Africa, with an opportunity to exchange ideas and learn from each other. Read more on the congress website.

THE PROGRAM The program will include lectures, debates and recorded cases from local and international faculty and is designed to address issues and topics specific to Central Africa. Topics will include: • Paravalvar leak closure • Left atrial apendage closure • Pulmonary valve replacement • Echo evaluation of ASDs and VSDs • Coarctation stenting

• ASD closure • VSD closure • Transseptal puncture • PDA closure • Pulmonary valvuloplasty • Mitral valvuloplasty

• How to develop structural, congenital and valvar interventions in Africa • Challenging cases, problems & complications

WHO SHOULD ATTEND? The meeting is designed for adult and pediatric interventional cardiologists, cardiothoracic surgeons, anaesthetists, imaging specialists & colleagues of other disciplines, such as nursing staff, who wish to know more about this field.

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Nuclear cardiology practices and radiation exposure in Africa: results from the IAEA Nuclear Cardiology Protocols Study (INCAPS) Salah E Bouyoucef, Mathew Mercuri, Thomas NB Pascual, Adel H Allam, Mboyo Vangu, João V Vitola, Nathan Better, Ganesan Karthikeyan, John J Mahmarian, Madan M Rehani, Ravi Kashyap, Maurizio Dondi, Diana Paez, Andrew J Einstein, for the INCAPS investigators group

Abstract Objective: While nuclear myocardial perfusion imaging (MPI) offers many benefits to patients with known or suspected cardiovascular disease, concerns exist regarding radiationassociated health effects. Little is known regarding MPI practice in Africa. We sought to characterise radiation doses and the use of MPI best practices that could minimise radiation in African nuclear cardiology laboratories, and compare these to practice worldwide. Methods: Demographics and clinical characteristics were collected for a consecutive sample of 348 patients from 12 laboratories in six African countries over a one-week period from March to April 2013. Radiation effective dose (ED) was estimated for each patient. A quality index (QI) enumerating adherence to eight best practices, identified a priori by an IAEA expert panel, was calculated for each laboratory. We compared these metrics with those from 7 563 patients from 296 laboratories outside Africa. Results: Median (interquartile range) patient ED in Africa was similar to that of the rest of the world [9.1 (5.1–15.6) vs 10.3 mSv (6.8–12.6), p = 0.14], although a larger proportion of African patients received a low ED, ≤ 9 mSv targeted in societal recommendations (49.7 vs 38.2%, p < 0.001). Bestpractice adherence was higher among African laboratories (QI score: 6.3 ± 1.2 vs 5.4 ± 1.3, p = 0.013). However, median

ED varied significantly among African laboratories (range: 2.0–16.3 mSv; p < 0.0001) and QI range was 4–8. Conclusion: Patient radiation dose from MPI in Africa was similar to that in the rest of the world, and adherence to best practices was relatively high in African laboratories. Nevertheless there remain opportunities to further reduce radiation exposure to African patients from MPI. Keywords: myocardial perfusion imaging, radiation, effective dose, best practices, Africa Submitted 25/5/16, accepted 16/10/16 Cardiovasc J Afr 2017; 28: 229–234

www.cvja.co.za

DOI: 10.5830/CVJA-2016-091

The increasing burden of cardiovascular disease, affecting rates of morbidity and mortality, has brought with it a rise in technological innovations for diagnosing and managing disease. In recent decades, cardiovascular imaging modalities that use ionising radiation have become essential to cardiology practice. Myocardial perfusion imaging (MPI) is one such technology. Through the use of an injected radiopharmaceutical in conjunction with a single-photon emission computed tomography (SPECT) or positron emission tomography (PET)

Centre Hospitalo-Universitaire de Bab El Ouéd, Alger, Algeria

Quanta Diagnóstico & Terapia, Curitiba, Brazil

Salah E Bouyoucef, MD

João V Vitola, MD, PhD

Division of Cardiology, Department of Medicine, Columbia University Medical Center and New York-Presbyterian Hospital, New York, USA

Department of Nuclear Medicine, Royal Melbourne Hospital and University of Melbourne, Melbourne, Australia

Mathew Mercuri, PhD Andrew J Einstein, MD, PhD, andrew.einstein@columbia.edu

Section of Nuclear Medicine and Diagnostic Imaging, Division of Human Health, International Atomic Energy Agency, Vienna, Austria Thomas NB Pascual, MD, MHPEd Ravi Kashyap, MD Maurizio Dondi, MD Diana Paez, MD

Cardiology Department, Al Azhar University, Cairo, Egypt Adel H Allam, MD

Nathan Better, MB BS

Department of Cardiology, All India Institute of Medical Sciences, New Delhi, India Ganesan Karthikeyan, MB BS, MD, DM, MSc

Department of Cardiology, Houston Methodist DeBakey Heart and Vascular Center, Houston, Texas, USA John J Mahmarian, MD

Radiation Protection of Patients Unit, International Atomic Energy Agency, Vienna, Austria; and Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA

Department of Nuclear Medicine, Charlotte Maxeke Johannesburg Academic Hospital, University of the Witwatersrand, Johannesburg, South Africa

Madan M Rehani, PhD

Mboyo Vangu, MD, MMed, MSc, PhD

Andrew J Einstein, MD, PhD

Department of Radiology, Columbia University Medical Center and New York-Presbyterian Hospital, New York, USA

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camera, MPI provides information that can be used to both diagnose coronary artery disease and stratify risk, and thus guide patient management.1-3 While the benefits of MPI are apparent, there are concerns regarding potential harmful effects from radiation exposure as a result of undergoing this procedure.4 Therefore, organisations promoting radiation safety, such as the International Commission on Radiological Protection (ICRP), advocate practice to use radiation only when justified and to limit radiation to levels that are ‘as low as reasonably achievable’ (ALARA) without compromising on diagnostic information.5 While judicious application of imaging technology that employs ionising radiation is the best approach, numerous techniques or ‘best practices’ exist to assist practitioners in limiting the dose when its use is warranted.6-9 A recent study conducted by the International Atomic Energy Agency (IAEA) revealed significant variation in both the uptake of evidencebased best practices to reduce patient radiation exposure and patient radiation effective dose from MPI among nuclear cardiology laboratories worldwide.9 Beyond this study, little is known about nuclear cardiology practice with regard to radiation exposure around the world, especially among laboratories in Africa. The purpose of this study was to characterise the MPI practice and patient dose among African nuclear cardiology laboratories participating in the IAEA Nuclear Cardiology Protocols Study (INCAPS), and examine it relative to practice among laboratories worldwide.

Methods This study used patient and laboratory data collected as part of the worldwide INCAPS survey. INCAPS was initiated by an expert committee of physicians and medical physicists convened by the IAEA to characterise radiation doses and examine best-practice use to minimise dose in nuclear cardiology clinics around the world. INCAPS used a cross-sectional design whereby participating laboratories provided demographics, clinical characteristics and MPI study parameters for a consecutive sample of patients over a one-week period of the laboratory’s choice between 18 March and 22 April 2013. Nuclear cardiology laboratories were recruited through membership lists provided by a number of national and international cardiology or nuclear medicine societies. A designated local investigator prospectively acquired data using a standardised data-collection tool that was issued by the coordinating centre. This included information on the patient’s age, gender and weight, and MPI study parameters, such as injected radiopharmaceutical, administered activity, camera type, imaging position and protocol, and camera-based dose-mediating hardware or software. Full details regarding study design are presented elsewhere.9 The study was reviewed, approved and conducted in compliance with the Columbia University institutional review board, which deemed it exempt from the requirements of US federal regulations for the protection of human subjects (45 CFR 46) because no individually identifiable health information was collected. Radiation dose was calculated for each patient using the effective dose (ED), as per the dose coefficients provided by the ICRP.10 ED is a whole-body measure that reflects both estimated individual organ doses and their relative sensitivity to

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carcinogenic effects from radiation. Radiation dose from studies using rubidium-82 was calculated using Senthamizhchelvan’s conversion coefficients.11 All radiation doses are presented in units of millisieverts (mSv). Mean and median ED was calculated at the laboratory and regional (Africa vs rest of the world) level. Using current clinical practice guidelines, the expert committee convened by the IAEA identified eight ‘best practices’ for optimising radiation dose from MPI studies a priori. A laboratory’s adherence to each of these practices was evaluated from the acquired data. Details regarding how the best practices are defined and adherence scored were reported previously by Einstein et al.9 and are summarised in Table 1. Briefly, these best practices centred around the practice of avoiding administering higher-than-needed doses of radiopharmaceuticals, using a strategy of stress-only imaging where possible, avoiding dosing leading to ‘shine through’ artifact, and the use of camera-based dose-reduction software or hardware technology (e.g. resolution recovery software or two-position supine and prone imaging), which can reduce radiation dose. Stress-only imaging refers to a protocol whereby rest imaging is only acquired in the event that stress images, which are performed first, reveal abnormalities. The use of this protocol has been shown to reduce radiation exposure, as a significant proportion of the population will not require the subsequent rest imaging.12 When performing single-day, two-injection technetium studies, there is a possibility of residual activity from the first injection interfering with the interpretation of images from the second injection. This shine-through artifact can be avoided by ensuring the administered activity in the second injection is more than three times that of the first injection. A composite quality index (QI) was enumerated for each laboratory, based on the number of specified best practices followed during the observation period. The expert committee established a median laboratory ED of ≤ 9 mSv, as specified in professional society recommendations,13 and a QI score of ≥ 6 as benchmarks for desirable laboratory performance.

Statistical analysis The primary comparison examined patient ED and laboratory best-practice adherence differences between Africa and the rest of the world. As a second focus, ED was compared between laboratories within Africa. For continuous variables, normality was tested using the Kolmogorov–Smirnov test for patient-level comparisons, given the large sample size of 7 911, and using the Shapiro–Wilk test for laboratory-level comparisons. Continuous variables were compared in terms of means using the Student’s t-test or analysis of variance for normally distributed data and compared in terms of medians using the Kruskal–Wallis test for non-normally distributed data. The chi-squared test was used to compare categorical variables. All analyses were performed using Stata/SE 13.1 (StataCorp, College Station, TX) and a p-value < 0.05 was considered statistically significant.

Results Of the 30 laboratories performing MPI in Africa, identified in the IAEA Nuclear Medicine database, data collection yielded information on 348 consecutive MPI studies from 12 laboratories in Algeria, Egypt, Kenya, Senegal, South Africa and Tunisia. It

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Table 1. Scoring and explanations of the eight best practices. Adapted from Einstein et al.9 Best practice Scoring Avoid thallium One point if no thallium-201 studies were performed in stress patients ≤ 70 years old

Explanation SPECT imaging with thallium is associated with a considerably higher radiation dose to patients compared with technetium-based radiopharmaceuticals. This item excludes thallium viability studies and stress redistribution–re-injection stress and viability studies Avoid dual One point if no dual isotope (rest thallium and stress techneDual isotope imaging is associated with the highest radiation isotope tium) studies were performed in patients ≤ 70 years old dose of any protocol Avoid One point if (1) no study was performed with technetium activ- 1 332 MBq is the highest recommended activity in guidelines, too much ities > 1 332 MBq (36 mCi), and (2) mean total effective dose and 15 mSv is a very high radiation dose for a 99mTc study technetium was < 15 mSv for all studies with two technetium injections Avoid too One point if for each study with thallium, less than 129.5 MBq The expert committee maintained that 129.5 MBq should be the much thallium was administered at stress upper threshold for thallium activity Perform stress- One point if the laboratory performed at least one stress-only If stress images are completely normal, subsequent rest imaging only imaging study, in which rest imaging was omitted, or if the laboratory can be omitted did only PET-based stress tests Use cameraOne point if the laboratory performed at least one study using Each of these approaches reduces the administered activity based doseat least one of the following: (1) attenuation correction (CT or needed and facilitates performance of stress-only imaging reduction transmission source), (2) imaging patients in multiple positions, strategies e.g. both supine and prone, (3) high-technology software (e.g. resolution recovery and noise reduction), and (4) high-technology hardware (e.g. PET or a solid-state CZT SPECT camera) Weight-based One point if the laboratory had a statistically significant posi- Tailoring the administered activity to the patient weight offers an dosing for tive correlation between patient weight and administered activ- opportunity to reduce radiation dose technetium ity (MBq), for injections of technetium Avoid One point if the laboratory performed no SPECT studies with Shine through occurs in one-day technetium studies when residuinappropriate technetium rest and stress injections on the same day, in which al radioactivity from the first injection interferes with the images dosing that the activity of the second injection was less than three times for the second injection. To avoid shine through, guidelines can lead to that of the first injection recommend that the activity for the second injection should be ‘shine-through’ three to four times higher than the first injection. A second injecartifact tion of less than three times of the activity of the first injection constituted a dosing that can lead to shine through

based dosing and ensuring sufficient administered activity to avoid shine through were both higher in African laboratories but failed to reach statistical significance.

Discussion Africa is facing difficulties in developing nuclear medicine in general,14 and the continent has the lowest ratio of clinical nuclear medicine applications per capita. Few studies15,16 explicitly examine nuclear cardiology practice in Africa. The INCAPS worldwide cross-sectional study of MPI provides a valuable

Number of patients

was compared with 7 563 studies from 296 laboratories in 59 countries around the world. Patient demographics, clinical characteristics and radiation dose information for the African and non-African study cohorts are presented in Table 2. African patients were younger compared to patients from the rest of the world (60.2 ± 11.0 vs 64.3 ± 12.0 years; p < 0.0001). Median and mean patient ED were similar in both populations. However, a larger proportion of African patients received an ED ≤ 9 mSv (49.7 vs 38.2%, p < 0.001). The distribution of individual African patient EDs is presented in Fig. 1. African patients were more likely than non-Africans to undergo an MPI study using a stress-only protocol [odds ratio (OR): 3.4, 95% CI: 2.7–4.3, p < 0.001]. The use of PET imaging was lower in African patients (1.7 vs 6.1%, p < 0.0001). Patient volumes were similar for participating African and non-African laboratories, as were the laboratory mean and median ED and the proportion of laboratories with a median ED ≤ 9 mSv (Table 2). However, there was significant variation in the ED among African laboratories (median ED range: 2–16.3 mSv, p < 0.0001). African laboratory volumes and EDs are presented in Table 3. The overall adherence to best practices to minimise radiation exposure was higher among African laboratories, as reflected in the mean QI score (6.3 ± 1.2 vs. 5.4 ± 1.3, p = 0.013) and the proportion of laboratories with a QI score ≥ 6 (75.0 vs 44.9%, p = 0.041). However, while the adherence to each individual best practice was also higher among African laboratories, this difference failed to reach statistical significance (Table 4). The only exception was the use of stress-only imaging, which was used in 66.7% of African laboratories and only 28.7% of non-African laboratories (p = 0.005). The practices of weight-

0 0

10 15 Effective dose (mSv)

Fig. 1. Distribution of radiation-effective dose among observed African patients.

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Table 2. Patient and laboratory demographics and clinical characteristics Africa (n = 348) 135 (38.8)

Rest of world (n = 7 563) 3119 (41.2)

Patients Female, n (%) Age (years) Mean 60.2 64.3 SD 11 12 Effective dose (mSv) Median 9.1 10.3 IQR 5.1–15.6 6.8–12.6 Range 1.8–20.0 0.75–35.6 ≤ 9 mSv, n (%) 173 (49.7) 2892 (38.2) Stress-only, n (%) 109 (31.3) 896 (11.8) PET, n (%) 6 (1.7) 465 (6.1) Laboratories 12 296 Patients/laboratories Median 19 16 IQR 10–48 8–33 Range 4–73 1–250 Quality index score ≥ 6, n (%) 9 (75.0) 133 (44.9) Mean 6.3 5.4 SD 1.2 1.3 Laboratories with median dose ≤ 9 mSv, n (%) 5 (41.7) 86 (29.1) SD, standard deviation; IQR, interquartile range.

Table 4. Laboratory best-practice adherence

p-value 0.36 < 0.0001

0.14

< 0.001 < 0.001 < 0.001

0.402

0.041 0.013

0.35

opportunity to better appreciate radiation doses and use of best practices to reduce radiation among patients undergoing nuclear cardiology procedures on the African continent, and how Africa compares to the rest of the world in terms of patient dose and best-practice adherence. Analysis of data from INCAPS revealed that overall radiation dose to patients undergoing a procedure in Africa was similar to that among patients undergoing a procedure elsewhere in the world. Notably, African laboratories performed much better than the rest of the world with regard to best-practice adherence to minimise patient dose, as reflected in both a higher QI score and proportion of laboratories adhering to each best practice. However significant variation in ED and QI score was noted within Africa, specifically at the laboratory level. Table 3. African laboratory patient volume, radiation exposure and quality index score Laboratory Algeria 1 Algeria 2 Algeria 3 Algeria 4 Egypt 1 Egypt 2 Kenya 1 Senegal 1 South Africa 1 South Africa 2 Tunisia 1 Tunisia 2

No of patients 42 73 17 14 54 39 5 4 12 60 21 7

Effective dose (mSv) 25% Median 75% 5 8.4 9.5 1.8 2 6.2 2.5 4.5 5.1 11.3 11.9 12.5 8.2 16.3 17.2 7.3 15.3 16 11.4 11.6 11.8 6.3 8 8.9 9.4 9.4 9.4 14.8 16.1 17.8 8.2 9.4 9.9 3.1 3.6 9

Quality index (QI) score 7 7 7 6 8 8 4 5 5 6 7 6

Best practice Avoid thallium stress Avoid dual isotope Avoid too much technetium Avoid too much thallium Perform stress-only imaging Use camera-based dosereduction strategies Weight-based dosing for technetium Avoid shine through

Africa (n = 12) n % 12 100.0 12 100.0 11 91.7 12 100.0 8 66.7

Rest of world (n = 296) p-value n % 270 91.2 0.61 286 96.6 1 252 85.1 1 294 99.3 1 85 28.7 0.005

66.7

198

66.9

50.0

27.7

0.108

58.3

129

43.6

0.313

The eight-fold range in median patient ED at the laboratory level is likely attributable to protocol use, specifically the practice of stress-only imaging. While this practice was used in the majority of African laboratories, the rate of use was higher in some than others. One laboratory in particular used a stress-only protocol in 73% of its cases and had the lowest median ED, and incidentally, the highest patient volume. The option of stress-only protocol could be a consequence of a few factors: the desire to lower radiation dose, the overload of patients due to insufficient nuclear cardiology facilities inducing a long waiting list, and/or for economic reasons to reduce the cost of MPI. But regardless of the laboratory’s motivation to commonly use a stress-only protocol, its salutary effect on radiation dose is undeniable. By contrast, the laboratory with the highest mean ED used a stress-only protocol in only 1.7% of cases. However while a practice of stress-only imaging is desirable where indicated, the correct rate is determined by the disease rate in the imaged population. Therefore it is difficult to determine the extent to which the observed rates of stress-only use reflect over- or under-use of this protocol, or of MPI imaging more generally. Overall there was good adherence in the use of specified best practices among the observed African laboratories. However, in contrast with the results of the worldwide study, there is a seemingly poor correlation between laboratory adherence to best practices and mean patient ED in Africa. Surprisingly, the two laboratories that adhered to all eight best practices were among the laboratories with the highest patient ED on the continent. These laboratories predominantly used two-day protocols, with rest imaging performed on the second day, a fact that might explain the relatively higher rates of stress-only use in these laboratories (29.6 and 38.5%), compared to other observed laboratories in INCAPS. This suggests that dose-minimisation strategies are not strictly limited to the best practices described. Likewise, adherence to a best practice as we have defined it does not mean it is optimally applied in the laboratory. For example, a laboratory might use a high-efficiency solidstate SPECT camera for every case, but may never use prone positioning (both camera-based dose-reduction strategies). Laboratories should continue to be vigilant in ensuring that patient doses are optimised, given the high doses involved in the MPI study. Still, the lack of complete adherence to best practices among the majority of laboratories suggests opportunity to further reduce patient EDs through those practices specified by the expert committee. Furthermore this should be possible

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even in environments with significant resource constraints, as all of the specified best practices can be implemented with no additional cost, and in some cases, a cost reduction. Changing demographics and increased socio-economic development on the African continent are contributing to a rise in chronic illness, especially cardiovascular disease.17,18 Commensurate with this rise will be increased demand for diagnostic imaging. Resource constraints and a lack of available expertise have been cited as challenges to providing nuclear cardiology procedures in Africa.15,19 Furthermore, few nuclear cardiology-capable centres exist in Africa, even compared to developing nations elsewhere in the world; their equipment is older, and practitioners perceive a high need for additional training in a variety of nuclear medicine techniques.16 The data presented here may reflect these challenges. For example, the use of PET imaging among observed African laboratories was quite low, likely owing to lack of access to the relatively expensive scanners and/or radiopharmaceuticals, which in many cases require on-site manufacture. Likewise, the high use of stress-only imaging may be a result of careful use of scarce radiopharmaceuticals and camera time on the part of African nuclear medicine physicians. On the other hand, the lack of nuclear cardiology infrastructure (and therefore opportunity for training physicians and developing expertise) relative to other regions in the world may have contributed to the development of regional centres of excellence.20 Despite the increasing prevalence of coronary artery disease in Africa, which has accompanied westernisation, owing to limitations in trained personnel and equipment, nuclear cardiology capabilities presently exist in few African countries. Even in those countries where there are MPI capabilities, there are few laboratories. These are concentrated in regional referral centres, many of which are university-based teaching hospitals receiving technical assistance from IAEA. This assistance is provided through the IAEA’s technical cooperation programme. Under this programme, every year regional training courses are organised on specific nuclear medicine topics, with a major focus on nuclear cardiology. Participants from all over the African region, financially supported by the technical cooperation programme, gather in the host centres to attend lectures and practical sessions given by international experts. Furthermore, the IAEA provides financial support to fellowships that may last two to three months or up to years, to train future leaders in the field and develop regional centres of excellence. For many centres, the programme also supports the purchase of equipment and even SPECT cameras. The high rate of adherence to best practices observed among African laboratories is consistent with the concept of centres of excellence.

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only eight countries, six of which are represented in this study. It is possible that those laboratories that did participate are more engaged with the international radiation protection community, and therefore patient ED and best-practice adherence data presented here may represent the best-case scenario among African laboratories. Unfortunately we could not determine the response rate for participation, as the multiple mechanisms used to contact laboratories contain some overlap. However our study did manage to recruit 12 of 30 (40%) of the laboratories performing MPI in Africa, identified by the IAEA database. In addition, this study did not assess image quality or patient outcomes. Therefore we cannot determine whether lower patient ED and high uptake to the specified best practices indeed translate to improved patient care. Finally, the fact that two laboratories that adhered to all eight best practices showed overall higher ED suggests that our metrics may not be sensitive to the African MPI environment. Future research should examine how to optimise dose-reduction best practices to the local context.

Conclusion Our study of nuclear cardiology practice reveals that African laboratories performed better than the rest of the world with regard to best-practice adherence to optimise patient radiation dose. However wide variation in practice still exists and greater uptake of stress-only imaging, use of camera-based dosereduction technologies, and optimised dosing protocols may provide additional opportunity to further reduce radiation exposure from MPI in Africa, often at no extra cost to care. The authors gratefully acknowledge funding from the International Atomic Energy Agency, the Margaret Q Landenberger Research Foundation (in memory of Prof A Donny Strosberg) and the Irving Scholars Program. We affirm not having entered into an agreement with the funders that may have limited our ability to complete the research as planned, and indicate that we have had full control of all primary data. We are grateful to the INCAPS Investigators Group members* and their institutions for efforts in collecting the data, and to the cooperating professional societies, including the American Society of Nuclear Cardiology, the Asian Regional Cooperative Council for Nuclear Medicine, Australian and New Zealand Society of Nuclear Medicine, British Nuclear Medicine Society/British Nuclear Cardiology Society, Comissão Nacional de Energia Nuclear, European Association of Nuclear Medicine, European Council of Nuclear Cardiology, IAEA and the Intersocietal Accreditation Commission. Dr Einstein has received research grants for other investigator-initiated studies from GE Healthcare, Philips Healthcare, Spectrum Dynamics and Toshiba America Medical Systems. The other co-authors have no disclosures. *Members of the INCAPS investigators group

Limitations

Executive committee: AJ Einstein (chair), TNB Pascual (IAEA project lead),

Our study has some limitations. There is no comprehensive list of laboratories performing nuclear cardiology procedures in many countries, therefore it is not clear to what extent data acquired in the INCAPS study represents typical MPI practice around the world. Furthermore, the low number of participating laboratories in Africa may further exacerbate this concern. One could argue that the participation rate in Africa reflects the relative lack of nuclear cardiology-capable laboratories on the continent – such laboratories are known by the IAEA to exist in

N Better, SE Bouyoucef, G Karthikeyan, R Kashyap, V Lele, VPC Magboo,

D Paez (IAEA section head), M Dondi (IAEA section head); (alphabetically) JJ Mahmarian, M Mercuri, F. Mut, M.M. Rehani, J.V. Vitola. Regional coordinators: (alphabetically): E Alexánderson (Latin America), A Allam (Africa/Middle East), MH Al-Mallah (Middle East), N Better (Oceania), SE Bouyoucef (Africa), H Bom (East Asia), A Flotats (Europe), S Jerome (United States), PA Kaufmann (Europe), V Lele (South Asia), O Luxenburg (Israel), J Mahmarian (North America), LJ Shaw (North America), SR Underwood (United Kingdom), J Vitola (Latin America).

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Members (alphabetically, by region):

noninvasive myocardial perfusion imaging using single-photon emis-

Africa: W Amouri, H Essabbah, SS Gassama, KB Makhdomi, GIE El

sion computed tomography, cardiac magnetic resonance, and positron

Mustapha, N El Ouchdi, N Qaïs, N Soni, W Vangu.

emission tomography imaging for the detection of obstructive coronary artery disease: a meta-analysis. J Am Coll Cardiol 2012; 59: 1719–1728.

Asia: RM Abazid, B Adams, V Agarwal, MA Alfeeli, N Alnafisi, L Bernabe, GG Bural, T Chaiwatanarat, JM Chandraguptha, GJ Cheon, I Cho, AS

Hachamovitch R, Hayes SW, Friedman JD, Cohen I, Berman DS.

Dogan, M Eftekhari, A Frenkel, I Garty, S George, P Geramifar, H Golan,

Comparison of the short-term survival benefit associated with revascu-

S Habib, R Hussain, H Im, H-J Jeon, T Kalawat, WJ Kang, F Keng, A

larization compared with medical therapy in patients with no prior coro-

Klaipetch, PG Kumar, J Lee, WW Lee, I Lim, CMM Macaisa, G Malhotra,

nary artery disease undergoing stress myocardial perfusion single photon emission computed tomography. Circulation 2003; 107: 2900–2907.

BR Mittal, MH Mohammad, P Mohan, ID Mulyanto, D Nariman, UN Nayak, K Niaz, G Nikolov, JM Obaldo, E Ozturk, JM Park, S Park, CD

International Atomic Energy Agency, 2012.

Sayman, AS Shinto, V Sivasubramaniyan, MH Son, P Sudhakar, GMS Syed, N Tamaki, K Thamnirat, T Thientunyakit, S Thongmak, DN Velasco, A

4. 5.

The 2007 recommendations of the International Commission on Radiological Protection. ICRP Publication 103. Ann ICRP 2007;

Europe: SC Adrian, D Agostini, S Aguadé, G Armitage, M Backlund, M

37(2–4): 1–332.

Backman, M Baker, MT Balducci, C Bavelaar, M Berovic, F Bertagna, R Beuchel, A Biggi, G Bisi, R Bonini, A Bradley, L Brudin, I Bruno, E Busnardo,

Einstein AJ, Knuuti J. Cardiac imaging: does radiation matter? Eur Heart J 2012; 33: 573–578.

Verma, U Vutrapongwatana, Y Wang, KS Won, Z Yao, T Yingsa-nga, R Yudistiro, KT Yue, N Zafrir.

International Atomic Energy Agency. Nuclear Cardiology: Its Role in Cost Effective Care. IAEA Human Health Series No 18. Vienna:

Patel, HK Phuong, AP Quinon, TR Rajini, Y Saengsuda, J Santiago, HB

International Atomic Energy Agency. Nuclear Cardiology: Guidance and

R Casoni, A Choudhri, C Cittanti, R Clauss, DC Costa, M Costa, K Dixon,

Recommendations for Implementation in Developing Countries. IAEA

M Dziuk, N Egelic, I Eriksson, G Fagioli, DB de Faria, L Florimonte, A

Human Health Series No 23. Vienna: International Atomic Energy Agency, 2012.

Francini, M French, E Gallagher, I Garai, O Geatti, D Genovesi, L Gianolli, A Gimelli, E del Giudice, S Halliwell, MJ Hansson, C Harrison, F Homans,

Mol Imaging 2005; 32: 855–897.

Kaminek, A Kiss, M Kobylecka, M Kostkiewicz, J Kropp, R Kullenberg, T Lahoutte, O Lang, YH Larsson, M Lázár, L Leccisotti, N Leners, O

Henzlova MJ, Cerqueira MD, Mahmarian JJ, Yao SS. Stress protocols and tracers. J Nucl Cardiol 2006; 13: e80–90.

Lindner, RW Lipp, A Maenhout, L Maffioli, C Marcassa, B Martins, P Marzullo, G Medolago, CG Mendiguchía, S Mirzaei, M Mori, B Nardi, S

Hesse B, Tagil K, Cuocolo A, et al. EANM/ESC procedural guidelines for myocardial perfusion imaging in nuclear cardiology. Eur J Nucl Med

F Horton, D Jędrzejuk, J Jogi, A Johansen, H Johansson, M Kalnina, M

Einstein AJ, Pascual TNB, Mercuri M, et al. Current worldwide nuclear

Nazarenko, K Nikoletic, R Oleksa, T Parviainen, J Patrina, R Peace, C Pirich,

cardiology practices and radiation exposure: results from the 65 coun-

H Piwowarska-Bilska, S Popa, V Prakash, V Pubul, L Puklavec, S Rac, M

try International Atomic Energy Agency (IAEA) Nuclear Cardiology

Ratniece, SA Rogan, A Romeo, M Rossi, D Ruiz, N Sabharwal, BG Salobir, AI Santos, S Saranovic, A Sarkozi, RP Schneider, R Sciagra, S Scotti, Z Servini, LR Setti, S-Å Starck, D Vajauskas, J Veselý, A Vieni, A Vignati, IM Vito, K Weiss, D Wild, M Zdraveska-Kochovska.

Protocols Study (INCAPS). Eur Heart J 2015; 36: 1689–1696. 10. Radiological protection in cardiology. ICRP Publication 120. Ann ICRP 2013; 42: 1–125. 11. Senthamizhchelvan S, Bravo PE, Esaias C, et al. Human biodistribution

Latin America: RN Agüro, N Alvarado, CM Barral, M Beretta, I Berrocal,

and radiation dosimetry of 82Rb. J Nucl Med 2010; 51: 1592–1599.

