Ajcc November 2013 by IJCP

In This Issue — Aortic Stenosis: Diagnosis and Treatment — Usefulness of Ankle–Brachial Index as a Cardiovascular Risk Factor in Patients of Acute Coronary Syndrome and Its Correlation with Conventional Cardiovascular Risk Factors —

Intraventricular Conduction Defects in Hypertensive Patients

— Atrial Septal Aneurysm with Transient Loss of Vision — Cyanosis in an Older Woman — Updated Recommendations on Daily Aspirin Use in Patients with Diabetes —

Reconstitution of the Body Following an Autopsy

— Reasons for Financial Planning

Volume 16, Number 7, November 2013 Pages 241-280

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 7, November 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 245 Signs of “Sudden” Cardiac Death Come Weeks Before

KK Aggarwal

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

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

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

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

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

REVIEW ARTICLE 246 Aortic Stenosis: Diagnosis and Treatment

CLINICAL STUDY 255 Usefulness of Ankle–Brachial Index as a Cardiovascular Risk Factor in Patients of Acute Coronary Syndrome and Its Correlation with Conventional Cardiovascular Risk Factors

Mittal LC, Sharma D

260 Intraventricular Conduction Defects in Hypertensive Patients

Anand NN, Padma V, Rajendran SM

CASE REPORT 264 Atrial Septal Aneurysm with Transient Loss of Vision

Anand Gopal Bhatnagar Editorial Anchor Advisory Bodies Heart Care Foundation of India Non-Resident Indians Chamber of Commerce & Industry World Fellowship of Religions

Brain H. Grimard, Jan M. Larson

Mittal SR

photo quiz 266 Cyanosis in an Older Woman

Sangil Lee, Toshinori Ozeki

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

268 Updated Recommendations on Daily Aspirin Use in Patients with Diabetes

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

Carrie Armstrong

medilaw

ÂŠ 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.

270 Reconstitution of the Body Following an Autopsy

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.

medifinance 271 Reasons for Financial Planning

FORTHCOMING CONFERENCES 272 International Conferences

Around the Globe 273 News and Views

lighter reading 274 Lighter Side of Medicine

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from the desk of group editor-in-chief

Dr KK Aggarwal

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

Signs of “Sudden” Cardiac Death Come Weeks Before Signs of approaching “sudden” cardiac arrest, an electrical malfunction that stops the heart, usually appear at least a month ahead of time, according to a study of middle-aged men in Portland, Oregon.

determined that 53% had symptoms beforehand. Among those with symptoms, 56% had chest pain, 13% had shortness of breath, and 4% had dizziness, fainting, or palpitations.

Over 3.6 lacs out-of-hospital cardiac arrests occur each year in the United States largely involving middleaged men, with only 9.5% surviving, according to the American Heart Association.

About 80% of symptoms occurred between 4 weeks and 1 hour before the cardiac arrest. Although most men had coronary artery disease, just half had been tested for it before their attacks.

Patients can survive if they are given CPR immediately and their hearts are jolted back into normal rhythm with a defibrillator.

The message here is, if you have these signs or symptoms, please do not ignore them; seek healthcare.

Earlier clinical trials have focused only on symptoms or warnings signs within an hour of such attacks. Among 567 men who had “sudden” arrests, researchers

The new findings from the 11-year-old “Oregon Sudden Unexpected Death Study” were presented at the Annual Scientific Sessions of the American Heart Association being held in Dallas, Texas.

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REVIEW ARTICLE

Aortic Stenosis: Diagnosis and Treatment Brain H. Grimard*, Jan M. Larsonâ&#x20AC;

Abstract Aortic stenosis is the most important cardiac valve disease in developed countries, affecting 3 percent of persons older than 65 years. Although the survival rate in asymptomatic patients with aortic stenosis is comparable to that in age- and sex-matched control patients, the average overall survival rate in symptomatic persons without aortic valve replacement is two to three years. During the asymptomatic latent period, left ventricular hypertrophy and atrial augmentation of preload compensate for the increase in afterload caused by aortic stenosis. As the disease worsens, these compensatory mechanisms become inadequate, leading to symptoms of heart failure, angina, or syncope. Aortic valve replacement should be recommended in most patients with any of these symptoms accompanied by evidence of significant aortic stenosis on echocardiography. Watchful waiting is recommended for most asymptomatic patients, including those with hemodynamically significant aortic stenosis. Patients should be educated about symptoms and the importance of promptly reporting them to their physicians. Serial Doppler echocardiography is recommended annually for severe aortic stenosis, every one or two years for moderate disease, and every three to five years for mild disease. Cardiology referral is recommended for all patients with symptomatic aortic stenosis, those with severe aortic stenosis without apparent symptoms, and those with left ventricular dysfunction. Many patients with asymptomatic aortic stenosis have concurrent cardiac conditions, such as hypertension, atrial fibrillation, and coronary artery disease, which should also be carefully managed.

Keywords: Aortic stenosis, left ventricular hypertrophy, aortic valve replacement, serial Doppler echocardiography, left ventricular dysfunction.

ortic valve stenosis affects 3 percent of persons older than 65 years and leads to greater morbidity and mortality than other cardiac valve diseases.1 The pathology of aortic stenosis includes processes similar to those in atherosclerosis, including lipid accumulation, inflammation, and calcification.2

The development of significant aortic stenosis tends to occur earlier in those with congenital bicuspid aortic valves.3 Although the survival rate in asymptomatic patients is comparable to that in age- and sex-matched control patients, survival notably worsens after symptoms appear.

*Instructor Family Medicine, Mayo Clinic College of Medicine, Jacksonville â&#x20AC; Assistant Professor Family Medicine, Mayo Clinic College of Medicine, Jacksonville Address for Correspondence Brian H. Grimard Mayo Clinic, 110 Southwood Lake Dr., St. Augustine, FL 32086 E-mail: grimard.brian@mayo.edu Source: Adapted from Am Fam Physician. 2008;78(6):717-724, 725

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Pathophysiology and natural history The natural history of aortic stenosis involves a prolonged latent period, during which progressive worsening of left ventricular (LV) outflow obstruction leads to hypertrophic changes in the left ventricle.4,5 As the aortic valve area becomes less than one half its normal size of 3 to 4 cm2 (about the size of a nickel), a measurable pressure gradient between the left ventricle and ascending aorta may be detected on echocardiography or by direct measurement at cardiac catheterization.6 This change reflects compensatory increases in LV pressures that contribute to the maintenance of adequate systemic pressures. One consequence is LV hypertrophy with subsequent diastolic dysfunction and increased resistance to LV filling.7,8 Thus, a strong left atrial contraction is needed to provide sufficient LV diastolic filling and support adequate stroke volume.9 Increasing overall myocardial contractility and augmenting preload with an increased atrial kick preserve LV systolic function, typically while the patient remains asymptomatic. As aortic stenosis worsens, with the aortic valve area decreasing to 1 cm2 or less (about the size of the head of a golf tee),10

review article Sort: Key Recommendations for Practice Clinical Recommendation

Evidence Rating

References

25, 26

28, 30, 31

Echocardiography is recommended in patients with classic symptoms of aortic stenosis accompanied by a systolic murmur and in asymptomatic patients with a grade 3/6 or louder systolic murmur. Aortic valve replacement is the only effective treatment for patients with severe symptomatic aortic stenosis. Watchful waiting is recommended for most patients with asymptomatic aortic stenosis, including those with severe disease. Serial Doppler echocardiography is recommended annually for severe aortic stenosis, every one to two years for moderate disease, and every three to five years for mild disease. Aspirin prophylaxis should be considered in adults with a 10-year risk of cardiovascular disease of 6 percent or greater, which is common with aortic stenosis. Intensive lipid-lowering therapy has not been shown to stop the progression of calcific aortic stenosis and is not recommended in the absence of other indications for statin therapy.

A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to http://www.aafp.org/afpsort.xml.

Aortic valve

Figure 1. Transesophageal echocardiograms of a normal aortic valve. (A) Axial view. (B) Horizontal four-chamber view.

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review article changes in LV function may no longer be adequate to overcome the outflow obstruction and maintain systolic function, even when complemented by an increase in preload. The resulting impairment in systolic function, alone or combined with diastolic dysfunction, may lead to clinical heart failure. Progressive LV hypertrophy from aortic stenosis also leads to increased myocardial oxygen needs11; concurrently, myocardial hypertrophy may compress the intramural coronary arteries as they carry blood toward the endocardium. These changes along with reduced diastolic filling of the coronary arteries may result in classic angina, even in the absence of coronary artery disease (CAD).12 In addition, as aortic stenosis becomes severe, cardiac output no longer increases with exercise.13 In this setting, a drop in systemic vascular resistance that normally occurs with exertion may lead to hypotension and syncope.14-16 Figure 1 shows echocardiograms of a normal aortic valve, and Figure 2 shows echocardiograms of severe aortic stenosis.

Diagnosis

Signs and Symptoms Classic symptoms of aortic stenosis include dyspnea and other symptoms of heart failure, angina, and syncope. The onset of these classic symptoms indicates hemodynamically significant aortic stenosis and is a critical point for making management decisions. It is also important to recognize that presentations may vary. Some patients with severe aortic stenosis, especially older patients, may present more subtly and initially experience a decrease in exertional tolerance without recognizing the classic symptoms. Others may have a more acute presentation, sometimes with symptoms precipitated by concurrent medical conditions. For example, new-onset atrial fibrillation with a resultant decrease in atrial filling may lead to symptoms of heart failure, or initiation of vasodilator medications may cause syncope. A classic physical finding of aortic stenosis is a harsh, crescendo-decrescendo systolic

Figure 2. Transesophageal echocardiograms of severe aortic stenosis. (A) The axial view shows diffusely thickened leaflets with a restricted opening motion. (B) The horizontal four-chamber view shows the resultant severe left ventricular hypertrophy and left atrial enlargement.

