Ajcc October 2013

In This Issue —

Radiologic Evaluation of Suspected Congenital Heart Disease in Adults

— Systolic and Diastolic Ratio and Rate Pressure Product in Anemia — Acute Renal Failure and Silent Myocardial Infarction Following Multiple Honey Bee Stings — Case of a Young Hypertensive with Recurrent Cerebrovascular Disease due to a Rare Etiology — What are the Factors Contributing to Resistant Hypertension?

— Guidelines for BP Control in Special Circumstances —

Skin Plaques in a Woman with Renal Disease

—

NICE Updates Guidelines on Management of Chronic Heart Failure

Volume 16, Number 6, October 2013 Pages 201-240

Asian

Journal of

IJCP Group of Publications

CLINICAL CARDIOLOGY

Dr Sanjiv Chopra Prof. of Medicine & Faculty Dean Harvard Medical School Group Consultant Editor

Volume 16, Number 6, October 2013

Dr Deepak Chopra Chief Editorial Advisor

Padma Shri and Dr BC Roy National Awardee Dr KK Aggarwal Group Editor-in-Chief Dr Veena Aggarwal MD, Group Executive Editor

from the desk of group editor-in-chief 205 Naprosyn Safest NSAID for Heart Patients

Dr Praveen Chandra Guest Editor, AJCC praveen.chandra@medanta.org

Clinical Review

Assistant Editors: Dr Nagendra Chouhan, Dr Dharmendar Jain

AJCC Speciality Panel International Dr Fayoz Shanl Dr Alain Cribier Dr Kohtian Hai Dr Tanhuay Cheem Dr Ayman Megde Dr Alan Young Dr Gaddy Grimes Dr Jung bo Geg Dr Rosli Mohd. Ali Dr S Saito National Dr Mansoor Hassan Dr RK Saran Dr SS Singhal Dr Mohd. Ahmed

Advisory Board Dr PK Jain Dr PK Gupta Dr Naresh Trehan Dr Sameer Shrivastava Dr Deepak Khurana Dr Ganesh K Mani Dr K S Rathor Dr Rajesh Kaushish Dr Sandeep Singh Dr Yugal Mishra Faculty Dr GK Aneja Dr Ramesh Thakur Dr Balram Bhargava Dr HK Bali Dr HM Mardikar

Dr Sanjay Mehrotra Dr Vivek Menon Dr Keyur Parikh Dr Ajit Mullasari Dr Kirti Punamiya Dr MS Hiramath Dr VS Narain Dr SK Dwivedi Dr Raja Baru Panwar Dr Vijay Trehan Dr Rakesh Verma Dr Suman Bhandari Dr Ravi Kasliwal Dr Atul Abhyankar Dr Tejas Patel Dr Samir Dani

KK Aggarwal

206 Radiologic Evaluation of Suspected Congenital Heart Disease in Adults

Vincent B. HO

Clinical Study 212 Systolic and Diastolic Ratio and Rate Pressure Product in Anemia

K Singh

IJCP Editorial Board

Obstetrics and Gynaecology Dr Alka Kriplani, Dr Thankam Verma, Dr Kamala Selvaraj Cardiology Dr Praveen Chandra, Dr SK Parashar Paediatrics Dr Swati Y Bhave Diabetology Dr CR Anand Moses, Dr Sidhartha Das, Dr A Ramachandran, Dr Samith A Shetty ENT Dr Jasveer Singh, Dr Chanchal Pal Dentistry Dr KMK Masthan, Dr Rajesh Chandna Gastroenterology Dr Ajay Kumar, Dr Rajiv Khosla Dermatology Dr Hasmukh J Shroff, Dr Pasricha, Dr Koushik Lahiri Nephrology Dr Georgi Abraham Neurology Dr V Nagarajan, Dr Vineet Suri Journal of Applied Medicine & Surgery Dr SM Rajendran, Dr Jayakar Thomas Orthopedics Dr J Maheshwari Anand Gopal Bhatnagar Editorial Anchor Advisory Bodies Heart Care Foundation of India Non-Resident Indians Chamber of Commerce & Industry World Fellowship of Religions

Case Report 215 Acute Renal Failure and Silent Myocardial Infarction Following Multiple Honey Bee Stings

Kavina Marian Fernandes, Gadwalkar Srikant R, Shyamala G

219 Case of a Young Hypertensive with Recurrent Cerebrovascular Disease due to a Rare Etiology

SM Rajendran, S Palaniandavar, Jamima Bhaskar, J Senthilnathan, Arun R, Jose Mathew

Expert's Opinion 223 What are the Factors Contributing to Resistant Hypertension?

Sameer Shrivastava, KK Aggarwal

Clinical Algorithm Published, Printed and Edited by Dr KK Aggarwal, on behalf of IJCP Publications Ltd. and Published at E - 219, Greater Kailash, Part - 1 New Delhi - 110 048 E-mail: editorial@ijcp.com

225 Guidelines for BP Control in Special Circumstances

Printed at New Edge Communications Pvt. Ltd, New Delhi E-mail: edgecommunication@gmail.com

photo quiz 226 Skin Plaques in a Woman with Renal Disease

Š Copyright 2013 IJCP Publications Ltd. All rights reserved.

The copyright for all the editorial material contained in this journal, in the form of layout, content including images and design, is held by IJCP Publications Ltd. No part of this publication may be published in any form whatsoever without the prior written permission of the publisher.

Editorial Policies The purpose of IJCP Academy of CME is to serve the medical profession and provide print continuing medical education as a part of their social commitment. The information and opinions presented in IJCP group publications reflect the views of the authors, not those of the journal, unless so stated. Advertising is accepted only if judged to be in harmony with the purpose of the journal; however, IJCP group reserves the right to reject any advertising at its sole discretion. Neither acceptance nor rejection constitutes an endorsement by IJCP group of a particular policy, product or procedure. We believe that readers need to be aware of any affiliation or financial relationship (employment, consultancies, stock ownership, honoraria, etc.) between an author and any organization or entity that has a direct financial interest in the subject matter or materials the author is writing about. We inform the reader of any pertinent relationships disclosed. A disclosure statement, where appropriate, is published at the end of the relevant article.

Practice Guidelines 228 NICE Updates Guidelines on Management of Chronic Heart Failure

mediLAW 231 When can Hospitals be Liable for Medical Negligence Deaths?

KK Aggarwal

Around the Globe 233 News and Views

Note: Asian Journal of Clinical Cardiology does not guarantee, directly or indirectly, the quality or efficacy of any product or service described in the advertisements or other material which is commercial in nature in this issue.

lighter reading 234 Lighter Side of Medicine

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from the desk of group editor-in-chief Dr KK Aggarwal

Padma Shri and Dr BC Roy National Awardee Sr. Physician and Cardiologist, Moolchand Medcity, New Delhi President, Heart Care Foundation of India Group Editor-in-Chief, IJCP Group and eMedinewS National Vice President, Elect, IMA Chairman, Ethics Committee, Delhi Medical Council Director, IMA AKN Sinha Institute (08-09) Hony. Finance Secretary, IMA (07-08) Chairman, IMA AMS (06-07) President, Delhi Medical Association (05-06) emedinews@gmail.com http://twitter.com/DrKKAggarwal Krishan Kumar Aggarwal (Facebook)

Naprosyn Safest NSAID for Heart Patients In patients who require high doses of a nonselective nonsteroidal anti-inflammatory drug (NSAID) for longterm use and who have known cardiovascular disease or are at high-risk for cardiovascular events. The current recommendation is to use naproxen rather than ibuprofen or diclofenac.

One should prefer naproxen to other nonselective NSAIDs, although there are few data evaluating nonselective NSAIDs other than ibuprofen and diclofenac in patients at high cardiovascular risk.

Most NSAIDs increase the risks of major cardiovascular events.

The magnitude of risk is best illustrated by a meta-analysis of data from over 3,00,000 participants in over 700 trials that compared nonselective NSAIDs (used at the upper end of their dose range) or coxibs with either placebo or another nonselective NSAID or coxib.

Compared with placebo, use of high-dose diclofenac or a coxib increased major cardiovascular events (nonfatal myocardial infarction, nonfatal stroke or vascular death) by 40%.

High-dose ibuprofen increased the risk of major coronary events but not major vascular events.

High-dose naproxen did not increase major cardiovascular events, major coronary events or vascular death.

The estimated excess absolute risk of a major vascular event or death with use of diclofenac, coxib and possibly ibuprofen was two events per 1,000 persons per year in patients at low baseline cardiovascular risk and 7-8 events per 1,000 persons per year, including two fatal events, in patients at high baseline cardiovascular risk.

Naproxen is therefore the preferred nonselective NSAID when long-term use is needed in patients at increased risk for cardiovascular disease. (UpToDate) ■■■■

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Clinical Review

Radiologic Evaluation of Suspected Congenital Heart Disease in Adults VINCENT B. HO

Abstract The population of adults with congenital heart disease is increasing in North America. Radiologic imaging is critical for the initial assessment and for surveillance in this population. Chest radiography and echocardiography are valuable first-line tools for evaluation. However, magnetic resonance imaging and computed tomography are often necessary, particularly for assessment of extracardiac anatomy or specific vascular connections or relationships, which may be complex in postoperative patients.

Although magnetic resonance imaging and computed tomography can provide volumetric data for more comprehensive evaluation of cardiac anatomy and function, magnetic resonance imaging does not require patient exposure to ionizing radiation or nephrotoxic iodinated contrast media. Magnetic resonance imaging also can measure blood flow for quantification of leftto-right shunts, regurgitant fractions, and pressure gradients. Although noninvasive imaging techniques have limitations, they can evaluate most lesions and preclude the need for cardiac catheterization. Noninvasive imaging is particularly useful for serial evaluation of patients with surgically corrected congenital heart disease, because nearly one half of these patients will require two or more surgeries.

Keywords: Congenital heart disease, electrocardiography, atrial septal defect, cardiac catheterization, angiography

T

he number of adults in North America who have congenital heart disease (CHD) has steadily increased over the past 30 years.1,2 Although this increase is partly because of the growth of adult population, it may be more attributable to improvements in surgical management, which have resulted in a greater than 90 percent 10-year survival rate in persons with CHD.3 Between 1979 and 1997, mortality from CHD decreased by 39 percent in the United States.4 In North America, at least 500,000 adults have had surgical correction of CHD, with nearly 50 percent requiring two or more surgeries, and 23 percent requiring three or more.2,3,5 Congenital heart lesions may become symptomatic any time from birth to adulthood. At least 10 percent of persons with CHD have lesions that are typically not diagnosed until adulthood, such as secundum atrial septal defect (ASD) and congenitally corrected transposition of the great arteries (a condition in which the aorta and pulmonary artery are transposed, as are the ventricles, resulting in congenital correction of circulation).1,2 Patients with some types of common CHD lesions often survive into adulthood (e.g.,

VINCENT B. HO, MD, MBA, FAHA, is vice chair and professor of radiology at the Uniformed Services University of the Health Sciences, Bethesda, Md. Source: Adapted from Am Fam Physician. 2009;80(6):597-602.

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those with bicuspid aortic valve, congenital forms of mitral valve prolapse, coarctation of the aorta, ASDs, pulmonary valve stenosis, patent ductus arteriosus, or tetralogy of Fallot).2 Diagnostic imaging procedures for adults with suspected CHD include chest radiography, echocardiography (transthoracic and transesophageal), nuclear scintigraphy, cardiac-gated computed tomography (CT), magnetic resonance imaging (MRI), and cardiac catheterization and angiography. The evaluation of CHD often requires the accurate assessment of not only intra- and extracardiac anatomy, but also hemodynamics and function. Adults with CHD have the additional clinical considerations of acquired comorbidities (e.g., hypertension, atherosclerosis, occlusive coronary artery disease, pulmonary disease, renal disease) that may complicate their medical or surgical treatment.2 Illustrative Case A 40-year-old woman presented with a one year history of worsening dyspnea on exertion that was sometimes associated with vague chest pain. She had no history of cardiopulmonary disease and was not taking any medications. Electrocardiography was nonspecific, and the physical examination was significant only for a mild systolic murmur at her left lower sternal margin.

Chest radiography suggested right heart enlargement.

clinical review

RV

LV RA

LA

Figure 1. Long-axis, four-chamber, systolic bright blood magnetic resonance imaging reveals one of the atrial septal defects (short arrow), and enlargement of the right atrium and right ventricle. This image also shows a systolic regurgitant flow jet (long arrow) emanating from the tricuspid valve, consistent with tricuspid insufficiency. (LA = left atrium; LV = left ventricle; RA = right atrium; RV = right ventricle.)

Transthoracic echocardiography (TTE) revealed mild to moderate enlargement of the right atrium and right ventricle, and moderate tricuspid insufficiency. Left ventricular function was normal (ejection fraction of 55-60 percent). Transesophageal echocardiography (TEE) was performed to evaluate for left-to-right shunt.

TEE revealed two ASDs and probable right upper partial anomalous pulmonary venous return (PAPVR).

The left superior and inferior pulmonary veins were noted to drain normally to the left atrium, but the right inferior pulmonary vein was not identified.

