Ajcc December 2013

In This Issue — High Blood Pressure in Children and Adolescents

— Role of Atorvastatin in Dyslipidemia: A Clinical Study

— Cerebral Venous Thrombosis Due to Abrin Toxicity: A Case Report

— Coronary Artery Air Embolism

— ACC and AHA Update on Chronic Heart Failure Guidelines

— A Subtle ECG

Volume 16, Number 8, December 2013 Pages 281-316

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 8, December 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 285 Cardiology Update

KK Aggarwal

Dr Praveen Chandra Guest Editor, AJCC praveen.chandra@medanta.org Assistant Editors: Dr Nagendra Chouhan, Dr Dharmendar Jain

AJCC Specialty 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

REVIEW ARTICLE 286 High Blood Pressure in Children and Adolescents

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

Margaret Riley, Brian Bluhm

CLINICAL STUDY 294 Role of Atorvastatin in Dyslipidemia: A Clinical Study

Pooja BA, Bhatted S, Chaturvedi N, Deekshit S, Bhojani MK

CASE REPORT 297 Cerebral Venous Thrombosis Due to Abrin Toxicity: A Case Report

KV Rajalakshmi, G Shivkumar, S Karthikeyan, V Punitha, K Sangeetha

300 Coronary Artery Air Embolism

Maheshwari M, Agarwal A

PRACTICE GUIDELINES 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

302 ACC and AHA Update on Chronic Heart Failure Guidelines

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

photo quiz 306 A Subtle ECG

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.

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.

Around the Globe 308 News and Views

lighter reading 310 Lighter Side of Medicine

IJCP’s Editorial & Business Offices Delhi

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Mr. Nilesh Aggarwal Dr Veena Aggarwal Ritu Saigal 9811036687 9818421222 Sr. BM 9831363901 E - 219, Greater Pravin Dhakne Kailash, Part - I, 8655611025, 24452066 Flat 7E New Delhi - 110 048 Merlin Jabakusum Unit No. 210 Cont.: 011-40587513 28A, SN Roy 2nd Floor Shreepal editorial@ijcp.com Road Complex, Suren Road, drveenaijcp@gmail.com Kolkata - 700 038 Near Cine Magic Subscription Cont.: 24452066 Cinema Dinesh: 9891272006 ritu@ijcp.com Andheri (E) subscribe@ijcp.com Mumbai - 400 093 Ritu: 09831363901 nilesh.ijcp@gmail.com ritu@ijcp.com 284 Asian Journal of Clinical Cardiology, Vol. 16, No. 8, December 2013 Sr.: Senior; BM: Business Manager; GM: General Manager

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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 Member, Ethics Committee, Medical Council of India (2013) 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)

Cardiology Update zz

Bleeding with cardiac implantable electronic device insertion in patients on warfarin for high risk of thromboembolism: For patients requiring cardiac implantable electronic device insertion and who are at the highest risk of thromboembolic events (greater than 5% per year), one should continue chronic warfarin therapy rather than a bridging strategy using heparin.1

zz

Statins in patients with ventilator-associated pneumonia: In a multicenter randomized trial to evaluate statin therapy in patients with ventilator-associated pneumonia, patients were assigned to either simvastatin or placebo, to be continued through intensive care unit (ICU) discharge or up to 28 days.2 The trial was stopped early for futility.

After enrollment of 300 patients, day 28 mortality was not lower in the statin group compared with the placebo group (21% vs 15%). There were also no significant differences in day 14, ICU, or in-hospital mortality rates; duration of mechanical ventilation; or changes in sequential organ failure assessment (SOFA) score.

zz

Increased risk of deep vein thrombosis with peripherally inserted central catheters (PICCs): A meta-analysis of 11 nonrandomized studies comparing PICCs with centrally inserted catheters found an increased risk of deep vein thrombosis with PICCs (odds ratio 2.6).3 Risk was highest in critically ill patients and those with malignancy.

There were no pulmonary embolism events for comparison.

zz

Chlorhexidine bathing for intensive care unit patients: In a large, randomized, multicenter trial that involved over 74000 patients in 74 ICUs, universal decolonization with chlorhexidine bathing reduced both MRSA-positive clinical cultures and bloodstream infections due to any pathogen to a greater extent than either screening and contact isolation alone or targeted decolonization of carriers, when compared to baseline pre-intervention rates.4

REFERENCES 1. Wolff AC, Hammond H, Hicks DG, et al. J Clin Oncol 2013; Online 10/7/2013.

2. Papazian L, Roch A, Charles PE, et al. JAMA 2013; 310:1692.

3. Chopra V, Anand S, Hickner A, et al. Lancet 2013; 382:311.

4. Huang SS, Septimus E, Kleinman K, et al. N Engl J Med 2013; 368:2255.

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review article

High Blood Pressure in Children and Adolescents MARGARET RILEY, BRIAN BLUHM

Abstract High blood pressure in children and adolescents is a growing health problem that is often overlooked by physicians. Normal blood pressure values for children and adolescents are based on age, sex, and height, and are available in standardized tables.

Prehypertension is defined as a blood pressure in at least the 90th percentile, but less than the 95th percentile, for age, sex, and height, or a measurement of 120/80 mm Hg or greater. Hypertension is defined as blood pressure in the 95th percentile or greater. A secondary etiology of hypertension is much more likely in chil­dren than in adults, with renal parenchymal disease and renovascular disease being the most common. Overweight and obesity are strongly correlated with primary hypertension in children. A history and physical examination are needed for all children with newly diagnosed hypertension to help rule out underlying medical disorders. Children with hypertension should also be screened for other risk factors for cardiovascular disease, including diabetes mellitus and hyperlipid­emia, and should be evaluated for target organ damage with a reti­nal examination and echocardiography. Hypertension in children is treated with lifestyle changes, including weight loss for those who are overweight or obese; a healthy, low-sodium diet; regular physi­cal activity; and avoidance of tobacco and alcohol. Children with symptomatic hypertension, secondary hypertension, target organ damage, diabetes, or persistent hypertension despite nonpharmaco­logic measures should be treated with antihypertensive medications. Thiazide diuretics, angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, beta blockers, and calcium channel blockers are safe, effective, and well tolerated in children.

Keywords: High blood pressure, secondary etiology, obesity, diabetes mellitus, hyperlipid­emia, antihypertensive medications

H

ypertension in children and ado­lescents is a growing health prob­lem. In persons three to 18 years of age, the prevalence of prehy­pertension is 3.4 percent and the prevalence of hypertension is 3.6 percent.1 The combined prevalence of prehypertension and hyperten­ sion in adolescents who are obese is greater than 30 percent in boys and is 23 to 30 percent in girls.2 High blood pressure in childhood commonly leads to hypertension in adult­hood,3 and adult hypertension is the leading cause of premature death around the world.4 Children with hypertension may have evi­dence of target organ damage, including left ventricular hypertrophy and pathologic vas­ cular changes.5,6 Primary hypertension in chil­dren is also commonly associated with other risk factors for cardiovascular disease (CVD), such as hyperlipidemia and diabetes mellitus.7,8

MARGARET RILEY, MD, is an assistant professor in the Department of Fam­ily Medicine at the University of Michigan Medical School in Ann Arbor.

BRIAN BLUHM, MD, is a practicing family physician with Integrated Health Associates in Ann Arbor. At the time this article was written, he was com­pleting an academic fellowship at the University of Michigan.

Source: Adapted from Am Fam Physician. 2012;85(7):693-700.

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Despite the high prevalence and potential risks of hypertension in children, physicians often do not recognize the condition in this population. In one study, hypertension was diagnosed in only 26 percent of children with documented high blood pressure in an elec­tronic medical record.1 Normal blood pressure values in children vary by age, sex, and height; therefore, increased awareness about how to diagnose and treat hypertension in children is needed to combat this increasingly common condition. An approach is outlined in Figure 1.9 Definition of Hypertension Normal blood pressure values in children increase with body size. Tables of normal and abnormal blood pressure values based on age, sex, and height are available from the National Institutes of Health at http://www.cc.nih.gov/ccc/pedweb/pedsstaff/bptable1.

PDF for boys, and at http://www.cc.nih.gov/ccc/ pedweb/pedsstaff/bptable2.PDF for girls. Applica­tions for handheld devices to help physicians quickly and accurately determine if a child’s blood pressure is in the normal range are commercially available.

The National High Blood Pressure Educa­ tion Program (NHBPEP) has published defi­nitions of prehypertension and hypertension in children and

review article Managing High Blood Pressure in Children and Adolescents Measure blood pressure*

Normal blood pressure: < 90th percentile

Patient’s systolic or diastolic blood pressure is ≥ 90th percentile for age, height, and sex†

Repeat measurement at subsequent office visits

Prehypertension: 90th to < 95th percentile or ≥ 120/80 mm Hg

Stage 1 hypertension: 95th to < 99th percentile plus 5 mm Hg

Recommend therapeutic lifestyle changes If patient is overweight, screen for CVD risk factors with fasting glucose and lipid measurements If patient is normal weight or prepubescent, consider screening for secondary causes of high blood pressure Repeat blood pressure measurement in six months

Evaluate primary vs. secondary etiology Screen for underlying renal disease Screen for CVD risk factors with fasting glucose and lipid measurements Evaluate for target organ damage with echocardiography and retinal examination

Primary hypertension Recommend therapeutic lifestyle changes Prescribe antihypertensive medication if patient has target organ damage or diabetes mellitus, or if the blood pressure remains elevated despite weight loss and lifestyle changes *Blood

Stage 2 hypertension: > 99th percentile plus 5 mm Hg Evaluate primary vs. secondary etiology Consider referral to a subspecialist in childhood hypertension Screen for underlying renal disease Screen for CVD risk factors with fasting glucose and lipid measurements Evaluate for target organ damage with echocardiography and retinal examination Recommend therapeutic lifestyle changes and prescribe antihypertensive medication

Secondary hypertension Treat underlying cause Refer to a subspecialist if appropriate Recommend therapeutic lifestyle changes and prescribe antihypertensive medication if hypertension persists

pressure should be measured at every office visit beginning at three years of age. during the same office visit, then confirm the elevation at three separate office visits.

†Remeasure

Figure 1. Algorithm for the management of high blood pressure in children and adolescents. (CVD = cardiovascular disease.)

Information from reference 9.

Table 1. NHBPEP Classification of Prehypertension and Hypertension in Children and Adolescents Classification

Systolic or diastolic blood pressure*

Normal Prehypertension

< 90th percentile 90th to < 95th percentile or ≥ 120/80 mm Hg†

Stage 1 hypertension

95th to < 99th percentile plus 5 mm Hg

Stage 2 hypertension

> 99th percentile plus 5 mm Hg

NHBPEP = National High Blood Pressure Education Program. *Based on sex, age, and height; measured on at least three separate occasions. †Blood pressure of 120/80 mm Hg or greater is prehypertension regardless of whether it is less than the 90th percentile. If 120/80 mm Hg is in the 95th percentile or greater, then the patient has hypertension.

Information from reference 9.

adolescents (Table 1).9 Hyper­tension is defined as an average systolic or dia­stolic blood pressure level that is in the 95th percentile or greater based on at least three separate readings. After hypertension is diag­nosed, it is classified as either stage 1 or 2 to assist in evaluation and treatment decisions.

Children and adolescents have a much higher incidence of secondary hyperten­ sion compared with 9-11 Younger children or children with stage adults.