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review article murmur that is loudest over the second right intercostal space and radiates to the carotid arteries. This may be accompanied by a slow and delayed carotid upstroke, a sustained apical impulse, and an absent or diminished aortic second sound. However, in older persons, the murmur may be less intense and often radiates to the apex instead of to the carotid arteries. Also, with an increased incidence of atherosclerosis and hypertension in older persons, the classic carotid pulse changes may be masked. It is difficult to rule out aortic stenosis with physical examination findings alone. Reliable auscultatory indicators of the absence of aortic stenosis include a grade 1/6 or softer systolic murmur, absence of a radiating systolic murmur heard over the head of the right clavicle, and presence of a split second heart sound.17,18 It is essential that primary care physicians consider aortic stenosis in adults who present with any of the classic symptoms accompanied by a systolic murmur. Older patients with vague complaints, such as fatigue or decreased exercise tolerance, and asymptomatic patients undergoing preoperative medical assessment should receive further evaluation when physical examination reveals a grade 2/6 or louder systolic murmur. American College of Cardiology/American Heart Association (ACC/AHA) practice guidelines recommend echocardiography in asymptomatic patients with a grade 3/6 or louder systolic murmur.19

Diagnostic Testing Doppler echocardiography is the recommended initial test for patients with classic symptoms of aortic stenosis. 19 It is helpful for estimating aortic valve area, peak and mean transvalvular gradients, and maximum aortic velocity. These are the primary measures for assessing disease severity, and they have been well validated compared with measurement obtained with cardiac catheterization.20 Echocardiography also provides useful information about LV function, left ventricular filling pressure, and coexisting abnormalities of other valves. Guidelines for relating these hemodynamic measures to severity of aortic stenosis are presented in Table 1.19 Isolated aortic stenosis rarely becomes symptomatic until the aortic valve area is less than 1 cm2, the mean gradient is greater than 40 mm Hg, or the aortic jet velocity is greater than 4 m per second.

surgery has an average perioperative mortality rate of 4 percent21-23 and a risk of prosthetic valve failure of approximately 1 percent per year.24 Figure 3 is an algorithm for the management of severe aortic stenosis.19

Symptomatic Patients Mortality dramatically increases after aortic stenosis becomes symptomatic. The average overall survival rate is two to three years in symptomatic patients without surgical treatment. Among older members of this population, one- and three-year mortality rates of 44 and 75 percent, respectively, have been reported.24 Although there are no prospective randomized trials comparing aortic valve replacement with medical management, retrospective observational studies have shown that surgical repair leads to significant improvement in survival, usually accompanied by symptom improvement.25,26 The 10-year survival rate in Medicare-age patients after aortic valve replacement is almost identical to that in age- and sex-matched persons who do not have aortic stenosis.27 Although these observational studies may have limitations, such as selection bias, a greater than four-fold difference in survival between surgically and medically treated patients supports the well-accepted recommendation that aortic valve replacement should be performed promptly in symptomatic patients.19 Additionally, it is unlikely that prospective randomized trials will be completed. In symptomatic patients with echocardiographic measures consistent with severe aortic stenosis, symptoms must be presumed to be a result of aortic stenosis, even if other potentially causative conditions, such as CAD, are present. However, if echocardiographic findings suggest only moderate aortic stenosis, further diagnostic testing (e.g., coronary angiography, pulmonary function testing, arrhythmia evaluation) may be needed. Table 1. Classifications of Aortic Stenosis Severity Severity

Normal Mild

Treatment

Moderate

Aortic valve replacement is the only effective treatment for hemodynamically significant aortic stenosis. The

Severe

Aortic jet velocity

Mean gradient

Aortic valve

(m per second)

(mm Hg)

< 2.5

â&#x20AC;&#x201D;

3 to 4

2.5 to 2.9

< 25

1.5 to 2

3 to 4

25 to 40

1 to 1.5

> 40

area (cm2)

Information from reference 19.

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review article

Management of Severe Aortic Stenosis Aortic valve area less than 1 cm2, mean gradient greater than 40 mm Hg, or aortic jet velocity greater than 4 m per second

Patient already plans to undergo CABG or other heart surgery?

Symptoms present?

Yes

Equivocal findings

Exercise stress test

Normal measurement

Symptoms, decreased blood pressure

Left ventricular ejection fraction

Less than 50 percent

Normal result

Severe valve calcification, rapid progression, or expected delays in surgery?

Yes Class I

Class I

Class IIb

Class I

Class IIb

Aortic valve replacement; preoperative coronary angiography

No Clinical follow-up, patient education, risk-factor modification, annual Doppler echocardiography

Reevaluation

Class I = evidence for, and/or general agreement that, the procedure or treatment is beneficial, useful, and effective; Class II = onflicting evidence and/or a divergence of opinion about the usefulness or effectiveness of the procedure or treatment; Class IIb = usefulness or effectiveness is less well established by evidence or opinion.

Figure 3. American College of Cardiology/American Heart Association algorithm for the management of severe aortic stenosis. (CABG = coronary artery bypass graft.) Adapted from Bonow RO, Carabello BA, Kanu C, et al. ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines [published correction appears in Circulation. 2007;115(15): e409]. Circulation. 2006;114(5):e108.

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review article Asymptomatic Patients

Monitoring and Referral

Aortic valve replacement is also recommended for asymptomatic patients with severe aortic stenosis accompanied by LV systolic dysfunction (i.e., ejection fraction of less than 50 percent). When severe aortic stenosis is shown to be the primary pathology in this setting, aortic valve replacement is a lifesaving therapy and improves LV function.20,28,29

Watchful waiting until symptoms are detected is appropriate in most patients with asymptomatic aortic stenosis. ACC/AHA guidelines recommend that serial Doppler echocardiography be performed annually for severe aortic stenosis, every one to two years for moderate aortic stenosis, and every three to five years for mild aortic stenosis.19 Because symptoms are the best indicator of hemodynamic significance, a careful patient history should be obtained at regular intervals. Most importantly, patients should be educated about symptoms and the importance of promptly reporting them to their physicians. Cardiology referral is recommended for all patients with symptomatic aortic stenosis, for patients with aortic stenosis accompanied by LV dysfunction, and for asymptomatic patients with very severe or rapidly progressive calcification. Cardiology evaluation should also be considered in patients with subtle or atypical presentations, such as decreased exercise tolerance or an episode of congestive heart failure precipitated by new-onset anemia.

However, watchful waiting is recommended in most asymptomatic patients with aortic stenosis, including those with severe disease. Survival in patients with aortic stenosis that is managed with watchful waiting is comparable to that in patients without aortic stenosis. Additionally, the surgical risk outweighs the approximately 1 percent annual risk of sudden death in asymptomatic patients with aortic stenosis. Attempts have been made to identify those who are more likely to have poor outcomes without “early” aortic valve replacement. Patients with very severe aortic stenosis (aortic valve area of 0.6 cm2 or less or an aortic jet velocity of 5 m per second or more), a more rapid increase in aortic jet velocity over time (0.3 m per second or more per year), or severe valve calcification have a high risk of developing symptoms and of needing aortic valve replacement within the next one to two years. High-risk patients, including patients who do not live near a medical care facility, may need closer monitoring or consideration of early valve replacement if the predicted operative mortality rate is 1 percent or less (i.e., in patients 70 years or younger without significant comorbidities).28,30,31 It is important to distinguish patients who are truly asymptomatic from those who have a routine activity level that has decreased to below their symptom threshold. This is especially important in older patients who may attribute their symptoms to normal aging or concurrent illness. When the symptom status is unclear, ACC/AHA guidelines recommend that exercise stress testing be performed under the direct observation of an experienced cardiologist.19 Aortic valve replacement should be considered if symptoms occur when the patient is at less than 80 percent of the predicted maximum heart rate or if the patient has an abnormal blood pressure response.32-34 Although exercise stress testing to detect concurrent CAD or to determine exercise tolerance is safe in patients with mild to moderate aortic stenosis, some cardiologists may be reluctant to perform the tests in those with significant aortic stenosis because of the risk of death during the test.

Medical Management During Watchful Waiting No medical treatments have been proven to delay the progression of aortic valve disease or to improve survival. However, many patients with asymptomatic aortic stenosis have concurrent cardiac conditions, including hypertension, atrial fibrillation, and CAD; these conditions should be carefully controlled.19,28

Hypertension Approximately 40 percent of patients with aortic stenosis also have hypertension.28,35 With concurrent hypertension, LV afterload is elevated as a result of the “double load” that is created by aortic stenosis plus increased vascular resistance. Because it appears that the degree of valvular opening and stroke volume can increase in response to afterload reduction, treatment of hypertension is recommended in patients with asymptomatic aortic stenosis.36-38 However, patients with aortic stenosis can be particularly sensitive to the manipulation of preload, contractility, or systemic vasomotor tone.39 Blood pressure–lowering agents should be initiated at low doses and gradually titrated to achieve the desired effect. Angiotensin-converting enzyme (ACE) inhibitors are well tolerated, improve effort tolerance, and reduce dyspnea in symptomatic patients with severe aortic stenosis.38 However, routine use of ACE inhibitors

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review article in patients with asymptomatic aortic stenosis cannot be recommended at this time. Second-generation dihydropyridine calcium channel blockers do not appear to depress LV function, as older calcium channel blockers do, and may be safe to use in patients with aortic stenosis. Diuretics should be used with caution because of the potential for reducing LV diastolic filling, which may reduce cardiac output. Peripheral alpha-blocker use may lead to hypotension or syncope and should be avoided.

Atrial Fibrillation Atrial fibrillation occurs in 5 percent of patients with aortic stenosis. Its presence may make echocardiographic assessment of aortic stenosis more challenging. Newonset atrial fibrillation may precipitate heart failure in a previously asymptomatic patient with significant aortic stenosis. Heart rate control is important to allow time for optimal diastolic filling. However, physicians should be aware of the possible hemodynamic effects of some rate-controlling medications in patients with aortic stenosis. In particular, beta blockers and rateslowing calcium channel blockers may depress LV systolic function.

Coronary Risk Reduction Concurrent CAD is common in patients with aortic stenosis. ACC/AHA guidelines recommend evaluation and modification of cardiac risk factors in these patients.19 This includes discontinuation of tobacco use, initiation of aspirin prophylaxis in adult patients with a 10-year risk of cardiovascular disease 6 percent or greater, and participation in regular exercise.40 Patients with mild aortic stenosis should not be restricted from physical activity. Asymptomatic patients with moderate to severe aortic stenosis should avoid competitive or vigorous activities that involve high dynamic and static muscular demands, although other forms of exercise are safe.19,41 Although initial observational studies suggested a significantly lower rate of aortic stenosis progression in patients treated with statins,42,43 a more recent randomized prospective study showed no statistical difference in hemodynamic progression of aortic stenosis between patients receiving aggressive atorvastatin therapy and those receiving placebo.44 Because these studies were relatively small, it is too early to draw firm conclusions about the value of statin therapy for aortic stenosis. Larger prospective studies are expected to conclude in 2009.45

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Finally, antimicrobial prophylaxis for bacterial endocarditis is recommended in patients who have undergone aortic valve replacement, but is no longer recommended for patients with aortic stenosis or other acquired valve diseases.46 REFERENCES 1. Lindroos M, Kupari M, Heikkilä J, Tilvis R. Prevalence of aortic valve abnormalities in the elderly: an echocardiographic study of a random population sample. J Am Coll Cardiol. 1993;21(5):1220-1225. 2. Otto CM, Knuusisto J, Reichenbach DD, Gown AM, O’Brien KD. Characterization of the early lesion of “degenerative” valvular aortic stenosis. Histological and immunohistochemical studies. Circulation. 1994;90(2):844-853. 3. Lewin MB, Otto CM. The bicuspid aortic valve: adverse outcomes from infancy to old age. Circulation. 2005;111(7):832-834. 4. Tobin JR Jr, Rahimtoola SH, Blundell PE, Swan HJ. Percentage of left ventricular stroke work loss. A simple hemodynamic concept for estimation of severity in valvular aortic stenosis. Circulation. 1967;35(5):868-879. 5. Pantely G, Morton M, Rahimtoola SH. Effects of successful, uncomplicated valve replacement on ventricular hypertrophy, volume, and performance in aortic stenosis and in aortic incompetence. J Thorac Cardiovasc Surg. 1978;75(3):383-391. 6. Grossman W, Jones D, McLaurin LP. Wall stress and patterns of hypertrophy in the human left ventricle. J Clin Invest. 1975;56(1):56-64. 7. Hess OM, Ritter M, Schneider J, Grimm J, Turina M, Krayenbuehl HP. Diastolic stiffness and myocardial structure in aortic valve disease before and after valve replacement. Circulation. 1984;69(5):855-865. 8. Hess OM, Villari B, Krayenbuehl HP. Diastolic dysfunction in aortic stenosis. Circulation. 1993;87(5 suppl):73-76. 9. Stott DK, Marpole DG, Bristow JD, Kloster FE, Griswold HE. The role of left atrial transport in aortic and mitral stenosis. Circulation. 1970;41(6):1031-1041. 10. Ross J Jr. Afterload mismatch and preload reserve: a conceptual framework for the analysis of ventricular function. Prog Cardiovasc Dis. 1976;18(4):255-264. 11. Johnson LL, Sciacca RR, Ellis K, Weiss MB, Cannon PJ. Reduced left ventricular myocardial blood flow per unit mass in aortic stenosis. Circulation. 1978;57(3):582-590. 12. Marcus ML, Doty DB, Hiratzka LF, Wright CB, Eastham CL. Decreased coronary reserve: a mechanism for angina pectoris in patients with aortic stenosis and normal coronary arteries. N Engl J Med. 1982;307(22):1362-1366. 13. Bache RJ, Wang Y, Jorgensen CR. Hemodynamic effects of exercise in isolated valvular aortic stenosis. Circulation. 1971;44(6):1003-1013.