JF Batista Cuellar, T-M Cabral Chang, LO Cabrera Rodríguez, J Canessa,

12. Mercuri M, Pascual TNB, Mahmarian JJ, et al. Estimating the reduc-

G Castro Mora, AC Claudia, GF Clavelo, AF Cruz júnior, FF Faccio, KM

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Fernández, JR Gomez Garibo, U Gonzalez, PE González, MA Guzzo, J

of stress-only imaging in the United States and worldwide. J Am Med

Jofre, M Kapitán, G Kempfer, JL Lopez, TV Massardo, I Medeiros Colaco,

Assoc Int Med 2016; 176: 269–273.

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14. San Luis TOL, Bouyoucef SE, Padhy AK. World radiopharmaceutical

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Pilot study of risk factors associated with cardiovascular disease in northern and southern Cameroonians Jeanne Durendale Chiadak, Jason Perret, Hilaire Macaire Womeni, Jules Roger Kuiaté, Pierre Cullus, Christelle Senterre, Christine Delporte

Abstract Aim: The aim of the study was to evaluate whether the risk factors for cardiovascular disease (CVD) are similar in the northern and southern regions of Cameroon. Methods: The participants answered a questionnaire concerning their lifestyle. Anthropometric and blood pressure measurements were evaluated in 192 individuals and biochemical parameters in 50 randomly selected volunteers. Results: Northerners displayed low alcohol and tobacco consumption, little practice of sport but physically demanding professions, and consumption of soybean, refined palm and other polyunsaturated oils. Southerners consumed alcohol, practiced sport, had intellectually based professions, and consumed crude and refined palm oils. Waist circumference and body mass index were higher in the southerners compared to the northerners. Blood glucose levels, and systolic and diastolic blood pressures were higher among the northerners than the southerners. Among the southerners, there were positive correlations between total cholesterol levels and systolic or diastolic blood pressure, low-density lipoprotein cholesterol and blood glucose levels or diastolic blood pressure, triglyceride levels and systolic blood pressure. Conclusion: Providing region-adapted, health-related advice for northern and southern Cameroonians would contribute to reducing risk factors for CVD. Keywords: cardiovascular diseases, risk factor, lifestyle, nutrition, diet, fatty acids

Laboratory of Pathophysiological and Nutritional Biochemistry, Faculty of Medicine, Université Libre de Bruxelles, Brussels, Belgium Jeanne Durendale Chiadak, PhD Jason Perret, PhD Christine Delporte, PhD, cdelport@ulb.ac.be

Department of Biochemistry, Faculty of Sciences, University of Dschang, Cameroon Jeanne Durendale Chiadak, PhD Hilaire Macaire Womeni, PhD Jules Roger Kuiaté, PhD

Biostatistics and Medical Informatics Service, Faculty of Medicine, Université Libre de Bruxelles, Belgium Pierre Cullus

Research Centre of Epidemiology, Biostatistics and Clinical Research, School of Public Health, Université Libre de Bruxelles, Belgium Christelle Senterre, PhD

Submitted 24/6/16, accepted 30/10/16 Published online 17/5/17 Cardiovasc J Afr 2017; 28: 235–241

www.cvja.co.za

DOI: 10.5830/CVJA-2016-094

Cardiovascular disease (CVD) remains the leading cause of death worldwide, accounting for around 17 million deaths per year.1 In sub-Saharan Africa, CVD is responsible for 20% of all global deaths,2 where in the past, CVD was considered a rare ailment among black African populations. However, the incidence of CVD has recently been rising with the increasing shift to Western lifestyle and habits, notably with an increased sodium and calorie intake. These changes account for the rising prevalence of obesity, the metabolic syndrome and diabetes. Between 1990 and 2020, the increase in mortality rates from CVD is estimated to be 140% in men and 118% in women in sub-Saharan Africa, compared to 53% in men and 31% in women in developed countries.1,3 Monitoring of CVD is based on the evaluation of non-modifiable risk factors (age, gender, race, family history), behavioural risk factors (physical inactivity, excessive alcohol consumption, smoking, diet high in saturated fat, salt and cholesterol), and modifiable risk factors (obesity, diabetes, hypertension, low- and high-density lipoprotein cholesterol levels).4 In developing countries, relationships between malnutrition and CVD have been poorly explored.5-7 Cameroon is considered a miniature Africa due to its diverse climate (ranging from southern tropical forests to northern savannah and western mountains) and its ethnic diversity (366 ethnic groups and 240 languages). The various ethnic groups distributed across 10 regions, including rural and urban zones, are characterised by distinct eating habits. The second Cameroonian household survey assessed the average energy intake per capita to be 3 241, 2 721 and 2 887 kcal/day for far north, far south and the whole country, respectively.8 Contribution to energy requirements results from three main nutrient uptakes; protein, fat and carbohydrates. The percentage energy from protein per unit of consumption was 11.9% in the far north, 9.4% in the far south and 10.5% overall for Cameroon. The percentage energy from fat per unit of consumption was 19.8% in the far north, 28.8% in the far south and 27.1% overall for Cameroon. Finally, the percentage energy from carbohydrate per unit of consumption was 68.3% in the far north, 61.7% in the far south and 62.4% overall for Cameroon.8 The percentage recommended for these three nutrients are 50 to 55% for carbohydrates, 12 to 15% for proteins and 30 to 38% for fat. In Cameroon, crude palm oil represents 10.6%, cottonseed oil 2.1%, refined palm oil 0.9% and peanut oil 0.4% of the total energy intake.8 Changes in the amount and/or type of fatty acids

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ingested can contribute to the development of many diseases, including obesity and diabetes, and thereby CVD. It appears that fatty acids could be implicated in the pathogenesis of these diseases; either by altering the composition of membrane phospholipids, or by modulating the expression of genes.9 Plasma omega-3 fatty acid levels were correlated to the eating habits in the three European countries investigated.10 The consumption of palm oil, which is rich in saturated fatty acids, is a well-recognised risk factor for cardiovascular and metabolic diseases; palm oil induces a larger increase in plasma concentrations of total cholesterol and low-density lipoprotein cholesterol.11 It has been suggested that a 20% increase in the tax on palm oil in India would reduce mortality rates from CVD by 1.3% and reduce total cholesterol levels by 0.08 mmol/l without substitution of palm oil with other oils.12 Furthermore, if palm oil could be substituted by an oil rich in polyunsaturated fatty acids, total cholesterol levels would then be reduced by 0.10 mmol/l. A reduction of 0.009 mmol/l in cholesterol level has been considered clinically significant, with a noticeably beneficial impact on health.13 In this context, the impact of dietary lipids on the development of CVD represents the focus of current health concerns, not only in economically developed countries but also in developing countries. While eating behaviours differ between the north and south of Cameroon, the energy intake remains comparable between the two regions, 3 241 kcal/day in the north and 2 721 kcal/day in the south.8 The aim of this study was therefore to evaluate whether the risk factors for CVD are similar in north and south Cameroonians displaying different food habits (regarding fat intake) but characterised by equivalent average energy intake.

Methods This study was performed on 192 volunteers, composed of 101 women and 91 men aged 35 to 65 years. They were distributed between 89 volunteers from the north (45 men and 44 women) and 103 volunteers from the south (46 men and 57 women). The volunteers answered a questionnaire concerning their lifestyle. In addition, their anthropometrics and biochemical parameters were measured. This study (P2013/164) was approved by the ethics committee of the Université Libre de Bruxelles, Erasme University Hospital and was conducted in compliance with the Declaration of Helsinki. All volunteers gave written informed consent before participation. The sample size was calculated using the following standard formula: [n = t² × p × (1–p)/m2] where n is the minimum sample size to obtain significant results for an event and a fixed level of risk; t is the confidence level (typical value of the confidence level of 95% is 1.96); p is the estimated prevalence of CVD, based on the literature (14% mortality rate due to CVD in Cameroon14) and m is the margin of error (usually set at 5%). Due to logistical and financial reasons, the biochemical parameters were measured in 50 randomly selected volunteers (25 north, 25 south, with equal numbers of men and women from the different cities). Anthropometric and blood pressure measurements were performed on all 192 volunteers. All volunteers were living in the urban zone from different cities of the south (S): Douala, Yaoundé, Bafang and Dschang;

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and the north (N): Garoua and Ngaoudéré. All volunteers belonged to the working and middle social classes. The volunteers were randomly recruited in their home or work place. Basic information was collected and included the following: gender: female (F) and male (M); age: volunteers were grouped by age: 35–50 and 51–65 years; tobacco consumption: defined as never smoked (no); former smoker or smoker (yes); alcohol consumption: defined as no consumption (none); consumption once or twice a week (occasionally); consumption more than twice a week (regularly); physical activity (sport and professional) was defined as sport: never practice (no); practice intense or moderate activity once or more than once a week (yes); for profession, domestic workers, farmers and traders were considered physically active, whereas office workers were considered intellectual; oil consumption: the oils mostly used for cooking were recorded. Various anthropometric parameters were collected for all volunteers. Height was collected from the ID card and weight was measured using an electronic scale. Body mass index (BMI) was calculated using the formula: weight (kg)/height2 (m) and BMI categories were defined as underweight with BMI ≤ 18.5 kg/m2; normal was BMI 18.5–24.9 kg/m2; overweight was BMI 25–29.9 kg/m2; and obese was BMI ≥ 30 kg/m2.15 Waist circumference (WC) was measured with a tape measure at the navel while standing. The recommended WC thresholds for assessing abdominal obesity for sub-Saharan African was: women ≥ 80 cm; men ≥ 94 cm.15 Systolic and diastolic blood pressure measurements were performed on all volunteers in a seated position at rest and monitored for at least five minutes using an electronic medical wrist blood pressure monitor (Omron M2 Basic; Omron Electronics SA, Knokke-Heist, Belgium). Two measurements were performed on each subject and the mean value was used. Blood pressure ranges were for systolic blood pressure (SBP): normal < 140 mmHg, and high ≥ 140 mmHg; for diastolic blood pressure (DBP): normal < 90 mmHg, and high ≥ 90 mmHg.16 Biochemical parameters such as blood glucose (BG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C) and triglycerides (TG), were measured in 50 randomly selected volunteers, using an equal number of men and women from different cities, who were advised to fast prior to and up to the time of measurement (not having eaten and/or drunk during the last 12 or eight hours, respectively). Disposable test strips were used with a Cardio Chek Analyser (Polymer Technology systems Inc, Indianapolis, USA). Low-density lipoprotein cholesterol (LDL-C) was calculated using Fridewald’s formula: LDL-C = TC – (HDL-C + TG/5). Blood glucose values were defined as normal < 100 mg/dl (5.55 mmol/l); limit 100–125 mg/dl (5.55–6.94 mmol/l); diabetic > 125 mg/dl (> 6.94 mmol/l). TC ranges were defined for women as normal: 155–255 mg/ dl (4.01–6.6 mmol/l); hypocholesterolaemia: < 155 mg/dl (< 4.01 mmol/l) and hypercholesterolaemia: 255 mg/dl (> 6.6 mmol/l). TC ranges were defined for men as normal: 130–250 mg/dl (3.37–6.48 mmol/l); hypocholesterolaemia: < 130 mg/dl (< 3.37 mmol/l) and hypercholesterolaemia: > 250 mg/dl (> 6.48 mmol/l). HDL-C ranges were defined for women as normal: 50–92 mg/ dl (1.3–2.38 mmol/l); hypocholesterolaemia: < 50 mg/dl (< 1.3 mmol/l), and hypercholesterolaemia: > 92 mg/dl (> 2.38 mmol/l). HDL-C ranges were defined for men as normal: 37–65 mg/

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dl (0.96–1.68 mmol/l); hypocholesterolaemia: < 37 mg/dl (0.96 mmol/l) and hypercholesterolaemia: > 65 mg/dl (1.68 mmol/l). LDL-C ranges were defined for women as normal: 100–150 mg/dl (2.59–3.89 mmol/l), hypocholesterolaemia: < 100 mg/ dl (< 2.59 mmol/l) and hypercholesterolaemia: > 150 mg/dl (> 3.89 mmol/l). LDL-C ranges were defined for men as normal: 110–160 mg/dl (2.85–4.14 mmol/l), hypocholesterolaemia: < 110 mg/dl (< 2.85 mmol/l) and hypercholesterolaemia: > 160 mg/dl (> 4.14 mmol/l). Triglyceride ranges were defined for women as normal: 35–140 mg/dl (0.4–1.58 mmol/l), hypotriglyceridaemia: < 35 mg/ dl (< 0.4 mmol/l) and hypertriglyceridaemia: > 140 mg/dl (> 1.58 mmol/l). Triglyceride ranges were defined for men as normal: 45–175 mg/dl (0.51–1.98 mmol/l), hypotriglyceridaemia: < 45 mg/dl (> 0.51 mmol/l) and hypertriglyceridaemia: > 175 mg/dl (> 1.98 mmol/l).15

Statistical analysis All statistical tests were performed using SPSS software (version 22.0.0.0; IBM Corp). For quantitative variables, data are presented as mean or median ± standard error of means (SEM). The Student’s t-test for independent samples or Wilcoxon– Mann–Whitney test were used to compare the means or medians of two groups, while one-way ANOVA or the Kruskal–Wallis test were used to compare the means or medians of more than two groups. For qualitative variables, data are presented in tables using numbers and percentages, and chi-squared or Fisher’s exact tests were used to compare characteristics between the groups. Spearman’s correlations were used to test possible correlations between two parameters. The results were considered statistically significant for p < 0.05.

Results The study population was distributed equally between men and women in the two regions, north and south. The distribution according to age group showed a significant difference (p < 0.001) between the two regions. Populations from the south consumed more alcohol than those in the north, who drank little or nothing (p < 0.001). The tobacco consumption was zero in the north and in the south very low (p < 0.03). The intense or moderate practice of sport was very low in the north compared to the south (p < 0.001). However, northerners had physical rather than intellectual professions compared to people of the south (p < 0.001). The percentage consumption of polyunsaturated oils was higher among the northerners compared to southerners. The majority of the southern population consumed both crude and refined palm oils, while a small portion of the southern people consumed only crude palm oil. In the north, people consumed mainly soybean oil and refined palm oil (Table 1). WC and BMI were higher among southerners than northerners (p = 0.01 and 0.04, respectively). However, the percentage of obese population, determined by measuring either the WC (north 61%, south 69%) or BMI (north 21%, south 21%), was statistically comparable between the two regions. The average and range of TC, HDL-C, LDL-C and TG levels were not significantly different according to region. By

contrast, BG levels, SBP and DBP were higher in the northern populations than the south (p = 0.024, p < 0.001, respectively). The percentages of individuals with diabetes, 10% in the north and 2% in the south, were not statistically different. There was however an over-representation of hypertension (SBP and DBP) in the north compared to the south (p < 0.001) (Table 2). In men from the two regions, there was no statistically significant difference between WC and BMI. By contrast, women from the south had a WC and BMI statistically higher than northern women (p = 0.001 and 0.005, respectively). The percentage of obesity was statistically higher among northern than southern men, based on BMI (p = 0.03) but not WC. By contrast, the percentage of obese women was higher in the south compared to the north, based on WC (p < 0.001) but not BMI. BG, TC, HDL-C, LDL-C and TG levels were not significantly different between women and men in the two regions. Both SBP and DBP were higher in men from the north than from the south (p < 0.001), whereas those parameters were comparable in women from the two regions. Northern men had a higher incidence of diabetes (16%) than men from the south (4%) (p = 0.027). Similarly, a greater percentage of men from the north had a SBP and DBP higher than that of men from the south (p < 0.001). The incidence of hypertension was higher among women from the north than from the south (p = 0.01) (Table 3). The characteristics of the populations showed that there was a significant difference in age between the volunteers from the north and south. Taking this into consideration, anthropometric

Table 1. Characteristics of the study population Population Characteristics

Total number

North (n = 89)

Percentage (%) South (n = 103)

North

South

p-value

Gender Female Male

101

0.23

Age (years) 35–51

107

51–65

None

Occasionally

< 0.001

Alcohol use

Regularly

< 0.001

Tobacco use Yes

183

100

0.03

Sport Yes

157

146

< 0.001

Profession Physical Intellectual

< 0.001

Oils consumed Crude palm oil

Crude and refined palm oils

Soybean oil and refined palm

Other polyunsaturated oils

< 0.001

p-value of chi-squared or Fischer’s exact test for the comparison of percentages between the two regions.

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Table 2. Anthropometric and biochemical parameters according to region Parameters

North

South

Table 3. Anthropometric and biochemical parameters among subjects of the same gender from the two regions

p-value

Parameters

p-value

87 ± 10

95 ± 11

p-value

WC (cm) (n = 192)

WC (cm) (n =192) Mean ± SEM

88 ± 10

92 ± 10

0.01

Mean ± SEM

89 ± 9

88 ± 9

Normal, n (%)

35 (39)

32 (31)

0.32

Normal, n (%)

27 (60)

32 (70)

Obese, n (%)

54 (61)

71 (69)

Obese, n (%)

18 (40)

14 (30)

Mean ±SEM

25 ± 4

24 ± 2

Normal, n (%)

23 (52)

24 (52)

0.68

17 (39)

7 (12)

0.01

Overweight, n (%)

12 (27)

19 (41)

0.23

18 (41)

31 (54)

0.27

9 (21)

3 (7)

0.03

9 (20)

19 (34)

0.13

98 ± 38

92 ± 17

Mean ± SEM

26 ± 4

28 ± 5

0.04

Normal, n (%)

40 (45)

31 (30)

0.10

Overweight, n (%)

30 (34)

50 (49)

Obese, n (%)

19 (21)

22 (21)

105 ± 51

92 ± 18

Obese, n (%)

[5.83 ± 2.83]

[5.11 ± 1.00]

Normal, n (%)

67 (75)

81 (79)

Limit, n (%)

13 (15)

20 (19)

9 (10)

2 (2)

Diabetes, n (%)

0.02 0.31

196 ± 56

193 ± 44

[5.08 ± 1.45]

[5.00 ± 1.14]

18 (80)

18 (72)

Hypocholesterolaemia, n (%)

4 (8)

3 (12)

Hypercholesterolaemia, n (%)

3 (12)

4 (16)

60 ± 16

61 ± 16

[1.55 ± 0.41]

[1.58 ± 0.41]

[mmol/l] Normal, n (%)

0.83 1

HDL-C (mg/dl) (n = 50) Mean ± SEM [mmol/l] Normal, n (%)

15 (60)

17 (68)

Hypocholesterolaemia, n (%)

6 (24)

3 (12)

Hypercholesterolaemia, n (%)

4 (16)

5 (20)

111 ± 48

109 ± 38

[2.87 ± 1.24]

[2.82 ± 0.98]

7 (28)

8 (32)

Hypocholesterolaemia, n (%)

15 (60)

14 (56)

Hypercholesterolaemia, n (%)

3 (12)

0.89 0.71

LDL-C (mg/dl) (n = 50) Mean ± SEM [mmol/l] Normal, n (%)

0.83

[mmol/l] Normal, n (%)

121 ± 91

116 ± 56

[1.37 ± 1.03]

[1.31 ± 0.63]

Mean ± SEM [mmol/l]

112 ± 61

91 ± 20

[6.22 ± 3.39] [5.05 ± 1.11]

Normal, n (%)

27 ± 5

30 ± 6

0.09 0.07

[5.44 ± 2.11] [5.11 ± 0.94]

34 (75)

35 (76)

33 (75)

42 (74)

Limit, n (%)

4 (9)

9 (20)

11 (19)

Diabetes, n (%)

7 (16)

2 (4)

4 (7)

Mean ± SEM [mmol/l]

0.02

214 ± 71

196 ± 48

[5.54 ± 1.84] [5.08 ± 1.24]

0.87 1

181 ± 34

191 ± 41

[4.69 ± 0.88] [4.95 ± 1.06]

Normal, n (%)

9 (75)

9 (69)

9 (75)

Hypocholesterolaemia, n (%)

0 (0)

1 (7)

4 (30)

2 (16)

Hypercholesterolaemia, n (%)

3 (25)

3 (23)

0 (0)

1 (8)

0.005

1 0.86

58 ± 15

58 ± 17

62 ± 18

65 ± 14

0.89 0.64

HDL-C (mg/dl) (n = 50) Mean ± SEM [mmol/l]

[1.50 ± 0.39] [1.50 ± 0.44]

1 1

[1.61 ± 0.47] [1.68 ± 0.36]

Normal, n (%)

6 (50)

7 (53)

9 (69)

10 (83)

Hypocholesterolaemia, n (%)

2 (16)

1 (7)

4 (31)

2 (16)

Hypercholesterolaemia, n (%)

4 (33)

5 (38)

0 (0)

127 ± 54

112 ± 42

0.81 0.49

Mean ± SEM [mmol/l]

96 ± 38

105 ± 35

[2.49 ± 0.98] [2.72 ± 0.91]

3 (23)

4 (30)

5 (41)

7 (58)

8 (61)

6 (50)

Hypercholesterolaemia, n (%)

2 (17)

2 (15)

1 (7)

1 (8)

1 0.64

1 0.83

TG (mg/dl) (n = 50)

18 (72) 0 (0)

Mean ± SEM

Hypercholesterolaemia, n (%)

4 (15)

7 (28)

[mmol/l]

146 ± 25

132 ± 20

< 0.001

Normal, n (%)

42 (47)

76 (74)

< 0.001

47 (53)

27 (26)

Hypocholesterolaemia, n (%) Hypercholesterolaemia, n (%)

Mean ± SEM

96 ± 18

84 ± 15

< 0.001

Normal, n (%)

26 (29)

68 (66)

< 0.001

Hypertensive, n (%)

63 (71)

35 (34)

and biochemical parameters among subjects from the two age groups were statistically compared. The results showed no significant difference between the two age groups for WC, BG, SBP and DBP. However, BMI was higher among people in the 35–51-year age group compared to people in the 51–65-year age group (p = 0.01). The percentage of obese people and people with normal SBP tended to be higher among people in the 35–51-year age group compared to people in the 51–65-year age

3 (25)

0 (0)

p-value for the comparison of means by Student’s t-test for independent samples or Wilcoxon–Mann–Whitney test and chi-squared or Fischer’s exact test for the comparison of the percentages in the two regions. WC, waist circumference; BMI, body mass index; BG, blood glucose; TC, total cholesterol; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; TG, triglycerides; SBP, systolic blood pressure; DBP, diastolic blood pressure.

Hypocholesterolaemia, n (%)

21 (84)

DBP (mmHg) (n = 192)

[3.29 ± 1.40] [2.90 ± 1.09]

Normal, n (%)

Hypocholesterolaemia, n (%) SBP (mmHg) (n =192) Mean ± SEM Normal, n (%) Hypertensive, n (%)

57 (100)

LDL-C (mg/dl) (n = 50)

TG (mg/dl) (n = 50) Mean ± SEM

36 (82)

0.001 < 0.001

TC (mg/dl) (n = 50)

TC (mg/dl) (n = 50) Mean ± SEM

0 (0)

BG (mg/dl) (n = 192)

BG (mg/dl) (n =192) [mmol/l]

8 (18)

BMI (kg/m2) (n = 192)

BMI (kg/m2) (n =192)

Mean ± SEM

0.19

137 ± 124

125 ± 67

106 ± 45

106 ± 42

[1.55 ± 1.4]

[1.41 ± 0.76]

10 (83)

9 (60)

11 (84)

9 (75)

0 (0)

2 (16)

4 (30)

2 (15)

3 (25)

Mean ± SEM

152 ± 27

129 ± 19

< 0.001 139 ± 22

134 ± 22

Normal n (%)

16 (35)

36 (78)

Hypertensive, n (%)

29 (64)

10 (22)

Mean ± SEM

98 ± 18

80 ± 14

Normal, n (%)

11 (34)

32 (70)

Hypertensive, n (%)

34 (75)

14 (30)

0.64

[1.20 ± 0.51] [1.20 ± 0.47]

1 0.64

SBP (mmHg) (n = 192) < 0.001

26 (59)

40 (71)

18 (40)

17 (29)

0.28

< 0.001

93 ± 17

87 ± 15

0.32

< 0.001

15 (24)

36 (63)

0.01

29 (66)

21 (37)

DBP (mmHg) (n = 192)

p-value for comparison of means by one-way ANOVA or Kruskal–Wallis test and the chisquared test or Fischer’s exact test for the comparison of percentages between groups. NM, northern men; NW, northern women; SM, southern men; SW, southern women; WC, waist circumference; BMI, body mass index; BG, blood glucose; TC, total cholesterol; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; TG, triglycerides; SBP, systolic blood pressure; DBP, diastolic blood pressure.

group (16 vs 8%; 37 vs 25%, respectively), but these were not statistically significant (p = 0.08; p = 0.05, respectively) (Table 4). In the north, there was a positive correlation between TC and TG levels (r = 0.61, p = 0.001); SBP and DBP (r = 0.82, p

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Table 4. Anthropometric and biochemical parameters among subjects of two age groups Parameters

35–50 years

51–65 years

p-value

WC (cm) (n = 192) Mean ± SEM

91.48 ± 1.77

91.01 ± 1.92

0.86

Normal, n (%)

37 (19)

69 (36)

0.50

Obese, n (%)

37 (19)

49 (26)

Mean ± SEM

29.42 ± 0.86

26.00 ± 0.93

0.01

Normal, n (%)

37 (19)

33 (17)

0.08

Overweight, n (%)

38 (20)

39 (20)

Obese, n (%)

31 (16)

14 (8)

Mean ± SEM

92.46 ± 11.63

117.48 ± 12.60

[mmol/l]

[5.13 ± 0.65]

[6.52 ± 0.70]

Normal, n (%)

78 (41)

65 (34)

Limit, n (%)

22 (11)

12 (6)

6 (3)

9 (5)

BMI (kg/m2) (n = 192)

< 0.001); SBP and WC (r = 0.30, p = 0.004); SBP and BMI (r = 0.24, p = 0.03) and DBP and WC (r = 0.26, p = 0.01). There was a negative correlation between HDL-C and TG levels (r = –0.45, p = 0.02) (Table 5). In the south there was a positive correlation between TC and TG levels (r = 0.48, p = 0.02); TC and SBP or DBP (r = 0.44, p = 0.03; r = 0.54, p = 0.006, respectively); LDL-C and BG (r = 0.43, p = 0.03); LDL-C and DBP (r = 0.49, p = 0.01) and TG and SBP (r = 0.54, p = 0.006) (Table 6).

Discussion

p-value for the comparison of means by Student’s t-test for independent samples or Wilcoxon–Mann–Whitney test and chi-squared test for the comparison of percentages between the two age groups. WC, waist circumference; BMI, body mass index; BG, blood glucose; SBP, systolic blood pressure; DBP, diastolic blood pressure.

To the best of our knowledge, CVD risk factors in northern and southern Cameroonians have not been studied before. Average WC and BMI from the studied population were significantly higher in the south than the north. However, the prevalence of obesity, determined by either BMI (± 21%) or WC (± 65%), was comparable between northern and southern Cameroonians, but based on BMI, higher than that in the entire Cameroonian population (± 10%).14 In addition, our data are in agreement with a study performed on the urban labour force from Douala (south) showing an obesity prevalence of 23%, based on BMI.17 The range limits used to establish each category (normal, overweight and obese) could explain the lack of difference in obesity prevalence between southerners and northerners, despite differences in average BMI and WC values. Based on BMI measurements, southern women displayed higher prevalence of obesity compared to northern women (34 vs 20%). Obesity prevalence determined in southern women (34%) was close to

Table 5. Correlations between parameters in the northerners

Table 6. Correlations between parameters in the southerners

BG (mg/dl) (n = 192)

Diabetes, n (%)

0.15 0.42

SBP (mmHg) (n = 192) Mean ± SEM

115.61 ± 8.80

135.17 ± 9.53

Normal, n (%)

71 (37)

47 (25)

Hypertensive, n (%)

35 (18)

39 (20)

0.14 0.05

DBP (mmHg) (n = 192) Mean ± SEM

88.65 ± 2.44

94.14 ± 2.65

0.13

Normal, n (%)

53 (28)

41 (21)

0.43

Hypertensive, n (%)

53 (28)

45 (23)

BG BG

HDL-C

LDL-C

SBP

DBP

BMI

BG BG

Sig n TC

0.13

Sig

0.54 25

n 1

0.17

–0.03

Sig

0.41

0.87

–0.45

Sig

0.27

0.001

0.02 25

0.95

–0.21

0.49

0.98

< 0.001

0.32

0.01

–0.18

–0.19

Sig

0.39

0.32

0.75

0.39

0.36

0.14

–0.16

0.10

0.03

–0.24

0.82

Sig

0.21

0.44

0.64

0.88

0.26

< 0.001

0.02

–0.06

0.36

–0.38

–0.05

0.30

0.26

Sig

0.87

0.77

0.08

0.06

0.81

0.004

0.01

DBP

BMI

0.29

–0.11

–0.04

0.24

0.19

Sig

0.93

0.92

0.15

0.61

0.86

0.03

0.07 < 0.001

89 0.72

0.951

CC, correlation coefficient; n, sample size; Sig, p-value; WC, waist circumference; BMI, body mass index; BG, blood glucose; TC, total cholesterol; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; TG, triglycerides; SBP, systolic blood pressure; DBP, diastolic blood pressure.

