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Volume 14, Number 1, May 2011, Pages 1-36

Dr KK Aggarwal Group Editor-in-Chief

Dr Praveen Chandra Guest Editor

Head Office: E - 219, Greater Kailash, Part I, New Delhi - 48 , India. e-Mail: emedinews@gmail.com, Website: www.ijcpgroup.com

eMedinewS is now available online on www.emedinews.in or www.emedinews.org From the Desk of Editor-in-Chief Padma Shri and Dr BC Roy National Awardee

Dr KK Aggarwal

President, Heart Care Foundation of India; Sr Consultant and Dean Medical Education, Moolchand Medcity; Member, Delhi Medical Council; Past President, Delhi Medical Association; Past President, IMA New Delhi Branch; Past Hony Director. IMA AKN Sinha Institute, Chairman IMA Academy of Medical Specialities & Hony Finance Secretary National IMA; Editor-in-Chief IJCP Group of Publications & Hony Visiting Professor (Clinical Research) DIPSAR

21 May 2011, Saturday Dear Colleague, Importance of water in Jyestha Month Jyestha and Ashadh are two months of Grishma Ritu (summer). In the month of Jyestha, days are the longest in the year and the nights are the shortest. It is a known saying that more the heat in the month of Jyestha, more will be the rains in the month of Shravan (sawan).

The month of Jyestha is worshipped as month of worshipping water. It is a month for conserving water, maintaining water hygiene as well as donating water as charity to those who have scarcity of water. People who have servants at home or establishments with fourth class employees should see to it that their employees maintain personal, food and water hygiene. During scarcity of water, people may not wash their hands after going to toilets, take baths for days, wash their clothes for days or wash their utensils regularly. The end result is – a person may suffer from diarrhea, typhoid and jaundice. Heat disorders are also likely to occur in this season which may manifest as heat cramps, heat exertion or heat stroke.

Dr KK Aggarwal Editor-in-Chief ATS: Daily use of antibiotic keeps COPD at bay Chronic obstructive pulmonary disease (COPD) patients at high risk of an acute exacerbation can postpone the event by taking a daily antibiotic, a researcher said here. In a randomized, placebo– controlled trial, the time to a COPD exacerbation was significantly delayed for patients taking azithromycin (Zithromax), according to Richard Albert, MD, of Denver Health Medical Center. The frequency of exacerbation was also lower among azithromycin patients compared with those who got only standard COPD care, Albert told a late–breaking abstract session at the American Thoracic Society meeting. (Source: Medpage Today).

FDA panel recommends new rules for kids’ paracetamol FDA has recommended that children’s medications containing paracetamol provide weight-based dosing instructions, specific instructions for infants, and just one dose for pills, chewables, and melt away tablets.

Infertility Update What are Indications for Use of Donor Oocytes? 

Women with hypergonadotropic hypogonadism



Women of advanced reproductive age.



Women who have diminished ovarian reserve.





Women who are known to be affected by a significant genetic defect.

Women with poor oocyte and/or embryo quality or multiple previous failed attempts to conceive via ART —Dr Kaberi Banerjee, Director Precious Baby Foundation

Pediatric Update What is Bronchiolitis?

Bronchiolitis is a clinical syndrome characterized by the acute onset of respiratory symptoms in a child younger than 2 years of age. Typically, the initial symptoms of upper respiratory tract viral infection, such as fever and coryza, progress within 4 to 6 days to include evidence of lower respiratory tract involvement with the onset of cough and wheezing. It is a clinical diagnosis based on typical history and examination findings, with no specific confirmatory or exclusionary diagnostic test or gold standard.

—Dr Neelam Mohan, Director Pediatric Gastroenterology, Hepatology and Liver Transplantation, Medanta – The Medicity

Obesity Update Which Exercises are Best for Weight Loss?  Perform exercises that target the major muscles groups, such as your chest, back and shoulders. In addition to weight machines







and dumbbells, rubber tubing or elastic bands to provide the resistance can be used.

Aquatic exercises/swimming offer resistance for muscles while placing little impact on the joints. Perform these exercises twice a week and gradually increase to three times per week.

Begin with one set of 12 to 15 repetitions per exercise and gradually progress to two sets per exercise using enough resistance so that it’s a slight struggle to complete the last couple of repetitions.

Slowly warm up body before resistance training. For example, walk or do light calisthenics for at least 10 minutes.

—Dr Parveen Bhatia and Dr. Pulkit Nandwani

Spiritual Update Hanuman Chalisa Prabhu Mudrika Meli Mukha Maaheen Jaladhi Langhi Gaye Acharaj Naheen Meaning: You crossed the ocean keeping Rama’s ring in your mouth as a token for Sita.