Cardiac MRI was ordered to assess the pulmonary venous drainage (especially the right pulmonary veins) and intracardiac anatomy, to evaluate for additional extracardiac lesions, and to quantify the left-to-right shunt (i.e., pulmonic to systemic blood flow [Qp:Qs] ratio). MRI confirmed the echocardiographic diagnosis of ASDs, right heart enlargement, and tricuspid insufficiency (Figure 1). MRI and gadolinium-enhanced three-dimensional magnetic resonance angiography (MRA) revealed normal left superior and inferior pulmonary veins, and a diminutive right inferior pulmonary vein draining normally to the left atrium, with the remainder of right pulmonary venous return draining via a large right upper PAPVR to the junction of the superior vena cava and right atrium (Figures 2 and 3).

RA LA

RA RV

Figure 2. Axial bright blood magnetic resonance imaging (left) reveals a large right upper PAPVR (arrow) draining into the right atrium. An oblique coronal bright blood image (right) better demonstrates the direct drainage of the right upper PAPVR (long arrow) to the right atrium at its junction with the superior vena cava (short arrow). (LA = left atrium; PAPVR = partial anomalous pulmonary venous return; RA = right atrium; RV = right ventricle.)

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Clinical review Chest Radiography

LSPV * LIPV

PAPVR

LA *

Posteroanterior and lateral chest radiography is widely available and remains a basic first-line imaging technique for adults with suspected CHD. Chest radiography may provide the first suggestion of a congenital lesion, such as a great vessel anomaly.1,8 Chest radiographs can readily illustrate cardiopulmonary and mediastinal contours, pulmonary vascularity, pathologic calcification, and evidence of previous intervention (e.g., metallic surgical clip, valve, stent), but they typically provide insufficient information for definitive diagnosis of CHD.

Echocardiography Figure 3. Reformatted posterior view from gadoliniumenhanced three-dimensional magnetic resonance angiography reveals three pulmonary veins draining into the left atrium: a left superior pulmonary vein, a left inferior pulmonary vein, and a small right inferior pulmonary vein (long arrow). The inferior pulmonary vein drains the right lower lobe. The remainder of the right lung (i.e., right middle and right upper lobes) drains via the large right upper PAPVR that empties anteriorly into the right atrium (*). (LA = left atrium; LIPV = left inferior pulmonary vein; LSPV = left superior pulmonary vein; PAPVR = partial anomalous pulmonary venous return.)

MRI showed the Qp:Qs ratio to be greater than 3:1 (i.e., a significant left-to-right shunt). An exercise stress-rest, dual-isotope (thallium 201 and technetium 99m sestamibi) single photon emission CT (SPECT) examination was performed before surgery to exclude the possibility of concomitant occlusive coronary artery disease. The stress-rest SPECT examination was normal, and the patient subsequently underwent surgical closure of the ASDs and rerouting of the right upper PAPVR to the left atrium.

Imaging The American College of Radiology Appropriateness Criteria for the imaging tests used in the evaluation of adults with suspected CHD are listed in Table 1.6,7 A more detailed discussion has been published previously.7 The illustrative case above highlights an application of imaging used in the evaluation of adults with CHD. Chest radiography was initially performed but was nonspecific, requiring TTE and then TEE for the identification of the underlying ASDs and PAPVR. Cardiac MRI with MRA played an important adjunctive role by delineating the pulmonary venous return, excluding the presence of additional cardiovascular lesions, and quantifying the left-to-right shunt.

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TTE is a crucial initial imaging study in adults with suspected CHD. Two-dimensional TTE using color Doppler is well suited for rapid evaluation of cardiac morphology, function, and blood flow. Threedimensional TTE can supply more information than traditional two-dimensional TTE,9 but it may be nondiagnostic in up to 27 percent of patients.10 TTE has several limitations, such as high operator dependence that diminishes its reproducibility.11 In adults, especially postoperative patients, the acoustic windows may be poor and can preclude adequate CHD assessment.2,12,13 In these situations, TEE and MRI have important roles.

Compared with TTE, TEE can provide a new or alternative diagnosis (14 percent) or new information (56 percent) in adults with CHD.14 Limitations include limited planes of view, poor visualization of specific regions (e.g., apicoanterior septum and right ventricular outflow tract, pulmonary valve, distal right pulmonary artery, proximal left pulmonary artery), and blind areas such as those created by masking of blood flow by implanted prosthetic material.14 TEE is also an invasive examination and is operator-dependent.15

Radionuclide Imaging Historically, radionuclide imaging has been used for the evaluation of ventricular function and quantification of cardiac shunts in adults with CHD.16,17 However, many of these indications are now more readily evaluated with MRI, which provides superior anatomic illustration of CHD lesions and does not require the radiation exposure inherent with radionuclide imaging.

In patients who are unable to undergo MRI, nuclear scintigraphy is a viable alternative. As the illustrative case shows, stress-rest radionuclide SPECT imaging is a valuable adjunctive study to exclude concomitant ischemic heart disease.

clinical review Table 1. Radiologic Evaluation of Suspected Congenital Heart Disease in Adults Procedure

Appropriateness rating*

Comments

Chest radiography

9

Recommended in combination with TTE

Ultrasound TTE with Doppler

9

Recommended in combination with chest radiography

Heart MRI

8

May be performed as adjunct to TTE by trained operator if additional information is required; see comments regarding contrast in referenced article under “Anticipated Expectations”7

Coronary artery CT angiography

7

Preferred technique for suspected coronary anomalies; can also be used for evaluation of coronary artery disease

Ultrasound TEE

7

May be performed as adjunct to TTE by trained operator if additional information is required

Chest magnetic resonance angiography

6

To evaluate associated vascular abnormalities; see comments regarding contrast in referenced article under “Anticipated Expectations”7

Heart CT with contrast

6

May be an alternative to MRI and TTE or TEE

Cardiac catheterization with angiography

5

Adjunctive to noninvasive testing, for hemodynamic measurements or coronary artery status, or if other diagnostic information is required

Heart nuclear scintigraphy

4

May be used for perfusion in patients with suspected ischemic heart disease

Nuclear shunt detection

4

Alternative to MRI for shunt quantification

CT = Computed tomography; MRI = Magnetic resonance imaging; TEE = transesophageal echocardiography; TTE = transthoracic echocardiography. *American College of Radiology Appropriateness Criteria scale: 1 = least appropriate to 9 = most appropriate.

Computed Tomography Cardiac-gated CT scanners can quickly evaluate the entire heart and great vessel region as a threedimensional volume.18-20 Most types of congenital cardiac malformations have been described using this technique. Cardiac-gated CT can provide a variety of cardiac functional measurements, such as ventricular volumes, ejection fraction, regurgitant volumes, and myocardial mass. CT angiography (CTA) can identify congenital abnormalities of the coronary arteries.

However, CTA and cardiac CT require exposure to iodinated contrast material and ionizing radiation.

Magnetic Resonance Imaging MRI is particularly useful for evaluating CHD.4,12,13,21-30 MRI can provide essential morphologic and functional information for the management of CHD, without the concerns of ionizing radiation and iodinated contrast material associated with cardiac CT. MRI can show turbulent blood flow (e.g., a flow jet) associated with septal or valvular lesions (Figure 1). Unlike CT, MRI allows direct measurement of blood flow for quantification of left-to-right shunts, regurgitant fractions, and pressure gradients across stenoses and valves.30 Unlike echocardiography, MRI is not limited by an imaging “window,” and images can be obtained in essentially any plane for improved three-dimensional visualization of cardiac anatomy, which can be particularly complex in postoperative patients.25-27

Similar to CT, MRI can provide volumetric coverage of cardiac chambers for determination of cardiac metrics, such as ventricular volumes, ejection fractions, regurgitant volumes, and myocardial mass.

MRI has some contraindications and limitations. Some patients have claustrophobia, but most can tolerate MRI with mild sedation. The presence of certain metallic devices, such as pacemakers, is generally considered a contraindication, although MRI has been performed safely under rigorous safeguards in patients with pacemakers.31 The administration of gadolinium chelate contrast agents may be problematic in some patients, such as those with a severe allergy to these agents or those at significant risk for nephrogenic systemic fibrosis (e.g., renal failure with an estimated glomerular filtration rate of less than 30 mL per minute per 1.73 m2). However, unlike for cardiac CT, the use of contrast agents for MRI evaluation of patients with CHD is often unnecessary. Detection of calcification is a limitation of MRI, so adults with homografts or bioprosthetic valved conduits in which the detection of calcification implies deterioration may not be optimally imaged.

TTE/TEE vs. MRI MRI often provides information that is additive to that of TTE.13 In some evaluations, MRI can more reliably assess lesion severity and can be more successfully performed than TTE.32 MRI is comparable with TTE

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Clinical review in the evaluation of isolated intracardiac defects, but MRI is often more useful in the diagnosis of complex congenital lesions, as well as lesions involving the right ventricular outflow tract or pulmonary arteries, and systemic-to-pulmonary shunts.33-35 TEE is superior to MRI in the evaluation of intracardiac anatomy in adults with CHD, but MRI is superior in assessing extracardiac anatomy.36 The two techniques provide similar overall diagnostic information.

However, when TEE and MRI are used in combination, they provide important complementary information in all diagnostic categories.36

Cardiac Catheterization and Angiography Cardiac catheterization and angiography have been the diagnostic gold standard for CHD for 50 years.

For the past two decades, this technique has been increasingly supplemented by noninvasive diagnostic modalities—initially, echocardiography and, more recently, MRI and cardiac CT. In 2001, a task force of the 32nd Bethesda Conference suggested the use of diagnostic catheterization primarily to resolve specific issues related to surgical intervention, such as the preoperative evaluation of coronary arteries; the assessment of pulmonary vascular disease and its response to vasoactive agents for traditional surgical intervention and/or heart or heart/lung transplantation; and as an adjunct to noninvasive assessment for further delineation of morphologic and functional characteristics of complex congenital lesions.

disparities, 2376-2381.

1979-1997.

Circulation.

2001;103(19):

5. Wren C, O’Sullivan JJ. Survival with congenital heart disease and need for follow up in adult life. Heart. 2001; 85(4):438-443.

6. American College of Radiology. ACR Appropriateness Criteria: suspected congenital heart disease in the adult. http://acsearch.acr.org/VariantList.aspx?topicid=68689.

Accessed August 3, 2009.

7. Ho VB. ACR Appropriateness Criteria on suspected congenital heart disease in adults. J Am Coll Radiol. 2008; 5(2):97-104.

8. Baron MG. Plain film diagnosis of common cardiac anomalies in the adult. Radiol Clin North Am. 1999;37(2):401-420.

9. Salustri A, et al. Transthoracic three-dimensional echocardiography in adult patients with congenital heart disease. J Am Coll Cardiol. 1995;26(3):759-767.

10. Cheng TO, et al. Real-time 3-dimensional echocardiography in assessing atrial and ventricular septal defects: an echocardiographic-surgical correlative study [published correction appears in Am Heart J 2005;149(2):208]. Am Heart J. 2004;148(6):1091-1105.

11. Salehian O, et al. Assessment of systemic right ventricular function in patients with transposition of the great arteries using the myocardial performance index: comparison with cardiac magnetic resonance imaging. Circulation.

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12. Rebergen SA, de Roos A. Congenital heart disease.

Evaluation of anatomy and function by MRI. Herz.

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Although diagnostic cardiac catheterization continues to be performed, many patients with simple congenital cardiac defects now undergo surgery based on noninvasive preoperative evaluation alone. Technical advances in echocardiography, cardiac CT, and MRI have been significant, and further advances will likely expand the roles of these techniques in the evaluation of CHD and diminish the need for invasive diagnostic catheterization and angiography.

13. Simpson IA, Sahn DJ. Adult congenital heart disease: use of transthoracic echocardiography versus magnetic resonance imaging scanning. Am J Card Imaging.

1995;9(1):29-37.

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Systolic and Diastolic Ratio and Rate Pressure Product in Anemia K Singh

Abstract Anemia, a common clinical entity is associated with hyperdynamic circulation and may be involved in etiopathology of heart failure. So, the current study was carried out in 30 patients in the age group 20-40 years with hemoglobin level <6 g/dl and of at least 3-month duration of anemia (using WHO definition) and compared with 30 age- and sex-matched healthy subjects.

Duration of systole and diastole was estimated by recording of electrocardiogram, apexcardiogram and phonocardiogram on polyrite with the paper speed of 50 mm/sec. Duration of cardiac cycle was reduced (18.22%) and heart rate was increased (p < 0.001) in anemia compared to controls. On comparison of duration of systole and diastole, there was more decrement in diastole (26.76%, p < 0.001) compare to systole (6.45%, p < 0.01) in anemia versus healthy subjects. Similarly, when fraction occupied by systole and diastole in cardiac cycle were compared, the systolic fraction was increased, diastolic fraction in cardiac cycle was reduced and systole/diastole ratio was increased (p < 0.001) in anemics compared to controls. Rate pressure product and double product were elevated (p < 0.001) in anemia versus controls, imposing mechanical load on heart. So, it is concluded that patients of severe anemia are at the brink of heart failure and should be treated promptly.