BMI

0.95 25 0.43

25 0.89

0.03 < 0.001 25

1 25

–0.14

0.25

0.51

0.23

1 25

CC –0.18

0.44

0.29

0.54

0.22

Sig

0.03

0.16

0.006

0.28

0.08 103

1 103

CC –0.02

0.54

0.02

0.39

0.49

0.71

Sig

0.006

0.92

0.06

0.01

< 0.001

0.85 103

103

1 103

0.19

0.03

–0.37

0.13

0.12

0.13

Sig

0.07

0.88

0.90

0.07

0.54

0.25

0.21

n 1

25 0.013

n 1

0.02

0.01

DBP

25 0.02

n 1

SBP

Sig

SBP

0.48

LDL-C CC

0.88

CC –0.01

Sig

0.07

LDL-C

25 0.23

n 1

0.25

0.004

–0.20

Sig TG

0.09

BMI

0.07

n 1

0.36

Sig

HDL-C CC –0.03

0.61

Sig

DBP

0.23

HDL-C

103

CC n

LDL-C CC

SBP

HDL-C CC

Sig 89

CC n

103

1 103

0.13

–0.09

0.03

–0.21

0.04

0.15

0.16

Sig

0.22

0.68

0.90

0.10

0.86

0.16

0.12 < 0.001

103

0.80 103

1 103

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the values determined in the women’s labour force from Douala (36%, based on BMI),17 and similar to the prevalence of obesity among urban southern women (33%)18 and rural southern women (33%).19 Based on WC measures, in our study, the prevalence of obesity in southern women was 100%, versus 82% for northern women. Our data are higher than that obtained in urban southern women (43%), based on WC.17 Based on BMI, our data showed that the prevalence of obesity in northern men was 21%, versus 7% for southern men, which were higher and lower, respectively, than that from the men’s labour force from Douala (18%, based on BMI).17 Based on WC measures, in our study, northern men displayed higher prevalence of obesity compared to southern men (40 vs 30%). These values were higher or lower than the obesity prevalence determined for the men’s labour force from Douala (32%, based on WC).17 Recruitment methods, population sizes and/or cut-off values for determination of obesity prevalence may have accounted for these differences. Strong and positive correlations existed between SBP and WC, SBP and BMI, and DBP and WC among the northerners. In the southern rural zone of Cameroon, obesity in women was not correlated with blood pressure and blood glucose values due to their farming activities, which can be equated with permanent physical exercise.19 Increased DBP and BMI in the north may have been due to a lack of physical activity (95%), which appeared to be much higher among northerners than among southerners (70%) or the overall Cameroonian population (39%).14 Higher WC and BMI values observed among southerners could have been related to their food habits and/or lifestyle, despite comparable total energy intakes observed in south and north Cameroon.8 Southerners were characterised by a significantly higher fat consumption than northerners.8 In addition, our study showed that crude and refined palm oils rich in saturated fatty acids (45–55%) and mono-unsaturated fatty acids (38–45%)20 were the oils mostly used by southerners. A recent report has shown that the replacement of polyunsaturated fatty acid with saturated fatty acid during a hypercaloric state was accompanied by modest weight gain as well as increased markers of endothelial dysfunction and insulin resistance in healthy, normal-weight individuals.21 The higher prevalence of obesity among southerners could also have been related to the high percentage of individuals consuming alcohol occasionally or regularly (92%), compared to the low percentage (1%) of northerners consuming alcohol, for cultural reasons. Our data corroborate a previous study performed on Cameroonians from urban workplaces, showing that the prevalence of obesity was positively correlated with excessive alcohol consumption.17 Among southerners, strong positive correlations existed between lipid parameters and other cardiovascular risk factors studied (hypertension and diabetes). Palm oil, rich in saturated fatty acids and consumed by southerners, is a well-recognised risk factor for CVD and metabolic diseases, as it induces a larger increase in plasma concentrations of TC and LDL-C.11 According to Keys, food composition, not only rich in cholesterol but also in fatty acids, controlled plasma TC concentrations.22 Brady et al. showed that consumption of omega-6 poly-unsaturated fatty acids is likely to contribute to insulin resistance.23 Diets with a high omega-3/omega-6 fatty acid ratio improve the plasma lipid

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profile and are known to reduce obesity and improve insulin resistance.24 While fish and shellfish are the main sources of omega-3 fatty acid,25 the energy intake from fish in Cameroon represents only 0.4% of the total energy intake.8 BG, SBP and DBP were significantly higher among northerners than southerners, with northerners being characterised by high carbohydrate consumption compared to southerners.8 Consumption of food with a high glycaemic index may account for increased BG levels and blood pressure among northerners. Similarly, consumption of high glycaemic index foods in Japan increased the risk of developing type 2 diabetes.26 In our study, the prevalence of diabetes in northern and southern Cameroonians was similar or lower, respectively, compared to the world global prevalence of diabetes estimated in 2004 at 9% among adults aged 18 years and over.27 More than 80% of deaths related to diabetes occur in low- and middle-income countries.28 It has been shown that a healthy diet, regular physical activity, maintenance of a normal weight and stopping smoking can prevent or delay the onset of type 2 diabetes.29 Providing adapted health-related advice to northern and southern Cameroonians would certainly contribute to reducing risk factors for CVD. Age has been considered a non-modifiable risk factor for the onset of CVD.4 However, the CVD risk factors monitored in our study did not increase with age. On the contrary, we observed that BMI was higher in the 35–51-year age group, compared to people in the 51–65-year age group; this could have been linked to a modification of lifestyle. In a recent report, the increase in mortality rate from CVD between 1990 and 2020 is estimated to be 140% in men and 118% in women in sub-Saharan Africa compared to 53% in men and 31% in women in developed countries. This is probably due to a shift to a Western lifestyle and an increased intake of calories in sub-Saharan Africa.1,3

Conclusion The prevalence of obesity was higher in southern Cameroonians (especially women) compared to northern Cameroonians. Lipid parameters (TC, LDL-C and TG) were positively correlated with cardiovascular risk factors such as BG levels, SBP and DBP among southern Cameroonians. The prevalence of diabetes and high blood pressure was higher among northern than southern Cameroonians, despite the lack of correlation between lipid parameters and cardiovascular risk factors assessed among northern Cameroonians. The main objective of this pilot study was to attract the attention of national health authorities and medical communities to the impact of dietary habits on the increasing prevalence of cardiovascular risk factors by comparison of the two main regions of Cameroon. Hopefully, the risk factors uncovered by this study will encourage public health authorities to promote (financially and logistically) a widespread multicentre study, allowing healthcare personnel to assess the looming health issues and to eventually provide public health recommendations. Furthermore, additional studies aimed at assessing food consumption and lifestyle factors in these two populations would increase our understanding of cardiovascular risk factors in Cameroon. This study was supported by grants from the Van Buuren and JaumotteDemoulin Foundation, de Meurs François Foundation and Defay Fund (Universite Libre de Bruxelles). JDC was a recipient of a doctoral fellowship

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from Fonds Xénophilia (Université Libre de Bruxelles) and a travel grant

Blood Institute. Diagnosis and management of the metabolic syndrome:

from the Féderation Wallonie Bruxelles.

an American Heart Association/National Heart Lung and Blood Institute Scientific Statement. Circulation 2005; 112(17): 2735–2752.

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tion of chronic diseases. Report of a World Health Organization Study

lation de femmes rurales de l’Ouest du Cameroun. Médecine d’Afrique Noire 2001; 48(10): 391–393. 20. Feinberg M, Favier JC, Ireland-Ripert J. Repertoire général des aliments.

Lemogoum D, Ngatchou W, Janssen C, Leeman M, van Bortel L,

Table de composition des corps gras. Ciqual/Regal 1987; 1: 16130–17420.

Boutouyrie P, et al. Effects of hunter–gatherer subsistence mode on

21. Iggman D, Rosqvist F, Larsson A, Arnlöv J, Beckman L, Rudling M,

arterial distensibility in Cameroonian pygmies. Hypertension 2012;

et al. Role of dietary fats in modulating cardiometabolic risk during

60(1): 123–128.

moderate weight gain: a randomized double-blind overfeeding trial

Institut national de statistique (INS). Pauvreté et Nutrition au Cameroun. Deuxième enquête camerounaise auprès des ménages (ECAM II). 2001.

Moyo DF, et al. Epidemiology of obesity in the work milieu Douala

Prévalence de l’obésité chez les femmes adultes en milieu urbain en

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vol. 1. Geneva: World Health Organization; 1999. 17. Fouda AA, Lemogoum D, Manga JO, Il Dissongo J, Tobbit R,

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Group Geneva. World Health Organization Technical Report Series, 7.

diabetes mellitus and its complications. Report of a WHO consultation,

developing world. Am Heart J 2004; 148(1): 7–15.

Global Burden of Disease Study. Science 1996; 274(5288): 740–743. 6.

16. World Health Organization. Definition, diagnosis and classification of

Pégorier JP, Le May C, Girard J. Control of gene expression by fatty acids. J Nutr 2004; 134(9): 2444–2449.

(LIPOGAIN study). J Am Heart Assoc 2014; 3(5): e001095. 22. Keys A. Serum cholesterol response to dietary cholesterol. Am J Clin Nutr 1984; 40: 351–359. 23. Brady LM, Lovegrove SS, Lesauvage SV, Gower BA. Increased n-6

10. Pounis G, De Lorgeril M, Salen P, Laporte F, Krogh V, Siani A, et al.

polyunsaturated fatty acids do not attenuate the effects of long-chain

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n-3 polyunsaturated fatty acids on insulin sensitivity or triacylglycerol

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reduction in Indian Asians. Am J Clin Nutr 2004, 79: 983–991. 24. Liu HQ, Qiu Y, Mu Y, Zhang XJ, Liu L, Hou XH, et al. A high ratio

11. Vega-Lopez S, Ausman LM, Jalbert SM, Erkkila AT, Lichtenstein AH.

of dietary n-3/n-6 polyunsaturated fatty acids improves obesity-linked

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TLR4 in SD rats. Nutr Res 2013; 33(10): 849–858. 25. Chowdhury R, Stevens S, Gorman D, Pan A, Warnakula S, Chowdhury

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and risk of cerebrovascular disease/ systematic review and meta-analysis.

economic-epidemiologic model. Br Med J 2013; 347: f6048.

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J Am Coll Cardiol 2004; 44(3): 720–732. 14. World Health Organization. Obesity: preventing and managing the

Prospective Study. Nutr J 2013; 12(1): 165. 27. World Health Organization study group. Global status report on noncom-

global epidemic. Report on a WHO Consultation (WHO Technical

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by Cause, Age, Sex and Country, 2000–2012. Geneva, WHO, 2014. 29. World Health Organization study group. Global status report on noncommunicable diseases 2010. Geneva, World Health Organization, 2011.

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A programme to increase appropriate usage of benzathine penicillin for management of streptococcal pharyngitis and rheumatic heart disease in Zambia Aidan Long, Joyce Chipili Lungu, Elizabeth Machila, Sherri Schwaninger, Jonathan Spector, Brigitta Tadmor, Mark Fishman, Bongani M Mayosi, John Musuku

Abstract Rheumatic heart disease is highly prevalent and associated with substantial morbidity and mortality in many resourcepoor areas of the world, including sub-Saharan Africa. Primary and secondary prophylaxis with penicillin has been shown to significantly improve outcomes and is recognised to be the standard of care, with intra-muscular benzathine penicillin G recommended as the preferred agent by many technical experts. However, ensuring compliance with therapy has proven to be challenging. As part of a public–private partnership initiative in Zambia, we conducted an educational and access-to-medicine programme aimed at increasing appropriate use of benzathine penicillin for the prevention and management of rheumatic heart disease, according to national guidelines. The programme was informed early on by identification of potential barriers to the administration of injectable penicillin, which included concern by health workers about allergic events. We describe this programme and report initial signs of success, as indicated by increased use of benzathine penicillin. We propose that a similar approach may have benefits in rheumatic heart disease programmes in other endemic regions. Keywords: rheumatic fever, rheumatic heart disease, benzathine penicillin, pencillin allergy Submitted 27/9/16, accepted 2/1/17 Cardiovasc J Afr 2017; 28: 242–247

www.cvja.co.za

DOI: 10.5830/CVJA-2017-002

Massachusetts General Hospital, Boston, USA Aidan Long, MD, aalong@mgh.harvard.edu

University Teaching Hospital, Lusaka, Zambia Joyce Chipili Lungu, RN Elizabeth Machila, RN John Musuku, MD

Novartis Institutes for BioMedical Research, Cambridge, USA Sherri Schwaninger, MBA Jonathan Spector, MD Brigitta Tadmor, PhD

Harvard Stem Cell and Regenerative Biology Department, Harvard University, Cambridge, USA Mark Fishman, MD

Department of Medicine, Groote Schuur Hospital and University of Cape Town, Cape Town, South Africa Bongani M Mayosi, MD

Rheumatic heart disease (RHD) is a major cause of morbidity and mortality in sub-Saharan Africa (SSA).1,2 Up to 3% of school-aged children have definite or borderline RHD,3-5 and congestive heart failure stemming from valve damage in RHD patients is a leading non-infectious cause of death in young adults.6,7 Acute heart failure from RHD in SSA has been associated with a 35% one-year mortality rate.8 Yet RHD is preventable and, to some degree, treatable. Evidence generated more than 60 years ago demonstrated that antibiotic treatment of group A Streptococcus (GAS) pharyngitis, a practice known as ‘primary prevention’, significantly reduced the risk of rheumatic fever (RF).9-11 Shortly thereafter, it was shown that ‘secondary prevention’, in which antibiotics are administered continuously for a period of many years to patients with RHD, was effective at suppressing new streptococcal infections and decreased the incidence of recurrent RF.10,12-14 The initial RF and RHD studies used penicillin as the antibiotic of choice and, to this day, GAS remains exquisitely sensitive to penicillin treatment.15-17 Penicillin continues to be the standard of care for primary and secondary prevention of RHD globally in non-allergic individuals.2 In resource-constrained parts of the world where RHD is still endemic, including SSA, the use of penicillin for RHD prevention and treatment is widely recognised to be suboptimal.18-20 The reasons for this are complex and related to a multitude of interacting factors, including drug supply, pharmaco-economics, health service infrastructure and possibly socio-cultural drivers.21 Indeed, a recent high-level report outlining the key actions required to eradicate RHD in Africa identified variable supply and suboptimal quality and use of penicillin as some of the major barriers to achievement of this goal,22 a position endorsed by the World Heart Federation.23 Penicillin comes in various formulations. Benzathine penicillin G (BPG), a World Health Organisation essential medicine, is an intramuscular injectable form with a long half-life, such that only a single dose is required for primary prevention (in contrast to a 10-day course of oral pills taken twice daily), and a single monthly dose is needed for secondary prevention (compared with a regimen of oral pills taken twice daily).10 In SSA, leading technical authorities, including the Pan-African Society of Cardiology (PASCAR), have advocated the use of BPG for the treatment of streptococcal pharyngitis and the management of RHD to maximise the likelihood of patient compliance with recommended regimens, an approach that has met with success in other low-resource settings.22,24,25 There is also evidence that BPG may be more effective than oral penicillin for secondary prophylaxis of RHD and, consequently, it is a commonly recommended therapy.14,26,27 In 2012, a public–private partnership was launched in Zambia with the goal of reducing and ultimately eliminating RHD.28 This

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multi-faceted initiative (called ‘BeatRHD Zambia’) is centred out of the University Teaching Hospital (UTH) in Lusaka, Zambia, and includes operational research (for example, to measure disease prevalence), public awareness, and health system-strengthening activities – in particular, efforts to increase appropriate BPG usage for primary and secondary prevention of RHD in government health facilities according to national guidelines. To explore and address factors contributing to possible low rates of BPG use among health workers in Zambia, we undertook an assessment of health workers’ attitudes and practices relating to BPG safety, appropriate use and effectiveness. The information obtained was used to inform education and training, and interventions for BPG access, which have been implemented in health centres across Lusaka, Zambia, and are now being rolled out in other provinces. This report describes the experience to date of supporting the use of BPG for primary and secondary prevention of RHD in Zambia.

Unmasking potential barriers to penicillin administration A two-day workshop was conducted at UTH in October 2014 in order to elicit participants’ knowledge, attitudes and practices relating to RHD and BPG, and to provide education and training on how to administer BPG. The workshop involved a classroom-based didactic and interactive programme directed at representatives from UTH and 20 government clinics in Lusaka. There were 29 attendees, mostly nurses and a few doctors.

Focus group discussion An initial focus group discussion (led by AL and JM) permitted course leaders to gain insight into current patterns of penicillin usage in cases of streptococcal pharyngitis and RHD. It allowed for an informal exploration of factors that were perceived to limit the use of BPG in these clinical circumstances. All 29 workshop participants expressed awareness of the existence of RHD and the majority reported having been involved in the care of such patients. While most participants reported prior experience with administration of oral penicillin VK and intramuscular penicillin G, no participant was able to relate first-hand experience in the administration of intramuscular BPG. Precise identification of the reasons for the non-use of BPG was challenging to ascertain but one theme appeared central: fear of penicillin allergy as a potential barrier to administration of BPG in Zambia. This concern had also been brought to light before the workshop by personal interactions between Zambian nurses and doctors and the head of Paediatrics at UTH (JM), which revealed anxiety over a perceived high risk of penicillin allergy associated with injectable penicillin (distinct from the oral form of penicillin). During the focus group, a significant number of the participants expressed grave fear of inducing an allergic reaction, apparently based on anecdotal information they had received secondhand about such events. No participant reported directly having encountered an adverse drug reaction (including allergic or anaphylactic reactions) with administration of any formulation of penicillin. Only one participant had previous training in drug-allergy recognition and management. There appeared to be prevalent misconceptions that anaphylactic reactions to BPG were common and were increased

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in individuals who were fasting or otherwise weak. Most programme participants were not aware that prior tolerance of other forms of penicillin (such as oral penicillin VK or intramuscular penicillin G) might have a bearing on the subsequent risk of anaphylaxis to BPG. A small number of participants inquired whether penicillin allergy testing would be necessary before BPG administration.

Educational session Informed by observations in the focus group, the educational component of the workshop covered the following topics: streptococcal pharyngitis and its relationship to RF and RHD; the role of penicillin in primary and secondary prevention; review of the various forms of penicillin, including BPG, penicillin VK and penicillin G; use of penicillin in previously documented RHD control programmes; the nature and likelihood of possible adverse reactions to penicillin (including IgE-mediated type I allergic reactions and other non-allergic adverse reactions); and how to recognise and intervene in acute anaphylaxis. The educational session also reviewed evidence that supported the lack of need to conduct penicillin allergy testing (often simply called ‘skin testing’ locally) before BPG administration to a patient in whom there was no prior history of adverse reaction to penicillin. Following the didactic programme, a hands-on, role-playing exercise was undertaken to teach recognition and management of acute anaphylaxis in a simulated patient (Fig. 1), based on algorithms developed by the World Allergy Organisation.29 Skills imparted included placing the patient in the supine position with the legs elevated, proper assessment of the patient’s airway, correct administration of intramuscular epinephrine, and determination of the potential need for additional medications such as antihistamines and bronchodilators. Educational activities were evaluated by pre- and posttesting of knowledge and skills. All participants demonstrated significantly improved anaphylaxis management skills, and in an anonymous post-course evaluation, every participant reported that their clinical practice would change as a result of the course.

Workshop learnings Important lessons learned from the initial educational workshop guided future programme activities. First, it was clear that health workers in Zambia had had misconceptions about the true frequency of severe penicillin allergic reactions. Second, health workers received scant, if any, training in drug-allergy recognition and management; therefore there was a need for programmes to improve health workers’ confidence in managing patients with drug allergy. Third, health workers were unclear about the precise indications and dosing for administering BPG, and were eager for opportunities to improve their diagnostic and treatment skills. These were each felt to be remediable contributory factors to the suboptimal use of BPG for primary and secondary prevention of RHD in Zambia.

Design and deployment of subsequent tailored interventions A core activity of the BeatRHD Zambia initiative is to work to help strengthen the Zambian health system in order that services for

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Fig. 2. The BeatRHD Zambia team conducts an on-site introductory workshop during enrollment of new health centres into the RHD control programme. The educational session was flipchart based and included allergy training as a core component. Fig. 1. A skills-building, role-playing exercise was conducted at the Lusaka workshop to help nurses and doctors build confidence in their ability to successfully recognise and manage medication-induced allergy. Placing the patient on the back and elevating the lower extremities is recommended for management of anaphylaxis, in addition to the immediate administration of adrenaline.31

primary and secondary prevention of RHD are reliably delivered. To achieve this, an RHD control programme was developed for implementation in individual health facilities, which includes an introductory on-site training workshop, dissemination of educational materials for staff and patients, ongoing supportive supervisory visits by UTH staff, and assessment of BPG stocks. Largely as a result of the lessons learned in the initial workshop described above, four main interventions were incorporated into the RHD control programme in Zambia.

training, to help physically prepare health workers to manage drug allergy, to help build their confidence so that they could successfully manage an allergic event, and to ultimately reduce barriers to the administration of injectable penicillin. The allergy kit contains a set of medications consistent with World Allergy Organisation guidelines for treating drug allergy,29 including injectable epinephrine with a sterile syringe and alcohol wipes; an oral non-sedating antihistamine; a short-acting beta-agonist bronchodilator inhaler; and oral prednisone tablets. These kits also include concise instructions for emergency steps to be taken in the event of a serious allergic reaction, a photocopy of figures from the World Allergy Organisation guidelines, a data sheet to record clinical events, a pen to complete the data sheet, and a patient handout. The components are packaged together in a locally procured, conspicuously labelled plastic box that was designed for ready availability and ease of transport. The

Creation of durable and accessible educational materials A user-friendly allergy-focused educational module, based on presentations delivered in the original workshop, was developed into a laminated paper flipchart format for subsequent teaching and reference in the field without need for electronic audiovisual support (Fig. 2). The flipchart reviews the topic of drug allergy; how to recognise and manage a severe allergic reaction; how the allergy kit is used (see below for description of allergy kit); and which medicines are indicated for patients with a known allergy to penicillin. A professionally produced video recording of the allergy module content was also developed for free electronic distribution, and a link to the video file was posted to the PASCAR website for educational purposes.30

Compilation and provision of penicillin allergy kits Every health centre that is enrolled in the RHD control programme is provided with a bundled â&#x20AC;&#x2DC;penicillin-allergy kitâ&#x20AC;&#x2122; that contains the key materials needed to initiate management of a penicillin-induced allergic reaction (Fig. 3). The allergy kit was conceived to be an additional mechanism that complements

Fig. 3. A specially designed, bundled allergy kit was assembled and distributed to each health centre enrolled in the RHD control programme. The kit contains key medicines and other materials, including pictorial instructions, needed to initiate management of a severe drug-allergy event.

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medicines in the allergy kit are clearly displayed and labelled to facilitate quick and proper use.

Ongoing supportive supervision in clinics Nurses from UTH provide on-site supportive supervision once or twice monthly to each clinic enrolled in the RHD control programme. These visits have been determined to be necessary in order to provide regular refresher education and training relating to drug allergy and other aspects of the RHD control programme (for example, primary and secondary prevention); to answer questions and help solve problems that invariably arise at the point of care; to check and re-stock the allergy kit as necessary; and to confirm that each health centreâ&#x20AC;&#x2122;s pharmacy has an adequate stock of penicillin, including BPG.

Assessment of BPG availability Through the RHD control programme, free penicillin treatment is offered to patients for primary and secondary prevention of RHD. To help ensure availability of high-quality medicine, in-country stocks of penicillin were augmented by a product grant of 25 000 doses from Sandoz, in accordance with World Health Organisation guidelines for medicine donations.31 The product grant was a supplement; we found that BPG procured through normal government processes was virtually always also available in enrolled clinics. Training followed by supportive and mentorship visits have also been commenced in provinces outside Lusaka, with the first one being in Choma (Southern Province), where ongoing supportive supervision in clinics and assessment of BPG availability will be replicated.

Initial outcomes Baseline information obtained from the initial workshop indicated an extremely low (and perhaps even zero) rate of usage of BPG for primary and secondary prevention of RHD among health workers at UTH and Lusaka area government health facilities. Now, two years later, we have observed substantial changes in the pattern of BPG usage as a result of the programmeâ&#x20AC;&#x2122;s interventions. We conducted structured interviews with 18 nurses, clinical officers and pharmacists in seven clinics that had been enrolled in the RHD control programme for four to six months. Ninety per cent of respondents had administered injectable penicillin since the training, and most of them reported that they had administered the medicine on many occasions. Six of the 18 participants reported that using injectable penicillin to treat pharyngitis was a new practice for them, which they had learned as a result of the programme. None of the health workers thought it was too much work to administer injectable penicillin compared with pills. Only one nurse had apprehension about giving injectable penicillin, and she requested from the programme nurses more training on allergy recognition and management; all other health workers reported that they felt comfortable recognising and managing penicillin allergy as a result of the knowledge and skills gained in the training. All heath workers interviewed believed that patients actually preferred injections to pills due to the perception that it was a

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more effective treatment. Many of the respondents also reported that they preferred the 1.2 million IU formulation to the 2.4 million IU formulation, since it was easier to dose in children. While the number of participants in this pilot evaluation was small, we believe that it provides an early signal on the impact of the programme. To date, 21 government health facilities in Lusaka have been enrolled in the RHD control programme and records indicate that more than 9 000 doses of BPG have been administered since the programme started, the majority of which was used for primary prevention of RHD (the incidence of pharyngitis was much higher than the number of patients with RHD who required secondary prophylaxis). Penicillin-allergy skin testing prior to BPG administration was not routinely undertaken. No case of anaphylaxis has been recorded. Further scale-up of the RHD control programme in Lusaka Province is underway, as is expansion to the Southern Province. Extension to additional provinces is anticipated during 2017.

Discussion Rheumatic fever and RHD are preventable and potentially eradicable conditions that still account for significant morbidity and mortality rates in Zambia, other countries in SSA and other underdeveloped areas of the world. Low rates of penicillin use, including BPG, in appropriate clinical circumstances are likely to be a factor accounting for the continuing high prevalence of these diseases.18 From our experience, included among the important underlying drivers that contribute to low rates of BPG usage are a lack of appropriate knowledge regarding the confirmed benefits to be derived from its use and the fear of potential adverse events, including allergic reactions. Similar observations have also been made in other regions of the world where RHD is endemic.32 That fear of penicillin allergy emerged as a significant barrier to BPG use, which came as somewhat of a surprise, since apprehension towards drug allergy has not been commonly described among health workers in SSA, and scant literature exists on adverse penicillin reactions in population-based studies of RF and RHD. A multinational study in 1991 that included 32 430 BPG injections in 1 790 patients estimated the risk of anaphylaxis to be exceedingly low, at approximately one in 10 000 injections,33 and a 2014 retrospective study of BPG treatment in RF in Turkey found confirmed allergy in one of 535 patients (0.18% of 17 641 injections) but documented no anaphylactic reactions.34 Three fatalities that were temporally related to BPG injection were reported from Zimbabwe more than 15 years ago, although clinical details were not well described and so it is not clear that drug allergy played a role.35 We document here that relatively simple interventions, including appropriate education of healthcare personnel, together with confidence building around the recognition and management of allergic drug reactions, followed by a number of low-cost ongoing supportive measures have the potential to significantly improve rates of BPG usage in the primary and secondary prevention of RHD in a low-resource setting. Our early data also suggest that there is no need to perform routine penicillin-allergy testing prior to BPG administration in patients without a prior history of adverse reactions to penicillin.

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This position is supported by several large published studies that evaluated interventions with BPG in RHD patients, where large numbers of BPG injections were administered without prior penicillin-allergy testing,33,34 and reported the incidence of adverse reactions, including anaphylaxis, was exceedingly low.36 A key action recommended in the plan to eradicate RHD in Africa includes appropriate training of health workers to safely and effectively deliver BPG.22 The preliminary experience in Zambia suggests that appropriate educational interventions in the setting of drug availability and ready access to medications to treat anaphylaxis can positively impact on rates of BPG usage. Future work will involve the exploration of innovative ways to scale up the RHD control programme, such as the use of electronic training modules, and determination of the impact of these types of interventions on health outcomes, including the incidence of RF and RHD.

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10. Stollerman GH, Rusoff JH, Hirschfeld I. Prophylaxis against group A streptococci in rheumatic fever; the use of single monthly injections of benzathine penicillin G. N Engl J Med 1955; 252: 787–792. 11. Chamovitz R, Catanzaro FJ, Stetson CA, Rammelkamp CH. Prevention of rheumatic fever by treatment of previous streptococcal infections. I. Evaluation of benzathine penicillin G. N Engl J Med 1954; 251: 466–471. 12. Tompkins DG, Boxerbaum B, Liebman J. Long-term prognosis of rheumatic fever patients receiving regular intramuscular benzathine penicillin. Circulation 1972; 45: 543–551. 13. Taranta A. Factors influencing recurrent rheumatic fever. A Rev Med 1967; 18: 159–172. 14. Manyemba J, Mayosi BM. Penicillin for secondary prevention of rheumatic fever. Cochrane Database Syst Rev 2002: CD002227. 15. Walker MJ, Barnett TC, McArthur JD, et al. Disease manifestations and pathogenic mechanisms of Group A Streptococcus. Clin Microbiol Rev 2014; 27: 264–301. 16. Horn DL, Zabriskie JB, Austrian R, et al. Why have group A strepto-

Conclusion

cocci remained susceptible to penicillin? Report on a symposium. Clin Infect Dis 1998; 26: 1341–1345.

A multi-faceted effort to combat RHD in Zambia included, as a core component, a novel programme to demystify concerns and dispel fears about safe administration of BPG. It appears that this approach contributed to increases in the rate of BPG use for primary and secondary prevention of RHD in government health facilities, according to national guidelines. Lessons from this experience may be applicable to other countries where RHD is endemic.

17. Abdissa A, Asrat D, Kronvall G, et al. Throat carriage rate and antimi-

SS, JS, BT and MF are or were employees of Novartis Institutes for

20. Zulhlke L, Engel ME, Karthikeyan G, et al. Characteristics, compli-

BioMedical Research, which is a corporate affiliate of Sandoz. JM receives

cations, and gaps in evidence-based interventions in rheumatic heart

grant funding from NIBR.

disease: The Global Rheumatic Heart Disease Registry (the REMEDY

crobial susceptibility pattern of group A Streptococci (GAS) in healthy Ethiopian school children. Ethiop Med J 2011; 49: 125–130. 18. Karthikeyan G, Mayosi BM. Is primary prevention of rheumatic fever the missing link in the control of rheumatic heart disease in Africa? Circulation 2009; 120: 709–713. 19. Robertson KA, Volmink JA, Mayosi BM. Lack of adherence to the national guidelines on the prevention of rheumatic fever. S Afr Med J 2005; 95: 52–56.

study). Eur Heart J 2015; 36: 1115–1122.

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33. International Rheumatic Fever Study Group. Allergic reactions to longterm benzathine penicillin prophylaxis for rheumatic fever. Lancet 1991;

sites/default/files/RHD Action_Global Status of BPG Report_Online Version.pdf (accessed Aug 22, 2016).