2 hypertension are more likely to have secondary hypertension, whereas primary hypertension becomes more prevalent in adolescence and young adulthood.11 Renal parenchymal disease and renovascular diseases account for most cases of secondary hypertension.12,13 Table 2 lists common causes of hypertension and associated findings.9,10

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review article Table 2. Etiologies of Hypertension and Suggestive Evaluation Findings Etiology

History findings

Physical examination findings

Possible findings on additional testing

Coarctation of the aorta

None

Difference between right and left arm blood Abnormal findings on echocardiography pressure Diminished femoral pulses Heart murmur Lower blood pressure in legs than in arms

Cushing syndrome

Family history of endocrinopathy

Acne, hirsutism, striae

Elevated cortisol levels

Moon facies Truncal obesity

Drug-induced

Illicit substance abuse Amphetamines Anabolic steroids Cocaine

Acne, hirsutism, striae (with anabolic steroid use)

Abnormal findings on urine drug screen

Sweating Tachycardia

Phencyclidine Over-the-counter agents Caffeine Diet pills Ephedra Performance-enhancing drugs Prescription medications Oral contraceptives Steroids Sympathomimetics Hyperthyroidism

Family history of thyroid disorder

Ophthalmopathy

Heat intolerance

Thyromegaly

Rash, sweating, pallor Mineralocorticoid excess (from congenital adrenal hyperplasia, aldosteronesecreting tumors)

Family history of endocrinopathy

Obstructive sleep apnea

Family history of sleep apnea

Tachycardia

Suppressed thyroid-stimulating hormone

Weight loss Ambiguous genitalia Muscle weakness

Elevated plasma aldosterone levels Hypokalemia Low plasma renin activity

Adenotonsillar hypertrophy

Abnormal findings on polysomnography

Snoring or disordered sleep Pheochromocytoma

Flushing, pallor, palpitations, sweating

Tachycardia

Elevated plasma and urine catecholamine levels

Primary hypertension

Diet high in fat and sodium

Acanthosis nigricans

Hyperlipidemia

Family history of essential hypertension or early cardiovascular disease

Obesity

Impaired glucose tolerance or type 2 diabetes mellitus

Limited physical activity Patient is in adolescence

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review article Renal artery stenosis

Prior umbilical artery catheterization

Abdominal bruit

Abnormal findings on renovascular imaging

Renal parenchymal disease

Enuresis

Abdominal mass

Family history of renal disease

Edema

Abnormal blood urea nitrogen or creatinine level

Fatigue

Growth retardation

Recurrent urinary tract infections Rheumatologic disorder

Gross hematuria

Anemia

Family history of autoimmune disease

Friction rub

Fatigue

Malar rash

Joint pain

Abnormal findings on urinalysis, urine culture, or renal ultrasonography

Joint swelling

Abnormal findings on autoimmune laboratory studies, elevated markers of inflammation

Rash Information from references 9 and 10.

Risk Factors Overweight and obesity are strongly correlated with primary hypertension in children.14-16 Family history of hypertension or CVD, male sex, and maternal smoking during pregnancy are additional risk factors, whereas children who were breastfed have a reduced risk of hypertension.14,17-19 Race and ethnicity have not been consistently linked to hypertension risk in children, although there is some evidence that black children with primary hypertension may be at increased cardiovascu­ lar risk compared with nonblack children.16,20 Diagnosis

Blood Pressure Measurement The NHBPEP recommends measuring blood pressure at every office visit beginning at three years of age.9 Ide­ ally, measurements should be performed using ausculta­tion, which is what standardized blood pressure tables are based on. If an oscillometric (automatic) device is used, then measurements that exceed the 90th percentile should be repeated using auscultation.9 Using the wrong size of blood pressure cuff is a com­ mon cause of inaccurate readings. A cuff that fits properly will have an inflatable bladder width that is at least 40 per­cent of the arm circumference at a point midway between the acromion and the olecranon, and a bladder length that is 80 to 100 percent of the arm circumference.9 Physicians who care for children and adolescents should have cuffs of varying sizes to ensure an appropriate fit. When a patient is in between cuff sizes, the larger of the two cuffs should be used.

Although a cuff that is too small may result in a falsely elevated reading, a cuff that is slightly too large

will still provide a relatively accurate measurement.

The patient should avoid stimulating drugs or foods before a blood pressure measurement, and should sit quietly for five minutes in a chair that has back support with his or her feet on the ground. Blood pressure should be mea­sured in the right arm while it is supported at heart level, because coarctation of the aorta may lead to falsely low readings in the left arm.

If blood pressure is greater than the 90th percentile, the measurement should be repeated during the same office visit to confirm validity. Blood pressure must be elevated on three separate occasions to diagnose prehypertension or hypertension.

Ambulatory blood pressure monitoring can differen­ tiate true hypertension from white coat hypertension, and can also determine the response to antihypertensive treatments.9,10,21 One study found a prevalence of white coat hypertension of 53 percent in children referred for hypertension evaluation.22 Ambulatory blood pressure monitoring should be considered if the office measure­ ment is only mildly or intermittently elevated, or if blood pressure values are normal when measured at home. Because ambulatory blood pressure monitoring involves only oscillometric measurements, there is some concern over what constitutes normal values in children. There­fore, the person interpreting the results should have sig­nificant experience with childhood hypertension.21 After prehypertension or hypertension is diagnosed, a history and physical examination can help determine if the child has primary or secondary hypertension. Very young children and children with stage 2 hypertension or with signs and symptoms suggesting an additional underlying systemic disorder require a more extensive evaluation for secondary

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review article hypertension. The NHBPEP and European Society of Hypertension guidelines for evaluation of children and adolescents with hyperten­sion are described below.9,10

History The patient’s medical history, including birth, growth, and developmental history, should be obtained, and screening for previous urologic, renal, cardiac, endo­ crine, and neurologic diseases should be completed.

Many drugs can increase blood pressure; therefore, a medication review that includes over-the-counter agents, nutritional supplements, performanceenhancing drugs, and illicit substances should be performed. Because dis­ordered sleep is associated with hypertension, a sleep history should be completed.

Patients should be screened for a family history of hypertension, other CVD risk factors, and renal or endocrine syn­dromes. Risk fac­tors such as a lack of physical activity, an unhealthy diet, smoking, and alco­hol use should be explored. A complete review of systems may suggest an underlying medical disorder or symptoms of hyperten­sive urgency (headache, vomiting) or hypertensive emer­gency (seizure, altered mental status), which require emergent evaluation and treatment.

Physical Examination Physical examination findings are normal in most chil­ dren with hypertension. Body mass index should be calculated because obesity is associated with primary hypertension, and poor growth may indicate an under­lying chronic illness. Blood pressure should be measured in both arms while the child is seated and in one leg while the child is in a prone position. Blood pressure should be roughly equal in both arms and is normally 10 to 20 mm Hg higher in the leg. If there is a significant differ­ence in blood pressure between the right and left arms, if leg blood pressure is lower than arm blood pressure, or if the femoral pulses are diminished, the child may have coarctation of the aorta. An abdominal bruit may indicate renovascular disease, and ambiguous genitalia can be associated with mineralocorticoid excess. The remainder of the examination should focus on detecting physical findings associated with other underlying con­ditions that cause hypertension (Table 2).9,10

Diagnostic Testing Initial laboratory studies are performed to evaluate for an underlying etiology, identify other CVD risk factors, and detect target organ damage. Table 3 summarizes

Table 3. Additional Testing for Children and Adolescents with Confirmed Prehypertension or Hypertension Target population

Recommended tests

Purpose

All children with confirmed hypertension

Blood urea nitrogen and creatinine levels

Rule out underlying renal disease

Complete blood count Electrolyte levels Renal ultrasonography Urinalysis Urine culture All children with confirmed hypertension

Fasting glucose level

Rule out diabetes mellitus or hyperlipidemia as comorbid risk factors for cardiovascular disease

Overweight children with prehypertension

Fasting lipid panel

All children with confirmed hypertension

Echocardiography

Children with prehypertension and diabetes or renal disease

Retinal examination

Identify target organ damage, including left ventricular hypertrophy and pathologic vascular changes

Children with prehypertension or hypertension and a history suggestive of sleep disorder

Polysomnography

Rule out obstructive sleep apnea

Children with prehypertension or hypertension and a history suggestive of substance use

Drug screen

Rule out underlying substances contributing to or causing elevated blood pressure

Further studies may be indicated if there is a high degree of suspicion for secondary hypertension.

Information from reference 9.

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review article additional testing recommended by the NHBPEP for children and adolescents with confirmed prehyperten­ sion or hypertension.9 If there is a high degree of suspi­cion that the child has secondary hypertension, further targeted workup may be indicated, typically in conjunc­tion with subspecialist consultation.

Treatment Blood pressure goals are determined by the etiology of the hypertension, presence of other medical disorders, and evidence of target organ damage. Children with uncomplicated primary hypertension and no target organ damage have a blood pressure goal of less than the 95th percentile. Children with chronic renal disease, diabetes, or evidence of target organ dam­ age have a goal of less than the 90th percen­tile.9 It is important to note that these blood pressure goals are based on expert opinion, rather than evidence from randomized tri­ als measuring patient-oriented, longterm outcomes. In many cases, the recommenda­tions are extrapolated from adult studies. Children with hypertension need periodic monitoring for target organ damage and development of other CVD risk factors.

Chil­dren with symptoms of hypertensive urgency or emergency require immediate treatment, typically with intravenous antihypertensive medications in a setting where they can be closely monitored.

Lifestyle Modifications All children with prehypertension or hyper­ tension should make therapeutic lifestyle changes (Table 49,23,24) to lower blood pressure and reduce the development of additional CVD risk factors. Weight loss should be encouraged for children who are overweight or obese,9 and children who are obese should be

referred for comprehensive, intensive behavioral interventions.23 Regular, sustained physical activity is most effective in lowering blood pressure,25,26 and the NHBPEP recom­mends 30 to 60 minutes of moderate aerobic physical' activity on most days and less than two hours of seden­tary activity per day.9 Children with prehypertension, stage 1 hypertension in the absence of target organ dam­age, or controlled stage 2 hypertension are eligible for participation in competitive sports.27 There is a lack of evidence that dietary interventions can significantly decrease blood pressure in children.

However, experts maintain that children with hyperten­ sion may benefit from consuming a diet high in fresh fruits and vegetables, fiber, and nonfat dairy products, in addition to reducing sodium intake.9 One study found that the DASH (Dietary Approaches to Stop Hyper­ tension) diet significantly lowered blood pressure in adolescents compared with standard dietary counsel­ ing.28 Tobacco and alcohol use should be avoided in all children, but this is particularly important in children with hypertension because smoking has been shown to increase the risk of CVD and excess alcohol intake has been shown to raise blood pressure in adult studies.24

Pharmacologic Therapy Children with symptomatic hypertension, secondary hypertension, target organ damage, diabetes, or persis­ tent hypertension despite nonpharmacologic measures require antihypertensive medications.9 There is no con­ sensus on the best initial antihypertensive medication to use in children, and there have been no clinical trials measuring patient-oriented, long-term outcomes in chil­dren. Therefore, recommendations are based on extrap­olations from adult studies. Thiazide diuretics, angiotensin-converting enzyme inhibitors,

Table 4. Lifestyle Modifications for Children and Adolescents with Prehypertension or Hypertension Modification

Comment

Weight reduction if overweight or obese

Refer for comprehensive, intensive intervention if obese23

Regular physical activity

Engage in 30 to 60 minutes of moderate aerobic physical activity on most days9 Restrict sedentary activities to less than two hours per day9

Healthy diet

Emphasize fresh fruit and vegetables, fiber, nonfat dairy9 Reduce sodium intake to 1.2 g per day in four- to eight-year-old children, and 1.5 g per day in children older than eight years and in adolescents9

Healthy habits

Avoid tobacco or alcohol use24

Family-based interventions

Involving the family in counseling on diet and physical activity to make changes for the entire household has been shown to improve success rates9

Information from references 9, 23, and 24.