review article 14. Grech ED, Ramsdale DR. Exertional syncope in aortic stenosis: evidence to support inappropriate left ventricular baroreceptor response. Am Heart J. 1991;121(2 pt 1): 603-606. 15. Schwartz LS, Goldfischer J, Sprague GJ, Schwartz SP. Syncope and sudden death in aortic stenosis. Am J Cardiol. 1969;23(5):647-658. 16. Kulbertus HE. Ventricular arrhythmias, syncope and sudden death in aortic stenosis. Eur Heart J. 1988;9 (suppl E):51-52. 17. Munt B, Legget ME, Kraft CD, Miyake-Hull CY, Fujioka M, Otto CM. Physical examination in valvular aortic stenosis: correlation with stenosis severity and prediction of clinical outcome. Am Heart J. 1999;137(2):298-306. 18. Etchells E, Glenns V, Shadowitz S, Bell C, Siu S. A bedside clinical prediction rule for detecting moderate or severe aortic stenosis. J Gen Intern Med. 1998;13(10):699-704. 19. Bonow RO, Carabello BA, Kanu C, et al. ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines [published correction appears in Circulation. 2007;115(15):e409]. Circulation. 2006;114(5):e84-e231. 20. Otto CM, Pearlman AS. Doppler echocardiography in adults with symptomatic aortic stenosis. Diagnostic utility and cost-effectiveness. Arch Intern Med. 1988;148(12):2553-2560. 21. Ambler G, Omar RZ, Royston P, Kinsman R, Keogh BE, Taylor KM. Generic, simple risk stratification model for heart valve surgery. Circulation. 2005;112(2):224-231. 22. Edwards FH, Peterson ED, Coombs LP, et al. Prediction of operative mortality after valve replacement surgery. J Am Coll Cardiol. 2001;37(3):885-892. 23. Society of Thoracic Surgeons. Executive Summary. STS Spring 2005 Report. http//www.sts.org/documents/ pdf/Spring2005STS-Executive Summary.pdf. Accessed November 2005. 24. Pellikka PA, Sarano ME, Nishimura RA, et al. Outcome of 622 adults with asymptomatic, hemodynamically significant aortic stenosis during prolonged follow-up. Circulation. 2005;111(24):3290-3295. 25. Schwarz F, Baumann P, Manthey J, et al. The effect of aortic valve replacement on survival. Circulation. 1982;66(5):1105-1110. 26. Horstkotte D, Loogen F. The natural history of aortic valve stenosis. Eur Heart J. 1988;9(suppl E):57-64. 27. Lindblom D, Lindblom U, Qvist J, Lundström H. Longterm relative survival rates after heart valve replacement. J Am Coll Cardiol. 1990;15(3): 566-573. 28. Otto CM. Valvular aortic stenosis: disease severity and timing of intervention. J Am Coll Cardiol. 2006;47(11): 2141-2151.

29. Vaquette B, Corbineau H, Laurent M, et al. Valve replacement in patients with critical aortic stenosis and depressed left ventricular function: predictors of operative risk, left ventricular function recovery, and long term outcome. Heart. 2005;91(10):1324-1329. 30. Rosenhek R, Binder T, Porenta G, et al. Predictors of outcome in severe, asymptomatic aortic stenosis. N Engl J Med. 2000;343(9):611-617. 31. Pellikka PA, Nishimura RA, Bailey KR, Tajik AJ. The natural history of adults with asymptomatic, hemodynamically significant aortic stenosis. J Am Coll Cardiol. 1990;15(5):1012-1017. 32. Amato MC, Moffa PJ, Werner KE, Ramires JA. Treatment decision in asymptomatic aortic valve stenosis: role of exercise testing. Heart. 2001; 86(4):381-386. 33. Das P, Rimington H, Chambers J. Exercise testing to stratify risk in aortic stenosis. Eur Heart J. 2005;26(13):1309-1313. 34. Alborino D, Hoffmann JL, Fournet PC, Bloch A. Value of exercise testing to evaluate the indication for surgery in asymptomatic patients with valvular aortic stenosis. J Heart Valve Dis. 2002;11(2):204-209. 35. Antonini-Canterin F, Huang G, Cervesato E, et al. Symptomatic aortic stenosis: does systemic hypertension play an additional role? Hypertension. 2003;41(6): 1268-1272. 36. O’Brien KD, Zhao XQ, Shavelle DM, et al. Hemodynamic effects of the angiotensin-converting enzyme inhibitor, ramipril, in patients with mild to moderate aortic stenosis and preserved left ventricular function. J Investig Med. 2004;52(3):185-191. 37. Jiménez-Candil J, Bermejo J, Yotti R, et al. Effects of angiotensin converting enzyme inhibitors in hypertensive patients with aortic valve stenosis: a drug withdrawal study. Heart. 2005;91(10):1311-1318. 38. Chockalingam A, Venkatesan S, Subramaniam T, et al. Safety and efficacy of angiotensin-converting enzyme inhibitors in symptomatic severe aortic stenosis: Symptomatic Cardiac Obstruction-Pilot Study of Enalapril in Aortic Stenosis (SCOPE-AS). Am Heart J. 2004;147(4):E19. 39. Zipes DP, Libby P, Bonow RO, Braunwald E, eds. Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine. 7th ed. Philadelphia, Pa.: Elsevier; 2005: 1582-1592. 40. U.S. Preventive Services Task Force. Guide to clinical preventive services. 3rd ed. 2000–2002. http://www.ahrq. gov/clinic/prevnew.htm. Accessed May 29, 2008. 41. Bonow RO, Cheitlin MD, Crawford MH, Douglas PS. Task Force 3: valvular heart disease. J Am Coll Cardiol. 2005;45(8):1334-1340. 42. Rosenhek R, Rader F, Loho N, et al. Statins but not angiotensin-converting enzyme inhibitors delay progression of aortic stenosis. Circulation. 2004; 110(10):1291-1295.

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review article 43. Bellamy MF, Pellikka PA, Klarich KW, Tajik AJ, Enriquez-Sarano M. Association of cholesterol levels, hydroxymethylglutaryl coenzyme- A reductase inhibitor treatment, and progression of aortic stenosis in the community. J Am Coll Cardiol. 2002;40(10):1723-1730. 44. Cowell SJ, Newby DE, Prescott RJ, et al., for the Scottish Aortic Stenosis and Lipid Lowering Trial, Impact on Regression (SALTIRE) Investigators. A randomized trial of intensive lipid-lowering therapy in calcific aortic stenosis. N Engl J Med. 2005;352(23):2389-2397. 45. Freeman RV, Otto CM. Spectrum of calcific aortic valve disease: pathogenesis, disease progression, and treatment strategies. Circulation. 2005;111(24):3316-3326.

46. Wilson W, Taubert KA, Gewitz M, et al. Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council onCardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group [published correction appears in Circulation. 2007;116(15):e376-377]. Circulation. 2007;116(15):1736-1754.

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CLINICAL STUDY

Usefulness of Ankle–Brachial Index as a Cardiovascular Risk Factor in Patients of Acute Coronary Syndrome and Its Correlation with Conventional Cardiovascular Risk Factors Mittal LC*, Sharma D†

Abstract The aim of this study was to determine the relationship between ankle–brachial index (ABI) and acute coronary syndrome (ACS) patients with or without major cardiovascular risk factors in MBS Hospital, Kota, Rajasthan. High-resolution B-mode vascular color Doppler ultrasonography has proved to be a valid and reliable method for measuring ABI. ABI was measured in all studied patients. ABI ≤ 0.9 (ABI+) was considered as peripheral vessel disease and ABI > 0.9 (ABI−) was considered as normal. Characteristics of studied subjects including demographics, familial history, past medical history, and atherosclerotic risk factors, such as diabetes mellitus, hypertension, dyslipidemia, and smoking, were obtained using a standard questionnaire. The results of the questionnaire and value of ABI were compared in ABI+ and ABI− groups. Data were analyzed by SPSS 15 using ANOVA, t-test, and Spearman’s rank correlation coefficient. In this study, 100 patients with ACS of age group 35–75 were investigated. ABI ≤ 0.9 was seen in 28 patients (28%). The prevalence of ABI+ among men and women was 33.8.9% and 17.1%, respectively (p = 0.01). The prevalence of atherosclerotic risk factors was significantly higher in ABI+ patients than in ABI− (p < 0.05). Greater the number of risk factors, lower the ABI. Peripheral arterial disease (PAD) in patients with coronary artery disease (CAD) is associated with a poor cardiovascular outcome. Ankle–brachial pressure index is a good predictor of subsequent cardiovascular events and could be included in routine screening of cardiovascular status. The findings of this research indicated that ABI could be a useful method in assessing both the atherosclerotic risk factors and PAD in ACS patients. However, in order to make more accurate decisions for using this method in diagnosing and preventing CAD, we should plan further studies in large sample sizes of general population.