Keywords: Systole, diastole, cardiac cycle, anemia

S

ystole and diastole are the fundamental periods of cardiac cycle. Intervals of cardiac cycle as measured by echocardiography, apexcardiography, i.e., isovolumic contraction time, isovolumic relaxation time are used to assess ventricular function.1 Recently importance of duration of systole and diastole is emphasized and it is advocated that they can be used to assess cardiac functions as prognosis of patients suffering from diastolic heart failure (DHF) is as ominous as prognosis of patients suffering from systolic heart failure (SHF).2

Anemia, a frequently encountered clinical entity, said to be a risk factor for functional and cognitive disease3 imposes mechanical load on heart and may be involved in pathogenesis and progression of heart failure,4 chronic angina5 and acute coronary syndrome.6 Moreover, it is associated with ventricular hypertrophy, ischemia and increased heart rate.6 So, the current study is planned to evaluate the duration of cardiac cycle, ratio of systole to diastole (S/D ratio), rate pressure product (RPP - since, Professor Dept. of Physiology Pt. BD Sharma, Postgraduate Institute of Medical Sciences (PGIMS), University of Health Sciences Rohtak (UHSR), Rohtak, Haryana Address for correspondence Dr K Singh 6J-11, Medical Campus, Rohtak - 124 001, Haryana E-mail: dr_rb_singh@rediffmail.com

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it is an easy measurable index of myocardial oxygen consumption and load on heart)7 and double product (DoP) in patients of anemia.

Methods The study was carried out in 30 patients of anemia (hemoglobin level was >6 g/dl for at least 3-month duration)8 using World Health Organization (WHO) definition of anemia - hemoglobin <13 g/dl for men and <12 g/dl in women9 in the age group of 20-40 years (mean age 32.65 ± 1.62) with body mass index (BMI) 22.9 ± 0.33 without clinical evidence of cardiac decompensation, and 30 age- (mean 31.49 ± 3.34 years) and sex-matched healthy subjects (hemoglobin level 11-14.02 g/dl) having BMI 22.2 ± 0.36.

Electrocardiogram (ECG), apexcardiogram (ACG) and phonocardiogram (PCG) were recorded with the paper speed of 50 mm/sec on polyrite (INCO). Systole was measured from onset of ventricular depolarization to first high frequency vibration of aortic sound. Diastole was measured from beginning of first high frequency of second heart sound to the beginning of sudden upstroke of ACG (Fig. 1). Duration of cardiac cycle, proportion of cardiac cycle occupied by systole and diastole, and S/D ratio were evaluated. Heart rate (HR) was assessed from ECG (lead II). Blood pressure (BP) was recorded manually by using sphygmomanometer.

Clinical Study RPP was calculated as SP × HR × 10-2, where SP is systolic pressure and value obtained was expressed as mmHg beats/min.7 Similarly, DoP was calculated as MP x HR, where MP is mean pressure and it was expressed in mmHg beats/min.10 Statistical analysis was done by unpaired ‘t’ test. Values were expressed as mean ± SD. A p value of <0.05 was accepted as significant.

Result Duration of cardiac cycle was 884.76 ± 87.54 msec. in normal healthy controls at the HR of 75.4 ± 12.5 beats/min in contrast to 723.5 ± 55.02 msec at the HR of 92.08 ± 18.19 beats/min in anemia. This reduction in duration of cardiac cycle (18.22%) was significant (p < 0.001). Duration of systole and diastole was 372.06 ± 29.41 versus 512.70 ± 110.14 msec, respectively in controls compared to duration of systole and diastole 348.04 ± 39.46 versus 375.46 ± 107.40 msec, respectively in anemic patients. On comparison of systole and Electrocardiogram

Apexcardiogram

Phonocardiogram Systole Diastole

Figure 1. Simultaneous recording of ECG, ACG and PCG in controls.

Electrocardiogram

Apexcardiogram

Phonocardiogram

Figure 2. Simultaneous recording of ECG, ACG and PCG in anemia.

diastole, there was more decrement in diastole (26.76%, p < 0.001) compared to systole (6.45%, p < 0.001) in anemic patients versus healthy controls (Fig. 2).

In healthy subjects systole and diastole constitute 42.05% and 57.94% fraction of cardiac cycle, respectively.

While in anemia systole and diastole constitute 48.1% and 51.89% fraction of cardiac cycle, respectively, indicating fraction of systole was increased and diastole was reduced in anemia (Table 1). S/D ratio was lengthened (p < 0.001) in anemia, i.e., 1.04 ± 0.23 versus 0.71 ± 0.06 in controls (Fig. 2). RPP and DoP were significantly (p < 0.001) elevated in anemia compared to controls (Table 1).

Discussion Anemia is said to be involved in the pathogenesis of heart failure (HF).4 It is hypothesized that relative duration of systole and diastole are altered and S/D ratio increases in HF.1 Duration of cardiac cycle in present study is about 0.88 second at normal HR in controls, which is in agreement with other authors.11 But in anemia, duration of cardiac cycle is shortened, which may be explained by hyperkinetic circulation. Reduction in duration of diastole is more (26%) than systole (6.4%), may be due to tachycardia. Tachycardia adversely affects the diastolic function by several mechanisms, as it diminishes the left ventricular filling, coronary perfusion time, increases myocardial oxygen demand, raises myocardial oxygen consumption and causes incomplete relaxation.12 It has to be noted that although duration of systole as such is reduced, proportion of cardic cycle occupied by systole is lengthened from 42.05% in controls to 48% in anemics.

In contrast proportion of cardiac cycle occupied by diastole is more reduced in anemia, from 57.9% to 51% in controls and anemics, respectively. All these changes result in enhanced S/D ratio in anemia in current study, which is consistent with the findings described by other authors in patients of HF. Myocardial perfusion occurs primarily in diastole. Myocardial blood flow in patients of left ventricular hypertrophy (LVH) (anemia can be associated with LVH) may depend upon diastolic perfusion time and perfusion pressure.

Myocardial remodeling induced by renin-angiotensin system activated due to decreased renal perfusion and increased catecholamine secretion in anemia predisposes the ischemic damage.13 Reduced oxygen carrying capacity of blood, increase in circulation time and HR with reduction in diastolic time may further complicate coronary perfusion and still worsen the cardiac function.1

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Clinical Study Table 1. Comparison of Parameters in Control and in Anemia (Mean ± SD) Parameters

Heart rate (beats/ min)

Systolic Diastolic BP BP (mmHg) (mmHg)

Cardiac cycle length (msec)

Duration of systole (msec)

Duration of diastole (msec)

Proportion of systole and diastole (%) in cardiac cycle

S/D ratio

RPP mmHg, beats/ min

DoP mmHg, beats/ min

Controls

75.4 ± 12.5

120.80 ± 8.90

71.10 ± 9.20

884.76 ± 87.54

372.06 ± 29.41

512.70 ± 110.14

42.05 and 57.94

0.71 ± 0.06

91.06 ± 12.32

7609.56 ± 190.5

Anemia

92.08** ± 18.19

111.04** ± 10.21

70.80 ± 9.27

723.5** ± 55.02

348.04* ± 39.46

375.46** ± 107.40

48.1 and 51.89

1.04** ± 0.23

Difference or p value

<0.001

<0.001

NS

18.22%

6.45%

26.76%

<0.001

102.24** 9029.37** ± 15.21 ± 260.1 0.001

< 0.001

P value * = <0.01, ** = <0.001, BP = Blood Pressure S/D ratio = Systolic/Diastolic ratio, RPP = Rate pressure product, DoP = Double product.

But clinical signs and symptoms pointing to HF were not evident in these patients.14 They were not taking treatment of it inspite of enhanced RPP and DoP in anemia indicating increase in O2 consumption and load on the heart. Enhanced O2 consumption of cardiac muscles in severe anemia is demonstrated by other authors also.15 But it is difficult to explain the reason for absence of features of HF, may be at this HR filling of LV is adequate enough to maintain cardiac output.11 As it is also stated that DHF is referred to as HF with normal left ventricular ejection fraction (LVEF), i.e.

HFNLVEF.12 Moreover, onsets of symptoms also depend on the rapidity with which the anemia develops as well as physical activity of patient.

So, our findings as lengthened systole, enhanced systolic and diastolic ratio and reduction in duration of diastole pointed out that patients of anemia are at the brink of HF. So, while treating the patient of HF and coronary artery disease, we should also have a look for anemia as treatment of systole and diastole failure is different.

References 1. Friedberg MK, Silverman NH. Cardiac ventricular diastolic and systolic duration in children with heart failure secondary to idiopathic dilated cardiomyopathy. Am J Cardiol 2006;97(1):101-5.

2. Aurigemma GP. Diastolic heart failure: a common and lethal condition by any name. N Engl J Med 2006;355(3):308-10.

3. Denny SD, Kuchibhatla MN, Cohen HJ. Impact of anemia on mortality, cognition, and function in communitydwelling elderly. Am J Med 2006;119(4):327-34.

4. de Silva R, Rigby AS, Witte KK, Nikitin NP, Tin L, Goode K, et al. Anemia, renal dysfunction, and their interaction in patients with chronic heart failure. Am J Cardiol 2006;98(3):391-8.

5. Sharma S, Gage BF, Deych E, Rich MW. Anemia: an independent predictor of death and hospitalizations

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among elderly patients with atrial fibrillation. Am Heart J 2009;157(6):1057-63.

6. Meneveau N, Schiele F, Seronde MF, Descotes-Genon V, Oettinger J, Chopard R, et al; Reseau de Cardiologie de Franche Comte. Anemia for risk assessment of patients with acute coronary syndromes. Am J Cardiol 2009;103(4):442-7.

7. Gobel FL, Norstrom LA, Nelson RR, Jorgensen CR, Wang Y. The rate-pressure product as an index of myocardial oxygen consumption during exercise in patients with angina pectoris. Circulation 1978;57(3): 549-56.

8. Agarwal V, Sachdev A, Lehl S, Basu S. Unusual haematological alterations in rheumatoid arthritis. J Postgrad Med 2004;50(1):60-1.

9. Felker GM, Gattis WA, Leimberger JD, Adams KF, Cuffe MS, Gheorghiade M, et al. Usefulness of anemia as a predictor of death and rehospitalization in patients with decompensated heart failure. Am J Cardiol 2003;92(5): 625-8.

10. Madanmohan, Udupa K, Bhavanani AB, Vijayalakshmi P, Surendiran A. Effect of slow and fast pranayams on reaction time and cardiorespiratory variables. Indian J Physiol Pharmacol 2005;49(3):313-8.

11. Ganong WF. Heart as a pump. Chapter 29. In: Review of Medical Physiology. 21st edition, A Lange Medical Book: McGraw-Hill, New Delhi 2010;Chap. 31, Sec.VI, p.570.

12. Chopra HK. Diastolic heart failure: a clinical challenge early recognition & timely intervention is the need of the hour. Indian Heart J 2009;61(2):138-45.

13. Schrier RW, Abraham WT. Mechanism of disease: Hormones and haemodynamics in heart failure. N Engl J Med 1999;341:577-85.

14. Braunwald E. Heart failure and corpulmonale. Chapter 216. In: Harrison’s Principle of Internal Medicine. Vol. II, 6th edition, McGraw-Hill: New York 2005:p.1370.

15. Levy PS, Quigley RL, Gould SA. Acute dilutional anemia and critical left anterior descending coronary artery stenosis impairs end organ oxygen delivery. J Trauma 1996;41(3):416-23.

Case Report

Acute Renal Failure and Silent Myocardial Infarction Following Multiple Honey Bee Stings Kavina Marian Fernandes*, Gadwalkar Srikant R**, Shyamala Gâ&#x20AC;

Abstract Massive envenomation by honey bee sting is capable of causing multiorgan dysfunction as a result of direct toxic effect of venom and secondary to systemic anaphylactic reactions. Myocardial infarction (MI) due to honey bee sting is rare, so is acute renal failure (ARF). The probable mechanism is severe coronary arterial spasm with secondary in situ thrombosis as a result of systemic anaphylaxis. This is a case of Kounis syndrome, which is the concurrence of acute coronary syndromes with conditions associated with mast cell activation. We describe a case of ARF and MI in a 58-year-old man after multiple honey bee stings; clinically silent and detected on electrocardiography and by cardiac biomarkers.

Keywords: Acute myocardial infarction, acute renal failure, massive honey bee envenomation, Kounis syndrome

H

ymenoptera sting envenomation may result in a number of clinical presentations: 1) nonallergic, local reactions (pain, minor edema, redness at the sting site); 2) allergic, large local reactions (extensive swelling >10 cm persisting for >24 hours); 3) anaphylaxis (generalized urticaria, angioedema, bronchospasm, hypotension, cardiovascular collapse and loss of consciousness); 4) systemic toxic reactions (edema, vomiting, diarrhea, headache, seizures and altered sensorium); and 5) unusual reactions (cardiac ischemia, encephalomyelitis and cerebral infarctions).1 We report a case of massive bee sting envenomation with unusual manifestations of acute myocardial infarction (AMI) and acute renal failure (ARF).

diabetes mellitus, ischemic heart disease or dyspnea on exertion or angina.