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review article Table 5. Recommended Dosages for Antihypertensive Agents Medication

Initial daily dosage

Maximum daily dosage

Dosing frequency

Benazepril (Lotensin), ≥ six years of age

0.2 mg per kg, up to 10 mg

0.6 mg per kg or 40 mg

Once daily

Enalapril (Vasotec)

0.08 mg per kg, up to 5 mg

0.6 mg per kg or 40 mg

Once or twice daily

Fosinopril (Monopril), ≥ six years of age and 5 to 10 mg weighing > 111 lb (50 kg)

40 mg

Once daily

Lisinopril (Zestril), ≥ six years of age

0.07 mg per kg, up to 5 mg

0.6 mg per kg or 40 mg

Once daily

Losartan (Cozaar), ≥ six years of age

0.7 mg per kg, up to 50 mg

1.4 mg per kg or 100 mg

Once daily

Valsartan (Diovan), ≥ six years of age

1.3 mg per kg, up to 40 mg

2.7 mg per kg or 160 mg

Once daily

Metoprolol, extended release, ≥ six years of age

1 mg per kg, up to 50 mg

2 mg per kg or 200 mg

Once daily

Propranolol

1 to 2 mg per kg

4 mg per kg or 640 mg

Two or three times daily

Hydralazine

0.75 mg per kg

7.5 mg per kg or 200 mg

Four times daily

Minoxidil

0.2 mg per kg, up to 5 mg (< 12 50 mg (< 12 years of age), years of age), 5 mg (≥ 12 years 100 mg (≥ 12 years of age) of age)

Once or twice daily

2.5 mg

5 mg

Once daily

Central alpha agonist: clonidine (Catapres), 0.2 mg 12 years of age

2.4 mg

Twice daily

Diuretic: hydrochlorothiazide

3 mg per kg, up to 50 mg

Once daily

Angiotensin-converting enzyme inhibitors

Angiotensin II receptor blockers

Beta blockers

Vasodilator

Other Calcium channel blocker: amlodipine (Norvasc), ≥ six years of age

1 mg per kg

Other medications within these classes are considered safe but are not approved by the U.S. Food and Drug Administration for treating hyper­tension in children and adolescents.

Information from references 9, 10, and 29.

angiotensin II receptor blockers, beta block­ers, and calcium channel blockers are safe, effective, and well tolerated in children.9 When choosing an ini­tial medication, concurrent medical conditions and the patient’s lifestyle should be considered. For example, an angiotensin-converting enzyme inhibitor would be a good choice for a child with proteinuric renal disease,9 and a beta blocker should not be given to a competitive athlete because it is prohibited in some athletic events.3 The NHBPEP recommends beginning with the lowest recommended dosage of the antihypertensive medica­ tion, and then titrating up until the blood pressure goal is achieved. If the goal is not achieved with a maximum dosage of a single medication, a second medication with complementary action should be added.9

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Table 5 includes dosing information antihypertensive medications.9,10,29

for

REFERENCES 1. Hansen ML, Gunn PW, Kaelber DC. Underdiagnosis of hypertension in children and adolescents. JAMA. 2007;298(8):874-879.

2. McNiece KL, Poffenbarger TS, Turner JL, Franco KD, Sorof JM, Portman RJ. Prevalence of hypertension and pre-hypertension among adoles­cents. J Pediatr.

2007;150(6):640-644.

3. Chen X, Wang Y. Tracking of blood pressure from childhood to adulthood. Circulation. 2008;117(25):31713180.

4. Chobanian AV, Bakris GL, Black HR, et al.; The seventh report of the Joint National Committee on Prevention,

review article Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report [published cor­rection appears in JAMA. 2003;290(2):197]. JAMA. 2003;289(19):2560-2572.

analysis of a longitudinal adolescent cohort [published correction appears in Circulation. 2007;116(9):e319].

Circulation. 2006;114(24):2663-2670.

5. Brady TM, Fivush B, Flynn JT, Parekh R. Ability of blood pressure to predict left ventricular hypertrophy in children with primary hyperten­sion. J Pediatr. 2008;152(1):73-78.

18. Lawlor DA, Najman JM, Sterne J, et al. Associations of parental, birth, and early life characteristics with systolic blood pressure at 5 years of age: findings from the Mater-University study of pregnancy and its out­comes.

Circulation. 2004;110(16):2417-2423.

6. Sorof JM, Alexandrov AV, Garami Z, et al. Carotid ultrasonography for detection of vascular abnormalities in hypertensive children. Pediatr Nephrol. 2003;18(10):10201024.

7. Duncan GE, Li SM, Zhou XH. Prevalence and trends of a metabolic syn­drome phenotype among U.S. adolescents, 1999-2000. Diabetes Care. 2004;27(10):2438-2443.

8. Boyd GS, Koenigsberg J, Falkner B, Gidding S, Hassink S. Effect of obe­sity and high blood pressure on plasma lipid levels in children and ado­ lescents. Pediatrics.

2005;116(2):442-446.

9. National High Blood Pressure Education Program Working Group on High Blood Pressure in Children and Adolescents. The fourth report on the diagnosis, evaluation, and treatment of high blood pressure in children and adolescents. May 2005. NIH Publication No. 05-5267. http://www.nhlbi.nih.gov/health/prof/heart/hbp/ hbp_ped.pdf. Accessed July 27, 2011.

10. Lurbe E, Cifkova R, Cruickshank JK, et al. Management of high blood pressure in children and adolescents: recommendations of the Euro­ pean Society of Hypertension. J Hypertens. 2009;27(9):1719-1742.

11. Vogt BA. Hypertension in children and adolescents: definition, patho­physiology, risk factors, and long-term sequelae. Current Therap Res. 2001;62(4):283-297.

12. Arar MY, Hogg RJ, Arant BS Jr, Seikaly MG. Etiology of sustained hyper­tension in children in the southwestern United States. Pediatr Nephrol. 1994;8(2):186-189.

13. Wyszyńska T, Cichocka E, Wieteska-Klimczak A, Jobs K, Januszewicz P. A single pediatric center experience with 1025 children with hyperten­sion. Acta Paediatr.

1992;81(3):244-246.

14. Din-Dzietham R, Liu Y, Bielo MV, Shamsa F. High blood pressure trends in children and adolescents in national surveys, 1963 to 2002. Circula­tion. 2007;116(13):1488-1496.

15. Falkner B, Gidding SS, Ramirez-Garnica G, Wiltrout SA, West D, Rap­ paport EB. The relationship of body mass index and blood pressure in primary care pediatric patients. J Pediatr. 2006;148(2):195-200.

16. Sorof JM, Lai D, Turner J, Poffenbarger T, Portman RJ. Overweight, ethnicity, and the prevalence of hypertension in school-aged children. Pediatrics. 2004;113(3 pt 1):475-482.

17. Dasgupta K, O’Loughlin J, Chen S, et al. Emergence of sex differences in prevalence of high systolic blood pressure:

19. Martin RM, Ness AR, Gunnell D, Emmett P, Davey Smith G; ALSPAC Study Team. Does breast-feeding in infancy lower blood pressure in childhood? Circulation.

2004;109(10):1259-1266.

20. Brady TM, Fivush B, Parekh RS, Flynn JT. Racial differences among chil­dren with primary hypertension.

Pediatrics. 2010;126(5):931-937.

21. Lurbe E, Sorof JM, Daniels SR. Clinical and research aspects of ambula­ tory blood pressure monitoring in children. J Pediatr. 2004;144(1):7-16.

22. Sorof JM, Portman RJ. White coat hypertension in children with ele­vated casual blood pressure. J Pediatr.

2000;137(4):493-497.

23. U.S. Preventive Services Task Force. Screening for obesity in children and adolescents. January 2010. http://www. uspreventiveservicestaskforce.org/uspstf/uspschobes. htm. Accessed January 20, 2011.

24. Klatsky AL, Friedman GD, Siegelaub AB, Gérard MJ. Alcohol consump­ tion and blood pressure KaiserPermanente Multiphasic Health Exami­nation data. N Engl J Med. 1977;296(21):1194-1200.

25. Hansen HS, Froberg K, Hyldebrandt N, Nielsen JR. A controlled study of eight months of physical training and reduction of blood pressure in children: the Odense schoolchild study. BMJ. 1991;303(6804):682-685.

26. Farpour-Lambert NJ, Aggoun Y, Marchand LM, Martin XE, Herrmann FR, Beghetti M. Physical activity reduces systemic blood pressure and improves early markers of atherosclerosis in pre-pubertal obese chil­dren. J Am Coll Cardiol. 2009;54(25):2396-2406.

27. McCambridge TM, Benjamin HJ, Brenner JS, et al.; Council on Sports Medicine and Fitness. Athletic participation by children and adolescents who have systemic hypertension.

Pediatrics. 2010;125(6):1287-1294.

28. Couch SC, Saelens BE, Levin L, et al. The efficacy of a clinicbased behav­ ioral nutrition intervention emphasizing a DASH-type diet for adoles­cents with elevated blood pressure. J Pediatr. 2008;152(4):494-501.

29. Lexicomp online. http://www.crlonline.com/crlsql/ servlet/crlonline [pass­word required]. Accessed January 27, 2011.

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Clinical Study

Role of Atorvastatin in Dyslipidemia: A Clinical Study Pooja BA*, Bhatted S*, Chaturvedi N†, Deekshit S†, Bhojani MK‡

Abstract This clinical study aimed to see the efficacy of atorvastatin in the management of dyslipidemia. It was a randomized observational clinical study involving 30 patients diagnosed with dyslipidemia. The patients were administered atorvastatin 10 mg tablet once-daily at bedtime and followed up for 12 weeks. This drug achieved the desired lipid profile at the end of the 12th week. Statistically strongly significant results were obtained in all the lipid profile levels. Thus, the present study showed this drug to be effective in the treatment of dyslipidemia.

Keywords: Dyslipidemia, atorvastatin

D

yslipidemia, defined as an abnormal amount of lipids (e.g., cholesterol and/or fat) in the blood,1 is an important risk factor for coronary heart disease and stroke (cerebrovascular disease).

In developed countries, most dyslipidemias are hyperlipidemias often due to faulty diet and lifestyle.

Dyslipidemia can be caused due to prolonged elevation of insulin levels and also due to increased levels of O-linked N-acetylglucosamine (O-GlcNAc) transferase.

The data from the US National Health and Nutrition Examination Survey conducted from 1999 to 2000 reported that 25% of adults either had total cholesterol greater than 239.4 mg/dL or were taking a lipidlowering medication.2 According to the World Health Report 1999, ischemic heart disease was the leading single cause of death in the world, the leading single cause of death in high-income countries, and second only to lower respiratory tract infections in low and middle-income countries. In 1998, it was the leading cause of death, with nearly 7.4 million estimated deaths per year in member states of the World Health Organization, and caused the eighth highest burden

of disease in low-and middle-income countries (30.7 million disability-adjusted life years).