Keywords: Ankle-brachial index, acute coronary syndrome, atherosclerotic risk factors, coronary artery disease, peripheral artery disease

therosclerosis is a disease of large and mediumsized muscular arteries and is characterized by endothelial dysfunction, vascular inflammation, and build up of lipids, cholesterol, calcium, and cellular debris within the intima of the vessel wall. Atherosclerosis is the underlying disease process leading to ischemic heart disease, cerebrovascular accidents, and peripheral vascular diseases.1 It is the leading cause of morbidity and mortality all over the world. It is a slowly progressive disease with multiple risk factors. Traditional cardiovascular risk factors include older age, male sex, family history of coronary artery disease (CAD), diabetes mellitus (DM),

*Senior Registrar Government Medical College, Kota, Rajasthan †Professor and Unit Head Government Medical College, Kota, Rajasthan Address for correspondence Dr Lal Chand Mittal 1503, Vasudhara Heights, Plot No. 5, Sec. 11 Sanpada-400705, Navi Mumbai E-mail: drlmittal@gmail.com

dyslipidemia, hypertension, smoking, obesity, and lack of physical activity, and nontraditional risk factors include hsCRP, homocysteine, lipoprotein (a), abnormal ABI, microproteinurea (albumin/creatinine ratio), metabolic syndrome, left ventricular hypertrophy, renal disease, increased calcium score, chronic inflammatory diseases, HIV, and blood natriuretic peptide (BNP).2 The ankle-brachial systolic blood pressure index is an established clinical test for the assessment of peripheral arterial disease (PAD) and an indicator of generalized atherosclerosis.3–5 A low ankle–brachial index (ABI) is associated with increased mortality and risk of myocardial infarction and stroke in the general population, independent of conventional cardiovascular risk factors and prevalent cardiovascular disease.6 Both symptomatic and asymptomatic PAD patients are at risk of cardiovascular disease and related mortality. Considering the increasing burden of atherosclerotic disease and its mortality, and also the usefulness of noninvasive, easy, and practical methods for identifying atherosclerotic risk factors for prevention or early

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Clinical Study treatment of atherosclerotic diseases, the aim of the current study was to determine the association of ABI by performing high-resolution B-mode ultrasonography color Doppler in patients of acute coronary syndrome (ACS) with and without conventional cardiovascular risk factors and its relation with the age and sexmatched control subjects.

or fasting blood glucose ≥ 126 mg/dL or 2-h blood glucose ≥ 200 mg/dL, and/or use of glucoselowering drugs. zz

Obesity: BMI and WHR were used as tests for obesity and abdominal obesity, respectively.

Methods Hundred subjects of ACS and 70 subjects of the control group were admitted in the male and female medical wards and ICU of MBS Hospital, Kota, Rajasthan, during January 2011 to June 2012. The study protocol was approved by the Ethical Committee of the Government Medical College, Kota. Written informed consents were obtained from all studied patients. Characteristics of the studied subjects including demographics, familial history, past medical history, and atherosclerotic risk factors, such as DM, hypertension, dyslipidemia, and smoking were obtained using a standard questionnaire (Table 1). zz

Smoking: Regular smoking of a tobacco product one or more times per day or having smoked in the past 30 days prior to admission.

Hyperlipidemia: Total cholesterol ≥ 200 mg/dL, LDL cholesterol ≥ 130 mg/dL, HDL cholesterol ≤ 40 mg/dL in men and ≤ 50 mg/dL in women, and triglyceride ≥ 200 mg/dL or using medications.

Hypertension: Systolic blood pressure ≥ 140 mmHg and/or diastolic blood pressure ≥ 90 mmHg and/or receiving antihypertensive treatment.

DM: Positive findings from any two of the following tests on different days: symptoms of DM plus casual plasma glucose concentration ≥ 200 mg/dL

BMI: Weight (kg)/Height (m2). BMI = 18–25: normal; 25–29.9: overweight; >30: obese. WHR: Waist circumference/Hip circumference. Waist–hip ratio of 0.85 and more in female, and 0.90 and more in males is considered as abnormal and subjects were considered as having abdominal obesity.

Trained radiologist, using a B-mode Doppler ultrasonic instrument with an 8-MHz vascular probe (a HewlettPackard 2000 high-resolution ultrasound unit with a 8-MHz transducer probe), measured systolic blood pressure readings in the right and left brachial arteries, right and left dorsalis pedis arteries, and right and left posterior tibial arteries. B-mode vascular color Doppler ultrasonography has proved to be a valid and reliable method for measuring ABI. The ankle–brachial pressure index for each leg was calculated by dividing the ankle systolic pressure by the brachial systolic pressure (ABI leg = SBP leg/SBP arm). The lower of the indices obtained for the two legs was used as the measure of disease severity in the analysis. We used a cut-off point of 0.9 to define a low index in our calculations because it is a sensitive and specific measure of peripheral vascular disease in a clinical setting. ABI ≤ 0.9 (ABI+) was considered as peripheral vessel disease and ABI > 0.9 (ABI−) was considered as normal. Statistical methods used were unpaired student’s t-test and determination of correlation coefficient (r value)

Table 1. Mean Values, Standard Deviation, and Standard Error of Mean of Various Parameters of All the Subjects of ACS and Controls Acute Coronary Syndrome

Control

(Total No. = 100)

(Total No. = 70)

Variables

Mean

Age (years)

55.79

1.041

10.406

55.64

1.137

9.51

BMI (kg/m2)

23.79

0.441

4.389

21.88

0.274

2.298

WHR

0.936

0.00737

0.0737

0.895

0.0036

0.0306

TC (mg/dL)

175.48

2.51

25.13

173.91

1.346

11.26

TG (mg/dL)

119.56

3.03

30.32

117.48

2.961

24.772

HDL (mg/dL)

41.89

0.296

2.96

42.68

0.1489

1.24

LDL (mg/dL)

115.13

1.977

19.77

106.11

2.248

18.8

ABI

0.963

0.0127

0.1268

1.034

0.0152

0.1276

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CLINICAL STUDY between ABI and other variables by using GraphPad InStat Version 3.10. A value of p > 0.05 is considered as not significant, p < 0.05 as mildly significant, p < 0.01 as significant, p < 0.001 as highly significant, and p < 0.0001 as very significant. Results In this study, 100 ACS subjects and 70 control subjects of the same age and sex-matched groups were investigated. ABI ≤ 0.9 was seen in 28 subjects of ACS and 7 subjects in the control group (28% vs 7%), respectively. The prevalence of ABI+ among males was 33.8% versus 5.7% and among females was 17.1% versus 1.42% in both groups, respectively (p = 0.01). The prevalence of atherosclerotic risk factors was significantly higher in ABI+ patients than in ABI− (p < 0.05). Greater the number of risk factors, lower the ABI. zz

There was statistically highly significant (p < 0.001) low ABI noticed in ACS patients when compared with the control subjects.

There was statistically significant (p < 0.05) low ABI noticed in ST segment elevation MI (STEMI) subjects when compared with the non ST segment elevation MI (NSTEMI)/unstable angina (UA) subjects (Table 2).

There was statistically significant negative correlation between ABI and increasing age in ACS group (p < 0.05) but not in control group (p > 0.05) with and without risk factor.

There was statistically highly significant (p < 0.001) low ABI noticed when comparisons were made between males and females of controls and ACS subjects.

There was statistically significant (p < 0.05) negative correlation between ABI and BMI in ACS subjects. BMI was statistically significant (p < 0.05) in ACS when compared with control subjects and linear decrease in ABI noticed with increasing BMI in ACS group. There was statistically highly significant negative correlation between ABI and waist–hip ratio in

Table 2. Mean ABI in Different Types of ACS Type

STEMI

NSTEMI

Total no.

ABI < 0.9

Mean ABI

0.953

1.008

1.03

Table 3. Prevalence of Atherosclerotic Risk Factors in ABI+ and ABI− Subjects Atherosclerotic Risk Factors

ABI+ Subjects N = 28

ABI− Subjects N = 72

Diabetes mellitus

11 (39.2%)

8 (11.1%)

Hypertension

17 (60.7%)

17 (23.6%)

Smoking

16 (57.1%)

32 (44.4%)

Obesity

15 (53.5%)

13 (18%)

Hyperlipidemia

5 (17.8%)

4 (5.5%)

males and females of both control and ACS groups (p < 0.001). zz

There was statistically significant difference in ABI between hypertensives subjects in control and ACS groups (p < 0.001). There was statistically significant difference between hypertension and normotensives subjects (p < 0.05) of ACS group (Table 3).

There was a statistically highly significant difference in ABI (p < 0.001) between diabetic subjects in both the groups and diabetic and nondiabetics subjects (p < 0.05) in ACS group (Table 3).

There was statistically highly significant difference in ABI between smoker in control and ACS groups (p 0.001). There was statistically significant difference in ABI between smoker and nonsmokers (p < 0.05) in ACS group (Table 3).

There was a significant negative correlation (p < 0.05) between ABI and total cholesterol, LDL, and triglyceride in both groups and positive correlation with HDL cholesterol in control and ACS groups (Table 3).

There were negative correlations with the number of risk factors to ABI, greater the number of risk factors lower the ABI noticed.

Discussion In this study, the relation between ACS and ABI was evaluated. The results indicated that the prevalence of atherosclerotic risk factors was significantly higher in ABI+ patients than in ABI patients (Table 4). Our study revealed a negative correlation between increasing age and mean ABI in ACS subjects (r = −0.807) that was statistically significant (p < 0.05). The studies of Hasimu et al7 and Doza et al8 also showed similar result as our study that observed prevalence of PAD more in older patients. Syvänen et al9 and Sadegh et al10 observed no statistically significant difference in ABI values among age groups. Different results were

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Clinical STUDY Table 4. ABI and Risk Factors in ACS Subjects Relation Between Different Risk Factors and ABI Total no.

ABI < 0.9

Mean ABI

0.823

0.833

0.897

0.957

1.02

1.049

0.015

0.18

0.093

0.103

0.119

0.078

p value

<0.05

<0.1

0.0049

0.078

reported by Ishida et al11, Farkouh et al, and Rooke et al that showed ABI to be lowest at <40 years, and increased with age; the maximum was at 60–69 years in both sexes. This different result could be due to selective group of patients, subclinical calcification of arteries in older age, and other undiagnosed factors. In our study, prevalence of low ABI was observed more in males than in females. Similar results were also showed in the Augsburg et al study that noticed prevalence of low ABI in men and in women, 18.1% and 4.3%, respectively. Sadeghi et al10 study results were similar to our study and showed 20% of the subjects had ABI ≤ 0.9, that was significantly higher in men than in women. Kweon et al12 study also showed the prevalence of low ABI, 2.2% in men and 1.8% in women. Our results were in line with the study of Papamichael et al13 and Ramos et al14 whereas study of Taylor-Piliae et al showed different results from our study who observed similar prevalence of ABI+ (ABI < 0.9) in both sexes. Different results were observed by Hasimu et al7, Ingelsson et al, and Ishida et al11 who noticed that prevalence was higher in females than in males. Different results could be due to variability of cardiovascular risk factors present, selection of subjects, and preexisting PAD. As mentioned, several studies reported that patients with PAD are at a higher risk of adverse cardiovascular events and other atherosclerotic diseases. ABI ≤ 0.9 has widely been used as an indicator of PAD and adjunct to the office-based assessment of cardiovascular risk in high-risk populations. In a systematic review, Doobay et al determined the sensitivity and specificity of ABI in predicting future cardiovascular events. They concluded that although ABI ≤ 0.9 is highly specific but not sensitive in this regard, it is considered a useful cardiovascular event risk prediction tool, especially in selected populations, due to its simple assessment. In our study, the prevalence of all studied risk factors was significantly higher in ABI+ patients than ABI−. Moreover, in agreement with our study, we reported a

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higher prevalence of smoking, hypertension, DM, and dyslipidemia in patients with PAD than those without PAD; similar results were also reported in a study in Taiwan by Chang et al, who found that diabetes, hypertension, and smoking were significantly higher in ABI+ patients. Conclusion The following can be concluded from the above study: zz

In our study, low ABI was noticed in ACS patients with or without conventional risk factors. It was concluded that low ABI is strong and independent reflection for ACS.

Symptomatic subjects who have low ABI but no conventional risk factors should be screened for emerging risk factors and preventive measures should be taken to decrease future cardiovascular events.