Conﬁdence Through Clinical and Real World Experience1-3 #1 Scripted Non-VKA Oral Anticoagulant by Cardiologists* Millions of Patients Treated Worldwide Across Multiple Indications4 REFERENCES: 1. Patel M.R., Mahaffey K.W., Garg J. et al. Rivaroxaban versus warfarin in non-valvular atrial fi brillation. N Engl J Med. 2011;365(10):883–91. 2. Tamayo S., Peacock W.F., Patel M.R., et al. Characterizing major bleeding in patients with nonvalvular atrial fi brillation: A pharmacovigilance study of 27 467 patients taking rivaroxaban. Clin Cardiol. 2015;38(2):63–8. 3. Camm A.J., Amarenco P., Haas S. et al. XANTUS: A Real-World, Prospective, Observational Study. 4. Calculation based on IMS Health MIDAS, Database: Monthly Sales January 2017. S4 Xarelto 15: Each film-coated tablet contains rivaroxaban 15 mg. Reg. No: 46/8.2/0111; Namibia NS2 : 12/8.2/0006; S2 Botswana: BOT1302296; Zimbabwe: PP10 Reg. 2017/10.2/5363 S4 Xarelto 20: Each film-coated tablet contains rivaroxaban 20 mg. Reg. No: 46/8.2/0112;Namibia NS2 : 12/8.2/0007; S2 Botswana: BOT1302297; Zimbabwe: PP10 Reg. 2017/10.2/5364 PHARMACOLOGICAL CLASSIFICATION: A.8.2 Anticoagulants. INDICATIONS: (1) Prevention of stroke and systemic embolism in patients with non-valvular atrial fibrillation (SPAF); (2) Treatment of deep vein thrombosis (DVT) and for the prevention of recurrent deep vein thrombosis (DVT) and pulmonary embolism (PE); (3) Treatment of pulmonary embolism (PE) and for the prevention of recurrent pulmonary embolism (PE) and deep vein thrombosis (DVT). For full prescribing information, refer to the package insert approved by the Medicines Regulatory Authority (MCC). HCR: Bayer (Pty) Ltd, Co. Reg. No.: 1968/011192/07, 27 Wrench Road, Isando, 1609. Tel: 011 921 5044 Fax: 011 921 5041. L.ZA.MKT.GM 06.2017.1808 © Bayer June 2017 *Impact RX Data 2016 NOAC: Non Vitamin K Oral Anticoagulant

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Clinical presentation and outcomes of patients with acute rheumatic fever and rheumatic heart disease seen at a tertiary hospital setting in Port Elizabeth, South Africa Zongezile Masonwabe Makrexeni, Lungile Pepeta

Abstract Background: The incidence of acute rheumatic fever (ARF) and rheumatic heart disease (RHD) has waned in Western countries, however that is not the situation in developing nations. Methods: Records were reviewed of patients from the Eastern Cape municipal districts who presented to the Paediatric Cardiology Unit with ARF and RHD from January 2008 to August 2015. Results: Total of 56 patients with ARF/RHD was reviewed. The majority of patients (n = 52) presented for the first time with RHD. Four patients presented with ARF and two had recurrent ARF. Six patients presented with a combination of RHD and congenital heart disease. Twenty-three patients were operated on for chronic rheumatic valve disease, with good outcomes. Conclusion: The true burden of ARF/RHD is unknown in the Eastern Cape. Prospective studies are needed to accurately determine the prevalence of RHD in this province. Keywords: acute rheumatic fever, rheumatic heart disease, left ventricular dysfunction, rheumatic valve surgery, disease outcomes, prevention Submitted 27/5/16, accepted 4/4/17 Published online 20/4/17 Cardiovasc J Afr 2017; 28: 248–250

www.cvja.co.za

DOI: 10.5830/CVJA-2017-019

Acute rheumatic fever (ARF) is a post-infectious, non-suppurative sequela of pharyngeal infection with Streptococcus pyogenes or a group A beta-haemolytic streptococcus.1 More than one-third of affected children develop carditis, followed by progressive and permanent valvular lesions.2 Devastating complications of rheumatic heart disease (RHD) include severe valvular regurgitation, heart failure, strokes and infective endocarditis, usually affecting both younger school-going children and economically active, child-bearing members of society.3 Industrialised countries have reported the virtual disappearance Paediatric Cardiology Unit, Walter Sisulu University, Port Elizabeth, South Africa Zongezile Masonwabe Makrexeni, MB ChB, FCPaed, mmmaso30@gmail.com

Faculty of Health Sciences, Nelson Mandela Metropolitan University, Port Elizabeth, South Africa Lungile Pepeta, DCH, MB ChB, FCPaeds, Cert. Cardiology, MMed, FSCAI

of RHD.4 The burden of RHD in developed countries declined drastically at the end of the 20th century, largely due to reduced overcrowding and improved sanitation and living conditions.5 By contrast, in developing countries, RHD remains a public health issue and is the principal cause of acquired heart disease in children and young adults.6-8 It is estimated that there are over 15 million cases of RHD worldwide, with 282 000 new cases and 233 000 deaths annually. There was a noticeable decline in cases of ARF/RHD among children under the age of 14 years in a tertiary care hospital in South Africa over a period of 17 years, from 63 cases in 1993 to three cases in 2010.3 It was postulated that the decline was probably due to improved access to medical care for the general population, and the introduction in 1994 of free healthcare to children under the age of six years. This decline was also demonstrated by Smit and co-workers in 2015 in an echocardiography-based prevalence study of RHD in another tertiary care setting in South Africa,9 where the prevalence rate was 4.9/1 000 learners in grades 10 to 12. This was much lower than the 12.2/1 000 clinical prevalence rate reported by McClaren et al. in a similar South African population in 1972.10 Smit et al. postulated that socio-economic and rural development in South Africa have initiated this decline in RHD prevalence in South Africa.9 Although RHD remains a public health issue in developing countries, it appears that in South Africa there has been a decrease in the prevalence of RHD since 1994, compared with earlier studies. However, we need more inclusive, multicentre, prospective studies to confirm the overall prevalence of RHD in South Africa. We therefore conducted a retrospective cohort study to document the clinical presentation and outcomes of patients with ARF/RHD who presented at a tertiary paediatric cardiology referral centre in the Eastern Cape Province, South Africa.

Methods This was a retrospective review of records of paediatric patients presenting with ARF and RHD at Dora Nginza Hospital, Eastern Cape, South Africa, from January 2008 to August 2015 (seven years and eight months). The study was conducted following ethics clearance from the Health Research Ethics and Biosafety committee of Walter Sisulu University and permission from the chief executive officer of Dora Nginza Hospital. Demographic data such as age, gender, origin and clinical presentation of either ARF or RHD, and disease severity and surgical interventions were recorded. The diagnosis of ARF and RHD was based on clinical and echocardiographic evidence of RHD, using the newly revised Jones criteria of the World Heart Federation of 2012.11 In addition, an antistreptolysin O titre

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(ASOT) was performed in all patients as an indication of recent streptococcal infection.12 Disease severity was defined according to the task force on the management of valvular heart disease of the European Society of Cardiology and the ESC committee for practice guidelines.13 The newly revised clinical criteria for the diagnosis of ARF/RHD by the World Health Federation 201211 can be seen in Table 1.

Results A total of 56 patients with ARF and RHD were seen and/or admitted at the Paediatric Cardiology Unit from January 2008 to August 2015. Ninety-three per cent (n = 52) of patients presented for the first time with RHD (all were new patients). The majority (n = 37) of patients in our cohort were from the OR Tambo district of the former Transkei region of the Eastern Cape. The average age at presentation is given in Table 2. Ninetythree per cent of patients (n = 52) were between the age of five and 15 years, and the remainder were below the age of five years (n = 4), with the youngest patient three years old. In terms of clinical disease presentation, most patients (n = 52) presented with chronic RHD. Out of this group, two presented with acute-on-chronic RHD in that, in addition to having echocardiographic evidence of chronic RHD, they had a raised ASOT, fever and raised levels of inflammatory markers (C-reactive protein and erythrocyte sedimentation rate). These patients were aged eight and nine years old. All the patients younger than five years old had ARF diagnosed by the revised Jones criteria.11,12 Six patients presented with a combination of RHD and congenital heart disease (three atrial septal defects, two patent ductus arteriosus and one ventricular septal defect). The most commonly involved valve was the mitral valve, followed by the aortic valve (Table 2). Of the total cohort, only four patients presented with isolated aortic valve disease. Table 1. Newly revised clinical criteria for the diagnosis of ARF/RHD by the World Health Federation 201211 Criteria

Symptoms

Major criteria for the diagnosis of ARF Low-risk population

Carditis (clinical and or subclinical), arthritis (polyarthritis only), chorea, erythema marginatum, subcutaneous nodules

Moderate- and high- Carditis (clinical or subclinical), arthritis (includrisk population ing mono-arthritis, polyarthritis or polyarthralgia), chorea, erythema marginatum, subcutaneous nodules Minor criteria for the diagnosis of ARF Low-risk population

Polyarthralgia, fever (≥ 38.5°C), ESR ≥ 60 mm/h and/ or CRP ≥ 3.0 mg/dl, prolonged PR interval on electrocardiogram

Moderate- and high- Mono-arthralgia, fever (≥ 38°C), ESR ≥ 30 mm/h and/ risk population or CRP ≥ 3.0 mg/dl, prolonged PR interval on electrocardiogram

All patients had assessment of left ventricular function preand post-operatively. Twelve of 23 (52%) patients had dilated left ventricular end-diastolic diameter (LVEDD > 50 mm) pre-operatively. Of those, nine out of 12 (75%) had improved to normal left ventricular end-diastolic diameter (LVEDD < 50 mm) post-operatively (p < 0.05). Six of 23 (26%) patients had left ventricular systolic dysfunction (ejection fraction < 55%) pre-operatively. The mean follow-up time for patients after surgery was six months. Over the study period 23/56 (41%) patients were operated on for chronic rheumatic valve disease. Twelve patients had mitral valve repair, five mitral valve replacement, three aortic valve repair and three double valve (mitral and aortic valve) replacement. The average age at surgery was 11 years. No patients had surgical valvotomy or balloon valvuloplasty. Four patients required re-operation with mitral valve replacement following failed mitral valve repair. A single patient with atrial flutter post operatively, who was treated with amiodarone, had good control of the arrhythmias. Only one patient died in this cohort, and the cause of death was non-cardiac related (suicide).

Discussion A total of 56 patients were reviewed in this study from 2008 to 2015. Of note, the majority of patients in our cohort (n = 37; 66%) were from the OR Tambo district, Eastern Cape. These patients started attending the cardiology clinic at Dora Nginza Hospital from 2012, and were included in the study from 2012 onwards. Our results suggest that RHD continues to be a scourge in children from the OR Tambo district, whereas the disease burden seems to be declining elsewhere in South Africa.3,9 A study done by Cilliers3 in the Chris Hani/Baragwanath Hospital from 1993 to 2010 showed a decline in the number of cases of RF/RHD from 64 in 1993 to three in 2010. This decline in numbers is thought to be due to improved access to medical care in South Africa since 1994. Although we did not have a reference study in our population, we do see more patients than was reported by Cilliers. Smit et al.9 also reported a decline in the prevalence of RHD in the preliminary results of the Wheels-of-Hope outreach programme, with a prevalence rate of 4.9/1 000 leaners in grades 10 to 12 in central South Africa. This was postulated to be due to improved rural and socio-economic development in South Africa since 1994. The majority (93%) of patients in our study were within the expected age range of patients affected by this disease.1 However there were patients younger than five years of age (n = 4) in our cohort. This is in line with the report by Tani et al.14 on children younger than five years who presented with ARF and were diagnosed using the revised Jones criteria.11 In our study, the Table 2. Extent of the valvular disease

Criteria for diagnosis of ARF: two major criteria required, or one major criterion with two minor criteria Echocardiographic diagnosis of RHD Pathological mitral regurgitation Pathological aortic regurgitation

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Defined as jet length > 2 cm in at least one view, velocity > 3 m/s for one complete envelope and a pansystolic jet in at least one envelope Defined as a jet length ≥ 1 cm in at least one view, velocity > 3 m/s in early diastole and pan-diastolic jet in at least one envelope

ESR, erythrocyte sedimentation rate; CRP, C-reactive protein

Extent of the disease Isolated MV regurgitation

Average age at Number (n = 56) diagnosis (years) 31

AV regurgitation

AV regurgitation with AV stenosis

MV regurgitation with MV stenosis MV regurgitation with AV regurgitation

MV, mitral valve; AV, aortic valve.

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median age was four years (range 1.9–4.9 years). This emphasises that even though ARF/RHD commonly presents at between five and 15 years of age, there are cases that present early (under five years) who meet the criteria for the diagnosis of ARF. Regarding clinical presentation, the majority (n = 52; 93%) of our patients presented for the first time with RHD. Only four patients presented with ARF as their first presentation. This may have be due to cases of ARF being missed at the primary healthcare level or patients not presenting early at the clinic with a sore throat. In the Soweto study, Sliwa et al.15 reported on adult cases who presented for the first time with RHD. No patients presented with ARF. This suggests that patients who are not diagnosed early with ARF may present later with established RHD. As a result, they made the suggestion that new cases of RHD should be notified in order to ensure registration and follow up of these patients. Lack of notification of ARF/RHD may result in underreporting. Nkgudi et al. mentioned under-reporting of ARF in their study16 and concluded it was due to poor administration of the ARF notification system. The majority of patients who underwent valvular surgery in our study had mitral and aortic valve surgery. Cilliers reported this as the commonest surgery for RHD.2 Timeous surgery for RHD has very good outcomes.17 A limitation of this study is that it was a retrospective chart audit of patients seen and admitted to one hospital. The fact that these patients were mostly referred from other hospitals made it very challenging to estimate the incidence of ARF/RHD, as there was no primary screening of subjects suspected to have ARF/RHD. Despite the limitations, the findings have important implications. RHD should be notifiable, as the majority of our patients presented with RHD. Prospective studies are required in the Eastern Cape to determine the true prevalence of ARF/RHD.

Conclusion

14. Tani LY, Veasy LG, Minich LL, et al. Rheumatic fever in children

Marijon E, Mirabel M, Celermajer DS, et al. Rheumatic heart disease. Lancet 2012; 379: 953–964.

Cilliers AM. Rheumatic fever and rheumatic heart disease in Gauteng on the decline: Experience at Chris Hani Baragwanath Hospital, Johannesburg, South Africa. S Afr Med J 22014; 104(9): 632–634.

Gordis L. The virtual disappearance of rheumatic fever in the United States: Lessons in the rise and fall of disease. T Duckett Jones memorial lecture. Circulation 1985; 72: 1155–1162.

Essop MR, Nkomo VT. Rheumatic and non-rheumatic valvular heart disease: Epidemiology, management, and prevention in Africa. Circulation 2005; 112: 3584–3591.

Zuhlke LJ, Steer AC. Estimates of the Global Burden of Rheumatic Heart Disease. Global Heart 2013; 8: 189–195.

Zuhlke LJ, Mirabel M, Marijon E. Congenital heart disease and rheumatic heart disease in Africa: Recent advances and current priorities. Heart 2013; 99: 1554–1561.

Seckeler MD, Hoke TR. The worldwide epidemiology of rheumatic fever and rheumatic heart disease. Clin Epidemiol 2011; 3: 67–84.

Smit FE, Botes L, Rossouw S, et al. The prevalence of rheumatic heart disease among Grade 10–12 learners in the Free State and Northern Cape – Preliminary results of the Wheels-of-Hope Outreach Programme. SA Heart J 2015; 12(3): 146–151.

10. McClaren MJ, Hawkins DM, Koornhof HJ, et al. Epidemiology of rheumatic heart disease in black school children of Soweto, Johannesburg. Br Med J 1975; 3(5981): 474–478. 11. Gewitz MH, Baltimore RS, Tani LY, et al. Revision of the Jones criteria for the diagnosis of acute rheumatic fever in the era of doppler echocardiography. A scientific statement from the American Heart Association. Circulation 2015; 131(20): 1806–1818. 12. Jones, TD. Diagnosis of rheumatic fever. J Am Med Assoc 1944; 126: 481–486. 13. Vahanian A, Baumgartner H, Bax J, et al. Task force on the management of valvular heart disease of the European Society of Cardiology, and ESC committee for practice guidelines. Guidelines on the management of valvular heart disease. Eur Heart J 2007; 28(2): 230–268.

The true burden of ARF/RHD in the Eastern Cape Province is unknown and therefore prospective studies are needed to determine the prevalence or incidence of ARF and RHD in this province.

younger than 5 years: is the presentation Different? Pediatrics 2003; 112(5): 1065–1068. 15. Sliwa K, Carrington M, Mayosi BM, et al. Incidence and characteristics of newly diagnosed rheumatic heart disease in urban African adults: insights from the heart of Soweto study. Eur Heart J 2010; 31: 719–727. 16. Nkgudi B, Mayosi BM, Robertson KA, et al. Notification of rheu-

References 1.

Carapetis JR, Sreer AC, Mulholland EK, et al. The global burden of group A streptococcal diseases. Lancet Infect Dis 2005; 5(11): 685–694.

matic fever in South Africa- Evidence for underreporting by health care professionals and administrators. S Afr Med J 2006; 96: 206–208. 17. Finucane K, Wilson, N. Priorities in cardiac surgery for rheumatic heart disease. Glob Heart 2013: 8: 213–220.

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Review Article Primary care in the prevention, treatment and control of cardiovascular disease in sub-Saharan Africa Dike B Ojji, Kim Lamont, Olubunmi I Ojji, Bibiana Nonye Egenti, Karen Sliwa

Abstract Cardiovascular disease (CVD) is the frontrunner in the disease spectrum of sub-Saharan Africa, with stroke and ischaemic heart disease ranked seventh and 14th as leading causes of death, respectively, on this sub-continent. Unfortunately, this region is also grappling with many communicable, maternal, neonatal and nutritional disorders. Limited resources and the high cost of CVD treatment necessitate that primary prevention should have a high priority for CVD control in subSaharan Africa. One major challenge of such an approach is how to equip primary care to respond promptly and effectively to this burden. We present a practical approach on how primary care in sub-Saharan Africa could effectively address the prevention, treatment and control of CVD on the subcontinent. For effective prevention, control and treatment of CVD in sub-Saharan Africa, there should be strategic plans to equip primary care clinics with well-trained allied healthcare workers who are supervised by physicians.

Keywords: cardiovascular disease, treatment, prevention, primary care

Department of Medicine, Faculty of Clinical Sciences, University of Abuja, and Cardiology Unit, Department of Medicine, University of Abuja Teaching Hospital, Gwagwalada, Abuja, Nigeria Dike B Ojji, MB BS, PhD, dikeojji@yahoo.co.uk

Soweto Cardiovascular Research Unit, University of Witwatersrand, Johannesburg, South Africa Dike B Ojji, MB BS, PhD Kim Lamont, MSc, MPhil, PhD Karen Sliwa, MD, PhD

Department of Community Medicine, University of Abuja Teaching Hospital, Gwagwalada, Abuja, Nigeria Olubunmi I Ojji, B Ed, M Ed

Department of Community Medicine, Faculty of Health Sciences, University of Abuja, and Department of Community Medicine, University of Abuja Teaching Hospital, Gwagwalada, Abuja, Nigeria

Submitted 26/4/16, accepted 14/8/16 Published online 18/7/17 Cardiovasc J Afr 2017; 28: 251â&#x20AC;&#x201C;256

www.cvja.co.za

DOI: 10.5830/CVJA-2016-082

The global burden of disease has continued to shift away from communicable diseases to non-communicable diseases, with cardiovascular disease (CVD) taking the lead. The latest Global Burden of Diseases, Injuries and Risk Factors (GBD 2010) study report1 shows ischaemic heart disease (IHD) is the leading cause of disability-adjusted life years (DALYs) worldwide, moving from fourth position in 1990 and increasing in incidence by 29%. The same report also ranks stroke as the third leading cause of global DALYs, moving from the fifth position in 1990 and increasing by 19%. In sub-Saharan Africa, stroke and IHD ranked seventh and 14th, respectively, in the southern region, while they ranked 16th and 20th, respectively, in the western region in 1990. Further projections by the World Health Organisation (WHO)2 indicate that by 2030, cerebrovascular and ischaemic heart disease will overtake HIV/AIDS as leading causes of death in this sub-region. It is further elaborated by WHO statistics that by 2030, both cerebrovascular and ischaemic heart disease will contribute to over 20% of the total deaths and 7% of DALYs in sub-Saharan Africa. In South Africa, cerebrovascular disease is the second commonest cause of death after HIV/AIDS, accounting for about 40% of adult deaths.3 Unfortunately this sub-continent is still grappling with many communicable, maternal, neonatal and nutritional disorders, which remain dominant causes of the burden of disease.1 The health system is therefore overstretched by the existing burden of communicable diseases and a large burden of fastemerging non-communicable diseases, especially CVD. Limited resources and the high cost of CVD treatment suggest that primary prevention should be a priority for CVD control in sub-Saharan Africa.4,5 One of the major challenges of such an approach is how to equip primary care to respond promptly and effectively to this burden. In this article, we present a practical approach on how primary care in sub-Saharan Africa could effectively address the prevention, treatment and control of CVD on this sub-continent.

Bibiana Nonye Egenti, MB BS, MPH

Hatter Institute for Cardiovascular Research in Africa, Department of Medicine, Faculty of Health Sciences, University of Cape Town, South Africa Karen Sliwa, MD, PhD

Primary care approach to the treatment and prevention of diabetes and CVD In spite of the increasing cardiovascular risk burden in sub-Saharan Africa, many healthcare systems in many parts of this

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sub-continent are designed to treat mostly acute communicable diseases, while neglecting the treatment and prevention of non-communicable diseases, especially CVD.6 This is partially due to lack of resources, as the healthcare system in this part of the world is often challenged by lack of sufficient resources and up-todate practical information for healthcare providers.7-9 Another major challenge to treating and controlling CVD is the large rural population, as there are few providers to serve that population, and distances to the facilities are large, thereby increasing transportation costs.10 This is of great concern since the majority of the populace in sub-Saharan Africa resides in rural settings. Therefore, for there to be any meaningful effect in the treatment and control of diabetes and CVD in sub-Saharan Africa, healthcare must be brought closer to the people. The best way to achieve this is to employ a primary care approach, which should not only be involved in prevention and control but also in treatment of patients. For this type of approach to succeed in sub-Saharan Africa where there is a dearth of physicians, it has to be built around a non-physician workforce, including nurses, community health workers and other allied health professionals in the primary care setting.11 In the next section of this review we will discuss the role of the non-physician workforce in this primary care approach. We will also address how the primary care setting can be used to recognise common cardiac problems, such as chest pain, breathlessness on exertion, oedema, palpitations and syncope. The importance of a thorough physical examination as well as relatively simple non-invasive investigations, such as a blood sugar test with a glucometer will be discussed. Furthermore, we will highlight how basic approaches to cardiovascular risk assessment, as developed by the WHO, health professional societies and other expert bodies can be used in the primary care setting. A section of the review will also tackle the important issue of age-appropriate screening for major risk factors, such as hypertension, diabetes mellitus and dyslipidaemia, and address the issue of speciality care referral and long-term primary care management of patients with established CVD and diabetes, using the Seychelles success story.

Non-physician workforce in primary care management of CVD Non-physician health workers can be trained in the simple skills of taking a detailed history from patients and good physical examination with the aid of WHO pocket guidelines for the assessment and management of cardiovascular risk.11 They should be trained on how to use the WHO pocket guide to recognise people with risk factors who have not yet developed clinically manifest cerebrovascular disease. The effectiveness of this type of model has been demonstrated in Rwanda, where non-communicable disease clinics are run at district level, with such clinics staffed by two or three nurses who see 10 to 20 patients each day.12 For effective utilisation of non-physician healthcare workers, they should be trained in the accurate use of basic instruments such as stethoscopes, blood pressure devices, measuring tapes and weighing scales. They should also be able to carry out basic non-invasive investigations such as testing for glucose using a glucometer, testing for albumin in urine using albustix, and

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blood cholesterol testing using strips. In Rwanda and some other sub-Saharan African countries,12 such training is provided at the district level where district hospital leaders, working closely with the staff of healthcare centres, provide in-service training, clinical mentorship and evaluation. Nurses are also trained at district clinics through daily direct patient management while working with physicians. Another model adopted in this training, which has also been used in Rwanda, involves the use of programme leaders in non-communicable diseases (NCDs), neuropsychiatry and infectious diseases (HIV and TB), who form a chronic care team that trains and mentors a group of healthcare centre clinicians in the basic management of non-infectious diseases.12 The main advantage of the use of the programme leader approach is cost effectiveness. In settings such as Rwanda, where there has been success in these training models, training has been formalised into a three-month curriculum in advanced chronic disease management. The effectiveness of such training has been demonstrated in Rwanda where nurses have been trained at the community and district level, not only in basic clinical and laboratory skills, but also in echocardiography for the evaluation of heart failure patients.12 The non-physician healthcare worker should also be trained in how to initiate medications such as thiazide diuretics, betablockers, angiotensin converting enzymes inhibitors, calcium channel blockers, aspirin, metformin, statins and insulin. For example, in a model in Rwanda, heart failure treatment initially takes place in district level NCD clinics with non-physicians using algorithms to make the diagnosis and initiate treatments such as frusemide, spironolactone and angiotensin converting enzyme inhibitors.13 However, in the use of these medications, the place of regular supervision by a trained physician cannot be over-emphasised. For example, in non-physician-based care of heart failure patients in Rwanda, the role of the cardiologist is restricted to supervision and mentoring of district level clinicians, and evaluation of patients who are potential surgery candidates.14 Non-physician clinicians should also be trained to identify serious clinical features in a patient, such as pedal oedema, severe chest pain, and breathlessness on mild exertion and at rest, which are pointers to patients needing referral to secondary and tertiary centres. For example, they should be taught to refer if there are clinical features suggestive of the following: acute cardiovascular events such as heart attack, angina, heart failure, arrhythmias, stroke and transient ischaemic attack, secondary or malignant hypertension, newly diagnosed or uncontrolled diabetes mellitus, and established CVD such as stroke and heart failure. The non-physician can play a large role in the prevention of CVD and diabetes by using the WHO/ISH risk-prediction charts.11 These charts are designed for 14 WHO epidemiological sub-regions and indicate 10-year risk of fatal or non-fatal major cardiovascular events, such as stroke and myocardial infarction, according to age, gender, blood pressure, smoking status, total blood cholesterol level and presence or absence of diabetes mellitus. There are two sets of charts: one set of 14 charts can be used in settings where cholesterol can be measured, while the second set of 14 is for settings where blood cholesterol cannot be measured. Each chart can be used only in countries in the specific WHO epidemiological sub-region. Before the non-physician health worker applies the WHO riskstratification chart, he/she must select the appropriate chart for

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the region. The following information should then be recorded: the presence/absence of diabetes mellitus, gender and age of the patient, history of smoking habits, systolic blood pressure and total cholesterol level. These charts are very useful tools that can help non-physician health workers to identify patients with high cardiovascular risk and motivate them, particularly on lifestyle changes and when appropriate, to take anti-hypertensive or lipidlowering drugs and aspirin. When using these WHO charts, the non-physician health worker must realise that risk stratification is not necessary for making treatment decisions in individuals who belong to the high-risk category, including patients with established CVD, those without established CVD who have a total cholesterol ≥ 8 mmol/l, those with low-density lipoprotein (LDL) cholesterol ≥ 6 mmol/l, those with total cholesterol/high-density lipoprotein (HDL) cholesterol ratios > 8, individuals without established CVD who have persistently raised blood pressure > 160–170/100– 105 mmHg, those with type 1 or 2 diabetes mellitus with overt nephropathy or other significant renal disease, and patients with renal failure and renal impairment.

Cardiovascular risk prevention at the primary care level In sub-Saharan Africa, the levels of some risk factors are still relatively low compared to levels in developed nations. For example, many people in rural settings have low-fat diets, regular physical activity and do not smoke.14 However, the prevalence of other risk factors such as hypertension and diabetes mellitus is of concern; for example, up to 35% of adults aged 25 to 64 years have hypertension.14 To prevent an explosion of the growing risks of CVD in sub-Saharan Africa, there must be interventions at the community level, targeting people who do not have established CVD, by reducing risk factors such as high blood pressure, diabetes mellitus and smoking.15 To prevent an unhealthy diet, the consumption of local fruit and vegetables should be promoted, as well as reduction of intake of salt, refined sugars and animal fat. People should be encouraged to use vegetables and cereals commonly found in their environment. The promotion of moderate physical activity should be encouraging and inactivity discouraged. Control of diet and physical activity will result in reduction in incidences of obesity, hypertension, high cholesterol levels and diabetes mellitus. At the primary care level, hypertension is also preventable through a proper diet and physical exercise. A well-tailored hypertension control programme could detect undiagnosed and unregulated hypertensive individuals and thereby significantly reduce the incidence of stroke, heart failure, renal failure and peripheral vascular disease. This could be achieved through regular awareness campaigns in the media, especially on radio and television, and through organised lectures at primary healthcare centres, out-patient departments of secondary and tertiary health care centres, and in community halls, churches and mosques.

Primary care prevention of CVD: the Seychelles example A national programme on the prevention of CVD was initiated in 199116 in the Republic of Seychelles, which consists of 115

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islands in the Indian Ocean and had a population of 78 846 in 1998. This programme was initiated following an epidemiological survey between 1985 and 1987,17 which showed very high rates of cerebrovascular disease (higher than in most European countries) and medium rates of ischaemic heart disease (similar to those in southern European countries) were prevalent in the country, especially in young and middle-aged men. There was also a high prevalence of the classic modifiable risk factors such as hypertension and diabetes mellitus in the adult population, and a substantial proportion of the children were overweight. The epidemiological survey further attributed the high burden of CVD in Seychelles to dramatic lifestyle changes such as larger consumption of saturated fatty foods, increased intake of salt and calories, and increased prevalence of smoking and sedentary lifestyles.18 The dramatic changes in lifestyle were attributed to accelerated socio-economic development and improved standards of living, with the gross national product (GNP) per capita multiplying by 10 (from 600 US$ to 6 000 US$) within 20 years. Although this programme was started by the Seychelles Ministry of Health-based Unit for the Prevention and Control of Cardiovascular Disease (UPCCD), it progressively involved other sectors such as communities, local parastatals, private companies, international agencies such as the WHO, and academia. The programme was community based, involving non-physician healthcare workers and it was aimed at the promotion of healthy lifestyles and the control of risk factors in the population, in an attempt to prevent and control premature morbidity from CVD, diabetes mellitus and cigarette smoking. The main approaches used in the Seychelles primary CVD programme included: • Campaigns to raise awareness in the country through the use of media, especially radio and television. • Screening of risk factors in schools through the systematic assessment of body mass index, blood pressure, smoking and other lifestyle habits within routine school medical visits administered to all school children aged five, nine, 12 and 15 years. This screening helped for detection and counselling of children with abnormal readings. • Through the World No Tobacco Day programme in the Seychelles, high-profile activities were organised involving large segments of the population, as a main tool for health education on tobacco control. Such events were organised to last several weeks or months, thereby exposing the public to prolonged health education. Although the Seychelles CVD prevention programme initially relied mostly on health-promotion activities, additional emphasis was progressively put on interventions targeting highrisk individuals, and such measures included the following: • Risk-factor screening in public places and work sites were organised, with a good response. Several companies even provided financial support, so that plasma cholesterol could be measured for all their workers, using point-of-care measurements. In order to ensure diagnosis of high blood pressure and to limit the number of referrals to health centres, screening procedures were extended to include follow-up visits along defined protocols for suspected cases of hypertension, diabetes mellitus and dyslipidaemia. • Health clubs were organised at the community level for high-risk individuals, to encourage them to adopt healthy

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lifestyles. Sessions were held at primary healthcare centres or in district community centres and were facilitated by staff from UPCCD, the Nutrition Unit of the Health Ministry and local healthcare centres. The sessions focused mainly on skills needed for the adoption of a healthy lifestyle, including demonstrations of healthy cooking. The need for adherence to prescribed pharmacological agents such as anti-hypertensive and oral hypoglycaemic agents was also emphasised. • A register for hypertension and diabetes mellitus was established in 1997. Doctors of all health centres were requested to update a summary form once a year, which was placed in the inner page of the medical file of all patients with hypertension and diabetes mellitus. The form prompted doctors to record one value per year for all major risk factors, including blood pressure, body mass index, total cholesterol, HDL cholesterol, glucose levels, smoking, previous stroke and myocardial infarction. Clerks who filled in the patients’ medical notes then updated a health centre-based register with the information recorded in the forms. Every year, all health centre registers are electronically compiled into a national register in the Ministry of Health. Summary statistics and selected analysis are fed back to health centres and other relevant offices for information and action. For example, the lists of diabetic patients are sent to ophthalmology departments to promote screening and treatment of eye diseases. Evaluation of the Seychelles primary health prevention programme showed that (1) more than 90% of adults aged 35–65 years were aware of most of the main activities in the prevention programme and a similar high proportion showed good knowledge of CVD; (2) the prevalence of smoking decreased significantly and this was linked to health education and tax increases as a result of strong campaigns against tobacco usage; (3) the active participation of a proportion of the community and the active involvement of key persons and sectors generated a broad coalition among the public, authorities and other organisations that will be very useful in the development of further healthcare interventions and relevant policies; (4) although blood pressure and cholesterol levels increased in the population, it is argued that the levels could have been worse without this intervention programme, bearing in mind the concomitant accelerated socio-economic development.