Lifestyle modifications should always be part of the treatment regimen for patients with dyslipidemia, regardless of pharmacologic intervention.

There are four main classes of lipid-lowering drugs: The bile acid sequestrants (resins), niacin/nicotinic acid, fibric acid derivatives (fibrates), and the 3-hydroxy-3methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins).

The statins, or HMG-CoA reductase inhibitors, have taken a major role in the management of dyslipidemia.

More specifically, this family of agents is considered first-line for the treatment of hypercholesterolemia in patients who have failed to adequately respond to dietary therapy.3 The statins are well-tolerated and there does not appear to be major differences in toxicity or adverse effect profiles.4,5 Hence, this study was undertaken to see the efficacy and tolerability of atorvastatin (a statin) in the treatment of dyslipidemia.

Methods

*PhD Scholar *Associate Professor Dept. of Panchakarma National Institute of Ayurveda, Jaipur, Rajasthan †Assistant Professor Dept. of Cardiology SMS Medical College and Hospital, Jaipur, Rajasthan ‡Professor Government Ayurvedic Medical College, Junagadh, Gujarat Address for correspondence Dr Pooja BA Dept. of Panchakarma National Institute of Ayurveda, Jaipur, Rajasthan E-mail: drpoojaba@gmail.com

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The present study was a randomized observational clinical trial carried out at the Sawai Mansingh Medical College and Hospital, Jaipur, Rajasthan, over a period of 6 months. The study protocol was approved by the Ethical Committee of the National Institute of Ayurveda, Jaipur. After obtaining written informed consent, 30 patients of either sex in the age group of 20–60 years with newly detected dyslipidemia were selected for the study. Patients with the following conditions were excluded from the study: pregnant and lactating women, and patients with history or evidence of systemic disorders like cardiac, hepatic, renal, or

Clinical Study neurological diseases. A detailed medical history, clinical examination, anthropometric measurements, and baseline laboratory investigations were carried out.

Patients fulfilling the study criteria were administered with atorvastatin 10 mg tablet once daily at bedtime for 90 days (12 weeks). The lipid profile was recorded at baseline and after the 12th week. The patients were monitored for adverse events throughout the study period.

Laboratory investigations like Hb%, fasting blood sugar, lipid profile, renal function tests, liver function tests, urine analysis, and electrocardiography were done at baseline and at the end of the 12th week.

The data were expressed in percentages and mean ± standard deviation (SD). ANOVA was used to find the significance of treatment on the lipid profile.

Results Out of 30 patients, 24 were men and 6 were women.

The mean age was 45 ± 8.0 years. Ninety-two percent of patients were from urban and the remaining 8% were from rural areas.

The most comorbid condition, obesity (BMI ≥ 25 kg/m2) was observed in 26.66% (n = 8) of patients.

Table 1 reveals that the mean cholesterol level was 303.33 ± 26.31 at baseline and 223.33 ± 34.77 after 12th week with p < 0.001**, which is statistically strongly significant. Mean triglyceride (TG) level was 232.00 ± 23.98 at baseline that reduced to 159.67 ± 23.27 at 12th week with p < 0.001**, which is strongly significant. The mean high-density lipoprotein (HDL) level was 50.37 ± 6.24 at baseline and 49.70 ± 5.86 at 12th week with p = 0.094†, which is significant. At the baseline, mean low-density lipoprotein (LDL) was 206.57 ± 24.71 and at 12th week it was 142.03 ± 32.74 with p < 0.001** showing statistically strongly significant result. The mean very-low-density lipoprotein (VLDL) level was 46.40 ± Table 1. Lipid Profile Analysis Between Basal and 12th Week Values

Table 2. Adverse Events During Study Symptoms

Number of patients

Constipation

3

Fatigue

2

Abdominal discomfort

4

Myalgia

3

4.80 at baseline and 31.93 ± 4.65 after 12th week with p < 0.001**, which is statistically strongly significant.

All other laboratory parameters, both at baseline and at the end of 12th week, were within normal limits.

Adverse events like constipation and myalgia were encountered in three patients; abdominal discomfort and fatigue was observed in four and two patients, respectively (Table 2). All these symptoms were mild, transient, and did not require any treatment, discontinuation of medication, or withdrawal from the study.

Discussion In this study, reduction in cholesterol level by 26.37%, TGs level by 31.17%, HDL level by 1.33%, LDL level by 31.24%, and VLDL level by 31.18% was achieved at 12th week when compared with baseline values.

Statistically, the results were strongly significant.

Atorvastatin calcium is a synthetic lipid-lowering agent and is an inhibitor of HMG-CoA reductase, which catalyzes the conversion of HMG-CoA to mevalonate. Inhibition of HMG-CoA reductase leads to upregulation of LDL cholesterol (LDL-C) receptors in the liver,6 mediated by activation of sterol regulatory element-binding proteins resulting in enhanced clearance of LDL from the circulation, thus playing an important role in preventing atherosclerosis.

In the present study, mild adverse events like constipation and fatigue were observed in few patients, which are considered as the common adverse reactions of atorvastatin. The patients did not require any medication to treat the same.

Lipid profile Basal value in mean ± SD

12th week value in mean ± SD

p value

Conclusion

Serum cholesterol

303.33 ± 26.31

223.33 ± 34.77

<0.001**

Serum TG

232.00 ± 23.98

159.67 ± 23.27

<0.001**

Serum HDL

50.37 ± 6.24

49.70 ± 5.86

0.094†

Serum LDL

206.57 ± 24.71

142.03 ± 32.74

<0.001**

31.93 ± 4.65

<0.001**

Dyslipidemia is a common high-risk factor of cardiovascular disease. Despite the widespread availability of safe and efficacious medications, the management of this condition is far from optimal.

Indeed, epidemiological studies have indicated that 90% of patients with dyslipidemia fail to achieve their therapeutic targets. Moreover, the optimal goal in

Serum VLDL 46.40 ± 4.80

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Clinical Study patients with risk factors has been steadily declining, necessitating the treatment of bigger population subsets.

Statin group of drugs have excellent efficacy and safety profiles for the treatment of dyslipidemia. The present study also suggested that atorvastatin is effective in controlling the lipid profile at the end of 12th week and is tolerated with few minor adverse symptoms.

References 1. Harrison TR. Harrison’s Principles of Internal Medicines.

12th International Edition. In: Braunwald E, Fanci AS, Hauser SL, Kasper DL, Longo DL, Jameson JL (editors).

New York: McGraw-Hill Medical Publishing Division, Vol. I, 2002.

2. Rosamond W, Flegal K, Furie K, et al. Heart disease and stroke statistics – 2008 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation 2008;117(4):e25-e146.

3. Heart Protection Study Collaborative Group. MRC/BHF Heart Protection Study of cholesterol lowering with

simvastatin in 20,536 high-risk individuals: a randomised placebo-controlled trial. Lancet 2002;360(9326):7-22.

4. Sever PS, Dahlof B, Poulter NR, et al. Prevention of coronary and stroke events with atorvastatin in hypertensive patients who have average or lowerthan-average cholesterol concentrations, in the AngloScandinavian Cardiac Outcomes Trial–Lipid Lowering Arm (ASCOT-LLA): a multicentre randomised controlled trial. Lancet 2003;361(9364):1149-58.

5. Pearson TA, Laurora I, Chu H, Kafonek S. The lipid treatment assessment project (L-TAP): a multicenter survey to evaluate the percentages of dyslipidemic patients receiving lipid-lowering therapy and achieving low-density lipoprotein cholesterol goals. Arch Intern Med 2000;160(4):459-67.

6. Delsing DJ, Jukema JW, van de Wiel MA, et al. Differential effects of amlodipine and atorvastatin treatment and their combination on atherosclerosis in Apo E* 3-Leiden transgenic mice. J Cardiovasc Pharmacol 2003;42(1): 63-70.

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Sodium in Drugs can be Dangerous Using effervescent, dispersible or soluble drugs on a regular basis leads to greater risk for heart attacks, strokes, and other cardiovascular events.

Regular use of prescribed effervescent and other sodium-containing drugs have a 16% greater risk for nonfatal stroke, nonfatal myocardial infarction (MI), and vascular death (P<0.01), compared with regular users of low or no-sodium versions of the same drug as per Dr Jacob George, at the University of Dundee in Scotland who wrote in BMJ. Taking the maximum daily dose of drugs like effervescent aspirin or acetaminophen may exceed the recommended daily limit of sodium. Effervescent paracetamol 500 mg can contain 18.6 mmol of sodium in each tablet.

Sodium-loaded effervescent, soluble or dispersible tablets should be avoided in patients at risk of hypertension.

Current U.S. guidelines recommend that people at low risk for CVD events limit their sodium intake to no more than 2,300 mg (1 teaspoon or 100 mmol/L) per day.

Certain populations, including people over 50, African Americans, diabetics, and people with high blood pressure or chronic kidney disease, should limit their daily sodium intake to 1,500 mg.

American Heart Association recommends intake of less than 1,500 mg of sodium a day for everyone. World Health Organization (WHO) recommendations call for limiting daily sodium intake to no more than 2,000 mg per day.

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case report

Cerebral Venous Thrombosis Due to Abrin Toxicity: A Case Report KV Rajalakshmi*, G Shivkumar†, S Karthikeyan, V Punitha, K Sangeetha

Abstract Abrus precatorius (jequirity bean) is a common cause of accidental or intentional poisoning in the tropics. The data on exact incidence of abrus poisoning is largely insufficient in our country, due to lack of reporting. The estimated lethal dose for humans is 0.1-1 µg/kg. The toxic component is the protein abrin that causes widespread endothelial damage. Abrin causes a variety of manifestations like hemorrhagic gastroenteritis with erosions, hemolysis, acute renal damage, dyselectrolytemia, hepatotoxicity with elevated liver enzymes and seizures. Apart from the common manifestation of hemorrhagic gastroenteritis, patients experiencing mental status perturbations have been identified and documented earlier. There have been previous reports of elevated intracranial tension (ICT) in abrus poisoning, however, the exact cause for this phenomenon had not been elucidated.

We herein report a case of intentional A. precatorius poisoning in a young girl that caused cerebral venous thrombosis (CVT).

Keywords: Abrus precatorius poisoning, abrin poisoning, cerebral venous thrombosis, increased intracranial tension

A

brus precatorius seeds are often ingested with suicidal intent in India, however, data on exact incidence is lacking. Abrin is a potentially fatal toxalbumin obtained from the seeds of A. precatorius (jequirity bean, gundumani [Tamil]), which is similar in structure and properties to ricin.1

We herein report a case of A. precatorius poisoning with cerebral venous sinus thrombosis and intracerebral bleed that has never been documented earlier.

CASE REPORT An 18-year-old girl, a school dropout, was brought with an alleged history of consumption of approximately 10-15 crushed abrus seeds on July 31, 2013 at 22:00 hours, following a family dispute. She was given local indigenous treatment and taken to Taluk HQ Hospital, Ulundurpet at 08:50 hours on August 1, 2013. There she was instituted emergency care and subsequently transferred to the Govt. Villupuram Medical College, at

*Associate Professor †Assistant Professor Dept. of Internal Medicine Govt. Villupuram Medical College, Villupuram,Tamil Nadu Address for correspondence Dr (Major) G Shivkumar Assistant Professor Dept. of Internal Medicine Govt. Villupuram Medical College, Villupuram, Tamil Nadu - 605 601 E-mail: majorshivk@yahoo.com

19:35 hours, the same day. Upon arrival, the patient was dehydrated and had recurrent diarrhea and vomiting.