Spiritual Significance: Crossing the ocean with Rama’s Ring (Beej Mantra) indicates the process of Chakra Meditative Pranayama. One needs a vehicle of mantra, image or sound to cross over the ocean of thoughts.

Medicolegal Update Postmortem examination: Ideal containers/preservative for viscera For preservation of viscera, clean, wide-mouthed glass bottles fitted with glass stoppers of one liter capacity should be used. Rubber inserts under caps should preferably not be used.  20-30 ml of blood taken from femoral artery or vein by skin puncture should be collected in 60ml screw–capped bottles or in plastic capped tubes/10 mg of sodium or potassium fluoride per ml of blood should be added in blood for preserving blood.  20-30 ml of urine is obtained from direct puncture of the bladder during the postmortem examination with a syringe and needle and should be collected in 60 ml screw-capped bottles or in plastic capped tubes and 20-30 mg of thymol blue or boric acid or acetic acid should be added as preservative  Saturated sodium chloride solution (common salt.) for all the visceral samples for chemical/toxicological examination  If there is an associated history of death due to acid intoxication then all the samples should be preserved in rectified spirit.

—Dr Sudhir Gupta, Additional Prof, Forensic Medicine & Toxicology, AIIMS

Online Submission

Volume 14, Number 1, May 2011

An IJCP Group Publication

Contents From the Desk of Group Editor-in-Chief

Yoga may Benefit Heart Disease Dr KK Aggarwal Group Editor-in-Chief IJCP Group emedinews@gmail.com

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

Assistant Editor: Dr Nagendra Chouhan

AJCC Speciality Panel Advisory Board 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 Dr PK Jain Dr PK Gupta Dr Naresh Trehan Faculty Dr GK Aneja Dr Ramesh Thakur Dr Balram Bhargava Dr HK Bali Dr HM Mardikar Dr Sanjay Mehrotra Dr Vivek Menon

Dr Sanjiv Chopra Prof. of Medicine & Faculty Dean Harvard Medical School Group Consultant Editor Dr Deepak Chopra Chief Editorial Advisor Anand Gopal Bhatnagar Editorial Anchor

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

Dr KK Aggarwal CMD, Publisher and Group Editor-in-Chief Dr Veena Aggarwal Joint MD & Group Executive Editor

KK Aggarwal

Review Article

Medical Management of Stable Coronary Artery Disease

Dr VP Sood, Asian Journal of Ear, Nose and Throat Dr Praveen Chandra, Asian Journal of Clinical Cardiology Dr Swati Y Bhave, Asian Journal of Paediatric Practice Dr Vijay Viswanathan, The Asian Journal of Diabetology Dr KMK Masthan, Indian Journal of Multidisciplinary Dentistry Dr M Paul Anand, Dr SK Parashar, Cardiology Dr CR Anand Moses, Dr Sidhartha Das, Dr Ramachandran, Dr Samith A Shetty, Diabetology Dr Ajay Kumar, Gastroenterology Dr Koushik Lahiri, Dermatology Dr Georgi Abraham, Nephrology Dr Sidharth Kumar Das, Rheumatology Dr V Nagarajan, Neurology Dr Thankam Verma, Dr Kamala Selvaraj, Obs and Gyne

Advisory Bodies Heart Care Foundation of India Overseas Indian Peoples Foundation

6

Matthew Pflieger, Bradford T. Winslow, Kyle Mills, Ira M. Dauber

Clinical study

A Study of Strength of Association of Smoking and Hypertension in Faridkot District, Punjab 14 Sanjay Gupta, Anita Goyal, KS Kajal, Parveen Kumar Gupta

Pattern of Cardiac Risk Factors in Rural Areas

17

CI Jhala, PC Joshi, Bhanu Naik

Case Report

Concurrent First- and Second-degree Sinoatrial Block

20

MK Jain, SS Kabde, AD Talele, D Jain

Expert opinion

IJCP Editorial Board Dr Alka Kriplani, Asian Journal of Obs & Gynae Practice

5

What is the Role of Primary Percutaneous Coronary Intervention in the Management of Acute MI?

23

Shrenik Shah

Research Review

From the Journals ...

25

Emedinews Section

From eMedinewS

27

Lighter Reading

Lighter Reading

31

Volume 14, Number 1, May 2011

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

Dr. Good and Dr. Bad Situation: A diabetic was found to have high night-time systolic blood pressure (BP) on ambulatory BP monitoring.