Lessons for other sub-Saharan African countries from the Seychelles experience There are many lessons for countries in sub-Saharan Africa to learn from the Seychelles experience. • The programme was initiated by the government of Seychelles through the health ministry. Other governments in the subcontinent need to play more active roles in the control and treatment of CVD, while not forgetting about communicable diseases. Governments should realise that they can only get support from other sectors such as private, parastatals, academia and international organisations if they are first seen to be committed. • The Seychelles programme was community based, with healthcare brought to the population at their door steps. For any CVD intervention programme to succeed in the subcontinent, a community-orientated approach must be taken, especially with rural areas where transportation is difficult and

•

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the population struggles to seek medical help in urban and semi-urban health facilities. Primary healthcare centres need to be equipped with trained non-physician personnel and basic tools such as blood pressure apparatus, glucometers, urinalysis strips and point-of-care machines for cholesterol checks. The programme succeeded in the Seychelles because it was non-physician based, involving nurses and community health workers, with physicians playing a supervisory role. For a CVD prevention and treatment programme to be effective in sub-Saharan Africa, nurses and healthcare workers, who can reach people at their homes, must be properly trained and empowered. This is also important in regions where there is a lack of trained physicians. The success of the Seychelles programme can be attributed to good public education. Governments in sub-Saharan Africa need to channel media activities to campaign on the prevention of CVD if we want to curb the coming epidemic. This should be easy in the sub-continent, since much of the media is government owned. The Seychelles has a comprehensive health insurance scheme for the majority of the population, which ensured success of the preventative measures. This type of programme would be difficult in countries where patients pay out of pocket for healthcare. For any such programme to succeed elsewhere, governments would need to implement comprehensive health insurance schemes. There was a good referral system in the Seychelles. Governments would need to develop such a system, flowing from primary to secondary healthcare centres and then to tertiary centres. The Seychelles government was stimulated to embark on the intervention programme as a result of data generated from an epidemiological survey. For countries in sub-Saharan Africa to make any headway regarding prevention of noncommunicable diseases, a non-communicable disease survey is periodically needed in each country.

Suggested model for the prevention and treatment of CVD and diabetes in sub-Saharan Africa In view of the success stories in countries such as the Seychelles and Rwanda, the following model may be useful for the sub-continent, with a little modification to suit each country. Firstly, it should be aimed at both the prevention of CVD and diabetes mellitus, and at detecting and treating high-risk patients. Secondly, it should be coordinated by the non-communicable disease units of the ministries of health. Thirdly, it should be community based and involve non-physician health workers such as nurses, community health officers and allied staff, and be coordinated by a physician. Fourthly, there should be an emphasis on primary care in the rural areas. Primary healthcare centres or clinics should be located near where people live in the rural areas, with a larger comprehensive health centre in the district headquarters, where physicians can supervise the primary health centres. Such primary health centres should be equipped with basic instruments such as weight and height scales, blood pressure apparatus, glucometers, urinalysis strips and strips for cholesterol measurement. The comprehensive health centres should have an electrocardiography machine. They should be attached to a

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general hospital to which referrals can be made, while each general hospital or secondary centre should be attached to a tertiary centre or teaching hospital. Furthermore, there should be annual reports for each primary and comprehensive health centre, and performance should be rewarded. Finally, governments should take the lead and involve the private sector, non-governmental organisations and academia. Such projects require constant funding and support.

Conclusion The high burden of CVD and diabetes mellitus in sub-Saharan Africa means that individual governments must develop strategic plans to equip their primary care clinics with well-trained non-physician healthcare workers and basic instruments, such as blood pressure apparatus, kits for urinalysis, and blood glucose and cholesterol checks if an epidemic of chronic non-communicable diseases is to be averted on the sub-continent. Governments should also set up a referral system whereby there is supervision and referral from primary care to secondary centres, and two to five primary care centres should be attached to a secondary centre. The Seychelles experience shows that the key drivers of effective primary care to yield population-level impacts on diabetes mellitus and CVD include research, a non-physicianbased approach, and integration of the media, the general

population, academia and non-governmental organisations. For such a programme to succeed there must be a holistic framework, developed by the government and coordinated by the NCD unit of the federal ministry of health, as shown in Fig. 1. It should involve research on CVD and diabetes, structured training of non-physician healthcare workers, appropriate equipping of primary healthcare centres and correct referral systems from primary to secondary centres. Limited resources were a disadvantage in the Seychelles programme and would also be in sub-Saharan Africa. This could be overcome with the support of non-governmental agencies and the private sector, however, they would invest in such programmes only if they had confidence in the government of the country.

Key points • CVD plays a leading role in the disease spectrum of subSaharan Africa, with stroke and ischaemic heart disease ranked as seventh and 14th leading causes of death, respectively, on this sub-continent. • Limited resources and the high cost of CVD treatment necessitate that primary prevention should have a high priority for CVD control in sub-Saharan Africa. • For any CVD intervention programme to succeed on the sub-continent, a community-orientated approach must be taken, especially in rural areas where transportation is difficult, deterring people from seeking medical help at urban and semi-urban health facilities. • Primary health centres therefore need to be equipped with trained non-physician personnel who are supervised by physicians, and also with basic tools such as blood pressure apparatus, glucometers, urinalysis strips and point-of-care machines for cholesterol checks.

Functional organisation of PHC services

Supermarket approach

Comprehensive healthcare

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One-stop shop

Determinants This project was supported by award number D43TW008330 from the

• The size and structural set up of the clinic • The availability and competency of nurses • Availibity of equipment and space

Fogarty International Centre. The content is solely the responsibility of the authors and does not necessarily represent the official view of the Fogarty International Centre or the National Institute of Health. Dr Dike Ojji is currently a Research Fellow at the Soweto Cardiovascular Research Unit, University of Witwatersrand, South Africa under the Wits Non-Communicable Disease Research Leadership Programme, funded by

Prerequisite

the NIH (Fogarty) training programme. Dr Kim Lamont was funded by the

PHC team PARC: Productivity, Availability, Responsibility, Competence

Organisational support SITE: Space, Infastructure, Transport, Equipment

Collaboration PHC team, Community, NGOs, Academia

NRF scarce skills award.

References 1.

Murray CJL, Global Burden of Disease study group 2010. Disabilityadjusted life years (DALYS) for 291 diseases and injuries in 21 regions, 1990–2010: a systematic analysis for the Global Burden of Disease study 2010. Lancet 2012; 380: 2197–2223.

Enabling work environment and proper supervision

Mathers CD, Loncar D. Projections of global mortality and burden of disease from 2002 to 2030. PLoS Med 2006; 3(11); e442.

Fig. 1. O rganisational structure showing how primary healthcare can be effective in preventing cardiovascular disease. PHC = primary healthcare. NGOs = nongovernmental organisations.

Opie LH, Mayosi BM. Cardiovascular disease in sub-Saharan Africa. Circulation 2005; 112: 3536–3540.

Expert Committee on Prevention of Coronary Heart Disease. WHO Technical Report Series No 678. World Health Organization, Geneva, 1982.

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edn. Boston MA: Partners in Health, 2011. Available at: http://act.pih.

Chockalingam A, Balaguer-Vintro I, Achutti A, de Luna AB, Chalmers

org/ncdguide.

J, Farinaro E, et al. The World Heart Federation’s white book:

Impending global pandemic of cardiovascular diseases: challenges and

13. Kwan GF, Bukhman AK, Miller AC, Ngoga G, Mucumbitsi J, Bavuma

opportunities for the prevention and control of cardiovascular diseases

C, et al. A simplified echocardiographic strategy for heart failure diag-

in developing countries and economies in transition. Can J Cardiol 2000;

nosis and management within an integrated non-communicable disease

16(2): 227–229.

clinic at district hospital level for sub-Saharan Africa. J Am Coll Cardiol 2013; 1: 230–236.

Yach D, Hawkes C, Gould C, Hofman K. The global burden of chronic diseases: overcoming impediments to prevention and control. J Am Med

14. Cardiovascular diseases in the African region: current situation

Assoc 2004; 291(21): 2160–2622. 7.

and perspectives. Report of the WHO Regional Director, 17 June 15. Stewart S, Sliwa K. Preventing CVD in resource-poor areas: perspec-

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tives from the ‘real-world’. Nat Rev Cardiol 2009; 6: 489–492.

Motala AA. Diabetes trends in Africa. Diabetes Metab Res Rev 2002; 18(Suppl 3): S14–20.

2005. http://www.afro.who.int.

Addo J, Smeeth L, Leon DA. Hypertension in sub-Saharan Africa: A systematic review. Hypertension 2007; 50(6): 1012–1018.

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collaborative long-term programme of reduction of cardiovascular

healthcare for diabetes in Africa. J Cardiovsc Risk 2003; 10: 103–110.

risk factors in the population of the Seychelles. SozPraventivmed 1991; 36(Suppl 1): S30–33.

Goudge J, Gilson L, Russel IS, Gumede T, Mills A. Affordability, avail17.

Bovet P, Perret F, Shamlaye C, Darioli R, Paccaud F. Seychelles Heart Study II: methods and selected basic findings. Seychelles Med Dent J

longitudinal case studies from South Africa. BMMC Health Serv Res

1997; 5; 8–24.

2009; 9(9): 75.

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Gervasoni JP, Bovet P, Shamlaye C, Paccaud F. Guidelines for a

Whiting DR, Hayes L, Unwin NC. Diabetes in Africa. Challenges to

ability and acceptability barriers to healthcare for the chronically ill:

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World Health Organization. Pocket Guidelines for the Assessment and

18.

Bovet P, Shamlaye C, Kitua A, Riesen WF, Paccaud F, Darioli R. High

Management of Cardiovascular Risk. Geneva: WHO, 2007.

prevalence of cardiovascular risk factors in Seychelles (Indian Ocean).

Bukhman G, Kidder A, eds. The partners. In: Health Guide to Chronic

Arterioscler Thromb 1991; 11: 1730–1736.

Care Integration for Endemic Non-Communicable Diseases. Rwanda

Joint PASCAR and Sudan Heart Society African Congress 2017 Khartoum, Sudan 8 to 11 October 2017 www.pascar.org info@pascar.org

“Join us for the next phase in Eradication of Heart Disease at the confluence of the White and Blue Nile”

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ECG Series Reviewing the causes of electrocardiographic pauses Charle Viljoen, Robert Smith, Ashley Chin

Abstract The electrocardiographic term ‘pause’ refers to the prolonged R-R interval that represents the interruption in ventricular depolarisation. This article presents a case of sinus node dysfunction and provides a diagnostic approach to pauses on the ECG. Keywords: ECG, sinus node dysfunction, SA exit block, sinus arrest Cardiovasc J Afr 2017; 28: 257–260

www.cvja.co.za

DOI: 10.5830/CVJA-2017-041

Division of Cardiology, Groote Schuur Hospital and the University of Cape Town, South Africa Charle Viljoen, MB ChB, MMed, FCP (SA), charleviljoen@gmail.com Ashley Chin, MB ChB, FCP (SA), MPhil

Department of Medicine, Groote Schuur Hospital and the University of Cape Town, South Africa Robert Smith, MB ChB

Fig. 1. T he 12-lead ECG is in keeping with sino-atrial exit block.

A 48-year-old man was referred to the Cardiac Clinic at Groote Schuur Hospital for evaluation of suspected symptomatic aortic stenosis. He had a medical history of hypertension, which was well controlled on amlodipine 10 mg and atenolol 50 mg once daily. He had presented with three episodes of syncope in the three months prior to assessment. The syncope was not related to exertion, standing or other specific situations and occurred without any prodrome. He was not troubled by any dyspnoea, and he denied chest pain and any palpitations. Examination excluded severe aortic stenosis. He had regular, good volume pulses, a normal jugular venous pressure and an undisplaced apex beat with normal character. There was a soft ejection systolic murmur, best heard at the lower left sternal border with no radiation. The lung bases were clear. An electrocardiogram (ECG) and echocardiography were performed. Echocardiography showed a normal aortic valve with no evidence of aortic stenosis. The ECG (Fig. 1) showed an irregular rhythm with intermittent pauses. There were no premature complexes preceding the pauses. However, during each of the pauses, there were no P waves at the expected time interval. The R-R interval during the pause was twice the R-R interval before and after the pause.

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Fig. 2. A 24-hour Holter ECG showing an episode of sinus arrest lasting seven seconds (starting just before 3:58:45) and intermittent sino-atrial exit block (just after 3:59:15).

Premature complexes

Premature atrial complex

Premature ventricular complex Sinus node dysfunction

Intermittent ectopic generation

P wave with different morphology and earlierthan-expected P wave Wide QRS with abnormal morphology, not preceded by P wave

Similarly, the P-P interval during the pause was twice that of the P-P interval before and after the pause. These ECG features are in keeping with sino-atrial (SA) exit block. A 24-hour Holter ECG was subsequently done (Fig. 2), which showed intermittent SA exit block and an episode of sinus arrest lasting seven seconds, which did not trigger any escape beats. The patient was diagnosed with symptomatic sinus node dysfunction and an AAIR pacemaker was implanted. The patient has been asymptomatic since.

Intermittent absent generation

Causes of pauses

SA exit block

P-P interval around the pause is a multiple of P-P interval without pause

Sinus arrest

P-P interval around the pause has variable or random lengths

The electrocardiographic term ‘pause’ refers to the prolonged R-R interval that represents the interruption in ventricular depolarisation. The differential diagnosis of a pause with the characteristic feature of each is shown in Fig. 3. In the presence of a pause, one should exclude premature complexes with compensatory pause. If the ectopic beat failed to reset the sinus node, the premature complex would be followed by a compensatory pause, i.e. the R-R interval after the premature complex is longer than the R-R interval between normal sinus beats. A premature atrial complex is recognised as an early P wave with a different morphology from the sinus P wave (Fig. 4), and a premature ventricular complex is the wide QRS complex with abnormal morphology that is not preceded by a P wave (Fig. 5). In the absence of premature complexes, one should determine whether the pause is caused by intermittent absent impulse generation (i.e. sinus node dysfunction) or intermittent absent impulse conduction [i.e. second-degree atrio-ventricular (AV)

2nd degree AV block

Intermittent absent conduction

Mobitz type 1

PR interval before pause longer than PR interval after pause

Mobitz type 2

Regular PR interval, usually followed by wide QRS complex

Fig. 3. A diagnostic approach to electrocardiographic pauses.

Sinus P wave

Compensatory pause

Premature atrial complex different morphology from sinus P wave

Fig. 4. P remature atrial complex with compensatory pause.

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block].1 Sinus node dysfunction refers to the pause in atrial depolarisation, which is either caused by sinus arrest or SA exit block.2 The hallmark of sinus node dysfunction is missing P waves on the 12-lead ECG.3 In SA exit block, the atria fail to depolarise after the SA node discharges, because the impulse cannot leave the SA node. Because the atria do not depolarise, there is no P wave visible on the ECG tracing each time the impulse fails to leave the SA node. The SA node discharge is too small to be seen on a 12-lead ECG, therefore there is no waveform visible during the SA exit block.

The P-P interval during SA exit block is a multiple of the normal P-P interval, because when P waves appear, they occur at their scheduled time (Fig. 6).1,3 In sinus arrest, the SA node does not discharge. If there is no other atrial ectopic that takes over as a pacemaker, there will be no atrial depolarisation, and therefore no P waves will be visible on the ECG for the duration of the sinus arrest. If sinus arrest is long enough, an escape beat or escape rhythm may be triggered, which will manifest as QRS complexes that are not preceded by P waves. In sinus arrest, the pause duration can be variable, and the

Premature ventricular complex wide QRS with abnormal morphology

Compensatory pause

Fig. 5. P remature ventricular complex with compensatory pause.

R-R interval

Pause with absent P wave

P-P interval All P waves are followed by QRS complexes

Fig. 6. Sino-atrial exit block.

Variable RR intervals

Pause with absent P wave

Pauses have variable lengths

Variable P-P intervals All P waves followed by QRS complexes

Fig. 7. Sinus arrest with no escape beats.

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Regular P waves

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Variable PR intervals PR before pause longer than PR after pause

Group beating predictable pauses

Pause with absent QRS

Fig. 8. M obitz type 1 second-degree AV block (Wenckebach).

Pause with absent QRS

Wide QRS (typical bundle branch morphology)

Regular P waves

Regular PR interval

Fig. 9. Mobitz type 2 second-degree AV block.

P-P interval is therefore not necessarily a multiple of the normal R-R interval (Fig. 7).1 In second-degree AV block, the atrial depolarisation intermittently fails to conduct to the ventricles. On the 12-lead ECG, this will manifest as intermittent absent QRS complexes, i.e. more P waves than QRS complexes. Mobitz type 1 second-degree AV block manifests with group beating, with variable PR intervals. The PR interval typically increases in length until the pause, with the PR interval after the pause shorter than the PR interval before the pause (Fig. 8). Mobitz type 2 second-degree AV block has constant PR intervals, with unpredictable loss of conduction of P waves not followed by QRS complexes. The QRS complexes in Mobitz type 2 are typically wide with typical bundle branch morphology (Fig. 9).

patients do not require treatment, patients who are symptomatic are treated by insertion of a permanent pacemaker. Pacemaker therapy does not prolong life but relieves symptoms.4 The authors thank Prof Rob Scott Millar for the ECG examples used in Figs 4–9, from the Rob Scott Millar ECG Library at the Groote Schuur Cardiac Clinic.

References 1.

Millar RS. The ECG Atlas of Cardiac Rhythms. Cape Town: Clinics Cardive Publishing, 2015.

Ferrer MI. The sick sinus syndrome. Circulation 1973; 47(3): 635–641.

Mangrum JM, DiMarco JP. The evaluation and management of bradycardia. N Engl J Med 2000; 342(10): 703–709.

Brignole M, Auricchio A, Baron-Esquivias G, Bordachar P, Boriani G, Breithardt OA, et al. 2013 ESC guidelines on cardiac pacing and

Management of sinus node dysfunction

cardiac resynchronization therapy: the Task Force on cardiac pacing

Management of sinus node dysfunction depends on whether the patient is experiencing symptoms or not. Whereas asymptomatic

(ESC). Developed in collaboration with the European Heart Rhythm

and resynchronization therapy of the European Society of Cardiology Association (EHRA). Eur Heart J 2013; 34(29): 2281–2329.

ECG rhythms CPD CPD developed by Prof Rob Scott Millar, Cardiac Clinic, UCT/Groote Schuur Hospital CPD overview: Following the introductory “Approach to Rhythms”, this online educational CPD quiz will consist of a series of ECGs with a variety of important cardiac rhythms. Each will be accompanied by a series of questions, followed by a detailed analysis and explanation. Target audience: Cardiologists, physicians, emergency unit doctors and anaesthetists. Including those studying for FCP and certificate in cardiology. Total time commitment: ± 30 to 60 minutes. Assessment information: A pass mark of 70% is required. A candidate has 60 days to complete the CPD after registration. CPD certificate: A PDF certificate of completion will be issued on successful completion the CPD. CPD enrollment fee: Free / no charge. Important notice: The CPD was made possible by an unrestricted educational sponsorship from Bayer Pharmaceuticals South Africa, which had no control over the content. Publisher information: This CPD is endorsed by the Cardiovascular Journal of Africa published by Clinics Cardive Publishing.

For more information please visit www.cvja.co.za

Cardiovascular Journal of Africa

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PASCAR Roadmap on Hypertension Roadmap to achieve 25% hypertension control in Africa by 2025 Anastase Dzudie, Brian Rayner, Dike Ojji, Aletta E Schutte, Marc Twagirumukiza, Albertino Damasceno, Seringe Abdou Ba, Abdoul Kane, Euloge Kramoh, Jean Baptiste Anzouan Kacou, Basden Onwubere, Ruth Cornick, Karen Sliwa, Benedict Anisiuba, Ana Olga Mocumbi, Elijah Ogola, Mohamed Awad, George Nel, Harun Otieno, Ali Ibrahim Toure, Samuel Kingue, Andre Pascal Kengne, Pablo Perel, Alma Adler, Neil Poulter, Bongani Mayosi, on behalf of the PASCAR task force on hypertension

Department of Internal Medicine, Yaoundé Faculty of Medicine and Biomedical Sciences, Yaoundé, Cameroon Anastase Dzudie, MD, PhD, FESC, aitdzudie@yahoo.com Samuel Kingue, MD, PhD

Department of Medicine, University of Cape Town, Cape Town, South Africa

Institut cardiologique d’Abidjan, Abidjan, Cote d’Ivoire Euloge Kramoh, MD Jean Baptiste Anzouan Kacou, MD

Department of Medicine, University of Nigeria Teaching Hospital, Enugu, Nigeria Basden Onwubere, MD

Anastase Dzudie, MD, PhD, FESC Karen Sliwa, MD, PhD Bongani Mayosi, MD

Knowledge Translation Unit, University of Cape Town Lung Institute and Department of Medicine, University of Cape Town, Cape Town, South Africa

Hatter Institute for Cardiovascular Research in Africa, Department of Medicine, Groote Schuur Hospital, University of Cape Town, Cape Town, South Africa

Ruth Cornick, MD

Anastase Dzudie, MD, PhD, FESC Karen Sliwa, MD, PhD

Benedict Anisiuba, MD

Division of Nephrology and Hypertension, Department of Medicine, Groote Schuur Hospital and University of Cape Town, Cape Town, South Africa Brian Rayner, MD

Department of Medicine, Faculty of Health Sciences, University of Abuja; Cardiology Unit, Department of Medicine, University of Abuja Teaching Hospital, Gwagwalada, Abuja, Nigeria Dike Ojji, MD

Hypertension in Africa Research Team (HART); MRC Unit for Hypertension and Cardiovascular Disease, North-West University, Potchefstroom, South Africa Aletta E Schutte, MD

College of Medicine and Health Sciences, University of Rwanda, Kigali, Rwanda and African Society of Hypertension (AfSoH) Initiative, Heymans Institute of Pharmacology, Ghent University, Ghent, Belgium Marc Twagirumukiza, MD

Faculty of Medicine, Eduardo Mondlane University, Maputo, Mozambique Albertino Damasceno, MD

Le Dantec University Teaching Hospital, Dakar, Senegal

Department of Medicine, University of Nigeria Teaching Hospital, Enugu, Nigeria National Health Institute, Mozambique and University Eduardo Mondlane, Maputo, Mozambique Ana Olga Mocumbi, MD

Department of Clinical Medicine and Therapeutics, University of Nairobi, Kenya Elijah Ogola, MD

Division of Cardiology, University of Khartoum, Khartoum, Sudan Mohamed Awad, MD

Pan-African Society of Cardiology (PASCAR), Cape Town, South Africa George Nel

Section of Cardiology, Department of Medicine, Aga Khan University Hospital, Nairobi, Kenya Harun Otieno, MD

Division of Cardiology, University of Khartoum, Sudan Ali Ibrahim Toure, MD

Medical Research Council, Cape Town, South Africa Andre Pascal Kengne, MD

Science Advisory Unit, World Heart Federation, Geneva, Switzerland and London School of Hygiene and Tropical Medicine, London, UK

Seringe Abdou Ba, MD

Pablo Perel, MD Alma Adler, MD

Service de cardiologie, Hôpital Général de Grand Yolf, Dakar, Senegal

International Centre for Circulatory Health, Imperial College, London, UK

Abdoul Kane, MD

Neil Poulter, MD

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Abstract Background and aim: The Pan-African Society of Cardiology (PASCAR) has identified hypertension as the highest area of priority for action to reduce heart disease and stroke on the continent. The aim of this PASCAR roadmap on hypertension was to develop practical guidance on how to implement strategies that translate existing knowledge into effective action and improve detection, treatment and control of hypertension and cardiovascular health in sub-Saharan Africa (SSA) by the year 2025. Methods: Development of this roadmap started with the creation of a consortium of experts with leadership skills in hypertension. In 2014, experts in different fields, including physicians and non-physicians, were invited to join. Via faceto-face meetings and teleconferences, the consortium made a situation analysis, set a goal, identified roadblocks and solutions to the management of hypertension and customised the World Heart Federation roadmap to Africa. Results: Hypertension is a major crisis on the continent but very few randomised, controlled trials have been conducted on its management. Also, only 25.8% of the countries have developed or adopted guidelines for the management of hypertension. Other major roadblocks are either government and health-system related or healthcare professional or patient related. The PASCAR hypertension task force identified a 10-point action plan to be implemented by African ministries of health to achieve 25% control of hypertension in Africa by 2025. Conclusions: Hypertension affects millions of people in SSA and if left untreated, is a major cause of heart disease and stroke. Very few SSA countries have a clear hypertension policy. This PASCAR roadmap identifies practical and effective solutions that would improve detection, treatment and control of hypertension on the continent and could be implemented as is or adapted to specific national settings. Keywords: hypertension, roadmap, Africa, prevalence, control, blood pressure, action Submitted 26/5/17, accepted 12/8/17 Cardiovasc J Afr 2017; 28: 261–272

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preventing and controlling non-communicable diseases (NCDs). Target six of the action plan aims to achieve a 25% relative reduction in the prevalence of raised blood pressure or to contain this by 2020, according to national circumstances. State and government heads in the UN Political Declaration are committed to preventing and controlling NCDs through the establishment and strengthening of multi-sectoral national policies and plans. The Pan-African Society of Cardiology (PASCAR) met several times to identify key actions for a hypertension roadmap on the continent. The PASCAR coalition identified several roadblocks hampering the control of hypertension on the continent, which exist at government/health-system, physician and patient levels and include the following.

Government- and health system-related roadblocks • lack of established policies for controlling hypertension • poor political willingness to implement policies on NCDs • poor universal health insurance coverage, leading to out-ofpocket payment by most patients, which leads to poor access and adherence to treatment • lack of policies on antihypertensive medication procurement and distribution, resulting in stock shortages • lack of ad hoc screening and proper referral systems for patients identified at routine screening • inability of governments to effectively work with the private sector, non-governmental organisations (NGOs) and academia in a coordinated plan to tackle the burden of hypertension.

Healthcare professional-related roadblocks • lack of appropriate evidence-based guidelines for healthcare professionals in individual countries • hypertension treatment guidelines are poorly implemented because of a lack of continuing medical education • a dearth of healthcare professionals (physicians, nurses and trained health workers) at primary care level with very low physician/patient ratio • lack of quality and affordable antihypertension medications.

www.cvja.co.za

Co-published in Global Heart

Patient-related roadblocks

DOI: 10.5830/CVJA-2017-040

• poor awareness about hypertension and its consequences • poor adherence to drug therapy because of limited access to medication • difficulty in changing lifestyles, and false health beliefs that hypertension is curable, due to poor patient education.

Executive summary The Word Health Organisation (WHO) estimated that the number of people affected by hypertension is highest in Africa, at about 46% of adults aged 25 years and older, compared to 35 to 40% elsewhere in the world. Many hypertensive Africans are unaware of their status, and are rarely treated or poorly controlled, making them at highest risk for stroke, and heart and renal disease. African Union member states at the 2004 Addis Ababa meeting described hypertension as one of the continent’s greatest health challenges after HIV/AIDS. An urgency was recognised to develop and share best practices, including affordable and effective community-based programmes to screen and treat hypertension. The WHO’s 2013–2020 global action plan calls upon the United Nations (UN) member states to take immediate action in

PASCAR 10-point action plan The PASCAR hypertension task force identified a 10-point action plan, to be implemented by African ministries of health to achieve 25% control of hypertension in Africa by 2025. 1. All NCD national programmes should additionally contain a plan for the detection of hypertension. 2. Allocate appropriate funding and resources for the early detection, efficient treatment and control of hypertension. 3. Create or adopt simple and practical clinical evidence-based hypertension management guidelines.

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4. Annually monitor and report the detection, treatment and control rates of hypertension, with a clear target of improvement by 2025, using the WHO STEPwise surveillance in all countries. 5. Integrate hypertension detection, treatment and control within existing health services, such as vertical programmes (e.g. HIV, TB). 6. Promote a task-sharing approach with adequately trained community health workers (shift-paradigm). 7. Ensure the availability of essential equipment and medicines for managing hypertension at all levels of care. 8. Provide universal access and coverage for detecting, treating and controlling hypertension. 9. Support high-quality research to produce evidence that will guide interventions. 10. Invest in population-level interventions for preventing hypertension, such as reducing high levels of salt intake and obesity, increasing fruit and vegetable intake and promoting physical activity. African ministries of health, in their leadership roles, are called to adopt the 10-point action plan and customise it at a country level using a multi-sectoral approach. PASCAR calls on NGOs, all fraternal organisations, healthcare leaders and other members of the international community to join in this ambitious endeavour to support efforts by African ministries of health in reducing the burden of hypertension in Africa. Effective advocacy towards policy makers and politicians in national governments is particularly encouraged.