She was actively resuscitated with oral and intravenous fluid replacement. Her hydration status improved and vital parameters were stabilized. Her blood counts, biochemical analysis and liver function tests (LFTs) were within normal limits. Serum Na+ 158 mEq/l, K+ 2.3 mEq/l, Cl‒ 126 mEq/l, HCO3‒ 26 mEq/l.

Patient’s vomit improved but diarrhea persisted despite supportive treatment. On day 4, patient developed bloody diarrhea for which 1 unit of compatible group blood was transfused. Biochemical analysis revealed serum creatinine of 1.1 mg%, Na+ 143 mEq/l, K+ 2.4 mEq/l, Cl‒ 110 mEq/l and HCO3‒ 23 mEq/l. Repeat LFTs including prothrombin time/INR (international normalized ratio) were within normal limits. Her blood pressure was 120/86 mmHg and urine output was 2,100 ml/24 hours. On day 6, the patient experienced one episode of generalized tonic-clonic seizures. She was managed with intravenous loading and maintenance dose of phenytoin. She became progressively drowsy thereafter with persistent depressed mentation.

Fundus examination revealed bilateral papilledema.

A noncontrast computed tomography (CT) scan of brain revealed a hyperdense lesion with perilesional edema in left occipital region with hyperdense appearance of sagittal sinus (filled delta sign). The features were suggestive of superior sagittal sinus thrombosis with hemorrhage in left occipital lobe. CT contrast study was advised. Anti-edema and anticoagulant treatment with unfractionated heparin commenced.

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case report On further follow-up, despite adequately titrated doses of more than two anticonvulsants, the patient had recurrent seizures on days 7 through 12. She also developed right-sided hemiparesis with left gaze preference. Patientâ&#x20AC;&#x2122;s blood glucose and renal values were not much altered. On day 13, she showed signs of recovery and seizures stopped. ECG revealed a normal sinus rhythm and was within normal limits.

Her platelet counts were consistently >2,00,000/mm3

and coagulation profile showed a normal value for prothrombin time and INR, however, activated partial thromboplastin time (aPTT) was prolonged (Control 24.9 test -29.5). D-dimer was 1,270 ng/ml (elevated), familial defective apolipoprotein B-100 (FDB) was within normal limits. Lupus anticoagulant was negative, anticardiolipin titer was normal.

On day 14, a magnetic resonance imaging (MRI) scan of the brain with magnetic resonance venography (MRV) and magnetic resonance arteriography (MRA) were done, which revealed superior sagittal sinus thrombosis and left occipital hemorrhagic infarct (Figs. 1 and 2).

On day 15, neurosurgical consult was obtained, wherein she was advised decompressive surgery for the hematoma and increased intracranial tension (ICT). Patient was referred to a superspecialty surgical center on the same day.

On further follow-up, she was admitted to a tertiary care center on the same date. The patient underwent a decompressive left hemicraniectomy for elevated ICT and was placed on supported ventilation in intermediate care unit (IMCU). Patient presently has residual right hemiparesis and aphasia and is on follow-up.

DISCUSSION

Figure 1. Gradient sequence MR showing hemorrhagic blood products along left parieto-occipital region.

Figure 2. MRV sequence showing absent flow signal intensity in superior sagittal sinus.

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Poisoning from A. precatorius is attributed to the protein abrin that acts by inhibiting protein synthesis intracellularly, thereby causing cell death.1 The estimated human lethal dose is 0.1-1 mg/kg. Many of the features observed in abrin poisoning can be explained by abrin-induced endothelial cell damage, which causes an increase in capillary permeability with consequent fluid and protein leakage and tissue edema (the so-called vascular leak syndrome).1 Abrus poisoning results in a variety of clinical manifestations like hemorrhagic gastroenteritis with erosions, hemolysis, acute renal damage, dyselectrolytemia, hepatotoxicity with elevated liver enzymes and seizures.2 Previous literature also document rare manifestations like increased ICT with papilledema and autoimmune demyelination.2,3 Subrahmanyam et al have recommended routine fundus examination in such patients to detect the same.2 We herein stress the need for brain imaging in such situations. In a series of 131 patients who presented with papilledema and clinically suspected idiopathic intracranial hypertension, 10% had cerebral venous thrombosis (CVT) when MRI/MRV was

case report performed.4 Imaging of the cerebral venous system has been recommended for all patients with the clinical picture of idiopathic intracranial hypertension, because the distinction between CVT and idiopathic intracranial hypertension has important prognostic and treatment implications, and the yield of imaging is significant.4,5

to avoid acute kidney injury. Delay in institution of treatment worsens prognosis. Also such patients should be ideally placed under close observation for a minimum period of 72 hours, since the toxic features of abrin can manifest late.6

However, abrin poisoning resulting in CVT has never been documented earlier. We performed a literature review using search terms in PubMed: (“Abrin toxicity” OR “abrin poisoning” OR “Abrus precatorius poisoning”) and randomized trial: (“Abrin poisoning” OR “Abrus precatorius poisoning”) and could not find a previous reporting of CVT in abrus poisoning.

Considering this fact and the frequent occurrence of increased ICT in these patients, we hypothesize that undetected CVT is probably the cause for this phenomenon.

A. precatorius poisoning is a common occurrence in the Indian subcontinent. The toxic component is abrin that causes cell lysis by inhibiting protein synthesis. Cerebral venous sinus thrombosis has never been reported in abrus poisoning, although the occurrence of increased ICT has been documented. The objective of this case report is to create awareness about this complication and to anticipate it when dealing with such patients.

The mechanism by which abrus causes CVT is still a matter of speculation and requires indepth chemoanalysis of its components and further histopathologic or immunologic research to elucidate the bioprocess. A possible explanation could be due to widespread vascular endothelial cell damage and a procoagulant state like dehydration. In our case, although dehydration could be implicated as a potential cause, patient was well-hydrated with adequate urine output. Furthermore, it cannot account for occurrence of increased ICT in other patients documented previously.2 The management is purely supportive since there is no specific antidote.6 If early first aid is instituted by way of gastric lavage and absorbents (activated charcoal), the outcome is favorable. Adequate hydration and maintenance of optimal urine output is desirable

CONCLUSION

REFERENCES 1. Dickers KJ, Bradberry SM, Rice P, Griffiths GD, Vale GA. Abrin poisoning. Toxicol Rev 2003;22(3):137-42.

2. Subrahmanyam D, Mathew J, Raj M. An unusual manifestation of Abrus precatorius poisoning: a report of two cases. Clin Toxicol (Phila) 2008;46(2):173-5.

3. Sahoo R, Hamide A, Amalnath SD, Narayana BS. Acute demyelinating encephalitis due to Abrus precatorius poisoning - complete recovery after steroid therapy. Clin Toxicol (Phila) 2008;46(10):1071-3.

4. Lin A, Foroozan R, Danesh-Meyer HV, De Saivo G, Savino PJ, Sergott RC. Occurrence of cerebral venous sinus thrombosis in patients with presumed idiopathic intracranial hypertension. Ophthalmology 2006;113(12):2281-4.

5. Biousse V, Ameri A, Bousser MG. Isolated intracranial hypertension as the only sign of cerebral venous thrombosis. Neurology 1999;53(7):1537-42.

6. Arena JM, Thomas CC. Abrus poisoning – toxicology, symptoms and treatments. Springfield, IL 1986:p.496.

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The Heart of the Matter: Rethinking Prevention of Cardiovascular Disease A new report by the Economist Intelligence Unit investigates the health challenges posed by CVD. Despite greater recognition of the problem, every indication is that the global burden of the disease will get worse before it gets better. Greater collaboration is needed to prevent the disease. CVD is the world’s leading killer, according to the World Health Organization (WHO). It accounted for 30% of deaths around the globe in 2010. A joint Harvard University and World Economic Forum study estimated the total economic cost to be over US$850bn per year - predicted to reach US$1tn by 2025. Dr Srinath Reddy, the president of the World Heart Federation, calls CVD “the dominant epidemic of the 21st century”. In India and China, the percentage of deaths caused by CVD increased by 20% between 1990 and 2010. The equivalent rate in the US and western Europe fell by at least 20% during that same period, although CVD still accounts for 43% of all deaths in 2010, according to the WHO. The common feature of the disease across the world is its disproportionate impact on individuals from lower socioeconomic groups.

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case report

Coronary Artery Air Embolism MAHESHWARI M*, AGARWAL A†

Abstract Coronary artery air embolization is a rare event leading to catastrophic hemodynamic compromise within seconds after introduction of air emboli within the coronary arteries. The management of massive air embolism should be extremely quick so as to save life of the patient. We present a case of a 35-year-old, diabetic, and hypothyroid female who had massive air embolism in both LAD and LCX arteries during coronary angiography, which resolved within a few minutes of prompt treatment.

Keywords: Coronary artery air embolism, angiography, percutaneous interventions, hemodynamic compromise

C

oronary artery air embolization is a rare event, with overall incidence ranging from 0.2% to 0.8% during percutaneous interventions.1 Catastrophic hemodynamic compromise can occur within seconds after introduction of air emboli within the coronary arteries and may resolve within a few minutes if prompt treatment is undertaken, as we did in our case.

CASE REPORT A 35-year-old, diabetic, and hypothyroid female with treadmill test (TMT) positive for inducible ischemia was planned for coronary angiography. The right radial artery was cannulated with 5F tiger catheter.

Engagement and initial injections of left coronary angiogram was uneventful showing a smooth, and normal left anterior descending (LAD) and left circumflex arteries (LCX). However, while subsequently shooting RAO cranial view, the patient on table suddenly began to experience severe chest pain and ST segments in leads V1‒V6 began to rise up to 3 mm in amplitude.

Angiography demonstrated massive air embolism in both LAD and LCX arteries with no contrast flow beyond the mid-segments of both arteries (Fig. 1).

The patient was soon hemodynamically unstable with hypotension and bradycardia. Immediately, an attempt was made to suck out the air from the left coronary

*3rd Year Resident †Assistant Professor Dept. of Cardiology Jawaharlal Nehru Medical College Address for correspondence Dr Monika Maheshwari Navin Niwas, 434/10, Bapu Nagar, Ajmer - 305 001, Rajasthan E-mail: opm11@rediffmail.com

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Figure 1. Massive air embolism with no contrast flow beyond the mid-segments of both arteries.

Figure 2. Showing TIMI-3 flow and no residual air embolism.

case report arteries via the guiding catheter. Cardiopulmonary resuscitation (CPR) was initiated with vigorous external cardiac massage. The patient was given 100% oxygen, intravenous (IV) atropine injections, and was also put on IV dopamine. External cardiac massage and prompt aspiration was maintained for almost 4 min by which time the patient recovered both her heart rate and blood pressure with settled ST-segment on ECG monitor. After ascertaining that the patient was hemodynamically stable and had fully recovered her consciousness, left coronary angiogram was retaken, which showed TIMI-3 flow and no residual air emboli (Fig. 2).