Printed at IG Printers Pvt. Ltd., New Delhi E-mail: igprinter@rediffmail.com Š Copyright 2011 IJCP Publications Pvt. 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 Pvt. Ltd. No part of this publication may be published in any form whatsoever without the prior written permission of the publisher.

Š IJCP Academy

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.

Lesson: A Japanese study has shown that the HOMA index and night-time systolic ambulatory BP are independent risk factors for the high visceral fat accumulation in Japanese patients with impaired glucose tolerance.

Diabetes Care 2011;34(3):e32.

Dr KK Aggarwal

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.

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From the Desk of Group Editor-in-Chief xxxxxxxxxxx

Yoga may Benefit Heart Disease

Y

oga could be a boon for people with high blood pressure, heart failure and other forms of cardiovascular disease. Yoga’s combination of stretching, gentle activity, breathing and mindfulness may have special benefits for people with cardiovascular disease. The word ‘yoga’ comes from a Sanskrit term that means union. It aims to join body, mind and the day-to-day challenges of life into a unified experience rather than keep them separate. There are different forms of yoga, from the gentle, peaceful hatha yoga to the active ‘power’ form called ashtanga.

Hatha yoga’s path to balancing the mind and the body involves three interconnected threads: Physical postures called ‘asanas,’ controlled breathing and calming the mind through relaxation and meditation. The three work together.

Getting into the various postures during a yoga session gently exercises the muscles. Anything that works your muscles is good for your heart and blood vessels. Activity also helps muscles become more sensitive to insulin, which is important for controlling blood sugar.

The deep-breathing exercises help slow the breathing rate. Taking fewer but deeper breaths each minute temporarily lowers blood pressure and calms the sympathetic nervous system, which is responsible for generating stress hormones. The postures and deep-breathing offer a kind of physical meditation that focuses and clears the mind.

Meditation and the mindfulness of yoga have both been shown to help people with cardiovascular disease. Studies suggest that yoga:  Reduces high blood pressure  Improves symptoms of heart failure  Eases palpitations  Enhances cardiac rehabilitation  Lowers cardiovascular risk factors such as cholesterol levels, blood sugar and stress hormones  Improves balance, reduces falls, eases arthritis and improves breathing for people with chronic obstructive pulmonary disease.

—Harvard Health Beat

Dr KK Aggarwal

Padma Shri and Dr BC Roy National Awardee Sr Physician and Cardiologist, Moolchand Medcity President, Heart Care Foundation of India Group Editor-in-Chief, IJCP Group Editor-in-Chief, eMedinewS Chairman Ethical 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) Asian Journal of Clinical Cardiology, Vol. 14, No. 1, May 2011

review article

Medical Management of Stable Coronary Artery Disease Matthew Pflieger, Bradford T. Winslow, Kyle Mills, Ira M. Dauber

Abstract All patients with stable coronary artery disease require medical therapy to prevent disease progression and recurrent cardiovascular events. Three classes of medication are essential to therapy: lipid-lowering, antihypertensive, and antiplatelet agents. Lipid-lowering therapy is necessary to decrease low-density lipoprotein cholesterol to a target level of less than 100 mg per dL, and physicians should consider a goal of less than 70 mg per dL for very high-risk patients. Statins have demonstrated clear benefits in morbidity and mortality in the secondary prevention of coronary artery disease; other medications that can be used in addition to statins to lower cholesterol include ezetimibe, fibrates, and nicotinic acid. Blood pressure therapy for patients with coronary artery disease should start with beta blockers and angiotensin-converting enzyme inhibitors. If these medications are not tolerated, calcium channel blockers or angiotensin receptor blockers are acceptable alternatives. Aspirin is the first-line antiplatelet agent except in patients who have recently had a myocardial infarction or undergone stent placement, in which case clopidogrel is recommended. Anginal symptoms of coronary artery disease can be treated with beta blockers, calcium channel blockers, nitrates, or any combination of these. Familiarity with these medications and with the evidence supporting their use is essential to reducing morbidity and mortality in patients with coronary artery disease.

Key words: Coronary artery disease, angina pectoris, myocardial infarction, cardiovascular events

S

table coronary artery disease (CAD) is defined as an established pattern of angina pectoris, a history of myocardial infarction (MI), or the presence of plaque documented by catheterization.1 CAD results when coronary artery plaque develops, reducing the oxygen supply to the myocardium. All patients with stable CAD require medical therapy to alleviate symptoms, prevent cardiovascular events, and reduce mortality. Almost 17 million patients in the United States have stable CAD, and nearly 800,000 more will experience an initial event each year. Although CAD caused one out of five deaths in 2005, improved management of the disease has achieved a 34 percent decline in CAD mortality since 1995.1 This article focuses primarily on optimal drug therapy for CAD; other aspects of CAD management, such as coronary revascularization MATTHEW PFLIEGER, DO, is a family physician at Clinica Family Health Services, Denver, Colo.