Hypertension definitions There is a graded relationship between blood pressure (BP) levels, as low as 115/75 mmHg, and cardiovascular disease (CVD) risk.1 However, hypertension is defined as the BP level

Patient preparation • No caffeine, smoking or alcohol for preceding 30 minutes • A quiet warm setting is required • Bladder and bowel should be emptied • No exogenous adrenergic stimulatns e.g. nasal decongestants or eye drops for papillary dilation • Patient should be calmly seated for 5 minutes If ausculatory method is used, more info on technique can be sought at https://www. youtube.com/watch?v=-LqKmrmaHsk

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above which treatments have been shown to reduce clinical events in randomised trials, which is accepted as ≥ 140 mmHg systolic and/or ≥ 90 mmHg diastolic BP. The classification of BP levels used for defining hypertension is presented in Table 1.

Hypertension burden in Africa Hypertension has progressively become a major threat to the well-being of people in sub-Saharan Africa (SSA). During the past four decades, the highest levels of BP worldwide have shifted from high-income countries (HIC) to low- and middle-income countries (LMIC) in South Asia and SSA.2 The WHO estimates that the prevalence of hypertension is highest in the African region, with about 46% of adults aged 25 years and older being hypertensive.3 This compares to 35% in the Americas and other HIC and 40% elsewhere in the world.3 High hypertension rates, ranging from 19.3% in Eritrea to 39.6% in the Seychelles, were reported for 20 African countries in WHO STEPS (STEPwise approach to surveillance) surveys conducted between 2003 and 2009.4 In a systematic review, the pooled prevalence in over 110 414 participants aged ± 40 years in 33 surveys was 30% (95% confidence interval: 27–34%).5 In Table 1. Definitions of classes of raised blood pressure Category SBP (mmHg) DBP (mmHg) Optimal < 120 < 80 Normal 120–129 80–84 High normal 130–139 or 85–89 Grade 1 hypertension (mild) 140–159 or 90–99 Grade 2 hypertension (moderate) 160–179 or 100–109 Grade 3 hypertension (severe) ≥ 180 or ≥ 110 Isolated systolic hypertension ≥ 140 and < 90 SBP, systolic blood pressure; DBP, diastolic blood pressure

Do not speak during the measurement

Arm supported at the level of the heart Put cuff on bare arm, 3 cm above the elbow Be seated, with back supported by the chair Legs uncrossed Feet supported by the ground

BP measurement • Prepare the patient • Choose the appropriate cuff size • Place the cuff and check that the tightness of the cuff is appropriate • Press the start button • The cuff will inflate and deflate, at the end of the measurement systolic, diastolic BP and pulse rate will be displayed • Record the reading, then deflate the cuff • Repeat the measurement after 1 minute • Take two readings and obtain the average

Fig. 1. P ASCAR recommendations for blood pressure measurement, thresholds and action required following appropriate office measurement.

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Africa, the number of people with hypertension increased from 54.6 million in 1990 to 92.3 million in 2000, and 130.2 million in 2010. Under prevailing circumstances, this could increase to 216.8 million by 2030.6

Gap in the care versus opportunity to control hypertension The PASCAR task force recommends key steps for appropriate office measurement (Fig. 1). BP-lowering strategies that have shown their efficacy in HIC are likely to succeed in Africa. In Table 2, a synopsis is provided of currently published treatment guidelines differing regarding treatment thresholds.

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A simple and practical treatment algorithm using these thresholds is recommended (Fig. 2). Our schedule should consider patient costs (including transport and loss of wages because of time off to attend clinic visits), which affect treatment adherence and burden to the healthcare system. Because of the asymptomatic nature of hypertension, longterm medication adherence is poor. Patients and healthcare practitioners must be educated on non-pharmacological BP control methods (see Fig. 2). We encourage patient education using text messages, e-mails or social media (WhatsApp or Facebook), all of which are progressively available and affordable in Africa. We also encourage face-to-face education by traditional and religious leaders.

Table 2. Blood pressure guidelines

Definition of hypertension (mmHg) Drug therapy in low-risk patients after non-pharmacological treatment (mmHg) First-line therapy

Beta-blockers as first-line drug

WHO PEN1

NICE 20112

ESH/ESC 20133

ASH/ISH 20144

AHA/ACC/ CDC 20135

US JNC 8 20146

South Africa 20157

≥ 140/90

≥ 140/90 and daytime ABPM (or home BP) ≥ 135/85

≥ 140/90

Not addressed

≥ 140/90

≥ 140/90 (high risk) – 150/95 (low risk) and daytime ABPM (or home BP) ≥ 135/85

> 160/100

≥ 160/100 or daytime ABPM ≥ 150/95

≥ 140/90

< 60 years, ≥ 140/90; ≥ 60 years, ≥ 150/90

≥140/90

≥ 140/90 for high risk and ≥ 160/100 for low risk

ACE inhibitor or ARB; CCB; diuretic CCB/diuretic in people of African ancestry

Any of diuretics, betablockers, CCB, ACEIs or ARBs. preferably a thiazide diuretic. In elderly (> 65 years) or in blacks, start with diuretic or CCB.

No (step 3)

No (step 4)

Yes, in specific e.g. young, particularly those with tachycardia

< 55 years, low< 55 years, ACE inhibitor or dose thiazide ACE inhibitor ARB; beta-blocker; diuretic and/or or ARB; ≥ 55 CCB; diuretic ACE inhibitor; years or African ≥ 55 years, CCB ancestry, CCB and/or low-dose thiazide diuretic No

No (step 4)

Thiazides,

Chlortalidone, indapamide

Thiazides, chlortaliThiazides, done, indapamide chlortalidone, indapamide

Thiazides

Thiazides, chlortalidone, indapamide

Thiazide or thiazide-like (indapamide)

Thiazides, chlorthalidone, amiloride or spironolactone

Not mentioned

In patients with markedly elevated BP or patients with high overall CV risk

≥ 160/100

Diuretic + beta-blockers/CCB/ACEIs/ARBs if BP > 170/105

Blood pressure target (mmHg)

< 140/90

< 140/90; ≥ 80 years, < 150/90

< 140/90; elderly < 80 years, SBP 140–150, SBP < 140 in fit patients; elderly ≥ 80 years, SBP 140–150

< 140/90; ≥ 80 years, < 150/90

< 140/90; lower targets may be appropriate in some patients, including the elderly

< 60 years, < 140/90; ≥ 60 years < 150/90

< 140/90

< 150/95 in low-risk patients and in elderly (> 65 years). < 140/90: ≥ 2 risk factors, CKD, TOD < 130/80: HF or CKD when associated with proteinuria > 1 g/24 hours.

Blood pressure target in patients with diabetes mellitus (mmHg)

< 130/80

Not addressed

< 140/85

< 140/90

< 140/90; lower targets may be considered

< 60 years, < 140/90; ≥ 60 years, < 150/90

< 140/90

< 140/90 mmHg or < 130/80 if associated with proteinuria > 1 g/24 hours

Diuretic

Initiate drug therapy with two drugs (mmHg)

Yes (in specific subgroups)

Low-dose diuretic

No (step 4)

Egypt 20138

ABPM, ambulatory blood pressure monitoring; ACC, American College of Cardiology; ACE inhibitor, angiotensin converting enzyme inhibitor; AHA, American Heart Association; ARB, angiotensin receptor blocker; ASH, American Society of Hypertension; BP, blood pressure; CCB, calcium channel blocker; CDC, Centers for Disease Control and Prevention; CKD, chronic kidney disease; CV, cardiovascular; ESC, European Society of Cardiology; ESH, European Society of Hypertension; ISH, International Society of Hypertension; NICE, National Institute for Health and Care Excellence; SBP, systolic blood pressure; TOD, target-organ damage; US JNC 8, Eighth US Joint National Committee; WHO PEN, World Health Organisation Package of Essential Non-communicable disease interventions. 1 World Health Organisation. Implementation tools: package of essential non-communicable (PEN) disease interventions for primary healthcare in low-resource settings. Available at: http://apps.who.int/iris/bitstream/10665/133525/1/9789241506557_eng.pdf. Accessed April 8, 2015. 2 National Institute for Health and Care Excellence. NICE guidelines [CG127]. Hypertension: clinical management of primary hypertension in adults. Available at: www. nice.org.uk/guidance/cg127/chapter/guidance. Accessed April 8, 2015. 3 Mancia G, Fagard R, Narkiewicz K, et al. 2013 ESH/ESC guidelines for the management of arterial hypertension: the task force for the management of arterial hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). Eur Heart J 2013; 34: 2159–2169. 4 Weber MA, Schiffrin EL, White WB, et al. Clinical practice guidelines for the management of hypertension in the community a statement by the American Society of Hypertension and the International Society of Hypertension. J Hypertens 2014; 32: 3–15. 5 Go AS, Bauman MA, Coleman King SM, et al. An effective approach to high blood pressure control: a science advisory from the American Heart Association, the American College of Cardiology, and the Centers for Disease Control and Prevention. J Am Coll Cardiol 2014; 63: 1230–1238. 6 James PA, Oparil S, Carter BL, et al. 2014 evidence-based guideline for the management of high blood pressure in adults: report from the panel members appointed to the Eighth Joint National Committee (JNC 8). J Am Med Assoc 2014; 311: 507–520. 7 Seedat Y, Rayner B, Veriava Y. South African hypertension practice guideline 2014. Cardiovasc J Afr 2014; 25(6): 288–194. 8 The Egyptian Hypertension Society: Egyptian hypertension guidelines. Egypt Heart J 2014; 66(2): 79–132.

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SCREENING

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CLINIC/HOSPITAL

In health centre, clinic, hospital, pharmacy, markets and churches

By physicians and nurses. If ≥ 180/110 mmHg, refer. If < 140/90 mmHg, recheck after 6 months

Systolic BP of 140–159 or diastolic BP 90–99 mmHg without target-organ damage* and no diabetes

Systolic BP ≥ 160 or diastolic BP ≥ 100 mmHg Systolic BP 140–159 or diastolic BP 90–99 mmHg AND diabetes/target-organ damage*

Lifestyle modification** as a trial for 3–6 months. If this fails, consider adding a thiazide or thiazidelike diuretic or long-acting CCB as monotherapy

Combination of two medications preferred: thiazide or thiazide-like diuretic plus ACEI or ARB or CCB, or CCB plus ACEI or ARB” AND lifestyle modifications

Recheck and review readings in 3 months

Recheck and review readings in 4 weeks

BP at goal (< 140/90 mmHg)?

YES

If currently on BP medications optimise therapy or add drug from different classes. If not on BP medications, commence thiazide or thizide-like diuretic

Recheck and review readings in 4 weeks

BP at goal (< 140/90 mmHg)?

Optimise current dosages or add medications from a different class. Also consider adding spironolactone or a vasodilating beta-blocker or a long-acting α-blocker Address adherence, advise on self-monitoring and request readings rom home and other settings.

YES

Encourage patient to carry out self-monitoring and adherence to medications Advise the patient to inform the physician or health centre if he or she notices BP elevation or side effects Patients should be advised to continue office visits 6 monthly as clinically appropriate

Consider referal to specialist if: • Patient with 3 medications (including a thiazide or thiazide-like diuretic) and BP not at goal • Secondary causes suspected • Heart disease, kidney disease, or stroke • BP > 180/110 mmHg

ACEI: angiotensin converting enzyme inhibitors, ARB: angiotensin receptor blocker, CCB: calcium channel blocker *Target-organ damage indicates people with evidence of hypertensive heart disease, stroke or renal disease. In these people and those with diabetes, ACEI or ARBs should be preferred. **Lifestyle modifications include a reduction in weight, a diet rich in fruits, vegetables and low fats, a moderation of alcohol consumption and smoking cessation, a lower sodium intake and a regular aerobic physical activity (at least 30 min per day for at least 5 days per week). We emphasise that this algorithm does not replace the treating healthcare provider’s best clinical judgement.

Fig 2. PASCAR hypertension treatment algorithm

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The discrepancy between best practice (based on highquality evidence) and the care provided in routine clinical practice is called the ‘care gap’. This includes situations in which interventions with proven efficacy are under-utilised. This description is most marked in Africa, where it is favoured by poverty and inadequate utilisation of existing resources. Despite strong evidence of the management benefit, this can reflect as poor awareness and control of CVD rates or risk factors. Current data on awareness and hypertension control rates in SSA are from a wide range of studies differing in methodology and limiting the opportunity for reliable comparisons. However, available data show that the high prevalence of hypertension in Africa, as in other LMICs, is coupled with low awareness and control rates (Fig. 3), a reflection of a maximal care gap.5-8 In 2011, UN member states acknowledged at the highest international level that premature deaths from NCDs reduce productivity and curtail economic growth, causing significant social challenges in most countries.9 In 2015, the previous target of 25% reduction in rate of premature mortality from NCDs by 2025 was extended to a reduction of 33% by 2030, through prevention, treatment and promotion of mental health and wellbeing.10 Since 2004, the African Union, in a pro-active approach, named hypertension one of the continent’s greatest health challenges after HIV/AIDS. After more than a decade, this political enthusiasm, which is crucial for the development and implementation of any healthcare policy, has yet to be translated into public health action. The role of hypertension experts is key to facilitate the states’ action to adequately contain this threat. In a simple and practical hypertension policy, the PASCAR approach emphasises working in collaboration with all other stakeholders to set clear goals and define priority actions and minimum standards of African healthcare systems.

The World Heart Federation roadmap and other relevant initiatives As part of the WHO’s target in reducing heart attacks and stroke by 2025, the World Heart Federation (WHF) launched a

Prevalence 30% (27–34%)

Awareness 27% (7–56%)

Treated 18% (14–22%)

Controlled* 7% (5–8%)

Not aware 73%

Untreated 82%

Uncontrolled 93%

*BP < 140/90 mmHg

Fig. 3. P revalence, awareness, treatment and control of hypertension in Africa. Numbers are from Ataklte et al. Burden of undiagnosed hypertension in sub-Saharan Africa: A systematic review and meta-analysis.5

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roadmap focusing on raised BP during the 2015 World Health Assembly in Geneva.11 Herein the routes are described towards reducing premature cardiovascular mortality rate by 25%,11 focusing on presenting practical steps for hypertension control. For effective hypertension control, four population groups were identified: people who are unaware of their BP status; those who are aware of having raised BP but it is uncontrolled; those who are aware of their raised BP, which is under control; and those who are aware of having normal BP. After identifying the target population, practical steps are provided for improving hypertension management. These include opportunistic screening for awareness of BP status and effective drug treatment for high BP. The use of generic antihypertensive medications rather than proprietary medications is encouraged, to substantially reduce the cost of care, but with a caveat for the need to ensure quality generic medications. Bearing in mind the holistic nature of healthcare delivery, this initiative identified health-system requirements to achieve BP management targets and include human, physical and intellectual resources, healthcare delivery, healthcare recipients, financing, and governance and information systems. With global information technology tools available, the suggestion of using e-health, particularly m-health, for patient education is a very feasible approach in the guidelines. If well applied, this could be a useful tool in hypertension control. This roadmap is anticipated to substantially bridge the gap between HIC and LMIC in terms of hypertension management and control policy. The WHO Package of Essential Non-communicable (PEN) Disease Interventions for Primary Healthcare in Low-Resource Settings is an integrated approach to NCDs focusing exclusively on primary healthcare in low-resource settings.12 The WHF roadmap provides a global framework to reduce CVD mortality, focusing on evidence-based interventions. Strong emphasis is placed on health systems, cost-effectiveness and subsequent evaluation of programmes. Hypertension as a single risk factor, and an entry point to prevent CVD rather than the absolute-risk approach, provides a framework to identify roadblocks in implementing evidence-based interventions. Hypertension seldom occurs in isolation, co-existing with other CVD risk factors, contributing to the absolute-risk status. The PASCAR roadmap strongly emphasises hypertension as a global health crisis and major threat. We hope that hypertension screening will increase in the next eight years, resulting in a paradoxical increase in the prevalence of hypertension. For this reason, the task force’s target is to increase treatment and control rates among the treated subjects by 25% in the SSA region by 2025. We identified roadblocks to the control of hypertension in the African region and proposed solutions to these roadblocks, thus defining the best strategy to achieve this in SSA. Because the epidemic of NCDs is driven by globalisation, urbanisation, demographic trends and socio-economic conditions,13 interventions to reach our targets are required from the health sector and other governmental sectors, along with civil society and the private sector. Therefore, guidance is provided for policy makers, healthcare professionals (nurses, general practitioners, family doctors, internists, cardiologists, nephrologists and other hypertension specialists), patients, the private sector and the public, including

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civil society, on controlling hypertension to reduce premature mortality from CVD. To guide the action of stakeholders, we also highlight the importance of reaching minimum standards (Table 3) for the health systems of countries to achieve the 25% hypertension control target. Implementation of these solutions and suggestions on customising the overall strategy at a country level are discussed. The WHF roadmap provides a general framework that could be useful for LMICs, however, to be implemented it should be customised according to the local context. With PASCAR’s leadership and the contribution of other professional organisations, this approach seems to be at the right time to turn the many hypertension challenges in Africa into immense opportunities. Although population-based strategies for lowering BP may be cost-effective, they are not the focus of this roadmap, but we recognise these would be beneficial.

Methods In January 2014, panel members who were appointed to develop the PASCAR roadmap were invited to join the PASCAR task force on hypertension. Based on their expertise and leadership in hypertension, 41 nominees from 21 countries received invitations, with 95% responding positively. These experts included cardiologists, nephrologists, public health physicians, researchers (including clinical trialists), nurses, pharmacologists, evidence-based medicine specialists and guideline developers. During the first face-to-face meeting held in Nairobi on 27 October 2014,14 the group acknowledged the lack of a continental strategy to address the hypertension crisis. A decision was taken to develop a roadmap for the prevention and management of hypertension in Africa as a matter of urgency under the auspices of the WHF. To customise the WHF BP roadmap for Africa, the core group performed a comprehensive literature search and communicated with the WHF from November 2014 to July 2015 via teleconference and e-mail. After receiving and comprehending the WHF roadmap document, task force members held a second face-to-face meeting in London on 30 August 2015, to make suggestions on its relevance and customisation. A detailed presentation of this roadmap was reviewed and discussed by PASCAR task force members, hypertension experts and leaders of hypertension societies via e-mail, with WHF feedback. Development of a warehouse for African guidelines and clinical trials on hypertension was also reviewed. Finally, the steps in developing the African roadmap for reducing CVD mortality rates through BP control was planned. The first draft of the PASCAR roadmap for hypertension management and control was presented in Mauritius on 4 October 2015. Attendees were 13 presidents of national cardiac societies or representatives, the president of the International Forum for Hypertension Control and Cardiovascular Disease Prevention in Africa and representative of the International Society of Hypertension, a representative of the African Heart Network, members of the PASCAR task force on hypertension, and scientists from the WHF. The draft was reviewed and oral and e-mail comments were received from participants. The WHO PEN programme12 was compared with the PASCAR hypertension roadmap to ensure complementarity between the two documents.

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Table 3. Minimum care for hypertension management at each healthcare level in Africa Basic staff, equipment, test and medication

Level of care Primary Secondary Tertiary Trained health Medical worker or nurse Practitioner Specialist

Basic equipment Automated blood pressure devices, or calibrated sphygmomanometer, either +++ +++ +++ mercury or oscillometric plus appropriate cuffs Home blood pressure + +++ devices Ambulatory blood +/– +++ pressure devices Tape measure for waist +++ +++ +++ circumference Scale for weight +++ +++ +++ Stadiometer for height +++ +++ +++ Standard 12-lead ECG ++ +++ Glucometer + +++ +++ Funduscope ++ +++ Stethoscope +++ +++ +++ Basic tests Urine dipsticks for +++ +++ +++ protein, blood and glucose Standard 12-lead ECG ++ +++ recording Glucometer strips for + +++ +++ testing glucose + + Na , K and creatinine + ++ +++ with calculation of eGFR Cholesterol + +++ Glycated haemoglobin + ++ +++ (HbA1c) Chest radiograph +/– +++ Basic medication classes with examples* Thiazide or thiazide-like diuretic (hydrochloro+++ +++ +++ thiazide, indapamide, chlorthalidone) Calcium channel blockers (amlodipine, nicardipine, +++ +++ +++ long-acting nifedipine) Angiotensin converting enzyme inhibitor + +++ +++ (enalapril, lisinopril, perindopril, ramipril) Angiotensin receptor blockers (candesartan, +++ +++ valsartan, losartan) Vasodilating beta-blockers (nebivolol, bisoprolol, +++ +++ carvedilol) Spironolactone +++ +++ Long-acting α-blocker + + (doxazocin) Combinations of blood pressure-lowering + +++ +++ medications +++: strongly recommended; ++ moderately recommended, +: recommended; –: not done; +/–: done if facilities are available. *Availability of drugs at each level of care has been indicated and recommended here for initiation only, all drugs can be used once initiated by a medical practitioner. A trained healthcare worker may initiate and follow up some medication.

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The second version of the roadmap draft was submitted to a core group for internal review from October to December 2015. In March 2016, a selected group of hypertension experts from 12 French-speaking countries met in Yaoundé to discuss the algorithm and the draft.15 Comments were received and the draft was amended. The task force reviewed the final draft of the roadmap in Mexico in June 2016, which was then submitted for external peer-review by three independent experts in hypertension and policy development. The subsequent review was done by a group of experts in cardiology, nephrology, primary care and research (including clinical trials). Comments were reviewed and discussed by the panel and incorporated into a revised and final document.

PASCAR searches and surveys on the status of hypertension policy programmes and clinical practice guidelines From May to July 2015, an internal PASCAR survey was conducted, aiming to determine which African countries ran hypertension control programmes focusing on policy. Using the Survey Monkey software tool,16 national hypertension experts from 40 countries were asked whether a hypertension policy programme was operating in their country and could be judged as being ‘dormant’, ‘not much active’, ‘active’, or ‘very much active’. Among the responders (n = 127) representing 27 SSA countries, we noticed that up to 63.7% did not have a hypertension policy programme or that it was dormant or not very active. This regrettable situation highlights the importance of a continental initiative to develop a hypertension policy to address BP control from a population-wide and high-risk approach. Evidence has shown that explicit clinical practice guidelines (CPGs) do improve the care gap by providing practitioners and health-service users with synthesised quality evidence regarding

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decision-making.17 In another PASCAR study, we assessed the existence, development and use of national guidelines for the detection and management of hypertension in the African region, regardless of quality. Between May and July 2015, CPGs for hypertension were searched, using a scientifically developed search strategy. Searches were done using Google and PubMed. Search terms included (country name) AND (hypertension OR HTN OR high blood pressure) AND (clinical practice guidelines OR treatment guide). French, Portuguese and Spanish translations were included in the search strategy. Websites of ministries of health, national medical associations and the WHO were hand-searched, authors were e-mailed, and requests were sent on Afronets to obtain copies of CPGs for hypertension. To be included in the search, the CPGs had to be available and provided in full-text versions for assessment by the review team, comprising three independent authors. CPGs from Europe or South America or those that could not be obtained were considered non-existent. Two national hypertension experts were contacted for confirmation on countries for which we could not find CPGs on hypertension. CPGs published in peerreviewed journals needed to be readily accessed by end-users. E-mail messages were used for further clarification. In Fig. 4, the 2015 map is presented of countries with clear evidence of the existence of national guidelines for detection and management of BP across Africa. Only 16 (25.8%) out of 62 countries had CPGs complying with our search criteria. No evidence of CPGs on hypertension management could be found for the other 46 (74.2%) countries. Given that the only existing multinational expert recommendations for the management of hypertension in Africa dates back to 2003 and has not been updated since,18 we concluded that there is a legitimate, pressing need to support African ministries of health with a clear hypertension roadmap.

PASCAR roadmap to decrease the burden of hypertension in Africa

Fig 4. 2 015 map of African countries with evidence of existing clinical practice guidelines for hypertension management and 10 actions to reduce the hypertension burden in Africa

To reduce the incidence of CVD through treating hypertension in the African region, it will be necessary to increase the rates of detection, treatment and control of the disease. The 10 actions that need to be undertaken by African ministries of health to achieve a 25% control of hypertension in Africa by 2025 (Fig. 4) are listed below and we include an explanation as to why (bullets) and how (dashes) this needs to be done. 1. All NCD national programmes should additionally contain a plan for the detection of hypertension. • The hypertension crisis has yet to receive an appropriate response in SSA.19 • Incidence of hypertension increased by 67% since 1990 and was estimated to cause more than 500 000 deaths and 10 million years of life lost in 2010 in SSA.20,21 • Hypertension is the main cause of stroke, heart failure and renal disease in SSA. • Stroke, which is a major complication of uncontrolled hypertension, has increased to 46% since 1990 and essentially affects breadwinners.20 • Failure to control hypertension and its economic repercussions through revising health policies and services endangers the economic prosperity of all African nations.22

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–– All SSA countries should have adopted and should follow the WHO global agenda of reducing NCDs by 2020. –– When reporting to the Ministry of Health and the WHO, stakeholders should report specifically on hypertension. –– National cardiac and hypertension societies should monitor the prevalence, awareness and control rates of hypertension and report to PASCAR. –– Government, private sector, academia and community organisations should pay attention to this report and work together for a reduction in hypertension prevalence. 2. Allocate appropriate funding and resources for the early detection, efficient treatment and control of hypertension. • The costs of priority interventions for NCDs, including hypertension, have been shown to be small and countries are receiving global funds. • No new global funding is needed to implement the 10 actions for controlling hypertension. • Comprehensive implementation to control hypertension and reduce salt intake is affordable in all countries. • The current increasing burden of uncontrolled hypertension is a barrier to the development of all African nations. • Funding to support civil society and health organisations will contribute to developing and implementing appropriate health policies to control hypertension. • Funding is needed to support dissemination of best practices to detect, manage and control NCDs within Africa. –– Increase healthcare budgets in Africa to align with the WHO global action plan of 2013–2020, which has already been adopted by all SSA countries. –– Realign existing funding with the emerging hypertension threat that SSA populations are experiencing. –– Dedicate a clear percentage of the health budget to hypertension policy. –– Use existing resources more efficiently. –– Develop innovative funding mechanisms, including additional alcohol and tobacco taxes. –– National cardiac and hypertension societies should monitor the hypertension/NCD-related budget every two years and advocate otherwise for improvement. 3. Create or adopt simple and practical clinical evidence-based hypertension management guidelines. • The role of simple and practical guidelines is crucial for managing NCDs at large, and hypertension specifically. • In 2015, only 25% of SSA countries had developed or adopted clinical guidelines for managing hypertension (Fig. 4). • New scientific knowledge guides implementation and efficiency in developing guidelines according to the best actual practices. –– PASCAR will develop and regularly update continental guidelines with a simple care algorithm (Fig. 2) for detecting, treating and controlling hypertension. National cardiac societies are called upon to adopt or adapt to the country’s circumstances where appropriate. –– Alternatively, the WHO HEARTS technical package for CVD management in primary healthcare overtakes WHO PEN12 and provides a comprehensive CVD

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control approach,23 with the possibility of integrating hypertension as a risk factor. –– PASCAR has defined and will regularly update the minimum standards (Table 3) to control hypertension, which need to be achieved by each SSA country. Countries are called upon to adopt and implement these. 4. Annually monitor and report the detection, treatment and control rates of hypertension, with a clear target of improvement by 2025, using the WHO STEPwise surveillance in all countries. • The success of all NCD interventions, including hypertension policy, will depend on how specific, measurable, achievable, realistic and time-bound the objectives are. • A framework for national and continental monitoring, reporting and accountability will ensure that the returns on investments in hypertension and other NCDs meet the expectations of all partners. –– The WHO STEPwise approach to NCD risk-factor surveillance should be strengthened in all African countries to report on detecting, treating and controlling hypertension annually. –– BP to be measured at all relevant clinical encounters.   –– Regular representative population surveys are effective in monitoring trends of key risk factors and the uptake of priority interventions, such as the WHO STEPS approach to monitor NCD risk factors. –– National cardiac and/or hypertension societies should measure the level of coverage for some sentinel sites (communities, industries, primary healthcare centres, etc.) and report to PASCAR. –– National cardiac and/or hypertension societies should take responsibility for reporting progress in hypertension control, mobilising resources, developing policy and identifying best practices. –– The monitoring and reporting team in sentinel sites will ensure that people know their BP, hypertensives receive appropriate treatment, BP is controlled and they remain on treatment. 5. Integrate hypertension detection, treatment and control within existing health services, such as vertical programmes (e.g. HIV, TB). • What the medical community learned from the large-scale management of TB and HIV/AIDS should be successful in managing hypertension. –– The government, private sector, academia and community organisations should work together to align plans for detecting, treating and controlling hypertension with other ongoing programmes. –– Emphasis should be placed on (1) standardised treatment protocols, (2) identification and availability of affordable and effective drugs, and (3) service delivery, as with TB and HIV programmes. 6. Promote a task-sharing approach with adequately trained community health workers (shift-paradigm). • SSA carries 11% of the world population, 25% of the global burden of disease, with only 3% of the world’s health labour force, and has a global health expenditure of less than 1%.24 • These health-worker shortages are a major barrier to controlling hypertension in Africa.

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• Clear evidence exists that health staff without formal professional training can be adequately trained to effectively detect people with severe hypertension.25 • Using trained community health workers (CHW) to detect hypertension would free health professionals in Africa to treat and control the condition. • Well-trained nurses, general and family physicians can adequately manage uncomplicated hypertension, freeing specialists for more severe cases. –– Design a course to train CHW in detecting hypertension, providing information and educating the community. –– Train 250 000 CHW to detect hypertension by 2025. –– Design special courses reinforcing health staff capacity to manage hypertension. –– Use an online system to train at least 50 000 certified nurses and 25 000 certified general physicians to take appropriate decisions regarding detecting, treating and controlling hypertension by 2025. –– PASCAR and national cardiac societies will design the course, and national recertification may be required after training. 7. Ensure the availability of essential equipment and medicines for managing hypertension at all levels of care. • Target 8 of the global action plan acknowledges the need to improve the availability of affordable BP machines and medicines for the poor.26 • Target 9 of the global action plan is an 80% availability of affordable basic technologies and essential medicines, including generics, required to treat major NCDs in public and private facilities.26 • Access to affordable and good-quality drugs for hypertension is important for all LMICs, and especially SSA.26 –– Governments and societies should be willing to prioritise hypertension control and provide low-cost BP machines and medications. –– PASCAR and national cardiac and hypertension societies have adopted a hypertension treatment algorithm, suggesting the use of high-quality antihypertensive medications (Fig. 2). –– The ongoing randomised clinical trial, Comparing Three Combination Therapies in Lowering Blood Pressure in Black Africans (Creole), will provide more evidence-based information on the most efficacious of three ‘free’ combinations of two antihypertensive agents on 24-hour ambulatory systolic BP.27 –– PASCAR has defined minimum standards for BP machines and drug availability and affordability to control hypertension in Africa (Table 3). –– PASCAR and national cardiac and hypertension societies should strongly advocate making antihypertensive medications available and more affordable to patients. –– Governments should encourage adding to and periodically updating the hypertension medications on their national essential medicine list. –– Governments should subsidise the cost of and remove import duties on these essential medications. –– Governments should put in place an efficient, highquality monitoring process of medicines.