Low ABI reflects the combined effect of many risk factors over time and, once atherosclerosis has developed, would be expected to be a better predictor than any one risk factor alone. It was concluded that there was not only single risk factor responsible for low ABI but also other risk factors could be simultaneously present.

In our study, there was higher prevalence of smoking, hypertension, DM, and dyslipidemia in patients with low ABI and linear decrease in ABI was noticed with increasing number of risk factors.

It can be concluded that asymptomatic subjects with low ABI should be screened for CAD and evaluated for conventional and emerging risk factors, and preventive measures should be taken to decrease the risk of future cardiovascular events.

ABI due to its simple assessment, ease of application, reproducibility, low cost, and strong correlation with CAD makes itself the most reasonable option for screening of PAD and CAD in high-risk population in general practice and can be considered as a cardiovascular risk prediction tool.

CLINICAL STUDY zz

The findings of this research have indicated that ABI could be a useful method in assessing both the atherosclerotic risk factors and the CAD in suspected patients. However, making more accurate decisions for using this method in diagnosing and preventing CAD needs further studies with large sample sizes of general population.

References 1. Ross R. Atherosclerosis: an inflammatory disease. N Engl J Med 1999;340:115-25. 2. Boudi FB, Ali YS. Risk factors for coronary artery disease. Article in Medscape, Jan 30, 2012. 3. Ankle Brachial Index Collaboration. Ankle brachial index combined with Framingham risk score to predict cardiovascular events and mortality: a meta-analysis. JAMA 2008;300:197-208. 4. Greenland P, Abrams J, Aurigemma GP, Bond MG, et al. Prevention Conference V. Beyond secondary prevention: identifying the high-risk patient for primary prevention. Non-invasive tests of atherosclerotic burden. Circulation 2000;101:e16-e22. 5. Heald CL, Fowkes FGR, Murray GD, Price JF. Risk of mortality and cardiovascular disease associated with the ankle-brachial index: systematic review. Atherosclerosis 2006;189:61-9. 6. Wild SH, Byrne CD, Smith FB, Lee AJ, Fowkes FG. Low ankle-brachial pressure index predicts increased risk of cardiovascular disease independent of the metabolic syndrome and conventional cardiovascular risk factors in the Edinburgh Artery Study. Diabetes Care 2006;29: 637-42.

7. Hasimu B, Li J, Nakayama T, et al. Ankle brachial index as a marker of atherosclerosis in Chinese patients with high cardiovascular risk. Hypertens Res 2006;29:23-8. 8. Doza B, Kaur M, Chopra S, and Kapoor R. Cardiovascular risk factors and distributions of the ankle-brachial index among type 2 diabetes mellitus patients. Int J Hypertens 2012;1-6. doi: 10.1155/2012/485812. 9. Syvänen K, Aarnio P, Jaatinen P, Korhonen P. Effects of age, sex and smoking on ankle-brachial index in a Finnish population at risk for cardiovascular disease. Int J Angiol 2007;16(4):128-30. 10. Sadeghi M, Heidari R, Mostanfar B, et al. The relation between ankle-brachial index (ABI) and coronary artery disease severity and risk factors: An angiographic study. ARYA Atheroscler 2011;7(2):68-73. 11. Ishida A, Miyagi M, Kinjo K, Ohya Y. Age- and sexrelated effects on ankle–brachial index in a screened cohort of Japanese: the Okinawa Peripheral Arterial Disease Study (OPADS). Eur J Prev Cardiol 2012. doi: 10.1177/2047487312462822. 12. Kweon SS, Shin MH, Park KS, et al. Distribution of the ankle-brachial index and associated cardiovascular risk factors in a population of middle-aged and elderly Koreans. J Korean Med Sci 2005;20:373-8. 13. Papamichael CM, Lekakis JP, et al. Ankle-brachial index as a predictor of the extent of coronary atherosclerosis and cardiovascular events in patients with coronary artery disease. Am J Cardiol 2000;86(6):615-8. 14. Ramos R, Quesada M, Solanas P, Subirana I, Sala J, Vila J, et al. Prevalence of symptomatic and asymptomatic peripheral arterial disease and the value of the anklebrachial index to stratify cardiovascular risk. Eur J Vasc Endovasc Surg 2009;38(3):305-11.

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Clinical Study

Intraventricular Conduction Defects in Hypertensive Patients Anand NN*, Padma Vâ&#x20AC; , Rajendran SM*

Abstract Hypertension is one of the leading causes of morbidity and mortality in the world. Electrocardiogram is one of the tests recommended by 7th Joint National Committee of hypertension. The aim of this article is to study the prevalence of intraventricular conduction disturbances and to identify the most common type of intraventricular conduction disturbance in patients with systemic hypertension. Five hundred and twenty patients attending hypertension clinic at Sree Balaji Medical College and Hospital, Chennai, from January 2010 to January 2012, were included in the study. Of 520 patients enrolled, 50 patients had conduction disturbances. The incidence of conduction defects in males was 6.37% and in females it was 4.03% among all hypertensive patients enrolled in our study. Of the patients with conduction disturbances, 41.82% were between 45 and 54 years of age. This is a cross-sectional study involving hypertensive patients attending hypertension clinic. Of the conduction disturbances, the most common type is LAFB followed by LBBB and RBBB. Conduction disturbances were found in 9.6% of hypertensive patients. High diastolic blood pressure and longer duration of hypertension was associated with more conduction disturbances.

Keywords: Hypertension, electrocardiogram, intraventricular conduction disturbances

To identify the most common type of intraventricular conduction disturbance.

ypertension is one of the leading causes of morbidity and mortality in the world.1 It is one of the common disease that can be easily detected and easily treated, and causes complications like chronic kidney disease, heart failure, and stroke, if not treated.2 Electrocardiogram (ECG) is one of the tests recommended by the 7th Joint National Committee of Hypertension for initial evaluation of hypertensive patients.3

Hypertension causes an increase in left ventricular mass and fibrous tissue resulting in increased stiffness of left ventricle, causing reduced coronary reserve, abnormal electrophysiological properties of hypertrophied myocytes, and conduction disturbances and silent myocardial ischemia.

Patients with constant elevation of blood pressure (BP) (systolic > 140/diastolic > 90 mmHg) over a period of 3 weeks were taken for ECG and echocardiogram analysis. Patients with ischemic heart disease, diabetes mellitus, associated dyslipidemia, hyperuricemia, and other secondary causes of hypertension were excluded from the study.

ECG is least expensive cost-effective way to diagnose not only myocardial infarction and ischemia but also conduction disturbances and left ventricular hypertrophy (LVH). The aim of this clinical study is: zz

To study the prevalence of intraventricular conduction disturbance in patients with systemic hypertension.

*Professor of Medicine Sree Balaji Medical College, Chromepet, Chennai, Tamil Nadu â&#x20AC; Associate Professor of Medicine Sree Balaji Medical College, Chromepet, Chennai, Tamil Nadu

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METHODS Five hundred and twenty patients attending hypertension clinic at Sree Balaji Medical College and Hospital, Chennai, from January 2010 to January 2012 were included in the study.

A detailed history and a clinical examination was done in all patients. Average of two BP readings recorded 5 minutes apart in sitting position at two visits separated by 1 week was noted. BP was measured in both upper limbs in supine, sitting, and standing positions and also in both lower limbs. Routine hemogram, urinalysis, blood urea, sugar, serum creatinine, uric acid, electrolytes, and lipid profile were done. Chest X-ray in the posterior-anterior view and echocardiogram were taken for the patients.

Clinical Study Results

Of 520 patients enrolled, 50 patients had conduction disturbances.

The incidence of conduction defects in males was 6.37% and in females it was 4.03% among all hypertensives enrolled in our study. Of the patients with conduction disturbances, 41.82% were between 45 and 54 years of age (Fig. 1). The increased incidence of conduction defects in older patients is due to age-related degeneration of conduction system in addition to subendocardial fibrosis due to hypertensive heart disease. Males had higher incidence of intraventricular conduction delay (IVCD) than females (Fig. 2).

15 >90 and <100 10

>100

5 0

LAFB

RBBB

LBBB

Figure 3. Incidence of conduction disturbances in patients with DBP >100 mmHg and those with DBP >90 and <100 mmHg. 40

Of the 50 patients with conduction disturbances, 30 had a diastolic BP >100 mmHg (21 LAFB, 6 RBBB, 3 LBBB) and 20 had a diastolic BP of >90 and <100 mmHg (13 left anterior fascicular block [LAFB], 6 right bundle branch block [RBBB], 1 left bundle branch block [LBBB]). Among the different conduction disturbances prevalent, 34 had LAFB, 12 had RBBB, and 4 had LBBB (Fig. 3).

35 30 25 >140 and <160

>160

15 10 5 0

35–44 45–54 55–64 65–75

Figure 1. Incidence of conduction disturbances in the different age groups.

RBBB LBBB

LAFB

Figure 4. Incidence of conduction disturbances in patients with DBP >100 mmHg and those with DBP >140 and <160 mmHg. 25

15 Males Males

Females

Females 5

Figure 2. Sex-wise distribution of conduction defects in the study patients.

RBBB

LBBB

LAFB

Figure 5. Sex-wise distribution of RBBB, LBBB, and LAFB in the study patients.

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Clinical Study

RBBB

Martin et al8 have demonstrated that conduction disturbances develop in hypertrophied ventricles in the presence of myocardial ischemia9 and ischemia occurs in spite of normal coronaries.

LAFB

Goldman10 suggested that left axis deviation in LVH and involvement of conduction from pathway in hypertension is due to subendocardial fibrosis of anterior fascicle of the left bundle and not due to hypertrophied mass.

Figure 6. Incidence of LAFB, RBB, and LBBB in patients with LVH.

Gopinath et al,11 in their 3-year follow-up study of hypertensive patients in Delhi recorded ECGs of 1417 patients out of which 237 patients (16.7%) had LVH and 100 patients (7.8%) had intraventricular conduction disturbances.

LBBB

Of 50 patients, 48 patients had a systolic BP >160 mmHg (36 LAFB, 10 RBBB, 2 LBBB) and 2 patients had a systolic BP of >140 and <160 mmHg (1 LAFB, 1 LBBB) (Fig. 4). Among patients with conduction disturbances, 60% had a diastolic BP â&#x2030;Ľ 100 and 40% had a diastolic BP < 100 suggesting that high diastolic pressure could contribute to conduction disturbances seen in hypertensive patients. Among patients with conduction disturbances, 96% had a systolic BP >160 and 4% had a systolic BP >140 and <160 mmHg. Of the 50 patients with conduction disturbances, 23 were female (19 LAFB, 2 RBBB, 2 LBBB) and 27 were male patients (20 LAFB, 2 RBBB, 5 LBBB) (Fig. 5). Thirty-seven patients with LVH had IVCD. Of them 33 had LAFB, 3 had RBBB, and 1 had LBBB (Fig. 6). Out of 520 patients enrolled, 135 patients had LVH by ECHO and ECG criteria. Out of these 135 patients, 37 patients had IVCD. Studies on hypertension have shown increased incidence of LVH in females.4-6 de Simone et al7 stated in his study that prevalence of LVH rises as age increases. Discussion It is well evident that intraventricular conduction disturbances and LVH form one of the main ECG changes in hypertension. The Framingham study has shown that the evidence of LVH and conduction disturbance is higher among hypertensive patients. Messerli et al4 stated that increased incidence of conduction disturbance in hypertensives is probably due to increased fibrous tissue or altered collagen content.