BRADFORD T. WINSLOW, MD, FAAFP, is residency director at Swedish Family Medicine Residency Program, Littleton, Colo., and assistant professor of family medicine at the University of Colorado–Denver, Aurora.

KYLE MILLS, PharmD, is a clinical pharmacist at Bend (Ore.) Memorial Clinic.

IRA M. DAUBER, MD, is associate clinical professor of medicine at South Denver Cardiology Associates, Denver.

Source: Adapted from Am Fam Physician 2011;83(7):819-826.

and treatment of comorbidities (e.g., diabetes mellitus), will not be covered here, although lifestyle modifications are briefly summarized in Table 1.2,3 Lipid Therapy Statins limit the synthesis of cholesterol and increase the catabolism of low-density lipoprotein (LDL) cholesterol. There is substantial evidence that statins can benefit patients with CAD, as shown in Table 2.4-7 Although serious adverse effects such as rhabdomyolysis are rare (less than 0.1 percent), myalgias are a relatively common adverse effect of statin therapy, with discontinuation rates of 5.3 to 7.8 percent in clinical trials (Table 3).8,9 The National Cholesterol Education Table 1. Lifestyle Modifications for Patients with Coronary Artery Disease Tobacco cessation Body mass index goal of 18.5 to 24.9 kg per m2 Moderate-intensity activity for 30 to 60 minutes seven days a week Alcohol consumption in moderation Low-sodium diet Two to three servings a day each of fruit and vegetables Saturated fat less than 10 percent of daily calories Information from references 2 and 3.

Asian Journal of Clinical Cardiology, Vol. 14, No. 1, May 2011

Review Article Table 2. Number Needed to Treat to Prevent One Death from Coronary Artery Disease Using Statins for Secondary Prevention Study Cholesterol and Recurrent Events Trial

4

Patient population

Years of follow-up

Number needed to treat

Mean age: 59 years

5

37

5

66

6.1

29

5.4

31

86 percent male United States, Canada Heart Protection Study

Mean age: 62 years

5

70 percent male United Kingdom Long-term Intervention with Pravastatin

Mean age: 62 years

6

83 percent male Australia, New Zealand Scandinavian Simvastatin Survival Study

7

Mean age: 58 years 81 percent male Norway

Information from references 4 through 7.

Table 3. Adverse Effect Rate with Moderate-dosage Statin Therapy* vs. High-Dosage Intensive Statin Therapy† Adverse effect

Effect rate with moderate daily dosage (%)

Effect rate with high daily dosage (%)

Rhabdomyolysis

< 0.1

< 0.1

Elevated creatine kinase > 10 times normal

0 to 1.8

0.53 to 2.2

Elevated liver function tests to > three times normal 0.4

1.3 to 1.5

Myalgia

1.4 to 2.8

1.5 to 3.3

Discontinuation rate (caused by adverse effects)

5.3

7.8

*Simvastatin (20 or 40 mg daily), pravastatin (40 mg daily), and atorvastatin (10 mg daily). † Simvastatin (80 mg daily) and atorvastatin (80 mg daily).

Information from references 8 and 9.

Program’s Adult Treatment Panel III recommends using statins to achieve LDL levels of less than 100 mg per dL (2.59 mmol per L) in patients with CAD.2 The American College of Cardiology recommends that patients with CAD have a target LDL measurement of less than 100 mg per dL, and for those at very high risk, a goal of less than 70 mg per dL (1.81 mmol per L) or treatment with intensive statin therapy should be considered.3,8 Several studies have examined optimal LDL levels in patients with CAD. In one trial, patients given intensive therapy with atorvastatin in a dosage of 80 mg per day had significantly lower mortality 30 days after MI than those given standard therapy of pravastatin in a dosage of 40 mg per day (number needed to treat [NNT] = 45 over two years).10 Another study assessed patients with CAD who had an initial LDL level of Asian Journal of Clinical Cardiology, Vol. 14, No. 1, May 2011