Discussion Air can be introduced in coronary vessels inadvertently by inadequate aspiration of the guiding catheters, rupture of balloon, and leakage of air via a defective manifold system.2 The management of massive air embolism should be extremely quick so as to save the life of the patient. Case reports have described mechanical methods in the treatment of an air embolus including disruption or dislodgement by the guidewire and,3 forceful injection of saline1 to fragment the air embolus and allow dispersal distally. Such interventions may result in main vessel patency but have a potential to damage the distal microvasculature due to widespread, smaller embolizations. In contrast, aspiration aims at resolving the blockage by removing the air. Aspiration has been attempted with nondedicated devices such as over the wire (OTW) balloons4 or the angiography catheter itself.1 The lumen of such an OTW balloon system is just large enough to allow 0.014-inch wire passage and this may limit rapid aspiration. Use of the angiography catheter is limited by the ability

to manipulate it deeply enough to affect the distal embolus and the risk of damage while attempting this.

In contrast, the export aspiration catheter is a dedicated system for coronary artery aspiration.5 As such, it has the favorable qualities of being a monorail system that has the flexibility and slenderness to reach distal lesions down tortuous vessels. Dudar et al6 reported a case of massive air embolism in which AngioJet catheter was utilized to aspirate coronary air embolus with successful restoration of coronary blood flow. Along with these mechanical efforts, supportive measures with 100% oxygen, opioid analgesia, external cardiac massage (CPR), DC cardioversion, and, if needed, intraaortic balloon support are warranted for life saving.

Treatment has to be rapid and prompt as we did in our case.

REFERENCES 1. Khan M, Schmidt DH, Bajwa T, Shalev Y. Coronary air embolism: incidence, severity, and suggested approaches to treatment. Cathet Cardiovasc Diagn 1995;36(4):313-8.

2. Dib J, Boyle AJ, Chan M, Resar JR. Coronary air embolism: a case report and review of the literature. Catheter Cardiovasc Interv 2006;68(6):897-900.

3. Inoue T, Yaguchi I, Mizoguchi K, Hoshi K, Takayanagi K, Morooka S, et al. Air embolism in the right coronary artery occurring during the left coronary angioplasty using the guiding catheter with a side hole. Catheter Cardiovasc Interv 2000;49(3):331-4.

4. Solodky A, Birnbaum Y, Assali A, Ben Gal T, Strasberg B, Herz I. Coronary air embolism treated by bubble aspiration.

Catheter Cardiovasc Interv 2000;49(4):452-4.

5. Patterson MS, Kiemeneij F. Coronary air embolism treated with aspiration catheter. Heart 2005;91(5):e36.

6. Dudar BM, Kim HE. Massive air embolus treated with rheolytic thrombectomy. J Invasive Cardiol 2007;19(7):E182-4.

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TOPAC trial The TOPCAT trial evaluating spironolactone in patients with heart failure and preserved ejection fraction did not meet its primary endpoint, but there was some evidence of benefit. Through an average follow-up of 3.3 years, the rate of cardiovascular mortality, aborted cardiac arrest, or heart failure hospitalization was 18.6% in the spironolactone group and 20.4% in the placebo group according to Marc Pfeffer, MD, PhD, of Brigham and Women’s Hospital in Boston. The rate of heart failure hospitalization was, however, significantly reduced in the spironolactone group (12% versus 14.2%) with no differences in the other components of the primary endpoint.

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practice guidelineS

ACC and AHA Update on Chronic Heart Failure Guidelines

I

n 2009, the American College of Cardiology (ACC) and the American Heart Association (AHA) published a focused update of the ACC/AHA 2005 guideline update for the diagnosis and management of chronic heart failure in the adult. The guidelines writing committee reviewed recent trial data and other clinical information in the revision process for the 2009 update.

Updated Recommendations Updates to the 2005 guidelines are included in sections about the evaluation of patients presenting with heart failure; patients with reduced left ventricular ejection fraction (LVEF); patients with refractory end-stage heart failure; and the treatment of special population groups (e.g., blacks). The updated guidelines also contain a new section with recommendations about heart failure in the hospitalized patient.

Evaluation of Heart Failure Updates to the section on the evaluation of patients presenting with heart failure were made to clarify the role of functional assessment beyond the New York Heart Association (NYHA) classification, and to expand on the use of brain natriuretic peptide (BNP) and N-terminal prohormone brain natriuretic peptide (NT-proBNP) testing for patient evaluation. According to the update, patients with left ventricular dysfunction or heart failure generally present in one of three ways: with a syndrome of decreased exercise tolerance; with a syndrome of fluid retention; or with no symptoms, or symptoms of another cardiac or noncardiac disorder.

2009 updated recommendation: Measurement of natriuretic peptides (i.e., BNP and NT-proBNP) can be useful in the evaluation of patients presenting in the urgent care setting in whom the clinical diagnosis of heart failure is uncertain.

Measurement of natriuretic peptides can be useful in risk stratification. (Level of Evidence: A) The 2005 guidelines

Source: Adapted from Am Fam Physician. 2010;81(5):654-665.

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also recommended measurement of BNP for evaluating patients who present in the urgent care setting with possible heart failure; the 2009 update expanded this recommendation to include the measurement of NTproBNP. The level of evidence remained the same for this recommendation. The 2009 update warns that, although elevated natriuretic peptide levels may help confirm a suspected diagnosis of heart failure, the results of this testing alone should not be used to confirm or exclude a heart failure diagnosis.

Reduced LVEF The section of the guidelines on patients with reduced LVEF included minor updates on recommendations about the use of angiotensin-II receptor blockers (ARBs) and exercise testing.

2009 updated recommendation: Use of ARBs is recommended in patients with current or previous symptoms of heart failure and reduced LVEF who have an intolerance to angiotensinconverting enzyme (ACE) inhibitors. (Level of Evidence: A) For this recommendation, the 2009 update modified the text in the 2005 guidelines by eliminating mention of specific agents tested.

2009 updated recommendation: Maximal exercise testing with or without measurement of respiratory gas exchange is reasonable to facilitate prescription of an appropriate exercise program for patients presenting with heart failure. (Level of Evidence: C) The 2009 update changed the class of recommendation from class I (i.e., treatment should be performed) to class IIa (i.e., treatment is reasonable to perform).

The section on patients with reduced LVEF also included several changes to recommendations concerning implantable cardioverter-defibrillator therapy and cardiac resynchronization therapy.

2009 updated recommendation: Implantable cardioverterdefibrillator therapy is recommended for the primary prevention of sudden cardiac death to reduce total mortality in patients with nonischemic dilated cardiomyopathy or ischemic heart disease at least 40 days after myocardial infarction (MI); an LVEF of 35 percent or less; and NYHA

practice guidelineS functional class II or III symptoms while receiving chronic optimal medical therapy, and who have reasonable expectation of survival with a good functional status for longer than one year. (Level of Evidence: A) This recommendation was modified in the 2009 update to be consistent with the 2008 Device-Based Therapy guidelines from the ACC, AHA, and Heart Rhythm Society (HRS).

It replaces recommendations from the 2005 guidelines on implantable cardioverter-defibrillator therapy for patients with ischemic heart disease at least 40 days after MI (2005 Level of Evidence: A) or nonischemic cardiomyopathy (2005 Level of Evidence: B) with an LVEF of 30 percent or less, and for patients with an LVEF of 30 to 35 percent of any origin (2005 Level of Evidence: B).

In two of the major trials reviewed by the guidelines committee, no survival benefit was observed from implantable cardioverter-defibrillator therapy until after the first year of recovery from an acute coronary event. Patients with heart failure and low ejection fraction are typically older than 70 years, although this patient population was not well represented in the trials.

Physicians should consider common comorbidities in older adults (e.g., previous stroke, chronic pulmonary disease, arthritic conditions) when discussing this type of therapy with patients.

Medication may substantially improve LVEF; therefore, consideration of implantable cardioverter-defibrillator therapy should follow documentation of sustained reduction of LVEF despite a course of b blockers and ACE inhibitors or ARBs. Implantable cardioverterdefibrillator therapy is not warranted in patients with refractory heart failure (stage D) or in those with concomitant diseases that would shorten their life expectancy independent of heart failure. Before implantation, physicians should inform patients of the effectiveness, safety, and mortality risks of implantable cardioverter-defibrillator therapy; of the morbidity associated with an implantable cardioverter-defibrillator shock; and that the therapy does not improve clinical function or delay progression of heart failure.

2009 updated recommendation: Patients with LVEF of 35 percent or less, sinus rhythm, and NYHA functional class III or ambulatory class IV symptoms despite recommended, optimal medical therapy and who have cardiac dyssynchrony (i.e., a QRS duration of 0.12 seconds or more) should receive cardiac resynchronization therapy, with or without an implantable cardioverterdefibrillator, unless contraindicated. (Level of Evidence: A) The 2009 recommendation was updated to clarify that cardiac resynchronization therapy may be

indicated for patients with or without an implantable cardioverter-defibrillator. Evidence shows that cardiac resynchronization therapy can improve symptoms, exercise capacity, quality of life, LVEF, and survival; it can also decrease hospitalizations in patients with persistently symptomatic heart failure receiving optimal medical therapy who have cardiac dyssynchrony. The use of an implantable cardioverterdefibrillator in addition to cardiac resynchronization therapy should be based on the indications for implantable cardioverter-defibrillator therapy.

End-Stage Heart Failure The section of the guidelines on patients with refractory end-stage heart failure (stage D) included a modified recommendation on intermittent infusions.

2009 updated recommendation: Routine intermittent infusions of vasoactive and positive inotropic agents are not recommended for patients with refractory end-stage heart failure. (Level of Evidence: A) The 2009 update changed the level of evidence from B to A for this recommendation, based on evidence from an additional multicenter trial. Intermittent outpatient infusions of vasoactive medications (e.g., nesiritide) or positive inotropic medications have not been shown to improve symptoms or survival in patients with advanced heart failure.

New Recommendations

Hydralazine/Nitrates New recommendation to 2009 update: The combination of hydralazine and nitrates is recommended to improve outcomes for patients with reduced LVEF whose ethnicity is self-described as African American and who have moderate to severe symptoms on optimal therapy with ACE inhibitors, beta blockers, and diuretics. (Level of Evidence: B) Analysis of vasodilator trials showed effectiveness of treatment with isosorbide dinitrate and hydralazine in black participants. Adding these medications to standard therapy with an ACE inhibitor, a beta blocker, or both proved to be beneficial in a subsequent trial.

Accordingly, this combination is recommended for black patients who remain symptomatic despite optimal medical therapy. However, patient compliance with this combination may be low because of the large number of tablets required and the high incidence of adverse reactions. The combination treatment should not be prescribed in patients who have not previously used an ACE inhibitor, nor should it be substituted for ACE inhibitors in those who are tolerating them

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practice guidelineS without difficulty. It is unclear if this combination is beneficial in non-black patients.

Atrial Fibrillation and Sinus Rhythm New recommendation to 2009 update: It is reasonable to treat patients who have atrial fibrillation and heart failure with strategies to maintain sinus rhythm or to control ventricular rate alone. (Level of Evidence: A) Four trials evaluated the effectiveness and safety of restoring and maintaining sinus rhythm in patients with atrial fibrillation. There were equivalent outcomes for restoring and maintaining sinus rhythm by electrical or pharmacologic conversion compared with controlling ventricular rate in patients with atrial fibrillation.

Most patients quickly relapse to atrial fibrillation unless they are treated with a class I or III antiarrhythmic medication, but patients with heart failure are not likely to respond favorably to class I medications.