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–– Donor organisations and pharmaceuticals should be engaged in making these medications affordable. –– PASCAR will regularly measure the proportion of the population with access to affordable, essential drugs in sentinel sites. 8. Provide universal access and coverage for detecting, treating and controlling hypertension. • There are proven cost-effective lifestyle and medical interventions to prevent and manage hypertension. However, in Africa, uptake is still unacceptably low.3 • Universal health coverage will be the main step forward to ensure that persons with hypertension have access to effective, affordable and accessible care. –– Governments must have the political will to acknowledge the hypertension crisis, and the commitment to convince their parliaments to approve budgets needed for universal coverage. –– Failure to implement universal coverage may result in increased healthcare expenditure on the complications of hypertension. 9. Support high-quality research to produce the evidence that will guide interventions. • Data from randomised, controlled trials on hypertension management are lacking in SSA. • Research is vital in formulating a sound healthcare policy to evaluate the performance of interventions in hypertension control and take managerial decisions in the overall NCD policy.28 • Research into hypertension in Africa should be essential, especially where it can inform resource-allocation decisions. –– African governments should encourage all multidisciplinary, multidirectional and collaborative approaches at national and international levels, and take a firm commitment to develop research guided through priority intervention, as suggested by the WHO.26 –– National cardiac and/or hypertension societies should take responsibility for identifying research priorities, building national and international research networks and partnerships, and advocating for investment in research to support best practices. –– PASCAR, with its good continental research network, will continue taking the leadership for research training and funding while ensuring to develop and sustain research activities to guide cost-effective interventions for hypertension control. 10. Invest in population-level interventions for preventing hypertension, such as reducing salt intake and obesity levels, increasing fruit and vegetable intake and promoting physical activity. • The relationship between BP and the risk of developing stroke or heart disease is ongoing, starting at a systolic pressure > 115 mmHg.1 • Hypertension is a preventable cause of morbidity and mortality. • High-quality evidence in non-acutely ill adults shows that reduced sodium intake reduces BP.29 • These two previous facts highlight the importance of highrisk and population-based strategies in BP management and control.

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–– Therefore, advocate for a healthy public policy and large national programme for hypertension prevention and control. –– Use national multi-sectoral policies and plans that specifically address physical activity and nutrition, including dietary salt, in preventing hypertension and NCDs. –– Wider implementation of successful governmental actions including smoke-free policies, marketing of unhealthy foods and alcohol, sin taxes (e.g. sugar taxes), and regulation of sodium content in processed foods.

How to adapt the PASCAR 10 actions at country level This roadmap can be implemented as is or adapted to overcome local barriers and develop solutions that are more relevant to specific national settings. In the latter case, we recommend that national roadmaps be developed, using a multi-sectoral approach in collaboration with inter-governmental organisations, heart health advocacy foundations, cardiovascular scientific organisations, healthcare leaders, providers from primary and specialised care, private-sector stakeholders and people affected by CVD. Effective advocacy towards policy-makers and politicians in national governments is mandatory for success. Screening among politicians might be an effective way to increase awareness and encourage governments to act. The PASCAR task force recommended the following steps: • Step 1: where applicable, national cardiac societies (otherwise national hypertension societies or cardiovascular specialists) should take the leadership to develop and convene a multisectoral coalition against hypertension. At this step, persuading the government and all other stakeholders to collaborate is essential. • Step 2: this coalition will then assess the epidemiological profile of hypertension and review and synthesise existing official data and published and unpublished literature. This step also includes a map of all existing policies. • Step 3: the coalition conducts policy dialogues with multiple local stakeholders. Local problems, specific barriers to hypertension control and potential solutions should be discussed and appropriate strategies selected according to context. At this step, it is important to understand existing policies and their current effect. Within the same nation, appropriate strategies may also need adaptation. Some stakeholders who will be invited to the policy dialogue include the ministry of health, various health sector staff (physicians and non-physicians), health workers, key opinion leaders such as politicians and religious people, and also alternative medicine specialists and traditional healers, who may have a significant influence on people with hypertension in some settings. • Step 4: the coalition develops a clear national strategy and time-bound plan for detecting, treating and controlling hypertension. The PASCAR coalition against hypertension takes responsibility for fostering the development of national roadmaps and supporting national cardiac and hypertension societies at all levels.

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Conclusions Although there is significant scientific evidence that costeffective lifestyle and medical interventions could control hypertension and prevent health-threatening complications, such as heart disease and stroke, the African region still bears a very high disease prevalence, coupled with poor rates of detection, treatment and control. This context is a barrier to the achievement of the universal global action plan and gives reasons for urgent action. The PASCAR task force on hypertension roadmap was conceived by a variety of leaders and stakeholders in the field to provide the most appropriate strategy to have 25% control of hypertension by 2025. The roadmap identifies major barriers to disease control and priority areas of intervention, and 10 actions to improve the control of hypertension by 2025 are proposed. The most important steps to put forth in this continental roadmap include: 1. Advocate for government leadership and policy. 2. Allocate funding and resources. 3. Design simple and practical guidelines. 4. Promote large-scale screening. 5. Integrate hypertension detection, treatment and control in all existing programmes. 6. Promote task sharing and expand the scope of practice. 7. Promote the use of inexpensive, good-quality BP machines and generic medications. 8. Promote universal coverage for hypertension diagnosis and management. 9. Support high-quality research to produce the best evidence for interventions. 10. Invest in population preventive measures. This is a unique moment in history for the African CVD community to have worked with global leaders in the field in defining a clear agenda to address the hypertension crisis. Support for this programme from the African Union and all stakeholders will help achieve the WHO global action plan of 2013–2020 for NCD reduction, specifically focusing on heart attack, stroke and other CVDs. The WHO and other UN organisations will support national efforts with upstream policy advice and sophisticated technical assistance, ranging from assisting governments to setting national targets in implementing relatively simple steps, which can make a huge difference. Our sincere thanks go to all fraternal organisations, including the WHF, the International Forum for Hypertension Control and Cardiovascular Disease Prevention in Africa, the Africa Heart Network, and all national cardiac societies for supporting this initiative. We are grateful to the Clinical Research Education, Networking and Consultancy for co-drafting the manuscript and providing first versions of some figures and tables, and all the reviewers for providing useful feedback. We also thank all members of the PASCAR task force on hypertension who worked on this project and provided feedback throughout the roadmap development, and all other partners who provided support. Dr Poulter’s institution has received grant support for research in hypertension from Pfizer and Servier and he has received speaker honoraria from AstraZeneca, Lri Therapharma, Napi and Servier. All other authors report no relationships that could be construed as a conflict of interest. The project was fully funded by PASCAR. The Pan-African Society of Cardiology received unrestricted educational grants from Servier and AstraZeneca.

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Conference News Illuminating the pathway for the next generation of cardiovascular medicine practitioners and researchers: Highlights of the Joint PASCAR–SCC clinical symposium on hypertension and heart failure, Cameroon Martin H Abanda, Anastase Dzudie, Ba Hamadou, Yves Monkam, Henry Luma, Marie Solange Douala, Loryane Nganhyim, Bonaventure S Dzekem, Theophile N Nana, George Nel, Ana O Mocumbi, Simon Stewart, Karen Sliwa, Eugene Belley Priso

Abstract The Pan-African Society of Cardiology roadmap aims to achieve a 25% control of hypertension by the year 2025. Whether this is attainable or not depends largely on the capacity of healthcare providers and policy makers to address the rising prevalence of hypertension and its complications, including heart failure. Task sharing is fundamental in optimising hypertension control. The Clinical Research Education, Networking and Consultancy (CRENC) engaged with the Pan-African Society of Cardiology (PASCAR) and the Cameroon Cardiac Society (SCC) in a joint hypertension and heart failure symposium at the Douala General Hospital in 2016. The primary aims were to foster clinical research in cardiovascular medicine by raising awareness on cardiovascular diseases, to provide evidence-based training of an international standard, to encourage the conduction and dissemination of high-quality research, and to build programmes for continuing medical education. The secondary aim was to potentiate

Clinical Research Education, Networking and Consultancy (CRENC), Douala, Cameroon Martin H Abanda, MD Anastase Dzudie, MD, PhD, FESC, aitdzudie@yahoo.com Loryane Nganhyim, MD Bonaventure S Dzekem, MD

Faculty of Medicine and Biomedical Sciences, University of Yaoundé 1, Cameroon Anastase Dzudie, MD, PhD, FESC, Ba Hamadou, MD Henry Luma, MD Marie Solange Douala, MD Eugene Belley Priso, MD

Douala General Hospital, Douala, Cameroon Anastase Dzudie, MD, PhD, FESC Yves Monkam, MD Henry Luma, MD Marie Solange Douala, MD Theophile N Nana, MD Eugene Belley Priso, MD

the 2nd Douala Research and Scientific Days. The symposium, which featured didactic lectures interspaced with oral/poster abstract presentations and a clinical visit, culminated in the launching of the book Heart of Africa, and the Young Investigator award. It is hoped that these served to capacitate existing cardiovascular structures, breed the next generation of cardiovascular physicians and researchers, and imprint a trail of clinical research excellence to be emulated in Cameroon and beyond. Sub-Saharan Africa bears about 80% of the global burden of cardiovascular disease (CVD).1,2 As the leading continental cardiovascular society, the Pan-African Society of Cardiology (PASCAR) has identified hypertension as the key area of priority action to reduce the burden of CVD in Africa. Shifting paradigms through task sharing has been highlighted among the 10 pillars to beat hypertension in Africa.3 Aligned with these strategies, the Clinical Research Education, Networking and Consultancy (CRENC) engaged with PASCAR at the Joint

Pan-African Society of Cardiology Anastase Dzudie, MD, PhD, FESC George Nel Ana O Mocumbi, MD Karen Sliwa, MD

Cameroon Cardiac Society Anastase Dzudie, MD, PhD, FESC Ba Hamadou, MD Yves Monkam, MD

Instituto Nacional de Saúde, and Eduardo Mondlane University, Maputo, Mozambique Ana O Mocumbi, MD

Mary Mackillop Institute of Health Research, Australian Catholic University, Australia Simon Stewart, MD

Hatter Institute of Cardiovascular Research, University of Cape Town, Cape Town, South Africa Karen Sliwa, MD

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PASCAR–SCC seminar on hypertension and heart failure at the Douala General Hospital (11–12 October 2016), supported by the National Institutes of Health (NIH) Fogarty International Center (Advancing Science for Global Health). Over 300 participants, including experienced, mid and early medical scientists, both national and international, were invited to discuss the science of hypertension and heart failure. This consisted of didactic lectures, abstracts (10 oral, 12 posters), a clinical visit and more than 50 oral communications for a target audience of about 300 participants. International faculty consisted of experts from the PASCAR task force on hypertension and heart failure and the Mary McKillop Institute for Health Research: Center for Research Excellence for reducing inequalities in cardiovascular disease burden at the Australian Catholic University (ACU). These experts were Profs Karen Sliwa, Simon Stewart and Ana O Mocumbi, Drs Dike Ojji and Kemi Tibazarwa, George Nel and Ms Ashley Kimberley Keates.

Pre-meeting activities: (9 October: pacemaker marathon; 10 October: mass media conference) These activities were aimed at increasing public and policy makers’ awareness on cardiac disease in general, as well as narrowing the gap between pacemaker needs and safety, and the current status of pacemaker implantation in Cameroon. There was a pacemaker marathon involving people with implanted pacemakers under close monitoring, and the launching of the ‘Pace4life Cameroon’ project.

Day 1: Joint PASCAR–SCC clinical symposium on hypertension and heart failure The opening ceremony was chaired by Dr Yves Monkam who offered a word of welcome to all participants and highlighted the importance of such an event for the advancement of medicine and research. He also commended young physician-researchers whose abstracts were accepted for presentation. The first part of this symposium was the PASCAR and Medtronic pacing and heart-failure training session, which was chaired by Drs Félicité Kamdem, Yves Monkam, Archange Nzali

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and Anastase Dzudie. Dr Loryane Nganhyim (CRENC affiliate) presented the LOng-TErm Prognosis of Patients with clinical indication for a cardiac Pacemaker Implantation (LOTEPPI) study, in which only about one in two patients had access to cardiac pacemakers but three in four patients with cardiac pacemakers had improved quality of life and likelihood of survival over three years. Re-using recycled cardiac pacemakers was suggested as an affordable alternative to new pacemakers in resource-limited settings such as Cameroon. Ms Kimberley Keates (Australia) gave a talk on the epidemiology of CVD in Africa. She highlighted that CVDs are common and that all regions in Africa are affected. However a major challenge remains the paucity of data, which limits detailed analyses of the spectrum and burden of CVD. Prof K Sliwa encouraged the publication of all studies conducted, as this will allow the possibility of future use of data, as well as a better or more realistic contextual analysis of CVD in Africa and Cameroon in particular. She also discussed the findings of the HOPE III trial.4-6 The second part was the hypertension and heart failure symposium, chaired by Emeritus Prof Walinjom FT Muna (Cameroon), Prof Simon Stewart (Australia), Prof Karen Sliwa (South Africa) and Dr Yves Monkam (Cameroon). Dr Monkam offered a word of welcome to international faculty, especially from PASCAR, on behalf of the Cameroon Cardiac Society. This was followed by Dr Biholong’s presentation ‘Management of mild–moderate hypertension’,7 and Dr Ba Ahmadou’s presentation on new recommendations from the European Society of Cardiology (ESC) on the treatment of heart failure in 2016.8 Dr Dzudie presented ‘What every general practitioner should know regarding the management of hypertension’ and he enumerated and explained the PASCAR 10 pillars to beat hypertension in Africa.3 The final part of this session was the NIH Fogarty non-communicable diseases leadership activity. Mr Ferdinant Mbidzenyuy presented ‘How to foster a research culture in limited-resource settings: the case of Cameroon Baptist Convention’. This was followed by Prof Mocumbi’s presentation ‘Building and maintaining a scientific reputation’. The talk was drawn from her own experience in Mozambique. She laid emphasis on the mentor–mentee system as one of the factors that facilitate building and maintaining a scientific reputation.

Fig. 1. G roup picture, PASCAR symposium on hypertension and heart failure.

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Dr Dzudie offered concluding remarks for day one. He highlighted the burden of CVDs in Africa, the antihypertensive effect of statins (Hope III trial), cardiovascular risk-factor stratification, the role of the general practitioner in the management of hypertension, being open to the mentor– mentee system, and the dissemination of research findings. He rendered tributes to the organisers and partners, both local and international, and gratitude to all participants.

Day 2: Grand rounds: cardiovascular diseases in pregnancy A clinical visit to the obstetrics and gynaecology ward of the Douala General Hospital was conducted. This was led by Profs Karen Sliwa and Eugene Belley Priso, among a delegation of about 40 clinicians. Three cases were identified on the ward and discussed: pregnancy and cardiac pacemakers, peripartum cardiomyopathy and postpartum cardiomyopathy. This activity took place in parallel with a scientific presentation of eight abstracts by early-career scientists. After the ‘grand rounds’, there was a symposium on cardiovascular disease in pregnancy, chaired by Profs Sliwa, Mocumbi and Priso. A most memorable presentation on cardiovascular diseases in pregnancy was given by Prof Sliwa. The burden of cardiac disease in pregnancy, common patterns of presentation, major signs and symptoms, and contributing factors were enumerated. This was followed by a presentation from Prof Mocumbi ‘When should women with cardiac disease in pregnancy give birth next?’ There were also presentations from Prof Mboudou and Dr Balla on the challenges of cardiac disease in pregnancy in Cameroon, and the management of diabetes in pregnancy, respectively.

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Conclusion The high burden of CVD warrants clinical research priorities such as the need for proper record archiving, dissemination of research findings, and preventative approaches to CVD. Emerging diseases such as cardiac disease in pregnancy also deserves strategies such as the establishment of good clinical registries. Bridging the gap between specialists and general practitioners will serve to improve the quantity and quality of healthcare delivery and by extension, the potential attainment of the 25 × 25 World Health Organisation objective for cardiovascular diseases. The Pan-African Society of Cardiology acknowledges the Mary Mackillop Institute for Health Research, Center for Research Excellence for reducing of inequalities in cardiovascular disease burden, the Clinical Research Education, Networking and Consultancy, and the Cameroon Cardiac Society. We are grateful to the NIH Fogarty International Center for travel support for the international faculty and we thank Douala General Hospital for hosting and sponsoring the event.

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Launching the Heart of Africa The book titled Heart of Africa was unveiled for the first time in Cameroon and senior editors present were Profs Sliwa, Stewart and Mocumbi, as well as associate editor Ms Kimberly Keates.9 Prof Sliwa presented all the authors with a copy of the book. Some of the authors present at the time were Drs Kemi Tibazarwa, Dike Ojji and Anastase Dzudie.

rate-of-hypertension-by-2025/. 4.

Blood-pressure and cholesterol lowering in the HOPE-3 trial. N Engl J Med 2016; 375(12): 1190–1194.

Yusuf S, Lonn E, Pais P, Bosch J, López-Jaramillo P, Zhu J, et al. Bloodpressure and cholesterol lowering in persons without cardiovascular disease. N Engl J Med 2016; 374(21): 2032–2043.

Yusuf S, Bosch J, Dagenais G, Zhu J, Xavier D, Liu L, et al. Cholesterol lowering in intermediate-risk persons without cardiovascular disease. N Engl J Med 2016; 374(21): 2021–2031.

National Institute of Health Fogarty Young Researcher awards

All oral/poster abstract presentations were evaluated on scientific merit (60%) and the quality of the oral/poster presentation (40%). The Heart of Africa was awarded to young investigators for the best abstract presentation. Of 20 oral/abstract presentations evaluated, the top three rated abstracts and presenters were awarded the Young Investigator award. Winners in order of merit were Dr Martin Abanda, Mr Ferdinant Mbidzenyuy and Dr Essama.

Filipovský J, Widimský J, Špinar J. Summary of 2013 ESH/ESC guidelines for the management of arterial hypertension. Cor Vasa 2014; 56(6): e494–518. 2016 ESC guidelines for the diagnosis and treatment of acute and chronic heart failure | Eur Heart J [Internet] [cited 2016 Nov 22]. Available from: http://eurheartj.oxfordjournals.org/content/37/27/2129.

Heart of Africa book launched 12 October 2016 Cameroon – News – Pascar [Internet] [cited 2016 Nov 21]. Available from: http://www.pascar. org/news/entry/heart-of-africa-book-launched-12-october-2016-cameroon.

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Case Report An unusual case of aorta–right atrial tunnel with windsock aneurysm: imaging, diagnosis and treatment Shehzaadi Aneesah Mohamed Khan, Leonie Scholtz, F Adriaan Snyders, Johan de Villiers Case report

Abstract The first successfully diagnosed and treated case of aorta– right atrial tunnel was reported by Coto et al. in 1980. The most common cause of aorta–right atrial tunnel is a ruptured aneurysm of the sinus of Valsalva. Sinus of Valsalva aneurysms had been reported as early as 1840 by Thurnam; these were diagnosed at autopsy. With the advances in radiology, many cases of aorta–right atrial tunnel have been reported since then, each with its own subtle variations. We report on a unique case of aorta–right atrial tunnel with a windsock aneurysm in the right atrium. A 55-yearold male presented with abdominal pain and the chest X-ray revealed cardiomegaly. On further investigation with echocardiography and computed tomography angiography, there was an incidental aorta–right atrial tunnel with a windsock aneurysm in the right atrium. He was treated successfully with surgery. A similar case has been reported only once before by Iyisoy et al. in 2014. Keywords: aorta–right atrial tunnel, aneurysms of the sinus of Valsalva Submitted 27/10/15, accepted 10/7/16 Published online 15/3/17 Cardiovasc J Afr 2017; 28: e1–e5

www.cvja.co.za

DOI: 10.5830/CVJA-2016-073

As early as 1840, aneurysms of the sinus of Valsalva were described by Thurnam; these were diagnosed through autopsies.1 The first successfully diagnosed and treated case of aorta–right atrial tunnel was reported by Coto et al. in 1980.2 Initially, diagnosis was limited to echocardiography and cardiac catheterisation, but with the advent of 64-slice computed tomography (CT) angiography, diagnostic accuracy and accessibility has improved. We present here a unique case of aorta–right atrial tunnel with a windsock aneurysm in the right atrium, diagnosed with echocardiography and CT angiography and successfully treated with surgery.

University of Pretoria, Pretoria, South Africa Shehzaadi Aneesah Mohamed Khan, MB ChB, aneesahkhan@hotmail.com Leonie Scholtz, MB ChB, MMed (RadD) F Adriaan Snyders, MB ChB, MMed (Int), FACC, FESC Johan de Villiers, MB ChB, MMed (thorax), GKC (thorax)

A 55-year-old male patient presented with abdominal pain and was admitted to hospital for the treatment of a kidney stone. Two days after the stone was removed and a stent was placed, he complained again of severe abdominal pain, nausea and vomiting. He was thoroughly examined; the abdominal CT and ultrasound were normal. The cause of abdominal pain was due to a urinary tract infection, which he had contracted after the urinary tract stone was removed. The abdominal symptoms were unrelated to the cardiac findings. The chest radiograph, however, demonstrated cardiomegaly. He was then referred to a cardiologist. The patient had no history of cardiac disease and reported no chest pain or palpitations. He had normal effort tolerance. In retrospect he recalled some ankle swelling during the afternoons and mild peri-orbital swelling during the mornings. His surgical history included a Nissen fundoplication. A transthoracic echocardiogram demonstrated a large left atrium and left ventricle. No left ventricular hypertrophy was reported. Ejection fraction on M-mode was normal. A significant finding was an impression on the enlarged right atrium from a possible adjacent lesion. The transoesophageal echocardiogram (TEE) confirmed normal valvular and left ventricular function. There was an aneurysm of the aortic sinus with a windsock in the right atrium, possibly increasing the pressure and volume in the right atrium (Figs 1–3). A CT angiogram was performed subsequent to the TEE. There was aneurysmal dilatation of the right coronary sinus with a tortuous dilated tunnel draining anteriorly into the right atrium. The distal end of the tunnel appeared to have a large sac/ windsock aneurysm, which protruded into the right atrium. The sac was not intact along its lateral border, forming a left-to-right shunt from the coronary sinus to the right atrium. There were extensive calcifications noted along the wall of the tunnel. The right coronary artery arose from the proximal part of the tunnel (Figs 4, 5). The patient was referred to the cardiothoracic surgeon for surgical repair of the aorta–right atrial tunnel, which was an incidental finding. The defect in the aorta was in the right coronary sinus and the lower border was approximately 4 mm from the aortic annulus (Fig. 6). The aneurysm formed a windsock with more than one opening, all of which were in the right atrium. The right atrium was opened and a retrograde cardioplegic cannula was placed in the coronary sinus. Retrograde cardioplegia was used due to the presence of the left-to-right shunt created by

CARDIOVASCULAR JOURNAL OF AFRICA • Volume 28, No 4, July/August 2017

Fig. 1. T wo-dimensional transoesophageal echocardiogram in long-axis view. 1, left atrium; 2, left ventricle; 3, aorta; 4, origin of tunnel. The origin of the tunnel arises from the proximal ascending aorta.

the aorta–right atrial tunnel. Anterograde cardioplegia was a less viable option while the shunt between the left and right side of the heart was still patent. The tunnel was approached and excised from both ends (Fig. 7), and it was closed directly with bovine pericardium and prolene sutures at the proximal aorta and right atrium. The aortic annulus was not damaged during the surgery and no valvuloplasty was necessary. There was a large saccular aneurysm in the right atrium. This was excised and the opening of the windsock was closed directly with sutures. There was no ventricular septal defect. The right coronary artery arose from the tunnel and had atherosclerosis around its origin, and when opened, the middle portion was also atherosclerotic. The right saphena magna vein was harvested for the bypass of the right coronary artery. It was not possible to re-implant the native right coronary osteum as it was too far removed from the ascending aorta. Therefore a distal end-to-side anastomosis was created between the graft and the right coronary artery.

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Fig. 3. Two-dimensional transoesophageal echocardiogram with Doppler in short-axis view. 1, right atrium; 2, right ventricle; 3, aneurysmal sac. Turbulent flow is demonstrated within the aneurysmal sac, which empties into the right atrium through a defect in the wall of the sac, thus creating the left-to-right shunt.

The patient followed up with the cardiologist four weeks after surgery. All had gone well, and he reported no dizziness or dysrhythmia. The transthoracic echocardiogram was normal.

Discussion Aorta–right atrial tunnel is an abnormal extra-cardiac vascular tunnel between any of the aortic sinuses and the right atrium.3 The differential diagnosis includes ruptured aneurysm of the sinus of Valsalva, coronary arteriovenous fistula, rupture of a dissecting aneurysm of the ascending aorta into the right atrium, and pseudo-aneurysm of the right coronary artery followed by

Fig. 2. T wo-dimensional transoesophageal echocardiogram in short-axis view. 1, right atrium; 2, right ventricle; 3, aneurysmal sac. The windsock arises from the terminal part of the tunnel and is demonstrated within the right atrium.

Fig. 4. CT angiogram axial image at the level of the left atrium. 1, distal end of the tunnel; 2, proximal end of tunnel; 3, right atrium; 4, right ventricle; 5, left ventricle; 6, left atrium. The tunnel is tortuous and dilated. Distally there are mural calcifications in the tunnel.

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Fig. 5. C T angiogram oblique sagittal image. 1, distal end of tunnel; 2, proximal end of tunnel; 3, left atrium; 4, inferior vena cava; 5, right ventricle; 6, pulmonary trunk; 7, descending aorta. There is a small dense calcification at the origin of the tunnel and dense mural calcifications at the distal end of the tunnel. The tunnel is long, tortuous and dilated.

formation of a fistula between the aneurysm and right atrium.2 A ruptured sinus of Valsalva aneurysm is by far the most common cause of aorta–right atrial tunnel.3 Aneurysms of the sinus of Valsalva were first described by Thurman in 1840 and remain relatively rare.1 The incidence of aneurysm of the sinus of Valsalva is reported to range between 0.1 and 3.5% of all congenital cardiac anomalies. Acquired

Fig. 7. Intra-operative image. Right atrium is opened and the windsock excised. The distal end of the tunnel is demonstrated opening into the right atrium with a thick collagenised wall due to the high pressure of the shunt. 1, distal end of the tunnel, the opening is within the right atrium; 2, right atrial appendage, which has been retracted; 3, superior vena cava; 4, retrograde cardioplegia cannula.

sinus of Valsalva aneurysms occur less frequently and causative factors include degenerative diseases (atherosclerosis, connective tissue disorders and cystic media necrosis), infections (syphilis, bacterial or fungal endocarditis and tuberculosis), or thoracic trauma.4 The aetiopathogenesis of congenital aneurysms is poorly understood.5 The right coronary sinus and the non-coronary sinus arise embryologically from the fusion of the bulbar septum and truncal ridges. Incomplete fusion can result in aneurysm formation within the septum when subjected to long-standing systemic arterial pressure (left-to-right shunt).6 Weakening of the aortic wall leads to rupture and the establishment of a fistulous tract that may communicate with any of the cardiac chambers, the right atrium being the most common.3 This is also closely related to membranous ventricular septum. Ventricular septal defects occur simultaneously in approximately 40% of patients with congenital aneurysms.4 The frequency of ruptured sinus of Valsalva aneurysm varies according to the location: 60% in the right sinus, 42% in the non-coronary sinus and only 10% in the left sinus.7 Aorta–right atrial tunnel can be classified according to the origin and course in relation to the ascending aorta, therefore termed anterior or posterior.8 Sakakibara and Konno10 proposed Table 1. Classification for SVA proposed by Sakakibara and Konno9

Fig. 6. I ntra-operative image. The right atrial appendage has been retracted and the tunnel is demonstrated originating from the proximal aorta. 1, aorta; 2, right atrial appendage; 3, tunnel; 4, superior vena cava.

Type I

Connect the right SV and the existing tract of the RV below the pulmonary valve

Type II

Connect the right SV and the VD in the supra ventricular crest

Type IIIa

Connect the right SV and the RA

Type IIIv

Connect the posterior zone of the right SV and the RV

Type IIIa + v Connect the right SV and both the RA and RV Type IV

Connect the non-coronary SV and the RA

SVA, sinus of Valsalva aneurysm; SV, sinus of Valsalva; RV, right ventricle; RA, right atrium.