He was brought to our emergency department eight hours after the bee stings. On admission, his pulse rate was 98 beats/minute, blood pressure was 90/60 mmHg, respiratory rate was 18/minute and oxygen saturation was 98% at room air. There were multiple stings on face, head, arms, chest, back and legs. There was

CASE PRESENTATION A 58-year-old forest official (Fig. 1), presented to us with a history of multiple bee stings (>200). He had been immediately admitted to a local hospital with swelling of lips and face. He was given preliminary care (treatment details are not known) and was referred to our hospital with dyspnea and decreased urine output.

He had dark colored urine. There was no history of chest pain, palpitations, syncope, seizure or altered sensorium. He was a chronic smoker. He was a known hypertensive on regular treatment. No past history of

*Postgraduate Student **Professor and Head â&#x20AC; Professor Dept. of General Medicine Vijayanagar Institute of Medical Sciences, Bellary, Karnataka

Figure 1. Patient with multiple stings and swelling of lips and face on third day of hospital admission.

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case report DISCUSSION

Figure 2. Electrocardiograph of the patient on the day of admission showing ST segment elevation in lead II, III and aVF, reciprocal ST depression was seen in lead I, aVL.

marked edema of face and lips with diffuse urticaria over the entire body. He had rhonchi in all lung fields.

Rest of the systemic examination was normal.

Hematological examination revealed total leukocyte counts (30,760 cells/mm3), and reduced platelet counts (58,000 cells/mm3). Renal parameters were elevated (urea, 62 mg/dl; creatinine, 3.3 mg/dl). Serum electrolytes were normal (sodium, 136 mmol/l; potassium, 4.2 mmol/l; chloride 106 mmol/l). Electrocardiograph showed ST segment elevation in lead II, III and aVF, reciprocal ST depression was seen in lead I, aVL (Fig. 2). Urine microscopy showed 10-12 pus cells and albuminuria 2+, troponin I was elevated (28.046 ng/ml).

ECG showed no further progression of ST elevation or poor progression of R waves. 2D-Echo showed normal cardiac chambers, normal cardiac valves, regional wall motion abnormality in inferior wall, ejaculation fraction (EF) was 55%.

His treatment with hydrocortisone 100 mg intravenous (IV) q6h, injection chlorphenaramine maleate 25 mg injection q12h and along with ranitidine 50 mg q8h.

He was hydrated with IV fluids. Injection epinephrine 0.3 mg IM was repeated thrice. Injection noradrenaline was given as an infusion at the rate of 1 Îźg/min. He was started on anticoagulants and oral antiplatelets.

Next day renal parameters increased (urea, 101 mg/dl; creatinine, 5.1 mg/dl). Ultrasonography of abdomen showed Grade I renal parenchymal disease with normal sized kidneys. Urine output did not improve inspite of above measures. He was dialyzed on alternate days.

His renal function gradually improved. ECG changes were reversed to almost normal limits.

Angioedema and urticaria also resolved completely.

Injection hydrocortisone was gradually tapered and stopped. He was switched to oral phenaramine maleate and ranitidine and discharged in 10 days. Patient was referred to higher center for further evaluation, where angiogram was done and reported to be normal.

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Massive honey bee envenomation is defined as more than 50 stings at a time. Individuals who are highly allergic to the venom may develop severe systemic anaphylaxis (type I hypersensitivity) from a single sting. Massive bee attacks can result in toxic reactions, regardless of pre-existing allergic conditions, by virtue of a high venom load potentially causing multiorgan dysfunction.1 The clinical and pathophysiological background of AMI after a bee sting is generally related to different mechanisms. Hymenoptera venom can cause acute myocardial injury by several mechanisms: (a) AMI occurring in subjects without significant coronary artery disease because of coronary thrombosis and vasospasm enhanced by intoxication.2 Release of allergenic proteins, vasoactive (epinephrine, dopamine), inflammatory (leukotrienes), thrombogenic peptides and amine constituents (histamine, serotonin, bradykinin, leukotrienes, thromboxane); which act on the coronary vasculature and induce coronary artery vasospasm and facilitate platelet aggregation as well as thrombosis. Paradoxical vasoconstriction could be an underlying mechanism. Severe coronary arterial spasm or secondary in situ thrombosis may also play a role in such a case;3 b) direct cardiotoxic effect of the venom and c) anaphylactic reaction. Anaphylactic reactions which result in acute coronary syndromes is also known as Kounis syndrome.4 Hymenoptera sting can lead to an AMI by different pathogenetic mechanisms depending on the presence of pre-existent coronary atherosclerosis, the development of shock or the therapeutic use of epinephrine.

Vasoactive amines, including histamine, dopamine and noradrenaline can provoke ischemia and even MI through profound hypotension and arrhythmia, or by increasing oxygen demands through direct inotropic and chronotropic effects in the presence of pre-existing ischemic heart disease.5 In patients with AMI after multiple bee stings as reported in literature, the coronary arteries were normal or insignificantly stenosed. Electrocardiographic changes consistent with acute myocardial ischemia or infarction, including ST depression or elevation and even the appearance of pathologic Q-waves, are seen in these patients. Rhythm abnormalities such as supraventricular arrhythmias, VPCâ&#x20AC;&#x2122;s, junctional rhythm and right bundle branch block may occur.4 Inflammatory mediators, adhesion molecules of neutrophils and monocytes, have been shown to be

case report increased in the plasma of patients presenting with acute coronary syndromes. Anaphylaxis is a systemic, immediate hypersensitivity reaction caused by rapid IgE-mediated release of mediators from mast cells and basophils. In 1991, Kounis and Zavras6 described the 'syndrome of allergic angina' as the coincidental occurrence of chest pain and allergic reactions accompanied by clinical and laboratory findings of classical angina pectoris caused by inflammatory mediators released during the allergic insult.

Allergic angina can progress to AMI, which was named 'allergic myocardial infarction'.7 In 1998, Braunwald,8 in an editorial, noted that vasospastic angina can be induced by 'allergic reactions with mediators such as histamine or leukotrienes acting on coronary vascular smooth muscle'.

There are two variants of this syndrome that have been described recently.9 Type Î&#x2122; variant includes patients with normal coronary arteries without predisposing factors for coronary artery disease in whom the acute release of inflammatory mediators can induce either coronary artery spasm leading to unstable angina or coronary vasospasm progressing to AMI. This variant might represent a manifestation of endothelial dysfunction. Type II variant includes patients with culprit but quiescent pre-existing atheromatous disease in whom acute allergic episode can induce plaque erosion or rupture manifesting as an AMI. If the clinical judgment favors the use of aspirin in these patients, it seems reasonable to give it after the initial treatment for Kounis syndrome has been started. Use of IV or sublingual nitroglycerin seems reasonable and safe if the blood pressure is satisfactory. b-blockers may offset some of the beneficial effects of epinephrine. Heparin bolus should be avoided.

Heparin should be used at low dose at a slow infusion rate. Calcium channel blockers may be considered the initial anti-ischemic drug of choice in patients with Kounis syndrome.10 Bee venom exposure may be associated with albuminuria.11 ARF following bee stings is a rare complication. Following bee stings, biphasic renal failure has been documented with early renal failure due to hemolysis and a second episode of azotemia about 10 days later occurring in conjunction with depressed serum complement C3 level and nephritic changes on renal biopsy. The major causes of renal failure are acute tubular necrosis (ATN) due to hypotension or pigment nephropathy resulting from rhabdomyolysis and intravascular hemolysis, and acute interstitial nephritis.12 Renal failure has resulted

from stings ranging from 22 to 1,000 in number.

The exact mechanism of rhabdomyolysis is not known but a direct toxic effect of venom on muscle is believed to be the main cause.13 However, other mechanisms postulated for renal damage due to bee stings are: 1) Direct nephrotoxicity due to toxin; 2) hypotension leading to ischemic tubular necrosis and 3) nephropathy due to hemoglobinuria and myoglobinuria.14 Reported systemic complications following multiple bee stings include ARF, myocarditis, MI, centrilobular necrosis of liver, acute encephalopathy, Guillain-Barre syndrome, vasculitis, disseminated intravascular coagulation and thrombocytopenia.15 CONCLUSION Of particular interest in the present case report is the silent presentation of MI. Clinical presentation may be quite different in AMI patients after bee stings. It may be completely silent, or ECG changes such as ST wave elevation may occur several hours after admission.

Therefore, a higher clinical suspicion is absolutely necessary to make a correct diagnosis. It follows that in any case of hymenoptera envenomation a standard ECG is advisable. Also, serial ECG recordings are recommended in every patient who complains of chest pain, regardless of the severity of the patient's reaction to a bee sting. Maintaining adequate urine output should be instituted with aggressive hydration to reduce the likelihood of rhabdomyolysis-induced renal insufficiency. In conclusion, massive bee envenomation can cause life-threatening complications like acute myocardial injury, rhabdomyolysis, hemolysis with ARF and systemic anaphylaxis.

REFERENCES 1. Betten DP, Richardson WH, Tong TC, Clark RF. Massive honey bee envenomation-induced rhabdomyolysis in an adolescent. Pediatrics 2006;117(1):231-5.

2. Ceyhan C, Ercan E, Tekten T, Kirilmaz B, Onder R. Myocardial infarction following a bee sting. Int J Cardiol 2001;80(2-3):251-3.

3. Massing JL, Bentz MH, Schlesser P, Dumitru C, Louis JP. Myocardial infarction following a bee sting. Apropos of a case and review of the literature. Ann Cardiol Angeiol (Paris) 1997;46(5-6):311-5.

4. Yang HP, Chen FC, Chen CC, Shen TY, Wu SP, Tseng YZ. Manifestations mimicking acute myocardial infarction after Honeybee Sting. Acta Cardiol Sin 2009;25:31-5.

5. Riches KJ, Gillis D, James RA. An autopsy approach to bee sting-related deaths. Pathology 2002;34(3):257-62.

6. Kounis NG, Zavras GM. Histamine-induced coronary artery spasm: the concept of allergic angina. Br J Clin Pract 1999;45(2):121-8.

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case report 7. Kounis NG, Zavras GM. Allergic angina and allergic myocardial infarction. Circulation 1996;94(7):1789.

12. Patil PL, Salkar HR. Wasp sting induced acute renal failure. Indian J Nephrol 2004;14:30-1.

8. Braunwald E. Unstable angina: an etiologic approach to management. Circulation 1998;98(21):2219-22.

13. Kim YO, Yoon SA, Kim KJ, Lee BO, Kim BS, Chang YS, et al. Severe rhabdomyolysis and acute renal failure due to multiple wasp stings. Nephrol Dial Transplant 2003;18(6):1235.

9. Nikolaidis LA, Kounis NG, Gradman AH. Allergic angina and allergic myocardial infarction: a new twist on an old syndrome. Can J Cardiol 2002;18(5): 508-11.

10. Cevik C, Nugent K, Shome GP, Kounis NG. Treatment of Kounis syndrome. Int J Cardiol 2010;143(3):223-6.

11. Elming H, Sølling K. Urine protein excretion after Hymenoptera sting. Scand J Urol Nephrol 1994;28(1): 13-5.

14. dos Reis MA, Costa RS, Coimbra TM, Dantas M, Gomes UA. Renal changes induced by envenomation with Africanized bee venom in female Wistar rats. Kidney Blood Press Res 1997;20(4):271-7.

15. Daher Ede F, da Silva Júnior GB, Bezerra GP, Pontes LB, Martins AM, Guimarães JA. Acute renal failure after massive honeybee stings. Rev Inst Med Trop Sao Paulo 2003;45(1):45-50.

■■■■

The subcutaneous implantable cardioverter-defibrillator (ICD) was safe and effective in the full pivotal trial results finally being published, but the device still has limitations. As per findings of Martin C. Burke, DO, of the University of Chicago Heart Rhythm Center, and colleagues, the S-ICD System met both its primary trial endpoints with a 180-day complication-free rate of 99% and induced acute ventricular fibrillation conversion rate of 100% in evaluable patients. According to the researchers, the subcutaneous ICD is a viable alternative to transvenous systems among patients who do not require pacing therapy for heart failure, bradycardia or ventricular tachycardia. The study is published in Circulation: Journal of the American Heart Association.

(Source: Medpage Today) Results from a readjudication of the Rosiglitazone Evaluated for Cardiovascular Outcomes and Regulation of Glycemia in Diabetes (Record) trial, supporting the original trial conclusion that the diabetes drug rosiglitazone does not increase the risk for adverse cardiovascular outcomes, have now been published in full in the August issue of the American Heart Journal, by Kenneth W. Mahaffey, MD, from Duke University, Durham, North Carolina and colleagues.

(Source: Medscape) A diet high in antioxidant-rich fruit may help protect against the development of an abdominal aortic aneurysm (AAA). A study from Karolinska Institute in Stockholm found that through 13 years of follow-up, men and women who said they ate more than two servings of fruit a day had a 25% lower risk of developing AAA (hazard ratio [HR] 0.75, 95% confidence interval [CI] 0.62-0.91) compared with those who ate <0.7 servings a day.

And those who ate the most fruit had a 43% lower risk of developing a ruptured AAA (HR 0.57, 95% 0.36-0.89), the researchers reported in the August 20 issue of Circulation: Journal of the American Heart Association. There were no such associations with vegetable intake.