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In our study, intaventricular conduction disturbances in hypertensive patients was 10.4%. Of them 39 patients had LAFB, 7 had LBBB, and 4 had RBBB. The incidence of conduction disturbance was more in men. Right bundle and anterior fascicle of left bundle are long thread-like structures. The anterior fascicle of left bundle passes below aortic valve in left ventricular outflow tract and receives blood from only one vessel, left anterior descending coronary artery. The main left bundle divides closer to its origin than the right bundle, hence is affected more than the right bundle. In hypertensive heart disease, left anterior fascicle and right bundle are affected that is confirmed by our study. Left posterior fascicle is not affected as the compactness of its position makes it least vulnerable segment to any injury. Left posterior fascicular block was not observed in our study population. High diastolic BP was associated with more conduction disturbances. Longer duration of hypertension is associated with more conduction disturbances. Conclusion This was a cross-sectional study involving hypertensive patients attending hypertension clinic. Of the conduction disturbances, the most common type is LAFB followed by LBBB and RBBB. Conduction disturbances were found in 10.4% of hypertensives. High diastolic BP and longer duration of hypertension was associated with more conduction disturbances. Early diagnosis and treatment of hypertension would prevent concentric LVH and conduction disturbances associated with hypertension.

Clinical Study 6. de Simone G, Daniels SR, Kimball TR, et al. Evaluation of concentric left ventricular geometry in humans. Hypertension 2005;45:64-8.

References 1. Murray CJ, Lopez AD. Lancet 1997;349:1498-504. 2. Kannel WB. BP as a cardiovascular risk factor: prevention and treatment. JAMA 1996;275:1571-6.

7. The JNC 7 report. JAMA 2003;289:2560-72.

3. Arnett DK, Bella JN, et al. The hyper GEN study. Am J Hypertens 2001;14:1226-30.

9. Martin, et al. Circulation 1987;1-49.

4. Post WS, Hill MN, et al. High prevalence of target organ damage in young. J Clin Hypertens 2003;5: 24-30. 5. East MA, Jolis JG, Nelson CL, et al. J Am College Cardiol 2003;4:949-54.

8. Messerli FH, et al. Cardiol Clinics 1998;13(4). 10. Goldman MJ. Principles of Clinical Electrocardiography. Los Altos, CA: Lange Medical Publications 1982:437 pages. 11. Gopinath N, Chadha SL, Shekawat S. A three year follow up of hypertension in Delhi. WHO Bulletin 1994;72(5):715-20.

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CASE REPORT

Atrial Septal Aneurysm with Transient Loss of Vision Mittal SR*

Abstract A 45-year-old male with sudden unexplained transient loss of vision is reported. Transesophageal echocardiography revealed an aneurysm of interatrial septum with a small fenestration. Such aneurysms are associated with significant risk of recurrent stroke due to transient right-to-left shunt or in situ thrombus formation. Transesophageal echocardiography is more sensitive than transthoracic echocardiography in detection and complete evaluation of such aneurysms.

Keywords: Atrial septal aneurysm, echocardiography, transesophageal echocardiography

45-year-old male was referred for cardiac evaluation. He was reported to have sudden transient loss of vision one day before being referred. An ophthalmologist, consulted after recovery, did not find any abnormality. There were no other symptoms. He did not have any cardiovascular risk factor. There was no family history of hypertension, diabetes, stroke, or ischemic heart disease. On clinical examination, serum biochemistry and electrocardiogram were normal. Doppler evaluation of the bilateral carotid artery was normal. Intima-media thickness was 0.6 mm on either side. Transthoracic echocardiography (TTE) did not reveal any abnormality in M-mode, 2-D, pulsed Doppler, color Doppler, and tissue Doppler imaging. Transesophageal echocardiography (TEE) revealed an aneurysm of interatrial septum with a small fenestration in its lower portion (Fig. 1). Color Doppler imaging revealed small left-to-right shunt across the fenestration (Fig. 2).

Figure 1. Transesophageal echocardiogram showing aneurysm of interatrial septum with fenestration (D).

Discussion Atrial septal aneurysm is a localized outpouching of interatrial septum. For the purpose of definition, maximum deviation of the aneurysm tissue should

*Department of Cardiology Mittal Hospital and Research Centre, Ajmer, Rajasthan Address for Correspondence Dr SR Mittal 11/101, Brahmpuri Ajmer, Rajasthan E-mail: sarweshwarm@gmail.com

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Figure 2. Transesophageal echocardiogram with color Doppler imaging showing flow across the fenestration.

case report be 10 mm or more from the plane of the interatrial septum.1 More than 70% of these aneurysms are associated with patent foramen ovale (PFO) or small fenestration. Small size of the defect allows only small and hemodynamically inconsequential left-toright shunt. Maneuvers such as valsalva and cough transiently increase right heart pressure and result in transient right-to-left shunt.2 It is also proposed that because of their tunnel-like structure, PFOs have propensity to stagnant flow and may serve as a nidus for in situ thrombus formation and subsequent systemic embolism.3 Presence of an interatrial septal aneurysm further increases the risk of an adverse event probably because of increased risk of in situ thrombus formation in the aneurysmal sac.3 This results in otherwise unexplained systemic embolic episode.2 PFOs have been implicated in the pathophysiology of cryptogenic stroke, decompression sickness, migraine headaches, and platypnea-orthodeoxia syndrome (dyspnea and arterial desaturation in the upright position, which improves when lying down).3 Etiological relationship of this echocardiographic finding with embolic episode is presumptive and cannot be proved. It could very well be a coincidence. However, atrial septal aneurysms with PFO have been found to be associated with a significantly higher incidence of recurrent stroke4 especially in younger patients without other risk factors. Large fenestrations with more substantial degree of shunt are at greater risk.2 Usual causes of stroke must be eliminated before considering PFO as a cause for unexplained systemic embolic episode.

Once an atrial septal aneurysm with PFO is considered as responsible, treatment modalities to prevent recurrent events include antiplatelets, anticoagulants, percutaneous device closure, or surgical closure. Conclusion Atrial septal aneurysms with PFO are associated with higher incidence of cryptogenic stroke especially in younger patients without other risk factors. TEE is more sensitive than TTE in detection and complete assessment of atrial septal aneurysms.2 TEE is, therefore, indicated in young patients with unexplained recurrent stroke. References 1. Feigenbaum H, Armstrong WF, Ryan T (editors). Left atrium, right atrium and right ventricle. Feigenbaum's Echocardiography, 6th edition. Philadelphia: Lippincott Williams & Wilkins;2005:181-213. 2. Feigenbaum H, Armstrong WF, Ryan T (editors). Contrast echocardiography. Feigenbaum's Echocardiography, 6th edition. Philadelphia: Lippincott Williams & Wilkins;2005:76-104. 3. Webb GD, Smallhorn JF, Therrien J, Redington AN. Congenital heart disease. In: Libby P, Bonow RO, Mann DL, Zipes DP (editors). Braunwald's Heart Disease, 8th edition. Philadelphia: Saunders;2008:1563-624. 4. Chen CW, Redberg RF. Echocardiographic evaluation of the patient with a systemic embolic event. In: Otto CM (editor). The Practice of Clinical Echocardiography, 3rd edition. Philadelphia: Saunders;2007:969-98.

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photo quiz

Cyanosis in an Older Woman Sangil LEE, Toshinori OZEKI

n 82-year-old woman presented to the emergency department with right-sided leg pain and paresthesias that had lasted for five days. The patient had been bedridden for several years because of dementia. Examination revealed diffusely scattered cyanosis on the foot (see accompanying figure), ankle, and calf, but sparing the knee. Peripheral pulses, including popliteal, posterior tibial, and dorsal pedis, were absent on the affected side.

Question Based on the patient’s history and physical examination, which one of the following is the most likely diagnosis?

C. Diabetic gangrene.

A. Blue toe syndrome.

D. Diffuse acute limb ischemia.

B. Buerger disease.

E. Postthrombotic syndrome.

SEE THE FOLLOWING PAGE FOR DISCUSSION.

Source: Adapted from Am Fam Physician. 2010 Jun 15;81(12):1491-1492.

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photo quiz Discussion The answer is D: diffuse acute limb ischemia. Diffuse acute limb ischemia is caused by a sudden decrease in limb perfusion that threatens limb viability within two weeks of the acute event. The condition is called critical limb ischemia when symptoms last for more than two weeks.1 Skin examination typically shows a cool, pale extremity with delayed capillary refill. The level of occlusion is generally one joint above the line of demarcation between the normal and ischemic areas. The classic symptoms of large artery occlusion are described as the five Ps: pain, paleness, pallor, paresthesia, and paralysis. Irreversible damage occurs within six hours of ischemia. When arterial occlusion occurs in the setting of well-developed collateral circulation, the symptoms may be less remarkable (e.g., intolerance to ambulation, modest pain, paresthesia). Limb ischemia is more common in lower extremities than in upper extremities. Diagnosis can be made using arterial Doppler evaluation and angiography. Angiography is confirmatory and demonstrates the location and severity of the obstruction.2 Acute limb ischemia is usually caused by embolic events, and therefore warrants investigation for an embolic source. Most embolic events are of cardiac or large artery origin. Cardiac disorders that can cause embolism include atrial fibrillation, myocardial infarction, and ventricular aneurysm. Atherosclerosis, or aneurysm of the aorta and other large arteries, is another embolic source of embolism. Although less common, a venous thrombus may enter systemic circulation through a patent foramen ovale or other septal defect.2 Arterial thrombosis may occur in atheromatous, aneurysmal, or traumatized vessels. Summary Table Condition

Characteristics

Blue toe syndrome

Acrocyanosis with strong pedal pulse and warm foot

Buerger disease

Small and medium vessel vasculitis causing ischemic pain and

Diabetic gangrene

Nonhealing ulcer, typically in persons with long-standing history of diabetes mellitus and multiple foot infections

Diffuse acute limb ischemia

Progressive pain, paleness, pallor, paresthesia, and paralysis

Postthrombotic syndrome

Pain, swelling, and heaviness; stasis ulcer may develop

Treatment of embolism includes prompt initiation of heparin to prevent propagation of the clot,1 followed by intra-arterial thrombolytic therapy with urokinase or surgical intervention (embolectomy or a bypass procedure). Nonviable tissue requires debridement, and amputation if necessary.3 Delayed amputation increases the risk of infection, myoglobinuria, acute renal failure, and hyperkalemia. After successful limb salvage, continuous anticoagulation with heparin followed by oral warfarin (Coumadin) is recommended to prevent recurrence.2 Blue toe syndrome is an acute embolic event at the digital artery that leads to sudden, painful cyanosis in the toe despite strong pedal pulse and a warm foot.4 This condition is analogous to transient ischemic attack in the central nervous system and leads to an impending ischemic event. Buerger disease is inflammation of distal arteries and veins causing ischemic pain and ulceration. Pathology shows inflammation of vessels; however, atherosclerosis is typically absent. Risk factors include Asian descent and cigarette smoking.2 Diabetic gangrene manifests as a nonhealing ulcer, typically on the toe. It is caused by the combination of arterial atherosclerosis and peripheral nerve damage. Diabetic gangrene typically develops after longstanding diabetes mellitus with multiple foot infections. Postthrombotic syndrome is a common complication of deep venous thrombosis. Typical features include pain, swelling, and heaviness; a stasis ulcer may develop.5 REFERENCES 1. Norgren L, Hiatt WR, Dormandy JA, Nehler MR, Harris KA, Fowkes FG; TASC II Working Group. Inter-Society Consensus for the Management of Peripheral Arterial Disease (TASC II). J Vasc Surg. 2007;45(suppl S): S5–67. 2. Creager MA, Dzau VJ. Vascular disease of the extremities. In: Fauci AS, Braunwald E, Kasper DL, et al., eds. Harrison’s Principles of Internal Medicine. 17 ed. New York, NY: McGraw-Hill; 2008. 3. Clagett GP, Sobel M, Jackson MR, Lip GY, Tangelder M, Verhaeghe R. Antithrombotic therapy in peripheral artery occlusive disease: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest. 2004;126(3 suppl):609S–626S. 4. Karmody AM, Powers SR, Monaco VJ, Leather RP. “Blue toe” syndrome. An indication for limb salvage surgery. Arch Surg. 1976;111(11):1263–1268. 5. Kahn SR. The post-thrombotic syndrome: progress and pitfalls. Br J Haematol. 2006;134(4):357–365.