Class III antiarrhythmic medications (e.g., sotalol, dofetilide, amiodarone can maintain sinus rhythm in some patients, although treatment is associated with an increased risk of organ toxicity (amiodarone) and proarrhythmia (dofetilide).

Cardiac Resynchronization Therapy New recommendations to 2009 update: For patients who have LVEF of 35 percent or less, a QRS duration of 0.12 seconds or more, and atrial fibrillation, cardiac resynchronization therapy, with or without an implantable cardioverter-defibrillator, is reasonable for the treatment of NYHA functional class III or ambulatory class IV heart failure symptoms on optimal recommended medical therapy.

(Level of Evidence: B) Cardiac resynchronization therapy is reasonable for patients with LVEF of 35 percent or less with NYHA functional class III or ambulatory class IV symptoms who are receiving optimal recommended medical therapy and who have frequent dependence on ventricular pacing.

(Level of Evidence: C) Cardiac resynchronization therapy recommendations were added to be consistent with the ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities.

New Section: The Hospitalized Patient The 2009 update includes a new section on the evaluation and treatment of heart failure in patients who are hospitalized. Patients may require hospitalization if they develop acute or progressive symptoms of heart failure. Generally there are three clinical profiles for these patients: those who have volume overload (manifested by pulmonary and/or systemic congestion and often precipitated by an acute increase in chronic

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hypertension); those with profound depression of cardiac output (manifested by hypotension, renal insufficiency, and/or a shock syndrome); and those with signs and symptoms of fluid overload and shock.

Patients with heart failure and preserved LVEF are just as likely to be admitted to the hospital as those with heart failure and low LVEF. Patients are usually admitted to the hospital following a concomitant cardiovascular or cerebrovascular event, and admission often is related to medical or dietary noncompliance. Other common factors that precipitate hospitalization for heart failure include acute myocardial ischemia; uncorrected high blood pressure; atrial fibrillation and other arrhythmias; recent addition of negative inotropic medications; pulmonary embolus; use of nonsteroidal anti-inflammatory drugs; excessive alcohol or illicit drug use; endocrine abnormalities (e.g., diabetes mellitus, hyperthyroidism, hypothyroidism); and concurrent infections (e.g., pneumonia, viral illnesses).

Inpatient Evaluation and Diagnosis The diagnosis of heart failure in hospitalized patients should be based primarily on signs and symptoms, including volume status, the adequacy of circulatory support or perfusion, and consideration of precipitating factors or comorbidities. Many of the evaluation steps are identical to those used in the initial evaluation of heart failure. For an uncertain diagnosis of heart failure, plasma BNP or NT-proBNP concentrations should be considered in patients being evaluated for dyspnea who have signs and symptoms compatible with heart failure. In patients who have already been diagnosed with heart failure, it is important to understand what has caused the clinical symptoms to worsen.

Acute MI is an important cause of worsening or new-onset heart failure, and criteria for an acute coronary event that might indicate the need for further intervention may be present in up to 20 percent of patients hospitalized for heart failure.

However, several other patients may have low levels of detectable troponins that do not meet criteria for an acute ischemic event, but that are typical of chronic heart failure with an acute exacerbation. For patients with newly discovered heart failure, physicians should keep in mind the causative role of coronary artery disease in heart failure and be certain that coronary structure and function are well delineated. Therefore, coronary visualization may be an important step in the evaluation of patients hospitalized with heart failure.

practice guidelineS Inpatient Treatment A careful review of each patient's maintenance medications for heart failure is important, and medication adjustments may be necessary as a result of the hospitalization. The majority of patients should continue taking their medications during hospitalization, and most are able to tolerate the continuation of beta blockers, which results in better outcomes.

Patients with substantial fluid overload on hospital admission should be treated with loop diuretics, initiated upon arrival to the emergency department.

After admission, careful and frequent evaluation and monitoring are important and include assessing volume status and circulatory support; monitoring daily weight and vital signs; managing daily fluid input and output; and assessing daily electrolyte levels and renal function, which should be performed while intravenous diuretics or active heart failure medication titration is being done.

Optimal dosing of diuretics should produce a rate of diuresis that will benefit volume status and relieve signs and symptoms of congestion without inducing an excessively rapid reduction in intravascular volume, possibly resulting in hypotension, renal dysfunction, or both. Limiting sodium intake and dosing the diuretic multiple times daily can enhance diuresis effectiveness.

Patients who present with congestion and moderate to severe renal dysfunction may have a blunted response to diuretics, requiring higher initial doses. If all diuretic strategies are unsuccessful, ultrafiltration or another renal replacement strategy may be considered, as well as consultation with a kidney subspecialist.

Intravenous vasodilators may be added to the treatment regimen in patients who have adequate blood pressure and ongoing congestion that does not adequately respond to diuretics and standard oral therapy. The goals of vasodilator therapy include a more rapid resolution of congestive symptoms; relief of anginal symptoms while awaiting coronary intervention; control of hypertension; and improvement of hemodynamic abnormalities before beginning oral medications for heart failure.

Patients presenting with predominantly low output syndrome or combined congestion and low output may be considered for intravenous inotropes (e.g., dopamine, dobutamine, milrinone), which may help relieve symptoms caused by poor perfusion and

preserve end-organ function in those with severe systolic dysfunction and dilated cardiomyopathy. These medications are most beneficial in patients with relative hypotension and who have intolerance or no response to vasodilators and diuretics. However, the use of inotropes indicates a poor prognosis, and a thorough hemodynamic assessment is necessary. There is no evidence of benefit for routine use of these agents in patients with acute heart failure caused by congestion only; therefore, inotropes should be limited to carefully selected patients with low blood pressure and reduced cardiac output, who will require close monitoring of blood pressure and heart rhythm.

Routine invasive hemodynamic monitoring is not indicated for most patients hospitalized with symptoms of worsening heart failure, but should be considered in those whose volume and filling pressures are uncertain or who are refractory to initial therapy, particularly when filling pressures and cardiac output are unclear.

Routine invasive hemodynamic monitoring also may be beneficial in patients with clinically significant hypotension (i.e., systolic blood pressure typically less than 90 mm Hg or symptomatic low systolic blood pressure) or worsening renal function during initial therapy. Invasive hemodynamic monitoring should be performed in patients with presumed cardiogenic shock that requires escalating pressor therapy and consideration of mechanical support; those with severe clinical decompensation in whom therapy is limited by uncertainty regarding relative contributions of elevated filling pressures, hypoperfusion, and vascular tone; those with apparent dependence on intravenous inotropic infusions after initial clinical improvement; or those with persistent, severe symptoms despite adjustment of recommended treatments.

As patients stabilize and volume status normalizes, oral therapy for heart failure should be initiated or resumed. Caution should be used when starting beta blockers in patients who were treated with inotropes while hospitalized, or when initiating ACE inhibitors in patients who had marked azotemia. Before discharge, patients should be fully transitioned off all intravenous therapy, and oral therapy should be adjusted and maximized. Patients should be given written discharge instructions or educational materials that address activity level, diet, discharge medications, follow-up appointments, weight monitoring, and what to do if symptoms worsen.

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photo quiz

A Subtle ECG Question The electrocardiogram shown at the side is most diagnostic of which one of the following conditions?

A. Hypokalemia.

B. Hypocalcemia.

C. Acute myocardial infarction.

D. First-degree atrioventricular block.

E. Wolff-Parkinson-White syndrome.

SEE THE FOLLOWING PAGE FOR DISCUSSION.

Source: Adapted From Am Fam Physician. 1999;59(9):2581-2582.

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photo quiz Discussion The answer is A: hypokalemia. Although subtle, this electrocardiogram (ECG) demonstrates a flattening of the T waves with development of U waves (see arrows) associated with hypokalemia. The ECG patterns seen in patients with hypokalemia range from slight T-wave flattening alone to the appearance of prominent U waves, occasionally with ST depressions or T-wave inversions.

This is usually a progressive pattern. When the U wave is greater than the T wave, the potassium level is usually less than 2.7 mEq per L (2.7 mmol per L). The most common causes of hypokalemia are medications (especially diuretics) or renal loss related to metabolic alkalosis or potassium loss in the stool secondary to diarrhea.1 Hypokalemia, although tolerated well in most patients, can be life-threatening in those with underlying cardiac disease. The potassium level in this patient was 2.3 mEq per L (2.3 mmol per L). Treatment includes potassium replacement and correction of the underlying cause when possible. Some patients require daily potassium supplementation. Interestingly, the hypokalemia occurring in this patient was a result of Bartter's syndrome, a rare hereditary disorder of renal

potassium wasting secondary to impaired electrolyte transport in the ascending loop of Henle.2 It is treated mainly by liberal potassium supplementation. The use of spironolactone can also help prevent potassium wasting.

As for the remaining multiple-choice answers, hypocalcemia manifests itself on ECG as a prolonged QT interval, which is not present in this tracing.

There are no ST elevations or other changes suggestive of acute myocardial infarction in this tracing.

First-degree atrioventricular block should also be ruled out because the PR interval on the ECG shown here is less than 0.20 mm. Finally, Wolff-Parkinson-White syndrome is a preexcitation syndrome characterized on ECG by wide QRS complexes, short PR intervals and delta waves, none of which are present on the ECG shown here.

REFERENCES 1. Gennari FJ. Hypokalemia. N Engl J Med. 1998;339:451-8.

2. Simon DB, Lifton RP. The molecular basis of inherited hypokalemic alkalosis: Bartter's and Gitelman's syndromes. Am J Physiol. 1996;271(5 pt 2):F961-6.

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around the globe

News and Views zz

The Union Cabinet recently cleared the health ministry’s proposal to institute a three-year degree programme for public health professionals. The bachelor in community health programme will act as a bridge between auxiliary nurse midwife and a doctor and overrides the objections raised by a parliamentary panel and the Medical Council of India.

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Chronic rhinosinusitis may be the result of an overactive immune response to normal microbes, not necessarily bacterial infection. A new study found that patients and healthy controls tended to have qualitatively similar microbiomes. While control lavage samples triggered interleukin (IL)-5 production in peripheral blood leukocytes from patients, this was not the case with leukocytes from controls.

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The US FDA has approved ibrutinib (Imbruvica, Pharmacyclics, Janssen Biotech), a “breakthrough” drug for mantle cell lymphoma (MCL) that has been hailed as a successor to traditional chemotherapy in treating hematological cancer. Ibrutinib is indicated for patients with MCL who have undergone at least one other therapy for this rare and aggressive form of blood cancer. The drug inhibits an enzyme that the cancer needs to multiply and spread.

According to a research from Sweden, women who have undergone bariatric surgery should be classified as at-risk during pregnancy, with a greater chance of giving birth to preterm or smallfor-gestational-age babies. The study is reported online in BMJ. A new analysis of the action to control cardiovascular risk in diabetes (ACCORD) trial published in the journal Diabetes Care has shown that response to standard or intensive glucose-lowering strategies appears to differ by age in individuals with type 2 diabetes. Cardiovascular mortality increased in the trial in middle-aged adults who received intensive versus standard glucose-lowering therapy, but this was not true for older adults. However, severe hypoglycemia occurred more often in the older individuals.

A novel variant of avian influenza A infected a 20-year-old woman in Taiwan, as reported by Ming-Tsan Liu, PhD, of the Taiwan Centres for

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Disease Control in Taipei, and colleagues in The Lancet Respiratory Medicine. It is the first reported case of an H6N1 avian virus infecting and causing disease in a human, although very similar viruses are endemic in chickens in the island nation.