(Source: Medpage Today)

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case report

Case of a Young Hypertensive with Recurrent Cerebrovascular Disease due to a Rare Etiology SM Rajendran*, S Palaniandavar**, Jamima Bhaskar†, J Senthilnathan‡, Arun R, Jose Mathew§

Abstract A young individual presented as hypertensive emergency due to a rare cause, a tumor arising from autonomic nervous system.

Screening test done in this patient revealed a case of extra-adrenal pheochromocytoma, which was confirmed by imaging studies. Pheochromocytoma usually manifests itself with paroxysmal symptoms and can be easily missed; therefore all young individuals with secondary hypertension must be screened for pheochromocytoma. This case presented clinically as recurrent cerebrovascular disease (CVD).

Keywords: Hypertensive emergency, pheochromocytoma, secondary hypertension, recurrent cerebrovascular disease

P

heochromocytoma is a tumor of the sympathetic or parasympathetic nervous system and is one of the causes of secondary hypertension, which is refractory to antihypertensive therapy. This is a curable cause of hypertension and its early detection and diagnosis is equally important.

Investigations

ÂÂ

Hemoglobin 13.2 g/dl, total leukocyte count 5,000 cells/mm3, differential leukocyte count P62L34E4, erythrocyte sedimentation rate 16 mm/hour.

Case Report

ÂÂ

Urea 35 mg/dl, creatinine 1 mg/dl, Na+ 134.1 mEq/l Cl- 85.2 mEq/dl, K+ 3.1 mEq/dl.

Chief Complaints

ÂÂ

Total cholesterol 138 mg/dl, triglycerides 119 mg/dl, high-density lipoprotein 38 mg/dl, low-density lipoprotein 76 mg/dl, very low-density lipoprotein 24 mg/dl. Cholesterol ratio 3.6.

ÂÂ

Antiphospholipid antibody 6.67 U/ml.

ÂÂ

24-hour urinary vanillylmandelic acid (VMA) 18.88 mg/24 hours (normal value <6-8 mg/dl in adults).

Mr. Suresh, a 22-year-old male was admitted to the hospital with the chief complaints of: a) Inability to use both his left upper and lower limbs for 3 days; b) inability to speak; c) deviation of angle of mouth to the right side; d) double vision and e) recurrent episodes of headache, palpitation and sweating.

There was history of similar episode two years ago.

He also had history of one episode of seizure seven years before. On examination, his blood pressure (BP) was 220/120 mmHg and pulse rate was 120/ min. Cardio-vascular system, respiratory rate and per abdomen examination revealed no abnormalities. On neurological examination, he had left-sided hemiplegia, horizontal nystagmus with lateral gaze, left-sided 3rd nerve palsy, right-sided 6th nerve palsy and right-sided lower motor neuron type of facial palsy and cerebellar signs. *Professor and Head **Professor, †Associate Professor ‡Assistant Professor, §Postgraduate Dept. of Medicine Sree Balaji Medical College and Hospital, Chennai

Blood Investigations

ECG Sinus tachycardia, electrical left atrial enlargement/left ventricular hypertrophy.

Chest X-ray Normal

MRI Abdomen Multiple relatively defined discrete lesions of varying sizes noted in the bilateral para-aortic region, extraadrenal pheochromocytoma, shrunken right kidney.

CT Brain Multiple infarcts

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case report Course in Hospital He was admitted to the intensive care unit (ICU) with a BP of 220/120 mmHg and nitroglycerin (NTG) infusion was started to control his BP. There was a very irregular response. NTG infusion was gradually tapered and he was put on prazosin, calcium channel blockers and angiotensin-converting enzyme (ACE) inhibitors.

Later, he was put on phenoxybenzamine, starting with 10 mg b.i.d. and increased to 20 mg t.i.d. After that, a b-blocker was added to control the tachycardia. He was advised low salt diet and adequate hydration. His BP was gradually reduced from 180/130-150/90 mmHg with episodes of wide fluctuations. After his BP was consistently below 160/90 mmHg for two weeks, he was taken up for surgery.

Laparotomy was done and multiple tumors were excised from the bilateral para-aortic region. There was an intraoperative rise in the BP associated with handling of the tumors, which was brought to control by NTG infusion.

A small portion of the tumor near the left renal vein was left behind because of difficulty in removing it without damaging the left renal artery. Postoperatively, the BP increased to 220/130 mmHg, which was managed by NTG infusion and magnesium sulfate regime. His BPwas stabilized to 130/100 mmHg within a week and was discharged with methyldopa 250 mg b.i.d. and vitamins. During follow-up, his BP was found to be within normal limits.

Histopathological Examination Specimen: Extra-adrenal pheochromocytoma.

Gross: Several fragmented dark brown masses in aggregates of size 7 Ă&#x2014; 4 Ă&#x2014; 3 cm. The cut surface showed a dark yellow to orange nodular lesion with a thin rim at the periphery.

Microscopy: Revealed small nesting growth pattern (zellballen appearance). Tumor cells were fairly uniform with finely granular cytoplasm.

Diagnosis: Extra-adrenal mass, excision-pheochromocytoma.

Discussion

Figure 1. MRI abdomen showing multiple relatively defined discrete bilateral lesions in para-aortic region and extra-adrenal pheochromocytoma.

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The patient was a young hypertensive who developed crossed hemiplegia due to brainstem lesion. Computed tomography (CT) brain showed multiple infarcts, which were secondary to hypertension. Urinary VMA was elevated and magnetic resonance imaging (MRI) abdomen showed multiple extra-adrenal masses. BP was refractory to antihypertensive therapy. Patient was put on a- and b-blockers, ACE inhibitor, methyldopa.

case report Inspite of these drugs, his BP did not come under control. Metaiodobenzylguanidine (MIBG) scan could not be done because the patient could not afford it.

Bilateral multiple extra-adrenal paraganglion masses were excised. In the postoperative period, BP started to come down and on follow-up, his BP was normal. ÂÂ

About 10% pheochromocytomas are extra-adrenal and most of them are <10 cm in diameter.

ÂÂ

It manifests as hypertension, which responds paradoxically to antihypertensive therapy.

ÂÂ

Patients have paroxysms during which they develop headache, sweating and palpitations.

ÂÂ

Cardiac manifestations are supraventricular tachycardia, ventricular arrhythmias, angina and cardiomyopathy.

ÂÂ

Some patients present with acute respiratory distress syndrome.

ÂÂ

There are reports of pheochromocytomas presenting as panic attacks, pre-eclampsia, impaired glucose tolerance and pulmonary edema.

ÂÂ

Biochemical assessment are done for urinary VMA, humovanillic acid, fractionated metanephrines and catecholamines.

ÂÂ

Plasma catecholamines, dopamine, free metanephrines (most sensitive) and chromogranin A may also be assayed.

ÂÂ

MRI/CT of the abdomen and MIBG scan help to localize the tumor.

ÂÂ

Patients should also be evaluated for other associated syndromes like multiple endocrine neoplasia 2A/2B, Von Hippel-Landau syndrome, neurofibromatosis, familial paraganglioma, familial pheochromocytoma with islet cell tumor, Sturge-Weber syndrome, ataxia telangiectasia, tuberous sclerosis and Carney’s triad.

Conclusion This case is being presented as a young hypertensive with recurrent cerebrovascular accident (CVA) and seizures who had resistant hypertension not amenable to antihypertensive therapy given in high dosage in different combinations. Urinary VMA was positive and further investigations confirmed pheochromocytoma.

Surgical removal brought complete cure to the patient.

Pheochromocytoma presenting as recurrent CVA is a very rare and unusual manifestation of the tumor.

Suggested Reading

Figure 2. Histopathology showing small nesting growth pattern (zellballen appearance).

1. Stein PP, Black HR. A simplified diagnostic approach to pheochromocytoma. A review of the literature and report of one institution’s experience. Medicine (Baltimore) 1991;70(1):46-66.

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case report 2. Adler JT, Meyer-Rochow GY, Chen H, et al.

Pheochromocytoma: current approaches and future directions. Oncologist 2008;13(7):779-93.

3. Luo A, Guo X, Ren H, et al. Clinical features and anesthetic management of multiple endocrine neoplasia associated with pheochromocytoma. Chin Med J (Engl) 2003;116(2):208-11.

4. Pacak K, Linehan WM, Eisenhofer G, et al. Recent advances in genetics, diagnosis, localization, and treatment of pheochromocytoma. Ann Intern Med 2001;134(4): 315-29.

5. Menger WM, Gifford RW Jr. Clinical and experimental pheochromocytoma. Blackwell Science: Cambridge, MA; 1996.

involvement with pheochromocytoma: a review. Chest 1999;115(2):511-21.

7. Whalen RK, Althausen AF, Daniels GH. Extra-adrenal pheochromocytoma. J Urol 1992;147(1):1-10.

8. Plouin PF, Chatellier G, Fofol I, et al. Tumor recurrence and hypertension persistence after successful pheochromocytoma operation.

Hypertension 1997;29(5):1133-9.

9. Scott HW Jr, Halter SA. Oncologic aspects of pheochromocytoma: the importance of follow-up.

Surgery 1984;96(6):1061-6.

10. d’Herbomez M, Gouze V, Huglo D, et al. Chromogranin A assay and (131)I-MIBG scintigraphy for diagnosis and follow-up of pheochromocytoma. J Nucl Med 2001;42(7):993-7.

6. Sandur S, Dasgupta A, Shapiro JL, et al. Thoracic ■■■■

New Way to Block Inflammation in Alzheimer’s, Atherosclerosis and Type 2 Diabetes Researchers at NYU Langone Medical Center have discovered a mechanism that triggers chronic inflammation in Alzheimer’s, atherosclerosis and type 2 diabetes. The results, published in Nature Immunology, suggest a common biochemical thread to multiple diseases and point the way to a new class of therapies that could treat chronic inflammation in these noninfectious diseases without crippling the immune system. Alzheimer’s, atherosclerosis and type 2 diabetes - diseases associated with aging and inflammation - affect more than 100 million Americans.

(Source: Science Daily)

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Expert's Opinion

What are the Factors Contributing to Resistant Hypertension?

Sameer Shrivastava*, KK Aggarwal**

R

esistant hypertension is somewhat uncommon in the modern management of hypertension. A majority of patients with primary hypertension respond favorably to one or more antihypertensive drugs. Definitions vary but hypertension is considered resistant if the blood pressure (BP) cannot be reduced below target levels in patients who are compliant with an optimal triple-drug regimen that includes a diuretic. When a hypertensive patient demonstrates resistance to standard antihypertensive drug therapy, proper management requires identification of possible etiologies. The major causes of resistant hypertension are described below.

Several classes of pharmacological agents can produce transient or persistent increases in BP. Nonsteroidal antiinflammatory drugs (NSAIDs) are a common cause of worsening BP control. They increase BP by an average of 5 mmHg, in part because of inhibition of renal prostaglandin production decreases in renal blood flow, followed by sodium and fluid retention.1 They also interfere with BP-lowering of all antihypertensive drug classes except calcium antagonists.2 The effect of NSAIDs on BP is more pronounced in patients with reduced kidney function. Selective cyclooxygenase-2 inhibitors have effects similar to those of NSAIDs on BP control.3 Sympathomimetic agents (nasal decongestants, anorectic pills, amphetamine-like stimulants), oral contraceptives, glucocorticoids, anabolic steroids, erythropoietin and cyclosporine are also commonly used agents that can interfere with BP control. The effect of these agents varies; most people manifest little or no effect, but certain persons may experience severe BP elevations. Lastly, illicit drugs can be a major unappreciated cause of resistant hypertension. Agents such as steroids and cocaine are common causes of resistant hypertension. *Associate Director Dept. of Cardiology, Fortis Escorts Heart Institute, New Delhi **Senior Physician and Cardiologist Moolchand Medcity, New Delhi

Although modest alcohol consumption does not generally increase BP, larger amounts (â&#x2030;Ľ3 drinks/day) have a dose-related effect on BP, both in hypertensive and normotensive persons. Alcohol intake in all hypertensive patients should be limited to no more than 1 oz of ethanol a day in most men (the equivalent of 2 drinks) and 0.5 oz of ethanol a day in women and lower-weight persons.

Another important factor responsible for many cases of resistant hypertension is excess dietary salt intake leading to volume overload. Data from small studies demonstrate that 90% of patients with resistant hypertension have expanded plasma volume.4 Majority of patients with resistant hypertension have higher salt intake than the general population, with an average dietary sodium intake exceeding 10 g/day.5 The optimal way to assess sodium intake is to measure sodium excretion in a 24-hour urine collection. Dietary salt reduction to <3 g/day is associated with modest BP reductions.

Current guidelines suggest that dietary sodium for a hypertensive person should be <100 mmol/day (2.4 g sodium or 6 g sodium chloride). This guidance is applicable to all patients with resistant hypertension, whereas for salt-sensitive patients, even lower amounts of sodium may be necessary.

Kidney disease is the most common secondary medical cause of hypertension. Failure to appreciate this relationship may lead to less than optimal choices of antihypertensive agents such as failure to use appropriately dosed or selected diuretics based on kidney function. This lack of diuretic use has been shown in referral practices to be the primary cause of resistant hypertension, with the use of these agents helping to achieve BP goals.