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practice guidelines

Updated Recommendations on Daily Aspirin Use in Patients with Diabetes Carrie ARMSTRONG

ersons with diabetes mellitus have two to four times the risk of cardiovascular events compared with persons of the same age and sex who do not have the disease. Coronary heart disease (CHD) is responsible for more than two-thirds of deaths in persons with diabetes who are older than 65 years. Although aspirin has been proven to reduce cardiovascular morbidity and mortality rates in highrisk patients with myocardial infarction or stroke, its benefit is unclear in patients without a history of cardiovascular events. In 2007, the American Diabetes Associa tion and American Heart Association rec ommended aspirin therapy (75 to 162 mg daily) for primary prevention in patients with diabetes who had increased CHD risk (e.g., older than 40 years, smoking, family history of cardiovascular disease). Since these recommendations were published, new evidence has raised questions about the effectiveness of this strategy. The U.S. Pre ventive Services Task Force recently recommended that physicians encourage aspirin use in men 45 to 79 years of age and in women 55 to 79 years of age, regardless of whether they have diabetes. To address the uncertainties about aspirin use in persons with diabetes, experts from the American Diabetes Association, American Heart Association, and American College of Cardiology Foundation reviewed the current evidence and updated the 2007 recommendations. The group organized its recommendations around the following questions:

What is the evidence for aspirin in preventing initial cardiovascular events in patients with diabetes?

How can the conflicting results of various primary prevention trials be reconciled?

What are the risks of aspirin therapy, and are these risks similar for patients with diabetes compared with those for patients without the disease?

What is the recommended dosage?

Source: Adapted from Am Fam Physician. 2010 Dec 15;82(12):1559-1563.

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How should the potential benefits and risks of aspirin therapy be integrated to determine which patients should take aspirin daily for the primary prevention of cardiovascular events?

The current evidence on aspirin therapy for prevention of cardiovascular disease includes three trials conducted in patients with diabetes, and six trials containing subgroups of patients with diabetes. None of these trials provides definitive results, so the group performed a meta-analysis to reconcile the available data. Data from subgroups of patients with diabetes from the six trials were included in a previous metaanalysis by the Antithrombotic Trialists’ Collaboration. These were combined with data from the Japanese Primary Prevention of Atherosclerosis With Aspirin for Diabetes study, the Prevention of Progression of Arterial Disease and Diabetes trial, and the Early Treatment of Diabetic Retinopathy Study. A randomeffects model showed that aspirin use is associated with nonsignificant decreases in the risk of CHD events (relative risk [RR] = 0.91; 95% confidence interval [CI], 0.79 to 1.05) and of stroke (RR = 0.85; 95% CI, 0.66 to 1.11). The results of the diabetes-specific analyses are consistent with the findings of the previous metaanalysis, and suggest that aspirin use likely reduces the risk of cardiovascular disease to a modest degree in patients with diabetes. Adverse effects of aspirin therapy include intracranial bleeding (hemorrhagic stroke) and extracranial bleeding (mainly gastrointestinal [GI]). Several cardiovascular risk factors also increase the risk of extracranial bleeding, which suggests that persons at higher risk of CHD events are also at higher risk of aspirinrelated adverse effects. Current evidence supports the use of proton pump inhibitors to decrease the risk of recurrent aspirin-related GI bleeding. However, routine use of these agents may not be cost-effective, and it is not clear whether they should be recommended for primary prevention of GI bleeding. The optimal dosage of aspirin for prevention of CHD events is not clear. The average daily dosage used in primary prevention trials that included persons with

practice guidelines diabetes ranged from 50 to 650 mg. The risk reductions achieved with low dosages (75 to 162 mg per day) seem to be similar to those obtained with higher dosages. Although platelets from patients with diabetes have altered function, it is not clear whether this affects the recommended dosage of aspirin for cardioprotection. There are alternate pathways for platelet activation and aggregation that are independent of thromboxane A2 and are therefore not sensitive to the effects of aspirin. The evidence is insuffi cient to empirically recommend higher dosages of aspirin for patients with diabetes. In adults with cardiovascular risk greater than 1 percent per year, the number of CHD events prevented will be approximately equal to or greater than the number of bleeding events induced, although these events (myocardial infarction, stroke, and GI bleeding) do not have equal effects on long-term health. Recommendations Low-dose aspirin therapy is reasonable in adults with diabetes and no history of vascular disease, whose 10year risk of CHD events is greater than 10 percent, and who are not at increased risk of bleeding (i.e., no history of GI bleeding or peptic ulcer disease, and no concurrent use of other medications that increase bleeding risk). Adults with diabetes who are at increased risk of CHD events include most men older

than 50 years and women older than 60 years who have at least one additional major risk factor (i.e., smoking, hypertension, dyslipidemia, albu minuria, or family history of premature cardiovascular disease). Aspirin should not be recommended in adults with diabetes who are at low risk of cardiovascular events (men younger than 50 years and women younger than 60 years with no additional major risk factors). The potential adverse effects from bleeding offset the potential benefits in these patients. Low-dose aspirin therapy may be considered for patients with diabetes who are at intermediate risk of CHD events (younger patients with at least one risk factor, older patients with no risk factors, or patients with a 10-year risk of 5 to 10 percent). These recommendations depend on the accurate assessment of CHD risk. Not all patients with diabetes are at high risk, and the use of a risk prediction tool is essential. There are several Web-based tools available, such as the UK Prospective Diabetes Study Risk Engine (http://www.dtu.ox.ac.uk/riskengine/index. php) and the Atheroscle rosis Risk in Communities CHD Risk Calculator (http://www.aricnews.net/ riskcalc/html/RC1.html). Risk should be reassessed periodically, because patients may acquire additional risk factors over time.

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medilaw

Reconstitution of the Body Following an Autopsy

n important component of the autopsy is the reconstitution of the body such that it can be viewed as normal following the autopsy procedure.

After the conduction of postmortem examination, the body has an open and empty chest cavity with chest flaps open on both sides, the top of the skull is missing, and the skull flaps are pulled over the face and neck. All organs and tissue must be returned to the body unless permission is given by the family to retain any tissue for further investigation.

Normally the internal body cavity is lined with cotton wool or an appropriate material; the organs are then placed into a plastic bag to prevent leakage and returned to the body cavity. The chest flaps are then closed and sewn back together and the skull cap is sewed back in place.

The cases of mutilation/dismembered corpse must be surgically repaired into a normal anatomical position. Then the body must be properly sutured and reconstructed by the doctor conducting the autopsy with a cosmetic and parlor touch and then only it should be handed over to the relative of deceased as a regard of human corpse for ritual cremation.

Impulse and Its Medicolegal Importance Impulse is a sudden and irresistible desire or force in a person, compelling him to the conscious performance of some act for which there is no motive; for example, kleptomania means an irresistible desire to steal articles which may be of small value and even, may be of no use to the person stealing the article. A sane person who has self–control and judgment capacity may not finally give shape to his impulsive or compulsive desire. But an insane person, who lacks in self–control and judgment capacity, cannot resist the impulse and may commit any offence. Thus, in connection with commission of an unlawful act, impulse is a good defense for an insane person which is not so for a sane person. Some types of impulses are: zz

Dipsomania: This is found in alcoholics who have an irresistible desire to take alcoholic drinks.

Pyromania: Here, there is an irresistible desire to set fire to things, which may be important and valuable. The person is not conscious or careful, at least temporarily, to the possible dangers of his act.

Mutilomania: This is an irresistible desire to injure and mutilate animals, commonly the domestic pets.

Sexual impulse: The person may feel compulsive urge to perform sexual intercourse, often in a perverted way. There may be some psychic problem concerning the sexual behavior; or the person may be a victim of mental sub normality.

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medifinance

Reasons for Financial Planning Confirming that financial objectives are being met

dedicated to his financial needs and who are in constant pursuit of his goals.

By evaluating a doctor’s total financial situation, the financial advisory team can coordinate strategies that do not interfere with any of the stated goals and objectives. By focusing on the whole, rather than on a part, recommendations can be made that are consistent with the long-term financial strategy.

Planning Process Components

Monitoring implementation A financial plan that is not implemented becomes merely an educational experience. The stated goals and objectives can never be met without putting the plan into action. Follow-through is crucial. A financial advisory team will ensure that all phases of your plan are properly implemented by selected agents, not only in terms of the types and categories of investments, but with respect to estate, tax and retirement planning. All areas of risk assessment are important. Any area if overlooked could wipe out the rewards of years of work and saving.

Review of your objectives and risk/reward attitudes: Short-term, medium range and longterm goals as well as perceptions of risks and expected rewards.

Asset structure: Review of current holdings, present value, cost basis, growth and expected purchases.

Liabilities: Present and anticipated debt obligations. Income tax analysis: Projections for 10 years, with review of personal tax returns for last two years.

Cash flow management: Projections for 10 years, determine effective use of anticipated surplus, managing deficits.

Investment review: Analysis and recommendations.

Insurance review: Analysis and recommendations.

Employee benefits: Review and recommendations; coordinate with personal assets and spousal plans.

Disability income: Analysis and recommendations; 10-year projections of taxes, cash flow and net worth.

Estate distribution: Costs and taxation analysis methods of reducing probate costs and estate duties.

Capital needs and survivor income analysis: Analysis and recommendations.

Retirement income: Analysis and recommendations inflation, qualified plans and increasing net cash flow.

Financial organizer file: For all documents, policy records.

Income tax organizer file: Used each year to accumulate and store vital records to support tax returns.

Master implementation checklist: To monitor your financial progress and be aware of advisor performance.

Periodic review sessions: Verify progress evaluation of investments, benefit plans and document completion.