The woman was treated in May and made a complete recovery, with no indication that she passed the novel virus to anyone else. zz

Not all polyunsaturated fatty acids (PUFAs) are created equal, according to a new report, so simply replacing dietary saturated fats with polyunsaturated fatty acids might not be enough to lower the risk of heart disease. In an analysis published November 11, 2013 in CMAJ, two researchers argue that to obtain the “heart benefits” of polyunsaturated fatty acids, the emphasis should be on a-linolenic acid, an omega-3 fatty acid, and not on linoleic acid, which is an omega-6 fatty acid.

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Fractional flow reserve, intravascular ultrasound, and optical coherence tomography all likely have a place in the interventional cardiologist’s armamentarium, according to a consensus statement from the Society for Cardiovascular Angiography and Interventions (SCAI).

The guideline published in Catheterization and Cardiovascular Interventions states that fractional flow reserve (FFR) is used to determine the functional significance of a coronary stenosis.

Intravascular ultrasound (IVUS) offers excellent visualization of intraluminal and transmural coronary anatomy. Optical coherence tomography (OCT) further improves vascular visualization.

zz

For children with juvenile idiopathic arthritis, early treatment with a combination of methotrexate and etanercept leads to sustained clinically inactive disease more often than methotrexate alone.

An exploratory analysis of data from the trial of early aggressive therapy in polyarticular juvenile idiopathic arthritis (TREAT) was presented at the American College of Rheumatology (ACR) 2013 annual meeting. TREAT was a double-blind placebo-controlled trial of 85 patients 2 to 17 years of age who had juvenile arthritis for less than a year.

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Young adults with major depressive disorder seemed to resolve depression after a 12-week exercise program with a motivational component.

around the globe In a small, pilot study of depressed 18- to 24-yearolds presented at the Society for Neurology meeting, exercise was associated with declines in depression severity of 63%, where 83% of participants were no longer considered depressed at the end of the 12-week program. zz

A small phase I study has reported that reduced sodium intake lowered blood pressure (BP) and improved indicators of kidney health in people with stage 3 and 4 chronic kidney disease (CKD).

Overall, salt restriction resulted in statistically significant and clinically important reductions in BP (mean reduction of systolic/diastolic BP 10/4 mm Hg), extracellular fluid volume, albuminuria and proteinuria. The study is published in the November 7 issue of the Journal of the American Society of Nephrology.

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A loss of peripheral bone mineral density (BMD) accompanied the spinal changes seen in patients with ankylosing spondylitis (AS), according to a study reported in the journal Arthritis Research and Therapy. High-resolution peripheral quantitative computed tomography revealed that AS patients had significantly less trabecular volumetric BMD at the ultradistal radius and at the ultradistal tibia compared with healthy controls.

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Successful hepatitis C (HCV) treatment before a liver transplant markedly reduced the risk of re-infection, according to research reported at the annual meeting of the American Association for the Study of Liver Diseases. Without treatment, HCV re-infection of the transplanted liver is “universal.”

But 64% of patients successfully treated with the investigational agent sofosbuvir along with the standard medication ribavirin remained virus-free 12-weeks after the transplant.

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A new prospective study has demonstrated a relationship between thyroid-function tests (TFTs) and mortality in elderly patients hospitalized for acute illness, then followed for 7 years.

Low triiodothyronine (T3) levels were associated with all-cause and cardiovascular death, illustrating that such hospitalized older people with low levels of this hormone face a slimmer risk for survival.

The findings are reported in the Journal of Clinical Endocrinology and Metabolism.

The US FDA has released a drug safety advisory with recommendations aimed at reducing the risk of spinal column bleeding after spinal intervention, including epidural procedures and lumbar puncture, in patients taking low-molecular-weight

heparins. The agency is recommending that “health care professionals carefully consider the timing of spinal catheter placement and removal, and delay dosing of anticoagulant medications for some time interval after catheter removal,” to decrease the risk of spinal bleeding and subsequent paralysis in these patients. The FDA said that these new timing recommendations, which can decrease the risk of epidural or spinal hematoma, will be added to the labels of anticoagulant drugs known as low molecular weight heparins, including lovenox and generic enoxaparin products and similar products. zz

Beta-trace protein (BTP), a biomarker that has been associated with both kidney damage and an increased cardiovascular risk, may help identify high-risk atrial fibrillation patients, as reported by researchers from University of Birmingham in England in the November 5 issue of Chest. Among patients with atrial fibrillation who were on stable oral anticoagulant therapy, high plasma levels of the protein were associated with significantly elevated risks of embolic events, adverse cardiovascular events, death, and major bleeding. Adding information about BTP levels modestly improved the predictive ability of models that included two established risk scores-CHAD2DS2-VASc and HAS-BLED-as indicated by higher C-statistics.

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Neovasc, the makers of a percutaneous treatment for refractory angina, have announced that the coronary sinus Reducer stent effectively reduced angina scores when compared with a sham procedure in patients with refractory angina.

The company reported that the 104-patient CORSIRA study achieved the primary end point, which is a decrease in two or more Canadian Cardiovascular Society (CCS) angina score grades from baseline to six months in Reducer-treated patients compared with patients who were treated with a control procedure.

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Two infectious disease experts have warned that a new polio outbreak in Syria caused by wildtype polio virus 1 (WPV1) and asymptomatic cases in Israel might endanger Europe and other neighboring regions, according to correspondence published online November 8 in the Lancet.

The WHO has confirmed an outbreak of at least ten cases of polio in Syria, where vaccination coverage has dramatically decreased during the civil war. WPV1 has been isolated from sewage and feces from asymptomatic carriers in Israel since February 2013.

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lighter reading

Two castle builders Hot sun. Salty air. Rhythmic waves.

A little boy is on his knees scooping and packing the sand with plastic shovels into a bright blue bucket. Then he upends the bucket on the surface and lifts it. And, to the delight of the little architect, a castle tower is created.

laugh a while

An Inspirational Story

Lighter Side of Medicine

All afternoon he will work. Spooning out the moat. Packing the walls. Bottle tops will be sentries. Popsicle sticks will be bridges. A sandcastle will be built.

Two builders of two castles. They have much in common. They shape granules into grandeurs.

They see nothing and make something.

They are diligent and determined. And for both the tide will rise and the end will come. Yet that is where the similarities cease. For the boy sees the end, while the man ignores it. Watch the boy as the dusk approaches.

As the waves near, the wise child jumps to his feet and begins to clap. There is no sorrow. No fear. No regret.

He knew this would happen. He is not surprised. And when the great breaker crashes into his castle and his masterpiece is sucked into the sea, he smiles. He smiles, picks up his tools, takes his father’s hand, and goes home.

The grown up, however, is not so wise. As the wave of years collapses on his castle, he is terrified. He hovers over the sandy monument to protect it. He blocks the waves from the walls he has made. Salt-water soaked and shivering he snarls at the incoming tide.

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2nd Person: "A little. What's wrong?"

1st Person: "Well, I sent a fax, and the recipient called back to say all she received was a coversheet and a blank page. I tried it again, and the same thing happened."

1st Person: "It's a pretty sensitive memo, and I didn't want anyone else to read it by accident, so I folded it so only the recipient would open it and read it."

QUOTE

HATRED weakens the liver; GRIEF weakens the lungs; WORRYING weakens the stomach; STRESS weakens both the heart and the brain and FEAR fails the kidneys…so stay HAPPY! LOOK GOOD, FEEL GOOD and DO GOOD! —Dr GM Singh

Dr. Good & Dr. Bad Situation : A diabetic patient was found to have low coronary flow reserve on Doppler Echo.

This test has no significance

Get your treadmill test done

© IJCP GROUP

All his life he will work. Formulating the plans.

Forecasting the future. Annuities will be sentries.

Capital gains will be bridges. An empire will be built.

1st Person: "Do you know anything about this fax-machine?"

2nd Person: "How did you load the sheet?"

Big city. Busy streets. Rumbling traffic.

A man is in his office. At his desk he shuffles papers into stacks and delegates assignments. He cradles the phone on his shoulder and punches the keyboard with his fingers. Numbers are juggled and contracts are signed and much to the delight of the man, a profit is made.

Modern Technology

Lesson : Coronary

flow reserve obtained by transthoracic Doppler echocardiography provides independent prognostic information in asymptomatic patients with T2DM without overt CAD. Patients with coronary flow reserve <2.5 had a worse long-term outcome.

Cardiovasc Diabetol 2013;12(1):121.

KK Aggarwal

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by Cheque/DD only, HeadJournal Office: E - 219, GreaterVol. Kailash, Part - 1, New Asian of Clinical Cardiology, 16, No. 8, December 2013Delhi - 110 048 Payable at New Delhi.

Telefax: 40587513 Mob.: 9891272006 Do not pay Cash.

Subscription Office: 7E, Merlin Jabakusum, 28A, S.N. Roy Road, Kolkata - 700 038 Tele No.: 033-23962055 Mob.: 9831363901, E-mail: subscribe@ijcp.com, Website: www.ijcpgroup.com

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 -

- -

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.

Manuscript - Three complete sets of the manuscript should be submitted and preferably with a CD; typed double spaced throughout (including references, tables and legends to figures).

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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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All pages should be numbered consecutively beginning with the title page.

departments and institutions where the work was performed, name of the corresponding authors, acknowledgment of financial support and abbreviations used.

- The title should be of no more than 80 characters and should represent the major theme of the manuscript.

A subtitle can be added if necessary.

- A short title of not more than 50 characters (including inter-word spaces) for use as a running head should be included.

- The name, telephone and fax numbers, e-mail and postal addresses of the author to whom communications are to be sent should be typed in the lower right corner of the title page.

- A list of abbreviations used in the paper should be included. In general, the use of abbreviations is discouraged unless they are essential for improving the readability of the text.

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

- It should not contain abbreviations, footnotes or references.

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.

- Ethical guidelines followed by the investigations should be described.

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).

- Method of allocating the subjects into different groups.

- Statistical methods used for presentation and analysis of data i.e., in terms of mean and standard deviation values or percentages and statistical tests such as Student’s ‘t’ test, Chi-square test and analysis of variance or non-parametric tests and multivariate techniques.

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

-

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.

Asian Journal of Clinical Cardiology, Vol. 16, No. 8, December 2013

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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.

- All photomicrographs should indicate the magnification of the print.

- Special features should be indicated by arrows or letters which contrast with the background.

- The back of each illustration should bear the first author’s last name, figure number and an arrow indicating the top. This should be written lightly in pencil only. Please do not use a hard pencil, ball point or felt pen.

- Color illustrations will be accepted if they make a contribution to the understanding of the article.

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Do not use clips/staples on photographs and artwork.

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Illustrations must be drawn neatly by an artist and photographs must be sent on glossy paper. No captions should be written directly on the photographs or illustration. Legends to all photographs and illustrations should be typed on a separate sheet of paper. All illustrations and figures must be referred to in the text and abbreviated as ‘Fig.’.

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.

Legends - These should be typed double spaces on a separate sheet and figure numbers (in Arabic numerals) corresponding with the order in which the figures are presented in the text.

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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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Asian Journal of Clinical Cardiology, Vol. 16, No. 8, December 2013

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

April 2012, Pages 545-596

Peer Reviewed Journal

Drug Review

Review Article

Original Article

Case Report

Photo Quiz

Lighter Reading

Asian Journal of Clinical Cardiology, Vol. 16, No. 8, December 2013

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

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