Obesity is also a very common feature of patients with resistant hypertension.6 The mechanisms by which obesity contributes to BP elevation and interferes with BP control are complex and not fully understood. Insulin resistance and hyperinsulinemia, impaired sodium

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Expert's Opinion excretion, increased sympathetic nervous system activity, increases in aldosterone sensitivity related to visceral adiposity and obstructive sleep apnea have all been implicated as potential causes.7 Weight loss achieved with both an appropriate exercise program and a reduced calorie diet is associated with modest BP reductions in obese hypertensive patients. These reductions are greater in patients already receiving antihypertensive therapy.

Increasing age, namely, >65 years old, is associated with a higher prevalence of resistant hypertension.8 Increasing age is associated with a higher prevalence of arterial stiffening, which is not only responsible for falsely elevated systolic BP readings but also a major cause of true elevations. Current guidelines for systolic BP goals of <140 mmHg are more difficult to achieve in patients with isolated systolic hypertension and are more difficult with increasing age because of the natural history of arteriosclerosis.

In patients with resistant hypertension, the presence of secondary hypertension must be considered; although its prevalence is largely unknown, previous studies have shown that 5-10% of patients with resistant hypertension have an identifiable cause.9

2. Conlin PR, Moore TJ, Swartz SL, et al. Effect of indomethacin on blood pressure lowering by captopril and losartan in hypertensive patients. Hypertension 2000;36(3):461-5.

3. Whelton A, White WB, Bello AE, et al; SUCCESS-VII Investigators. Effects of celecoxib and rofecoxib on blood pressure and edema in patients > or = 65 years of age with systemic hypertension and osteoarthritis. Am J Cardiol 2002;90(9):959-63.

4. Graves JW, Bloomfield RL, Buckalew VM Jr. Plasma volume in resistant hypertension: guide to pathophysiology and therapy. Am J Med Sci 1989;298(6):361-5.

5. Nishizaka MK, Pratt-Ubunama M, Zaman MA, et al.

Validity of plasma aldosterone-to-renin activity ratio in African American and white subjects with resistant hypertension. Am J Hypertens 2005;18(6):805-12.

6. Cushman WC, Ford CE, Cutler JA, et al; ALLHAT Collaborative Research Group. Success and predictors of blood pressure control in diverse North American settings: the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT). J Clin Hypertens (Greenwich) 2002;4(6):393-404.

7. Wong C, Marwick TH. Obesity cardiomyopathy: pathogenesis and pathophysiology. Nat Clin Pract Cardiovasc Med 2007;4(8):436-43.

References

8. Calhoun DA, Zaman MA, Nishizaka MK. Resistant hypertension. Curr Hypertens Rep 2002;4(3):221-8.

1. Johnson AG, Nguyen TV, Day RO. Do nonsteroidal anti-inflammatory drugs affect blood pressure?

A meta-analysis. Ann Intern Med 1994;121(4):289-300.

9. Garg JP, Elliott WJ, Folker A, et al. Resistant hypertension revisited: a comparison of two university-based cohorts.

Am J Hypertens 2005;18(5 Pt 1):619-26.

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Clinical Algorithms

Guidelines for BP Control in Special Circumstances

Hypertension In Myocardial Infarction Causes

Long standing HT

Acute Stress zz

(BP > 180/120mmHg with TOD)

No TOD*

Malignant HT zz

Severe HT with bilateral retinal hemorrhages

zz

Exudates with or without papilloedema

HT emergency

HT encephalopathy zz

Presence of signs of cerebral edema due to severe sudden rise in BP

Dissection of aorta with MI

*TOD – Target Organ Damage

Management of HT emergencies in MI ÂÂ

ÂÂ

Drugs used for acute myocardial ischemia

IV nitroglycerin

IV beta-blockers Drugs used for CHF with pulmonary edema IV nitroglycerin

IV furosemide (Lasix)

IV nitroprusside

IV ACE inhibitors

Do not reduce the BP abruptly as it can precipitate CVA or worsen coronary ischemia

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photo quiz

Skin Plaques in a Woman with Renal Disease

A

44-year-old woman was admitted to the hospital for severe pain localized to her lower extremities. She had a history of diabetes mellitus and end-stage renal disease requiring hemodialysis. On the sixth day of hospitalization, she developed tender, flat, hyperpigmented, violaceous plaques with irregular borders on her buttocks and thighs (Figure 1). Laboratory results included the following: ionized calcium level of 4.28 mg per dL (1.07 mmol per L), phosphorus level of 5.9 mg per dL (1.91 mmol per L), parathyroid hormone level of 483 pg per mL (483 ng per L), protein C activity of 41 percent, and protein S activity of 325 percent. The plaques increased in size, followed by blistering and sloughing of the skin (Figure 2). Skin biopsy showed focal necrosis of the deep dermis, microthrombi, and calcification of the vessel walls.

Question

Figure 1.

Figure 2.

Based on the patientâ&#x20AC;&#x2122;s history and physical examination, which one of the following is the most likely diagnosis?

C. Nephrogenic systemic fibrosis.

A. Calcific uremic arteriolopathy.

D. Peripheral arterial disease.

B. Necrotizing vasculitis.

E. Skin necrosis from warfarin therapy.

SEE THE FOLLOWING PAGE FOR DISCUSSION.

Source: Adapted from Am Fam Physician. 2010;82(10):1257-1258.

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photo quiz Discussion The correct answer is A: calcific uremic arteriolopathy.

Calcific uremic arteriolopathy, also known as calciphylaxis, is characterized by small vessel calcification and cutaneous necrosis. The condition occurs primarily in patients with end-stage renal disease who are on dialysis or who have recently received a renal transplant. It has also been reported in patients with primary hyperparathyroidism, alcoholic cirrhosis, or breast carcinoma treated with chemotherapy.1 The prevalence is approximately 4 percent among patients on dialysis.2 The mortality rate can be as high as 80 percent1,3 and is often due to secondary infection of ulcers and sepsis.

The pathogenesis of calcific uremic arteriolopathy is unclear, but hyperparathyroidism, vitamin D supplementation, hyperphosphatemia, hypercalcemia, and abnormalities of coagulation may be related.4 Clinically, calcific uremic arteriolopathy is suggested by painful skin lesions that progress quickly into necrotic, nonhealing ulcers. There are no specific laboratory tests, but laboratory findings, especially increased levels of calcium, phosphorus, and parathyroid hormone, in Summary Table Condition

Characteristics

Calcific Small vessel calcification and cutaneous uremic necrosis; progressive cutaneous lesions that arteriolopathy are painful and ulcerate; usually occurs in patients with end-stage renal disease who are on hemodialysis or have recently received a renal transplant Necrotizing vasculitis

Pruritic and painful lesions usually preceded by fever, arthralgia, and malaise; occurs in patients with collagen vascular disease, inflammatory bowel disease, or malignancy

Nephrogenic systemic fibrosis

Erythematous papules that coalesce into erythematous to brawny plaques; involved skin becomes thickened and woody in texture

Peripheral arterial disease

Ulcers typically occur on the toes, heels, and anterior shin; peripheral pulses absent; bilateral necrosis possible

Skin necrosis from warfarin (Coumadin) therapy

Necrotic lesions that usually appear in a distinct pattern three to six days after the initiation of therapy and regress after discontinuation; painful rash and petechiae progress to hemorrhagic bullae and necrotic eschar

the presence of suspicious lesions may suggest the diagnosis.

Histopathology reveals calcification of the vessel walls and sebaceous gland necrosis. Treatment includes correcting calcium and phosphorus levels,5 hemodialysis, wound debridement, hyperbaric oxygen therapy, and antibiotics. Parathyroidectomy may be required if hyperparathyroidism does not respond to medical management.

Necrotizing vasculitis occurs in patients with collagen vascular disease, inflammatory bowel disease, or malignancy. The lesions are usually pruritic and painful and are often preceded by fever, arthralgia, and malaise.

Nephrogenic systemic fibrosis occurs in patients with underlying renal disease. The lesions are typically erythematous papules that coalesce into erythematous to brawny plaques. The involved skin becomes thickened and woody in texture. Skin biopsy is essential for diagnosis.

Peripheral arterial disease can cause ulcers and necrosis.

Peripheral pulses are absent, and bilateral necrosis is possible. Ulcers typically occur on the toes, heels, and anterior shin, whereas the trunk and upper extremities usually are not involved.

Skin necrosis from warfarin therapy usually develops in a distinct pattern three to six days after therapy is initiated and regresses after the therapy is discontinued. Necrosis occurs in areas with significant underlying subcutaneous fat tissue. The rash is painful, and petechiae develop within 24 to 48 hours, progress to hemorrhagic bullae, and quickly change into full-blown necrotic eschar.

REFERENCES 1. Fine A, et al. Calciphylaxis is usually non-ulcerating: risk factors, outcome and therapy. Kidney Int. 2002;61(6):22102217.

2. Angelis M, et al. Calciphylaxis in patients on hemodialysis: a prevalence study. Surgery. 1997;122(6):1083-1089.

3. Weenig, et al. Calciphylaxis: natural history, risk factor analysis, and outcome. J Am Acad Dermatol.

2007;56(4):569-579.

4. Block GA. Prevalence and clinical consequences of elevated Ca x P product in hemodialysis patients. Clin Nephrol. 2000;54(4):318-324.

5. Moe SM, et al. Management of secondary hyperparathyroidism. Am J Nephrol. 2003;23(6):369-379.

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practice guidelines

NICE Updates Guidelines on Management of Chronic Heart Failure

H

eart failure is associated with poor prognosis and quality of life, as well as high health care costs. In 2010, the National Institute for Health and Clinical Excellence (NICE) updated its previous guideline on the management of chronic heart failure in adults. This update focuses on the role of signs and symptoms, serum natriuretic peptide levels, and echocardiography in the diagnosis of heart failure. It also discusses pharmacologic treatment of heart failure and management using cardiac resynchronization therapy and implantable cardioverter-defibrillators (ICDs), as well as disease monitoring. These recommendations apply to nonpregnant adults with symptoms of chronic heart failure, but not with acute heart failure or acute exacerbations of chronic heart failure.

Diagnosis Diagnosis of heart failure begins with a history and physical examination (Figure 1). To rule out other diagnoses, electrocardiography and consideration of chest radiography, peak flow measurement or spirometry, and blood tests are appropriate. Clinical signs and symptoms have limited use in diagnosing heart failure. Measurement of serum natriuretic peptide levels (brain natriuretic peptide [BNP] and N-terminal pro-BNP) has a high sensitivity but only moderate specificity for diagnosing heart failure.

In patients without previous myocardial infarction (MI), it is appropriate to measure serum natriuretic peptide levels and perform subsequent echocardiography.

Subspecialist evaluation is needed if levels are elevated. In patients with a history of MI, the physician should proceed directly to echocardiography with subspecialist evaluation. If the echocardiogram is normal, measurement of serum natriuretic peptide levels should be considered. Patients with previous MI or with high levels of serum natriuretic peptide should undergo echocardiography and subspecialist evaluation

Source: Adapted from Am Fam Physician. 2012;85(8):832-834.

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within two weeks of presentation. Those with no previous MI and raised (but not high) levels of serum natriuretic peptide should have echocardiography and subspecialist evaluation within six weeks of initial presentation. If an abnormality is discovered, the physician can begin assessing the severity and possible cause of cardiac dysfunction.

Treatment Management of chronic heart failure depends on whether the patient has heart failure with preserved ejection fraction or caused by left ventricular systolic dysfunction (Figure 2). In patients with preserved ventricular function, physicians should focus on managing comorbid conditions (e.g., hypertension, ischemic heart disease, diabetes mellitus) because there is insufficient evidence to recommend specific therapies in this population. Diuretics may be prescribed to manage fluid retention.

Patients with left ventricular systolic dysfunction should receive an angiotensin-converting enzyme (ACE) inhibitor and a beta blocker, regardless of symptom severity. High-quality evidence has shown that this treatment reduces morbidity and increases survival. Outcomes are the same regardless of whether ACE inhibitor or beta-blocker therapy is started first.

If patients cannot tolerate ACE inhibitors, angiotensin receptor blockers (ARBs) may be considered. Secondline therapy options include ARBs, aldosterone antagonists, and combination therapy with hydralazine and a nitrate. Hydralazine in combination with a nitrate is appropriate in patients who cannot tolerate ACE inhibitors or ARBs. When choosing a secondline therapy, physicians should consider the severity of heart failure, the patientâ&#x20AC;&#x2122;s ethnicity, and comorbid conditions. Monitoring renal function is important in patients taking any of these medications. Potassium levels should be monitored closely in those taking ARBs or aldosterone antagonists.