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a formal classification for sinus of Valsalva aneurysm, according to the coronary sinus affected and the area towards which they protrude or rupture (Table 1). A true aortico-cameral connection may be difficult to differentiate from a coronary cameral fistula. Levy stresses the origin of the abnormal tunnel above and separate from the coronary orifice.10 Bove and Schwartz, however, emphasise the separation of the orifice of the tunnel from the adjacent sinus of Valsalva by a small well-defined fibrous ridge.11 In our case, the tunnel gave rise to the right main coronary artery. To date, spontaneous closure of the aorta–right atrial tunnel has not been reported. The pressure that is created during a left-to-right shunt is too high to close spontaneously. Clinical presentation varies according to the degree of the left-to-right shunt, which can range from completely asymptomatic to symptoms related to the volume overload on the ventricles. Surgical and percutaneous interventions are the main therapeutic options. Transcatheter closure of a tunnel is technically straightforward in the hands of an experienced interventionist. It is cost intensive, but has low peri-procedural risk.12 Percutaneous intervention with a plug or coil is easiest when the coronary arteries arise separately from the tunnel. Complications of prolonged patency of the tunnel include calcification of its wall, biventricular volume overload or aneurysmal expansion, congestive cardiac failure, pulmonary vascular disease, infective endocarditis, and higher mortality rate during surgery if the lesion is left uncorrected until the patient ages.13 With regard to our patient, the CT angiogram demonstrated calcifications within the wall of the tunnel already. Multiple aortico-cameral tunnels have been reported once previously in an elderly male patient. Transthoracic echocardiogram, transoesophageal echocardiogram and cardiac catheterisation revealed separate tunnels from the right coronary sinus to the left ventricle, right ventricle and right atrium. Surgery was performed successfully.14 Mahesh et al. presented a case of pre-natal diagnosis of aorta–right atrial tunnel, subsequently treated with percutaneous coil embolisation.15

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Diagnosis Thurnam diagnosed all ruptured sinus of Valsalva aneurysms at autopsy.1 In 1951, Venning was possibly the first to diagnose an acute rupture of an aneurysm of the sinus of Valsalva in life.16 The first successfully diagnosed and treated case of aorta–right atrial tunnel was reported by Coto et al. in 1980.2 Aneurysm of the sinus of Valsalva may be difficult to diagnose clinically, and echocardiography is usually the first step to diagnosis.17 Two-dimensional echocardiography has been improved with the use of contrast, spectral Doppler and colourflow imaging.4 It is non-invasive and easily accessible. Chaing and co-workers were able to accurately diagnose a ruptured sinus of Valsalva aneurysm in 58% of patients using two-dimensional echocardiography alone. The addition of intravenously injected bubble contrast improved the sensitivity to 75%. One limitation of echocardiography is the inability to visualise the coronary anatomy.4 Transoesophageal echocardiography is more sensitive than transthoracic echocardiography due to the probe’s proximity to the relevant structures and it optimises echo graphic windows with distorted anatomy.18 Ultrasound has improved markedly in the past 15 to 20 years. Three-dimensional echocardiography offers the ability to improve and expand the diagnostic capabilities of cardiac ultrasound. Serial two-dimensional images are obtained and three-dimensional data are reconstructed from this data set, thereby complimenting and supplementing two-dimensional cardiac imaging. Thus far it has been successfully applied to the detection and assessment of several anatomical cardiac defects. This method has not yet been specifically applied to the detection or imaging of aorta–right atrial tunnel. Further technological improvements and additional clinical studies will broaden the list of appropriate applications of this exciting new ultrasound modality.19 Cardiac catheterisation and retrograde angiography have been considered necessary to differentiate these aneurysms from other cardiac anomalies, and also prove useful to map out the coronary arteries prior to surgery.4 The high cost,

Table 2. Descriptive summary of cases from 2003, diagnosed using electron-beam tomography, CT angiography and CMR Author

Imaging

Treatment

Turkay (2003)22

Age Gender 29

Type

Origin Termination RCS

lateral aspect proximal tunnel of right atrium

Coronary artery

electron beam tomography; echocardiography; angiography, intra-op images

surgery

Akar (2006)23

RCS

right atrium

separate

transoesophageal echocardiogram, cardiac catheterisation, CT angiogram, intra-op images

surgery

Krishna (2010)13

posterior

LCS

SVC/RA junction

separate

echocardiography, cardiac catheterisation, CT angiogram, intra-op images

surgery

Walker (2010)24

NCS

right atrium

transoesophageal echocardiogram, CT angiogram

surgery

Chandra (2011)8

RCS

posterior wall right atrium

separate

transoesophageal echocardiogram, CT angiogram, cardiac catheterisation

percutanous transcatheter occlusion of tunnel

Myers (2011)25

posterior

LCS

right atrium

tunnel

cardiac catheterisation, CT angiogram, intra-op images

surgery

Sung (2011)26

RCS

right atrium

separate

CT angiogram

surgery

Salehi (2013)18

RCS

right atrium

abutting origin of tunnel

cardiac catheterisation, transoesophageal echocardiogram, CMR

surgery

Tossios (2013)12

posterior

LCS

right atrium

separate

transthoracic echocardiogram, transoesophageal echocardiogram, cardiac catheterisation, CT angiogram, CMR

surgery

Iyisoy (2014)5

posterior

LCS

roof of right atrium

proximal tunnel

transoesophageal echocardiogram, cardiac catheterisation, CT angiogram

surgery

Kim (2014)27

RCS

right atrium

separate

transoesophageal echocardiogram, cardiac catheterisation, CT angiogram

surgery

CT, computed tomography; CMR, cardiac magnetic resonance; SVC, superior vena cava; RA, right atrial; RCS, right coronary sinus; LCS, left coronary sinus; NCS, non-coronary sinus

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and procedure-related morbidity and mortality associated with coronary angiography have motivated the search for alternatives to this invasive procedure.20 In an article published by Goldberg in 1990, CT and magnetic resonance (MR) were not widely used. It was reported to be limited by prolonged imaging time, slice thickness, radiation and cost.4 With the advent of 64-slice CT, cardiac CT has emerged as a useful diagnostic imaging modality for the assessment of cardiac anomalies. Imaging time has been cut down and the slices are thinner, allowing for accurate evaluation of the coronary arteries. CT angiography is now easily accessible in addition to it being non-invasive. A basic principle of radiation protection is to keep radiation exposure, ‘as low as reasonably achievable’ (ALARA).21 Tossios et al. were the first to image and document aorta– right atrial tunnel using cardiovascular magnetic resonance (CMR), which yielded excellent definition of the topographical anatomy of the tunnel with regard to its origin, course and termination. CMR angiography was an additional tool used to demonstrate blood flow and quantify the left-to-right shunt.12 Therefore the combination of CMR and other modalities has improved the diagnostic precision of aorta–right atrial tunnel and has also assisted in ruling out other associated lesions, such as septal defects.12 Prior to 2003, most cases of ruptured sinus of Valsalva aneurysms were diagnosed using echocardiography and cardiac catheterisation. Turkay et al. were the first to diagnose right coronary sinus tunnel to the right atrium using electron-beam tomography.22 Tossios and Salehi were the first to diagnose aorta–right atrial tunnel using CMR.12,18 Table 2 shows a descriptive summary of cases from 2003, diagnosed using electron-beam tomography, CT angiography and CMR.

Doty JR (eds). John Hopkins Textbook of Cardiothoracic Surgery. 2nd edn. New York: McGrawhill Education Medical, 2014. 7.

Galicia-Tornell MM, Marin-Solis B, Mercado-Astorga O, et al. Sinus of Valsava aneurysm with rupture. Case report and literature review. Cir Ciruj 2009; 77: 441–445.

Chandra S Vijay S, Kaur D, et al. Congenital aorta right atrial fistula: successful transcatheter closure with the Amplatzer occluder. Pediatr Cardiol 2011; 32(7): 1057–1059.

Sakakibara S, Konno, S. Congenital aneurysms of the sinus of Valsalva: A clinical study. Am Heart J 1962; 63: 708–719.

10. Levy MJ, Schachner A, Biciden LC. Aortico-left ventricular tunnel. Collective review. J Cardiovasc Surg 1982; 84: 102–109. 11. Bove KE, Schwartz DC. Aortico-left ventricular tunnel. Am J Cardiol 1967; 19: 696–709. 12. Tossios P, Sarlis G, Aidonidis G, et al. Aorta-right atrial tunnel: imaging and surgical repair in an adult patient. J Cardiothorac Vasc Anesth 2014; 28(5): 1314–1318 doi: 10.1053/j.jvca.2013.03.025. 13. Krishna CS, Baruah DK, Reddy GV. Aorta-right atrial tunnel. Texas Heart Inst J 2010; 37(4): 480–482. 14. Xing-biao QIU, Hong-yu SHI, Lan LIU, et al. Multiple aorticocameral tunnels associated with bicuspid aortic valve in aged: a case report. Chin Med J 2009; 122(18): 2184–2185. doi: 10.3760/cma.j.is sn.0366-6999.2009.18.021. 15. Mahesh K, Francis E, Kumar RK. Aorta to right trial tunnel. J Am Coll Cardiol 2008; 1(6): 716–717 doi:10.1016/j.jcin.2008.05.011. 16. Venning GR. Aneurysms of the sinuses of Valsalva. Am Heart J 1951; 42: 57–63. 17. Lee S, Lin T, Su H, et al. Ruptured aneurysm of the sinus of Valsalva into the right atrium without ventricular septal defect: a case report and literature review. Kaohsiung J Med Sci 2005; 21(11): 517–521. 18. Salehi A, Cui WW. Aorta–right atrial tunnel in an elderly patient. Cardiovasc Anesthesiol: Echo Rounds 2013; 117(6): 1282–1285. doi: 10.1023/ANE.0b013e3182a7479.

Conclusion Aorta–right atrial tunnel is a rare, congenital cardiac anomaly. The diagnosis can be improved using multi-modality imaging, and with the advent of live three-dimensional echocardiography, improved CT angiography and functional CMR, detailed non-invasive imaging may be a favourable adjunct to further treatment.

19. Hung J, Lang R, Flachskampf F, Shernan SK, NcCulloch ML, Adams DB, et al. 3D echocardiography: A review of the current status and future directions. J Am Soc Echocardiogr 2007; 20: 213–233. 20. Burrill J, Dabbagh Z, Gollub F, Hamady M. Multidetector computed tomographic angiography of the cardiovascular system. Postgrad Med J 2007; 83: 698–704. doi 10.1136/pgmj.2007.061804. 21. Hausleiter J, Meyer T, Herman, et al. Estimated radiation dose associated with cardiac CT angiography. J Am Med Assoc 2009; 301(5):

References 1.

Thurnam J. On aneurysms and especially spontaneous varicose aneu-

Cardiovasc Surg 2003; 125(5): 1058–1060. doi:10.1067/mtc.2003.87.

rysms of the ascending aorta and sinuses of Valsalva, with cases. Med

23. Akar AR, Sirlak M. Aortico-cameral communication form right sinus

Chir Tr (Lond) 1840; 23: 323–385. 2.

Otero-Coto E, Cafferena JM, Such M, Marques JL. Aorta–right atrial communication: report of an unusual case. J Thorac Cardiovasc Surg 1980; 80: 941–944.

2006; 59:(2): 73–76. 24. Walker J, Lee J. Congenital aorta to right atrial fistula. Cardiol J 2010; 17(5): 523–524. 25. Myers PO, Milas F, Panos A. Multimodality imaging in the evaluation

entation, diagnostic criteria, and surgical options. J Thorac Cardiovasc

of aorta–right atrial tunnel. Eur J Cardio-thorac Surg 2011; 40(4): 153.

Goldberg N, Krasnow N. Sinus of Valsalva aneurysms. Clin Cardiol 1990; 13: 831–836.

of Valsalva to right atrium. Ankara Üniversiti Tip Fakültesi Mecmuasi

Gajjar T, Voleti C, Matta R, et al. Aorta–right atrial tunnel: Clinical presSurg 2005; 130(5): 1287–1292. doi:10.1016/j.jtcvs.2005.07.021.

500–507. 22. Türkay C, Gölbasi I, Belgi A, et al. Aorta–right atrial tunnel. J Thorac

doi: 10.1016/j.ejcts.2011.05.044. 26. Sung YM, Merchant N. Imaging of congenital aorta–right atrial tunnel with electrocardiogram gated 64-multi-slice computer tomography. Ann

Iyisoy A, Celik T. Aorta–right atrial tunnel: An interesting type of a

Thorac Surg 2011; 92: 743. doi:10.1016/j.athoracsurg.2011.01.002.

congenital coronary artery anomaly. Korean Circ J 2014; 44(3): 193–195.

27. Kim KW, KIM JH, Choe WJ. Aorta–right atrial tunnel. Eur Heart J

doi:10.4070/kcj.2014.44.3.193.

Cardiovasc Imag 2013; 15(1): 112. doi:10.1093/ehjci/jet104 (accessed

Fitton TP, Moulick A, Vricella LA. Congenital anomalies of the sinuses

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of valsalva and aortico-left atrial tunnel. In: Yuh, D, Vricella L, Yang S,

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Case Report Management of a complicated redo giant dissecting aortic aneurysm Ibrahim Kara, Alper Erkin, Halil Ibrahim Erkengel, Kıyasettin Asil

Abstract Giant aortic aneurysm is defined as an aneurysm of the aorta of greater than 10 cm in diameter. This rare condition is associated with a high risk of morbidity and mortality and it may lead to fatal complications such as rupture and/or dissection if not managed with proper surgical planning and expertise. Other than atherosclerosis, the main causes of giant ascending aortic aneurysms include Marfan and Ehlers–Danhlos syndromes. Herein we report on a young male patient who had had an aortic valve replacement five years earlier due to a bicuspid aortic valve leading to aortic failure, accompanied by aortic coarctation. He had an aneurysmal expansion rate of 1.81 cm/year to reach a final aneurysmal diameter of 13.25 cm, which, to our knowledge, represents the largest size ever reported in the literature for such lesions, and in which the redo and aneurysmal wall were adjacent to the sternal margins. Keywords: giant aortic aneurysm, surgical procedures Submitted 19/5/16, accepted 28/9/16 Cardiovasc J Afr 2017; 28: e6–e8

www.cvja.co.za

Bicuspid aortic valve is a congenital condition requiring early valvular replacement due to accelerated valvular degeneration. It is a serious disorder of the aorta, frequently co-existing with dilation and rapid expansion of the ascending aorta. Therefore the ascending aorta should be regarded as a component of the pathology, and the type of surgical method to be performed should be carefully assessed in BAV patients requiring surgical intervention.4 Here we report on a young male patient who developed a giant ascending aortic aneurysm of 13.25 cm, against a background of the very rare occurrence of a chronic dissection five years after a valvular replacement that had been performed due to BAV failure.

Case report A 33-year-old male patient was admitted to the emergency room with headache, shortness of breath and sleeplessness. A consultation was requested from our unit due to extreme aortic and mediastinal dilatation, seen on chest X-ray (Fig. 1A) as well as a history of open-heart surgery. The patient had had a mechanical aortic valve replacement (23 no St Jude) five years earlier due to BAV failure.

DOI: 10.5830/CVJA-2016-087

Giant aortic aneurysm is a very rare clinical entity defined as an aneurysm of the aorta that is greater than 10 cm in diameter at its widest point.1 The risk of rupture closely parallels the diameter of the aneurysm, with a rupture risk of 31% in lesions in which the diameter of the ascending aorta is greater than 6 cm.2 Other main causes of ascending aortic aneurysms include Marfan and Ehlers–Danlos syndromes, in addition to atherosclerosis.1 Although the risk of dissection and/or aneurysm is lower in patients with a bicuspid aortic valve (BAV) than in patients with Marfan syndrome, the former condition bears higher clinical significance based on its much higher incidence.3

Department of Cardiovascular Surgery, Faculty of Medicine, Sakarya University, Sakarya, Turkey Ibrahim Kara, MD, ikara7881@hotmail.com Alper Erkin, MD Halil Ibrahim Erkengel, MD

Department of Radiology, Faculty of Medicine, Sakarya University, Sakarya, Turkey Kıyasettin Asil, MD

Fig. 1. Mediastinal widening seen in pre-operative chest radiography (A). Pre-operative thoracic CT scan: axial (B), coronal (C) and sagittal (D) views showing the giant dissecting aortic aneurysm of 13.25 cm in diameter.

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Fig. 3. Postoperative radiography (A). Postoperative thoracic CT scan: axial (B), coronal (C) and sagittal reconstructions – mediastinal window view (D).

Fig. 2. P re-operative (A) and postoperative (C, D) threedimensional reconstructions from CT scans, and intraoperative (B) view of the aortic aneurysm.

On physical examination, his blood pressure was 132/68 mmHg, heart rate was regular at 82 beats/min and electrocardiography was normal. Chest auscultation was normal but a chest X-ray revealed mediastinal widening and cardiomegaly. His family history was unremarkable. Transthoracic echocardiography (TTE) showed the presence of a mechanical aortic valve prosthesis in its normal anatomical position with normal function, excess dilatation of the proximal ascending aorta (132 mm) and normal left ventricular function. A thoracic contrast-enhanced computed tomography (CT) imaging study revealed a 132.5-mm non-ruptured giant aneurysm and an intra-luminal flap image confined to the ascending aorta (De Bakey type II) that was consistent with dissection (Fig. 1B–D). Surprisingly, despite a normal aortic arch and branches, there was an aortic coarctation just distal to the subclavian artery (Fig. 2A, D). The patient was haemodynamically and clinically stable and was admitted to our unit for surgery, which consisted of tubular graft interposition in the supracoronary ascending aorta (Fig. 2B–D). He was weaned from mechanical ventilation nine hours postoperatively, and was transferred to the ward on day two. He was discharged uneventfully at day seven. A follow-up thoracic CT at two months showed no problems, and the patient was subsequently followed up in the out-patient unit (Figs 2C, D, 3A–D).

Surgical technique As the wall of the ascending aorta was adjacent to the sternum (Fig. 1B, D), arterial cannulation from the right axillary artery was performed, as well as venous cannulation under transoesophageal guidance, from the right femoral vein extending up to the

right atrium. Cardiopulmonary bypass (CPB) and cooling was initiated. In such cases, CPB is instituted prior to resternotomy, using deep hypothermia in the event that circulatory arrest is required to gain control of the ascending aorta. As expected, the aneurysmatic aortic wall adjacent to the sternum was damaged during this procedure. In accordance with the pre-planned surgical strategy, CPB was suspended and deep hypothermia was used for a very short period of time (20°C), during which the aneurysmal sac was rapidly dissected in the distal direction and a clamp was placed at the origin of the aortic arch, which had normal dimensions. CPB was then re-initiated. Cardiac arrest with hypothermic blood cardioplegia was achieved via hypothermic blood given into the right and left coronary arteries using an osteal cannula, and myocardial protection was provided. Due to the adhesions, cardiac venting was performed through the pulmonary artery. After the body temperature was increased to 27°C, moderate hypothermic circulatory arrest was attained, followed by antegrade selective cerebral perfusion at a flow rate of 10 ml/kg. A selective cannula was then placed into the left main carotid artery to provide bilateral cerebral perfusion. Cranial oxygenation and perfusion were monitored using near-infra-red spectroscopy (NIRS). After ensuring cerebral protection, a distal aortic anastomosis was performed using no 32 Dacron tubular grafts with the double-Teflon felt technique during moderate hypothermia. A clamp was then placed on the Dacron graft and warming was initiated. Without complete resection of the aneurysmatic aorta from the supra-coronary region, the anastomosis of the proximal aorta was completed with pledgeted 4/0 sutures in the lower half, and the double-Teflon felt technique in the upper half. After air evacuation and completion of warming, the patient was gradually weaned off CPB. After bleeding was controlled, the patient was de-cannulated and was transferred to the intensive care unit.

Discussion This case is of interest from several points of view. First is the asymptomatic clinical course of a giant aneurysm of 13.25 cm

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with chronic dissection and very high risk of rupture. Second, despite previous reports on several patients with giant aneurysms without rupture, to our knowledge, our patient represents the first asymptomatic redo case of a giant dissecting ascending aortic aneurysm occurring five years after BAV replacement. Third, a surgical treatment of this giant dissecting ascending aortic aneurysm was performed with moderate hypothermic circulatory arrest without any subsequent neurological sequelae in the face of a high risk of aortic injury during sternotomy due to the close proximity to the sternum, caused by the previous aortic valvular surgery. Giant ascending aortic aneurysms may give rise to very severe clinical complications, among which, dissection and rupture are often fatal.1 The risk of rupture is related to the dimensions of the aneurysm and the expansion rate during follow up.1 An expansion rate exceeding 1 cm/year or an aneurysmal diameter greater than 6 cm is associated with a dramatic increase in the risk of rupture.5,6 The risk of dissection in aortic aneurysms is proportional to the increase in diameter, and nearly 25% of patients with chronic aortic dissections may develop aneurysms.7 Our patient seemed to have an aortic aneurysm secondary to chronic aortic dissection, based on the fact that the actual underlying pathology was BAV, the aneurysmal expansion rate was high, and the clinical course was of a chronic nature. The expansion rate and risk of rupture in ascending aortic aneurysms in patients with chronic aortic dissection is significantly higher compared to aneurysms on the same site due to other conditions. The average expansion rate of thoracic aortic aneurysms is 0.1 to 0.2 cm/year.1 By contrast, in our patient the ascending aortic diameter was 42 mm at the time of aortic replacement, and this increased to 132.5 mm within a five-year period, which corresponds to a significantly higher rate of expansion than usually reported, namely 18.1 mm/year.8 The probable cause of this high rate of expansion was the dissection, which was a complication of a BAV, and the subsequent rapid dilatation of the aneurysm. The lifetime risk of aortic dissection in patients

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with BAV disease is approximately 6.13%, which is nearly nine times higher than in the normal population.3

Conclusion Despite the rare occurrence and a very high risk of rupture, giant ascending aortic aneurysms may present with an asymptomatic clinical course, as was the case in our patient, who had a giant aneurysm of 13.25 cm. These challenging aneurysms are adjacent to the sternal wall, require redo operation and are associated with high mortality rates. Therefore adequate surgical planning and expertise are prerequisites for their proper management.

References 1.

Agarwal V, Yaliwal C, Ofo E, et al. Giant ascending aortic aneurysm – a case report and review. Heart Lung Circ 2007; 16: S385–388.

Elefteriades JA. Natural history of thoracic aortic aneurysms: indications for surgery, and surgical versus nonsurgical risks. Ann Thorac Surg 2002; 74: 1877–1880.

Edwards WD, Leaf DS, Edwards JE. Dissecting aortic aneurysm associated with congenital bicuspid aortic valve. Circulation 1978; 57: 1022–1025.

Bilgen F. Ascending aorta replacement in bicuspid aortic valve; when? Turkish J Thorac Cardiovasc Surg 2011; 19: 15–18.

Tadros TM, Klein MD, Shapira OM. Ascending aortic dilatation associated with bicuspid aortic valve: pathophysiology, molecular biology, and clinical implications. Circulation 2009; 119: 880–890.

Brown PM, Zelt DT, Sobolev B. The risk of rupture in untreated aneurysms: the impact of size, gender, and expansion rate. J Vasc Surg 2003; 37: 280–284.

Larson EW, Edwards WD. Risk factors for aortic disection: a necropsystudy of 161 cases. Am J Cardiol 1984; 53: 849–855.

Hiratzka LF, Bakris GL, Beckman JA. ACCF/AHA/AATS/ACR/ASA/ SCA/SCAI/SIR/STS/SVM Guidelines for the diagnosis and management of patients with thoracic aortic disease: executive summary. J Am Coll Cardiol 2010; 55: e27–e129.

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Case Report Left ventricular haematoma mimicking lateral wall myocardial infarction secondary to percutaneous coronary intervention Omer Senarslan, Necdet Batuhan Tamci, Umut Hasan Kantarci, Mehmet Eyuboglu, Dilsad Amanvermez Senarslan

Abstract Dissecting intra-myocardial haematoma is a rare disease and a potentially fatal complication after cardiac surgery. Patients with previous heart surgery have more risk for dissecting intra-myocardial haematoma after percutaneous coronary intervention. Management of this issue is challenging. We describe a rare case of a 63-year-old woman with a left ventricular wall-dissecting intra-myocardial haematoma, which developed 30 minutes after percutaneous coronary intervention. The patient was treated conservatively, with a successful outcome. Keywords: percutaneous coronary intervention, complication, dissecting intra-myocardial haematoma Submitted 10/4/16, accepted 16/10/16 Published online 10/11/16 Cardiovasc J Afr 2016; 27: e9–e11

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DOI: 10.5830/CVJA-2016-090

Intra-myocardial haematoma is a rare disease and is usually associated with multiple pathologies such as myocardial infarction, chest trauma, coronary artery bypass surgery and

Department of Cardiology, Medifema Hospital, Izmir, Turkey Omer Senarslan, MD, dromersen@yahoo.com

Department of Cardiology, Izmir Atasaglik Hospital, Izmir, Turkey Necdet Batuhan Tamci, MD

Department of Radiology, Izmir Esrefpasa Hospital, Izmir, Turkey Umut Hasan Kantarci, MD

Department of Cardiology, Special Izmir Avrupa Medicine Center, Karabaglar, Izmir, Turkey Mehmet Eyuboglu, MD

Department of Cardiovascular Surgery, School of Medicine, Celal Bayar University, Manisa, Turkey Dilsad Amanvermez Senarslan, MD

complications of percutaneous coronary intervention (PCI), or it could occur spontaneously.1 Dissecting intra-myocardial haematoma (DIH) is a potentially fatal complication that is characterised anatomically and pathologically into different forms. Sub-epicardial or intra-myocardial haematoma occurs rarely and has been reported mainly in patients with previous coronary artery bypass graft (CABG) who undergo PCI.

Case report A 63-year-old woman was admitted to our clinic with complaints of chest pain on effort. There was a record of CABG carried out in 2011. Coronary angiography revealed severe stenosis (99%) in the middle part of the circumflex artery (Cx) (Fig. 1A). PCI was chosen as the treatment option for the Cx lesion. We crossed the lesion with a 0.014-inch hydrophilic guidewire PT2-LS (Boston Scientific, Natick, MA) and it was advanced distally into the Cx. We performed pre-dilatation with a coronary balloon under nominal pressure, and a 2.75 × 23-mm Xience stent (Abbott Laboratories, Abbott Park, IL, USA) was implanted under nominal pressure. The final angiogram revealed acceptable results in the Cx with no abnormal findings or contrast dye leakage. The patient was taken to the cardiology department after PCI. Thirty minutes after the procedure, she suddenly complained of severe chest pain and discomfort. An ECG showed ST elevations in D1 and aVL deviations (Fig. 1B). We assumed acute stent thrombosis, so we took the patient back to the catheterisation laboratory. We saw no thrombus in the stent but noticed deterioration of blood flow in the intermediate artery (Fig. 1C). We checked the patient with echocardiography to see if there was a problem with the pericardium or myocardium. Two-dimensional echocardiography revealed a large 5.1 × 1.4-cm echolucent area without fluid in the pericardium (Fig. 2A). We presumed this echolucent area was a dissecting intra-myocardial haematoma in the lateral wall of the myocardium, which was compressing the intermediate artery. Repeated bedside echocardiography revealed no change in the size of the haematoma and no deterioration in left ventricular ejection fraction or valve function on the first two days of clinical follow up. Although the left ventricular lateral wall haematoma was large enough to cause complications, it was stable, so we decided to follow the patient conservatively with standard

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Fig. 1. A . Coronary angiography before PCI. B. ECG after PCI. C. Control angiography. Significant stenosis is seen in the circumflex artery (A) and there is no contrast dye leakage in the control angiography (C) in the right caudal position. There is ST segment elevation in D1 and aVL deviations, suggesting a new-onset acute coronary syndrome.

anti-anginal therapy, including intravenous nitroglycerin and morphine sulfate. In addition, we reversed the effects of heparin with protamine sulfate. On day three of the follow up, cardiac computed tomography revealed thickening of the lateral wall of the myocardium, a radiolucent centre without contrast dye, and bilateral pleural effusions with no pericardial effusion (Fig. 2B, C). The patient developed transient atrial fibrillation and dyspnoea on the third day. Sinus rhythm was achieved with intravenous amiodarone, and the heart failure symptoms and findings disappeared with diuretics. The patient did not complain of chest pain or arrhythmia after the third day, and she was discharged on the sixth day of follow up. There was no haematoma in the lateral wall of the left ventricle but this part of the left ventricle was akinetic in the control echocardiography after 45 days.

Discussion DIH can occur as a complication of myocardial infarction, PCI and cardiac surgery.1 Prediction and diagnosis of DIH is very

difficult after PCI and cardiac surgery. There are a few cases of DIH after PCI reported in the literature.2 Continued leakage of blood from the coronary artery after any kind of perforation and avulsion of the vessel can lead to dissection of the myocardium and it is characterised by dissection between the spiral planes of heart muscle, including laminated thrombi, myocytes and fibrous tissue.2 Self-propagation of the haematoma leads to more expansion, and it can be complicated by myocardial wall rupture.3 Patients with previous cardiac surgery may have a selflimiting DIH because of pericardial adhesions to the epicardium. Therefore, these patients may be protected from myocardial rupture.4,5 Since it is a rare situation, management of DIH is challenging in evidence-based medicine. Conservative management of DIH is associated with a mortality rate as high as 90 to 100%.2 Management strategies depend on the location and/or extent of the DIH. Left ventricular apical location of the DIH has higher spontaneous reabsorption rates so conservative management is preferable for this position. Evacuation of the DIH and surgical

Fig. 2. A . Transthoracic echocardiography. B, C. Axial and sagittal computed tomography sections of the heart. Intra-myocardial haematoma is seen in both echocardiography and computed tomography (asterisk). LV, left ventricle; LA, left atrium.

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repair of the myocardium are the main strategies for an unstable patient with haemodynamic impairment. However, reported surgical mortality rates range from 0–80%, presumably because of the complex patho-anatomy and friable myocardium.2 We decided to manage the patient conservatively due to the short period of haemodynamic instability, the size stabilised after protamine treatment, and there were no significant related complications.

References 1.

Rahman N, Sharif H, Jafary FH. Intramyocardial hematoma after coronary perforation during percutaneous coronary intervention–anticipated and treated. J Invasive Cardiol 2008; 20(7): E224–228.

Vargas-Barron J, Roldan FJ, Romero-Cardenas A, Molina-Carrion M, Vazquez-Antona CA, Zabalgoitia M, et al. Dissecting intramyocardial hematoma: clinical presentation, pathophysiology, outcomes and delineation by echocardiography. Echocardiography 2009; 26(3): 254–261.

Vargas-Barron J, Roldan FJ, Romero-Cardenas A, Vazquez-Antona CA. Intramyocardial dissecting hematoma and postinfarction cardiac

Conclusion Since there are high mortality rates and difficulties in the management of DIH, the main treatment strategies should be based on prevention of this disease in adults. Control of the guide-wire (especially hydrophilic ones) is very important during PCI. Management of DIH should be individualised, integrating the patient’s haemodynamic stability, the size, location and extent of the DIH, and development of DIH-related complications.

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rupture. Echocardiography 2013; 30(1): 106–113. 4.

Shekar PS, Stone JR, Couper GS. Dissecting sub-epicardial hematoma – challenges to surgical management. Eur J Cardiothorac Surg 2004; 26(4): 850–853.

Quan VH, Stone JR, Couper GS, Rogers C. Coronary artery perforation by cutting balloon resulting in dissecting subepicardial hematoma and avulsion of the vasculature. Catheterization Cardiovasc Int 2005; 64(2): 163–168.

Be part of the first-ever Global Evidence Summit 13–16 September 2017 Cape Town, South Africa Abstract submission closes on 1 March 2017 The Global Evidence Summit (GES) will be a unique gathering of five international organisations (Cochrane, Guidelines International Network, Campbell Collaboration, International Society for Evidence-based Healthcare and Joanna Briggs Institute) involved in evidence based practice, policy, methodology and advocacy. The theme of the conference is ‘Using evidence. Improving lives’. The GES aims to advance the use of reliable research evidence in addressing some of the world’s most serious health and social challenges. We expect up to 1500 participants to attend this conference. Bursaries and stipends will be available to help people based in developing countries, consumers and students attend the GES. Don’t miss out on this opportunity to exchange ideas with leaders in the field and discuss fresh thinking about how to generate and package evidence for health and society. Find out more at: www.globalevidencesummit.org Email: contact@globalevidencesummit.org Twitter: @GESummit, #GESummit17 Facebook: facebook.com/globalevidencesummit/

Need endurance when treating CVS disease?

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PUBLISHED ONLINE: • Aorta–right atrial tunnel with windsock aneurysm: diagnosis and treatment