Frequent reviewing to remain on schedule Financial planning is a dynamic process and should be reviewed on a continuing basis to verify that the goals are being met and that they are remaining on your financial schedule. Since “nothing is as constant as change itself” the goals, attitudes toward financial risks and family circumstances will change. Even if, we as individuals were to remain the same, the financial world around us changes so frequently that constant monitoring is a necessary part of the planning process. The political, tax, legislative and economic changes increase in frequency. Reviews also ensure that any necessary adjustments are made before it is too late. Providing peace of mind Dealing with a financial advisory team gives the doctor the peace of mind knowing that his financial situations are being handled by full-time professionals who are

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FORTHCOMING CONFERENCES

International Conferences 19th Annual Boston Atrial Fibrillation Symposium 2014 (BAFS 2014) Venue: Orlando World Center, Marriott Location: Orlando, FL http://afsymposium.com/ Start: 09 Jan, 2014 End: 11 Jan, 2014 24th European Days of the French Society of Cardiology 2014 (SFC 2014) Venue: Palais Des Congres Location: Paris, France http://www.sfcardio.fr/congres/journees-europeennes/ Start: 15 Jan, 2014

World Heart Failure Congress 2014 (WHFC 2014) Venue: Abu Dhabi National Exhibition Centre Location: Abu Dhabi http://www.worldheartfailure.org//WHFSCongress/ Start: 28 Jan, 2014 End: 30 Jan, 2014 6th Middle East Cardiovascular Disease and Intervention Conference 2014 Venue: Dubai International Convention Centre Location: Dubai http://www.arabhealthonline.com/en/AHCongress/ Conferences1/Conf2/Overview/ Start: 29 Jan, 2014

End: 18 Jan, 2014

End: 30 Jan, 2014

Malaysian Society of Hypertension 11th Annual Scientific Meeting 2014 (MSH 2014)

Rome Cardiology Forum 2014

Venue: Shangri-La Hotel Location: Kuala Lumpur, Malaysia http://www.msh.org.my/article.php?aid=367 Start: 17 Jan, 2014 End: 19 Jan, 2014 American Society of Echocardiography 25th Annual Echo Hawaii 2014 (ASE 2014) Venue: Hapuna Beach Prince Hotel Location: Kamuela, Hawaii http://www.asecho.org/echohawaii/ Start: 20 Jan, 2014 End: 24 Jan, 2014 Cell Therapy for Cardiovascular Disease 9th International Conference 2014 Venue: Nyph/Columbia University Medical Center Location: New York http://celltherapy.crf.org/ Start: 22 Jan, 2014 End: 24 Jan, 2014

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Venue: Rome Location: Rome, Italy http://www.escardio.org/education/live-events/courses/ rome-cardiology-forum/Pages/programme.aspx Start: 30 Jan, 2014 End: 01 Feb, 2014 Angiogenesis and Leukocytes in Atherosclerosis 2014 Venue: Uptown Geneva Location: Geneva, Switzerland http://www.abcam.com/index.html?pageconfig=resource &rid=15874&viapagetrap=geneva2014 Start: 30 Jan, 2014 End: 31 Jan, 2014 Belgian Society of Cardiology 33rd Annual Scientific Meeting 2014 (BSC 2014) Venue: Square Brussels Meeting Centre Location: Brussels, Belgium http://www.bscardio.be/Generic/servlet/Main.html?p_ modid=9284 Start: 30 Jan, 2014 End: 31 Jan, 2014

Around the Globe

News and Views zz

A new systematic review has identified nine variables associated with whether athletes will return to sport after undergoing anterior cruciate ligament (ACL) repair. These include: higher postoperative quadriceps strength; less knee effusion; less pain; fewer episodes of instability; greater tibial rotation; lower kinesiophobia; higher athletic confidence; higher preoperative knee self–efficacy; and higher preoperative self– motivation.

Testosterone therapy in veterans –both those who had coronary artery disease and those who didn’t –was associated with increased risk of mortality, myocardial infarction, and ischemic stroke, a retrospective cohort study found. The absolute rate of events was 19.9% in a group that did not receive testosterone therapy compared with 25.7% in the group that did, with an absolute risk difference of 5.8% (95% CI, 1.4% to 13.1%) 3 years after the cohort underwent coronary angiography.

Sugar intake was not associated with nonalcoholic fatty liver disease (NAFLD) in a population of overweight men who were otherwise healthy. In the study reported in the journal Gastroenterology, overweight men who consumed high–fructose or high–glucose diets did not see significant increases in insulin resistance (increase of 0.8 in a homeostasis model assessment versus 0.1), serum concentration of uric acid (22 mu–mol/L versus 23 mu–mol/L), concentration of hepatic triacylglycerol, or body weight.

Major depressive disorder (MDD) is the second leading cause of disability worldwide and a major contributor to the burden of suicide and ischemic heart disease, according to new data published online in November 5 in PLoS Medicine. The findings stem from the latest Global Burden of Disease (GBD) study and highlight the importance of including depressive disorders as a global health priority.

Total deaths worldwide from cirrhosis and liver cancer rose by 50 million per year over 2 decades, according to the first–ever WHO study of liver disease mortality. The liver disease–specific findings from the WHO Global Burden of Disease Study were presented at the Liver Meeting 2013.

Young and middle–aged women with diabetes have a significantly increased risk of coronary artery disease (CAD), according to the results of a new analysis published online October 31, 2013 in Diabetes Care. Although younger women were less likely to develop CAD than men if they didn’t have diabetes, the presence of diabetes upped their risk to the point where it equaled their male counterparts, report investigators. Dr Rita Kaylani, Johns Hopkins University, Baltimore, MD, the lead researcher said that while women have a far lower risk of heart disease in the absence of diabetes than men, diabetes effectively equalizes the risk by gender.

Treating obstructive sleep apnea (OSA) modestly brought down some measures of resistant hypertension beyond what blood pressure medications could achieve alone. In a small randomized trial reported in the November issue of Chest, 6 months of continuous positive airway pressure (CPAP) treatment cut daytime ambulatory blood pressure by 6.5/4.5 mmHg whereas it rose by 3.1/2.1 mmHg among controls on medical therapy alone.

Fine–tuning the ketogenic diet can have a modest effect on seizure control in children with refractory epilepsy. The retrospective study found that adjusting diet and changing medications had similar benefits and were helpful in meeting seizure control expectations in about 1 in 5 children. The study findings were presented at the Child Neurology Society (CNS) 2013 Annual Meeting.

According to a study presented at the annual meeting of the American Association for the Study of Liver Diseases, use of high–dose steroids as an adjuvant treatment after hepatoportoenterostomy for pediatric biliary atresia did not help prevent the need for liver transplantation. Of the 70 children assigned to receive corticosteroids following hepatoportoenterostomy, 58.6% achieved a total bilirubin of < 1.5 mg/dL at 6 months with his or her native liver vs 48.6% of the 70 children who were treated with placebo, for an adjusted relative risk of 1.14 in both the intention–to–treat analysis and in the per–protocol analysis. In the secondary endpoint, survival with the native liver at 24 months was 58.7% with steroids and 59.4% with placebo.

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lighter reading

As we waited for the signal to turn green, my eyes met up with a poor young boy, about 12 years old. He removed a piece of bread from his pocket and took a bite. As he was about to take his next bite, a stray dog wagged his tail looking at him. Without hesitation, he sat down and put the bread on the road for the dog to eat. The dog sniffed the bread and walked away. The boy waited until he was sure the dog was gone then he picked up the bread and ate it! My heart cried and wanted to walk up to the boy but before I could open the door the signal turned Green and our car drove away. I kept thinking about the boy and later during my evening meal I realized that I was thinking of approaching the boy but never did, I could have stopped the car and walked up to him which again I never did. All I did was “thinking” and this poor little boy who had only one piece of bread without any hesitation sharing it with the dog, though he himself seemed to be very hungry. I learnt one of the biggest lessons in my life which that boy taught me without a conversation. He taught me to share with love and happiness. I am so blessed to have learnt this beautiful lesson from my ‘little unknown master’. It is my moral duty to share this incident with all my friends across the globe and be blessed with happiness.

laugh a while

A few days ago I landed at the Bombay Airport (India) and took a cab to my scheduled destination in South Bombay. I was enjoying the busy traffic with people rushing in every possible direction then we got stranded at a very busy intersection.

The International Food Shortage

Recently, a worldwide survey was conducted and the only question asked was: “Would you please give your honest opinion about the solution to the food shortage in the rest of the world?” The survey was, not surprisingly, a huge failure. Because: In Africa they didn’t know what “food” meant. In Eastern Europe they didn’t know what “honest” meant. In Western Europe they didn’t know what “shortage” meant. In China they didn’t know what “opinion” meant. In the Middle East they didn’t know what “solution” meant. In South America they didn’t know what “please” meant. And, in the USA they didn’t know what “the rest of the world” meant.

Mind Trivia

A Poor Young Boy and the Dog

A woman and her husband are picking seashells on the beach. The wife says, “Give me seven of your shells and I will have twice as many as you!” The husband answers, “Are you crazy? Give me seven of yours and we’ll have the same amount!” How many seashells does each one have? zz

The wife has 12, the husband 5

The wife has 16, the husband 9

The wife has 49, the husband 35

The wife has 51, the husband 37 ANSWER: The wife has 49, the husband 35

An Inspirational Story

Lighter Side of Medicine

Dr. Good and Dr. Bad Situation : A patient with fever had low platelet count and raised SGOT/ SGPT with SGOT>SGPT.

This is viral hepatitis.

DENGUE NEEDS TO BE RULED OUT.

ICU

QUOTE

Thank you friends for making this world a beautiful place to dwell.

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"If we wait until our lives are free from sorrow or difficulty, then we wait forever. And miss the entire point. " —Dirk Benedict

Asian Journal of Clinical Cardiology, Vol. 16, No. 7, November 2013

Lesson : In dengue fever, SGOT can be raised 2-5 times

the upper limit of normal. But, in some cases it can be 15 times the upper limit of normal.

[Dr. KK Aggarwal, Padma Shri and Dr. BC Roy National Awardee; Chairman Legal Cell Indian Academy of Echocardiography; Chairman, Ethical Committee Delhi Medical Council; Editor, eMedinewS and President, Heart Care Foundation of India]

KK Aggarwal

Asian

Journal of

CLINICAL CARDIOLOGY

Information for Authors

Manuscripts should be prepared in accordance with the ‘Uniform requirements for manuscripts submitted to biomedical journals’ compiled by the International Committee of Medical Journal Editors (Ann. Intern. Med. 1992;96: 766-767). Asian Journal of Clinical Cardiology strongly disapproves of the submission of the same articles simultaneously to different journals for consideration as well as duplicate publication and will decline to accept fresh manuscripts submitted by authors who have done so. The boxed checklist will help authors in preparing their manuscript according to our requirements. Improperly prepared manuscripts may be returned to the author without review. The checklist should accompany each manuscript. Authors may provide on the checklist, the names and addresses of experts from Asia and from other parts of the World who, in the authors’ opinion, are best qualified to review the paper. Covering letter -

- -

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). -

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.

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.

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.

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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. -

Do not use clips/staples on photographs and artwork.

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. -

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. 7, November 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 Peer Reviewed Journal

Drug Review

Review Article

Original Article

Case Report

Photo Quiz

Lighter Reading

April 2012, Pages 545-596

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

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