Patients with left ventricular systolic dysfunction and persistent symptoms should be referred to a

practice guidelines Diagnosis of Heart Failure

Treatment of Heart Failure

Take a detailed history, and perform a clinical examination

Previous myocardial infarction

Heart failure

Heart failure with preserved ejection fraction

No previous myocardial infarction

Measure serum natriuretic peptide

High levels

Raised levels

Manage comorbid conditions, such as high blood pressure, ischemic heart disease, and diabetes mellitus, in accordance with NICE guidance

Consider measuring serum natriuretic peptide if levels are not known

Offer rehabilitation and education, and diuretics for congestion and fluid retention; consider an ICD where appropriate† For second-line treatment, consider adding one of the following:

Disease progression

Assess severity, cause, precipitating factors, type of cardiac dysfunction, and correctable causes

No clear abnormality

Offer ACE inhibitors and beta blockers licensed for heart failure as first-line treatment (consider an ARB if the patient cannot tolerate ACE inhibitors)

If symptoms persist despite optimal first-line treatment, seek subspecialist advice

Subspecialist assessment and Doppler echocardiography*

Abnormality consistent with heart failure

Heart failure caused by left ventricular systolic dysfunction*

Raised levels Normal levels Investigate other diagnoses

●●

An aldosterone antagonist licensed for heart failure (especially in patients with moderate to severe heart failure‡ or myocardial infarction in the past month)

●●

An ARB licensed for heart failure§ (especially in mild to moderate heart failure||)

●●

Hydralazine in combination with a nitrate (especially in persons of African or Caribbean origin¶ with moderate to severe heart failure‡; also may be considered if the patient cannot tolerate ACE inhibitors and ARBs)

If symptoms persist, consider the following: CRT (pacing with or without a defibrillator)** Digoxin Other Heart failure cardiac caused by abnormality left ventricular systolic dysfunction

Heart failure with preserved ejection fraction

Heart failure is unlikely; investigate other diagnoses

*Patients with previous myocardial infarction or high levels of serum natriuretic peptide should have subspecialist assessment and echocardiography within two weeks of presentation. Those without a previous myocardial infarction and raised levels of serum natriuretic peptide should have subspecialist assessment and echocardiography within six weeks of presentation.

Figure 1. Algorithm for the diagnosis of heart failure.

Normal serum natriuretic peptide levels are defined as brain natriuretic peptide (BNP) levels < 100 pg per mL (100 ng per L) or N-terminal pro-BNP levels < 400 pg per mL (400 ng per L). Raised serum natriuretic peptide levels are defined as BNP levels between 100 and 400 pg per mL (100 and 400 ng per L) or N-terminal pro-BNP levels between 400 and 2,000 pg per mL (400 and 2,000 ng per L). High serum natriuretic peptide levels are defined as BNP levels > 400 pg per mL or N-terminal pro-BNP levels > 2,000 pg per mL.

*For more information on drug treatment, see Appendix J to the NICE clinical guideline on heart failure and the NICE clinical guideline on chronic kidney disease. †Consider

using an ICD according to the recommendations described in the NICE technology appraisal on ICDs.

‡New

York Heart Association class III to IV.

§Not

all ARBs are licensed for use in heart failure in combination with ACE inhibitors.

||New

York Heart Association class II to III.

¶This

does not include persons of mixed race. For more information, see the full NICE chronic heart failure guideline. **Consider using CRT according to the recommendations described in the NICE technology appraisal on CRT.

Figure 2. Algorithm for the treatment of heart failure. The term “licensed for heart failure” refers to drugs that have been approved for use for the given indication by regulatory agencies in the United Kingdom. (ACE = angiotensinconverting enzyme; ARB = angiotensin receptor blocker; CRT = cardiac resynchronization therapy; ICD = implantable cardioverter-defibrillator; NICE = National Institute for Health and Clinical Excellence.)

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practice guidelines subspecialist for possible additional drug therapy (digoxin), cardiac resynchronization therapy, or an ICD. Criteria for cardiac resynchronization therapy include a left ventricular ejection fraction less than 35 percent and a QRS duration on electrocardiography of 150 milliseconds or higher, or between 120 and 149 milliseconds in those with mechanical dyssynchrony on echocardiography. Criteria for an ICD include sustained ventricular tachycardia or nonsustained ventricular tachycardia that is inducible on electrophysiologic testing if the left ventricular ejection fraction is less than 35 percent, or a QRS duration of 120 milliseconds or higher on electrocardiography if the left ventricular ejection fraction is less than 30 percent.

All patients with heart failure should be offered supervised group exercise–based rehabilitation that includes psychological and educational components, as long as they are stable and do not have a condition or device that precludes such a program. Moderatequality evidence has shown that exercise rehabilitation reduces hospital admissions for heart failure and increases long-term quality of life almost exclusively in patients with left ventricular systolic dysfunction.

Monitoring Patients with Heart Failure Because the clinical course of heart failure is unpredictable and fluctuating, physicians should monitor patients to make sure they are receiving optimal therapy and adjust treatment as necessary.

Serial monitoring of serum natriuretic peptide levels has been shown to be cost-effective when used by subspecialists. Moderate-quality evidence has shown that therapy guided by serum natriuretic peptide levels can lead to a medium-term reduction in hospitalization for heart failure, although there was no reduction in mortality in persons older than 75 years, in quality of life, or in hospitalization for any cause. Telemonitoring

can reduce mortality and hospitalization for any cause, but does not improve quality of life or decrease hospitalization for heart failure. However, the guideline does not make a recommendation on the use of telemonitoring because of heterogeneity of results from different trials.

New evidence Since publication of the 2010 update of the NICE clinical guideline on heart failure, some new evidence has emerged, although it is unclear whether these results would have affected guideline recommendations.

The Eplerenone in Mild Patients Hospitalization and Survival Study in Heart Failure investigated patients with chronic heart failure caused by left ventricular systolic dysfunction with mild symptoms (i.e., New York Heart Association class II heart failure). Results showed significant reductions in hospitalization and mortality when eplerenone therapy was started in patients hospitalized during the preceding six months or in those with persistent moderate elevation in serum natriuretic peptide levels. The Systolic Heart Failure Treatment with the If Inhibitor Ivabradine Trial showed that ivabradine, a blocker of the If channel in the sinoatrial node, significantly reduced unplanned hospitalization and mortality in patients with heart failure caused by left ventricular systolic dysfunction who had a heart rate above 70 beats per minute. A large trial of telemonitoring in patients with a recent hospitalization for heart failure found no evidence that it reduced hospital readmission or mortality. The Resynchronisation/Defibrillation for Ambulatory Heart Failure Trial found that adding cardiac resynchronization therapy in patients with an ICD who had mild to moderate heart failure reduced all-cause mortality and hospitalization, but increased adverse events.

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mediLAW

When can Hospitals be Liable for Medical Negligence Deaths?

KK Aggarwal

I

f a patient dies due to medical negligence in a hospital then its management cannot be prosecuted and it is only the doctors who should be penalized, the Delhi High Court has ruled. However, the court held that the management of the hospital would be liable in case of administrative negligence and failure to provide basic infrastructure to patients.

Justice SN Dhingra passed the order on a petition filed by Indraprastha Medical Corporation Limited challenging a metropolitan magistrate’s order for registration of a first information report against it for alleged Medical negligence resulting in the death of a patient in 2007.

Setting aside the trial court order, Justice Dhingra said: “The hospital or company cannot be held liable for the personal negligence of the doctor in giving wrong treatment.”

“If there is an administrative negligence or a negligence of not providing basic infrastructure, which results into some harm to an aggrieved person or such negligence which is impersonal, the hospital can be held liable”.

The court, said that it is the doctor who treats the patients and hospitals should not be punished due to error on part of its medical staff. “The offence of medical criminal negligence cannot be fastened on the company since the company can neither treat nor operate a patient of its own.”

“It is the doctor working in the hospital who treats and performs operations. It is the doctors who examine the patients and prescribe medicines. If there is a deliberate or negligent act of the doctor working in the hospital, it is the liability of the doctor and not of the hospitals for criminal negligence,” the court said.

In the present case, the company contended that the hospital could not be held responsible as the patient was being treated by three doctors from the Department of Cardiology a few years back.

Padma Shri and Dr BC Roy National Awardee President Heart Care Foundation of India Chairman Legal Cell Indian Academy of Echocardiography Editor - eMedinewS E-mail: emedinews@gmail.com

Judgment: Present petition has been filed by the petitioner for quashing of order dated 19th December, 2007, passed by learned Metropolitan Magistrate in a complaint case under section 336/337/471 read with section 34 IPC qua the petitioner. It is submitted that petitioner Indraprastha Medical Corporation Limited was a company incorporated under Companies Act and the company being only a juristic person was incapable of committing a crime of medical negligence, because it involved personal negligent act.

A complaint was filed before the learned M.M. against the petitioner company and the Doctors involved in the treatment of deceased wherein it was alleged that deceased died due to gross medical negligence of the Doctors. It is also submitted that Doctors involved in treatment advised wrong/superfluous treatments in order to extract extra money. The petitioner’s counsel stated that petitioner is not assailing the order as against Doctors but is assailing it so far as company was concerned on the ground that the company running the hospital, could not have acted in the manner in which it is assailed by the complainant.

In Standard Chartered Bank Vs. Directorate of Enforcement, 2005 SCC (Cri.) 961, SC made following observations regarding criminal liability of the Corporation: “6. There is no dispute that a company is liable to be prosecuted and punished for criminal offences. Although there are earlier authorities to the effect that corporations cannot commit a crime, the generally accepted modern rule is that except for such crimes as a corporation is held incapable of committing by reason of the fact that they involve personal malicious intent, a corporation may be subject to indictment or other criminal process, although the criminal act is committed through its agents.

8. Inasmuch as all criminal and quasi-criminal offences are creatures of statute, the amenability of the corporation to prosecution necessarily depends upon the terminology employed in the statute. In the case of strict liability, the terminology employed by the legislature is such as to reveal an intent that guilt shall not be predicated upon the automatic breach of the statute but on the establishment of the actus reus, subject to the defence of due diligence. The

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Medilaw law is primarily based on the terms of the statutes. In the case of absolute liability where the legislature by the clearest intendment establishes an offence where liability arises instantly upon the breach of the statutory prohibition, no particular state of mind is a prerequisite to guilt. Corporations and individual persons stand on the same footing in the face of such a statutory offence. It is a case of automatic primary responsibility. It is only in a case requiring mens rea, a question arises whether a corporation could be attributed with requisite mens rea to prove the guilt. But as we are not concerned with this question in these proceedings, we do not express any opinion on that issue.” In Kalpnath Rai Vs. State, 1998 AIR (SC) 201, SC made following observations: “The company is not a natural person. We are aware that in many recent penal statutes, companies or corporations are deemed to be offenders on the strength of the acts committed by persons responsible for the management of affairs of such company or corporations e.g. Essential Commodities Act, Prevention of Food Adulteration Act, etc. But there is no such provision in TADA which makes the company liable for the acts of its officers. Hence, there is no scope whatsoever to prosecute a company for the offence under Section 3 (4) of TADA. The corollary is that the conviction passed against A-12 is liable to be set aside.”

In Standard Chartered Bank Vs. Vinay Kumar Sood and Ors, 2009 (1) JCC 756, this court had observed as under: “Undisputedly, the petitioner is a bank incorporated in England with limited liability by Royal Charter, 1853 and, therefore, is a corporation/company. A company cannot be in any case held to have committed an offence under Section 500 IPC because; most essential ingredient of the said offence i.e. ‘mens rea’ would be missing as a company is a juristic entity or an artificial person, whereas a Director is not a company. The company may be made liable for offences, however, if there is anything in the definition or context of a particular Section or a particular statute which would prevent the application of the said section to a limited company, the limited company cannot be proceeded against.

There are number of provisions of law in which it would be physically impossible by a limited company to commit the offence. A limited company, therefore, cannot generally be tried for offences where mens rea is essential. Similarly, a company cannot face the punishment of imprisonment for obvious reasons that company cannot be sent to prison by way of a sentence.”

cannot be fastened on the company since the company can neither treat nor operate a patient of its own. It is the Doctor working in the company who treats and performs operations. It is the Doctor who examines the patients and prescribes medicines. If there is a deliberate or negligent act of the Doctor working in the Corporation/Hospital, it is the liability of the Doctor and not of the Corporation for criminal negligence despite the fact that due to the act of the Doctor of treating patients the Corporation was getting some revenue. These days, all Doctors with big hospitals, are on panels where they have fixed fee for examination of patients and for conducting operations. Out of this fee, a percentage is paid to the hospital. The hospital/ company cannot be held liable for the personal negligence of the Doctor in giving wrong treatment.

However, if there is an administrative negligence, or a negligence of not providing basic infrastructure, which results into some harm to an aggrieved person or such negligence which is impersonal, the hospital can be held liable. But, in the case of medical negligence, which is personal to the Doctor who gave treatment, the Corporation would not be liable and it is the Doctor who can be indicted for medical criminal negligence.

6. I therefore, allow this petition in respect of the petitioner. The order passed by learned M.M. qua the petitioner is hereby quashed.

Comments ÂÂ

This is an important judgment.

ÂÂ

Needs to be read in totality.

ÂÂ

It is applicable mainly for the criminal act and not for compensation purposes.

ÂÂ

A criminal negligence on the part of a resident will be the responsibility of the resident and not the hospital.

ÂÂ

But a fault of a resident where compensation is awarded will have to be paid by the hospital as he is the full time salaried staff of that hospital.

ÂÂ

The judgment lines “However, if there is an administrative negligence, or a negligence of not providing basic infrastructure, which results into some harm to an aggrieved person or such negligence which is impersonal, the hospital can be held liable” Covers a lot of situations. A mistake by the nurse, resident, pathology services, radiology services etc. will come under the “providing basic infrastructure services”.

5. The offence of criminal negligence requires a specific state of mind in respect of the person committing the offence. The offence of medical criminal negligence ■■■■

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Around the Globe

News and Views Does good cholesterol still predict heart risk after bad cholesterol is controlled by statin therapy?

Yes, according to a post-hoc analysis of data from the controversial COURAGE trial, appearing in the Journal of the American College of Cardiology. No, according to Dutch researchers whose report on the Secondary Manifestations of Arterial Disease (SMART) study also appears in the journal.

Optimal medical therapy after acute myocardial infarction Although nearly all heart attack patients leave the hospital on secondary prevention medications, only about a third get appropriate doses, registry data showed. Initial dose was key, because about threequarters of those who didn’t go home on a dose within 75% of the dose proven effective in landmark trials didn’t get an increase during follow-up care, Suzanne V. Arnold, MD, MHA, of St. Luke’s Mid America Heart Institute in Kansas City, Mo., and colleagues found. "Integration of dose intensity into performance measures may help improve the use of optimal medical therapy after acute myocardial infarction," the group suggested online in the Journal of the American College of Cardiology.

Face Recognition Test May Predict Early Dementia Patients who were unable to name or recognize culturally-relevant and age appropriate famous faces may be at risk for various deficits in early-onset dementias, researchers found. (Source: Medpage today) Coma Patients ‘Talk’ with Their Brains Researchers said they established a primitive type of communication with two nonresponsive patients using functional MRI (fMRI) to measure their attention to certain words, serving as responses to questions. Brain activity measured by fMRI in one patient with minimal consciousness and one in a persistent vegetative state demonstrated not only that they heard words spoken to them, but also could use their attention to the words to give 'Yes' or 'No' answers to questions about their names and location, according to Lorina Naci, PhD, and Adrian Owen, PhD, of Western University in London, Ontario. (Source: Medpage Today)

Coronary-Stenting Abuse A recent article highlights high-profile cases of alleged coronary-stenting overuse. It’s just the tip of the iceberg. "When stents are used to restore blood flow in heart-attack patients, few dispute they are beneficial," writes Peter Waldman, David Armstrong, and Sydney P Freedberg in Bloomberg BusinessWeek.

But heart attacks account for only about half of stenting procedures. Among the other half—elective-surgery patients in stable condition—overuse, death, injury, and fraud have accompanied the devices use. The article cites thousands of pages of court documents and regulatory filings, interviews with 37 cardiologists and 33 heart patients or their survivors, and more than a dozen medical studies. As per Texas Medical Board, Dr Samuel DeMaio is said to have implanted 21 coronary stents in one patient over an 8-month period.

The patient's later death was related to the placement of unneeded stents. Dr John McLean of Salisbury, MD, was convicted of billing for unwarranted stenting. He argued that inappropriate usage is widespread, and [he] was prosecuted for behavior that’s the industry norm. Baltimore cardiologist Dr Mark Midei, license was revoked in 2011 when the Maryland Board of Physicians found he falsified records to justify unwarranted stents. The hospital where Midei worked, St Joseph Medical Center in Towson, MD, paid the government $22 million without admitting liability as a part of settlement. Apart five other hospitals settled with the Justice Department over allegations that they paid illegal kickbacks to doctors for patient referrals to their cath labs. (Source: Medscape Cardiology) ------------------------------------------------------------------People with congenitally reduced triglyceride levels had about a 20% reduced risk of all-cause death compared with people without inherently low triglyceride levels during more than 30-years follow-up of nearly 14,000 people enrolled in the Copenhagen City Heart Study.

Data from the study also showed that people with higher triglyceride (TG) levels at the time they entered the study had significantly higher all-cause mortality during more than 30 years of follow–up than did people who entered with lower TG levels, Dr. Børge G. Nordestgaard said at the European Society of Cardiology annual congress.

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lighter reading

A woman baked a chapatti (roti) for members of her family and an extra one for a hungry passerby.

She kept the extra chapatti on the window sill, for whosoever would take it away. Every day, a hunchback came and took away the chapatti.

Instead of expressing gratitude, he muttered the following words as he went his way: "The evil you do remains with you: The good you do, comes back to you!" This went on, day after day.

Every day, the hunchback came, picked up the chapatti and uttered the words: "The evil you do, remains with you: The good you do, comes back to you!" The woman felt irritated. "Not a word of gratitude," she said to herself…

"Everyday this hunchback utters this jingle! What does he mean?" One day, exasperated, she decided to do away with him. "I shall get rid of this hunchback," she said. And what did she do? She added poison to the chapatti she prepared for him! As she was about to keep it on the window sill, her hands trembled. "What is this I am doing?" she said. Immediately, she threw the chapatti into the fire, prepared another one and kept it on the window sill. As usual, the hunchback came, picked up the chapatti and muttered the words: "The evil you do, remains with you: The good you do, comes back to you!" The hunchback proceeded on his way, blissfully unaware of the war raging in the mind of the woman.

Every day, as the woman placed the chapatti on the window sill, she offered a prayer for her son who had gone to a distant place to seek his fortune. For many months, she had no news of him. She prayed for his safe return. That evening, there was a knock on the door. As she opened it, she was surprised to find her son standing in the doorway. He had grown thin and lean. His garments were tattered and torn. He was hungry, starved and weak. As he saw his mother, he said, "Mom, it’s a miracle I’m here. While I was but a mile away, I was so famished that I collapsed. I would have died, but just then an old hunchback passed by.

I begged of him for a morsel of food, and he was kind enough to give me a whole chapatti. As he gave it to me, he said, "This is what I eat everyday: Today,

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I shall give it to you, for your need is greater than mine!" " As the mother heard those words, her face turned pale.

She leaned against the door for support. She remembered the poisoned chapatti that she had made that morning. Had she not burnt it in the fire, it would have been eaten by her own son, and he would have lost his life! It was then that she realized the significance of the words: "The evil you do remains with you: The good you do, comes back to you!" Do good and don’t ever stop doing good, even if it is not appreciated at that time.

"Three rules of work: Out of clutter find simplicity; From discord find harmony; in the middle of difficulty lies opportunity."

— Albert Einstein

"There are some people, who live in a dream world, and there are some who face reality; and then there are those who turn one into the other."

— Douglas H. Everettv

Dr. Good and Dr. Bad Situation : A patient with acute heart failure was admitted in the hospital.

he needs to be investigated

he needs immediate aggressive treatment

ICU

ICU

© IJCP GROUP

The Good you do, comes back to you

QUOTE

An Inspirational Story

Lighter Side of Medicine

Lesson : Very early treatment in heart failure includes

pre-hospital phase and the first 6-12 hours after presentation. These phase are critical for survival and early discharge of many patients.

Turk Kardiyol Dern Ars 2011;39(5):427-32.

KK Aggarwal

Asian

Journal of

CLINICAL CARDIOLOGY

Information for Authors

Manuscripts should be prepared in accordance with the ‘Uniform requirements for manuscripts submitted to biomedical journals’ compiled by the International Committee of Medical Journal Editors (Ann. Intern. Med. 1992;96: 766-767).

Asian Journal of Clinical Cardiology strongly disapproves of the submission of the same articles simultaneously to different journals for consideration as well as duplicate publication and will decline to accept fresh manuscripts submitted by authors who have done so.

The boxed checklist will help authors in preparing their manuscript according to our requirements. Improperly prepared manuscripts may be returned to the author without review. The checklist should accompany each manuscript.

Authors may provide on the checklist, the names and addresses of experts from Asia and from other parts of the World who, in the authors’ opinion, are best qualified to review the paper.

Covering letter -

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The covering letter should explain if there is any deviation from the standard IMRAD format (Introduction, Methods, Results and Discussion) and should outline the importance of the paper.

Principal/Senior author must sign the covering letter indicating full responsibility for the paper submitted, preferably with signatures of all the authors.

Articles must be accompanied by a declaration by all authors stating that the article has not been published in any other Journal/Book. Authors should mentioned complete designation and departments, etc. on the manuscript.

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The manuscript should be arranged as follow: Covering letter, Checklist, Title page, Abstract, Keywords (for indexing, if required), Introduction, Methods, Results, Discussion, References, Tables, Legends to Figures and Figures.

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A subtitle can be added if necessary.

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Summary - The summary of not more than 200 words. It must convey the essential features of the paper.

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Introduction - The introduction should state why the study was carried out and what were its specific aims/objectives.

Methods - These should be described in sufficient detail to permit evaluation and duplication of the work by others.

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Statistics The following information should be given: - The statistical universe i.e., the population from which the sample for the study is selected.

- Method of selecting the sample (cases, subjects, etc. from the statistical universe).

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Note: Please keep a copy of your manuscript as we are not responsible for its loss in the mail. Manuscripts will not be returned to authors.

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Title page Should contain the title, short title, names of all the authors (without degrees or diplomas), names and full location of the

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Confidence intervals for the measurements should be provided wherever appropriate.

Results These should be concise and include only the tables and figures necessary to enhance the understanding of the text.

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Discussion -

This should consist of a review of the literature and relate the major findings of the article to other publications on the subject. The particular relevance of the results to healthcare in India should be stressed, e.g. practicality and cost.

References These should conform to the Vancouver style. References should be numbered in the order in which they appear in the texts and these numbers should be inserted above the lines on each occasion the author is cited (Sinha12 confirmed other reports13,14...). References cited only in tables or in legends to figures should be numbered in the text of the particular table or illustration. Include among the references papers accepted but not yet published; designate the journal and add ‘in press’ (in parentheses). Information from manuscripts submitted but not yet accepted should be cited in the text as ‘unpublished observations’ (in parentheses).

At the end of the article the full list of references should include the names of all authors if there are fewer than seven or if there are more, the first six followed by et al., the full title of the journal article or book chapters; the title of journals abbreviated according to the style of the Index Medicus and the first and final page numbers of the article or chapter. The authors should check that the references are accurate. If they are not this may result in the rejection of an otherwise adequate contribution.

Examples of common forms of references are: Articles

Figures - Two complete sets of glossy prints of high quality should be submitted. The labelling must be clear and neat.

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Please complete the following checklist and attach to the manuscript: 1. Classification (e.g. original article, review, selected summary, etc.)_______________________________

Paintal AS. Impulses in vagal afferent fibres from specific pulmonary deflation receptors. The response of those receptors to phenylguanide, potato S-hydroxytryptamine and their role in respiratory and cardiovascular reflexes.

Q. J. Expt. Physiol. 1955;40:89-111.

2. Total number of pages ________________________

Books

6. Suggestions for reviewers (name and postal address)

Stansfield AG. Lymph Node Biopsy Interpretation Churchill Livingstone, New York 1985.

Indian 1.____________Foreign 1.________________

2.____________ 2.________________

Articles in Books

3.____________ 3.________________

Strong MS. Recurrent respiratory papillomatosis. In: Scott Brown’s Otolaryngology. Paediatric Otolaryngology Evans JNG (Ed.), Butterworths, London 1987;6:466-470.

4.____________ 4.________________

Tables -

These should be typed double spaced on separate sheets with the table number (in Roman Arabic numerals) and title above the table and explanatory notes below the table.

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The legend must include enough information to permit interpretation of the figure without reference to the text.

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3. Number of tables ____________________________ 4. Number of figures ___________________________ 5. Special requests _____________________________

7. All authors’ signatures________________________ 8.

Corresponding author’s name, current postal and e-mail address and telephone and fax numbers __________________________________________

Online Submission Also e-issue @ www.ijcpgroup.com For Editorial Correspondence

Dr KK Aggarwal

Group Editor-in-Chief Asian Journal of Clinical Cardiology E - 219, Greater Kailash, Part - 1, New Delhi - 110 048. Phone: 011-40587513 E-mail: editorial@ijcp.com, emedinews@gmail.com Website: www.ijcpgroup.com

Dr KK Aggarwal Group Editor-in-Chief Dr Veena Aggarwal MD and Group Executive Editor Dr Alka Kriplani Dr Praveen Chandra Dr Swati Y Bhave Dr CR Anand Moses Dr Sidhartha Das Dr Wiqar Sheikh Dr Ajay Kumar Dr A Ramachandran Dr Samith A Shetty Dr SK Parashar Dr Kamala Selvaraj Dr Georgi Abraham Dr V Nagarajan Dr Thankam Verma Dr KMK Masthan Dr Hasmukh J Shroff Dr Rajesh Chandna Dr SM Rajendran

Volume 22, Number 11 Peer Reviewed Journal

Drug Review

Review Article

Original Article

Case Report

Photo Quiz

Lighter Reading

April 2012, Pages 545-596

R.N.I. No. 71217/98 Date of Publishing 25 of Same Month Date of Posting 25-26 Same Month

REGISTRATION NO. DL (S)-01/3288/2013-2015 POSTED IN NDPSO NEW DELHI