130 mg per dL (3.37 mmol per L) or greater and were treated with atorvastatin to a goal of less than 70 mg per dL or less than 100 mg per dL. To avoid the combined outcome of cardiovascular death or MI, the NNT was 30 over five years in favor of the group with a goal of less than 70 mg per dL.11 In addition, a meta-analysis addressed whether a goal of less than 70 mg per dL or less than 100 mg per dL was better, and found that more intensive treatment resulted in an NNT of 20 over one to five years to prevent one MI or cardiovascular death.8 A reduction in LDL cholesterol, regardless of the specific number, is important as well. Another metaanalysis showed that a reduction of at least 40 mg per dL (1.04 mmol per L) yielded a 23 percent decrease in CAD mortality that was sustained over five years.12

Review Article Reducing triglyceride levels and increasing high-density lipoprotein (HDL) cholesterol levels also should be considered in the management of CAD. However, these are secondary interventions to incorporate after the LDL goal has been achieved.2,3,13 Nicotinic acid can be added to statin therapy when HDL levels are low or triglyceride levels are above goal. Nicotinic acid prevents the synthesis of very–low-density lipoproteins and LDL, and it alters LDL composition to promote its elimination. Nicotinic acid also raises HDL levels by 15 to 30 percent.2,14 The National Cholesterol Education Program’s Adult Treatment Panel III guidelines recommend adding nicotinic acid to statin therapy when triglyceride levels remain above 200 mg per dL (2.26 mmol per L) or HDL cholesterol is less then 40 mg per dL.2 Fibrates also lower non-HDL cholesterol (i.e., total cholesterol minus HDL) and triglyceride levels.

Fibrates increase the production of proteins that transport and promote catabolism of fatty acids and triglycerides.14 Evidence supporting the use of fibrates for secondary prevention in patients with CAD has been mixed. Gemfibrozil reduced nonfatal MI and cardiovascular death in patients with CAD (NNT = 22), but bezafibrate was unable to reproduce significant benefits unless triglyceride levels were more than 200 mg per dL.9,15 One study compared fenofibrate and placebo in patients with CAD who were already taking statins, and no difference was detected in cardiovascular outcomes. However, the patients with triglyceride levels higher than 200 mg per dL and HDL levels lower than 35 mg per dL (0.91 mmol per L) after statin therapy did have reduced cardiovascular outcomes with added fenofibrate.13 American Heart Association guidelines recommend adding fibrates if triglyceride levels are 200 mg per dL or higher after a statin trial in patients with CAD.3 Ezetimibe can lower LDL levels in patients who have not achieved their goal despite maximal statin dosing and those in whom statins are not tolerated. However, the effect of ezetimibe on cardiovascular events in patients with CAD has not been studied, and a reduction in intermediate outcomes, such as carotidintima thickness, has not been noted.16 Antihypertensive Agents The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment

of High Blood Pressure recommends lowering blood pressure to 140/90 mm Hg or less for patients with CAD; however, the American Heart Association recommends a goal of 130/80 mm Hg or less, just as for patients with diabetes or chronic kidney disease.17,18 According to observational studies, for every increase of 20 mm Hg in systolic blood pressure or 10 mm Hg in diastolic blood pressure above the goal of 130/80 mm Hg, the risk of CAD mortality doubles.

These data apply to patients 40 to 89 years of age, supporting blood pressure reduction in older patients with hypertension.19 The reduction should be limited to a minimum diastolic pressure of 55 mm Hg.17 Besides reducing blood pressure, antihypertensive drugs improve mortality in patients following MI and can relieve anginal symptoms. Antihypertensive treatment works by decreasing myocardial oxygen demand (which is increased in patients with CAD because of atherosclerosis), lowering left ventricular ejection fraction, and preventing left ventricular hypertrophy.17,18 Beta Blockers

Beta blockers are first-line antihypertensive agents for patients with CAD20; if tolerated, beta blockers are also indicated for patients who do not have hypertension (Table 414). These drugs block and β1 and β2 adrenergic receptors, causing a decrease in heart rate, an increase in diastolic filling time, and a decrease in cardiac contractility. This negative inotropic and chronotropic effect decreases myocardial oxygen demand.17 Cardioselective beta blockers, or those that affect only β1 receptors, are preferred to minimize adverse effects, especially the bronchoconstriction that can be caused by beta2 antagonism18,21 (Table 414). In one metaanalysis that evaluated beta-blocker therapy in patients with CAD, investigators found a 23 percent reduction in the risk of death (NNT = 42 over two years to avoid one additional death).22 A recent meta-analysis with 464,000 patients confirmed that beta blockers should be first-line therapy in patients with CAD. In the first two years after MI, beta blockers can double the reduction in cardiovascular events compared with all other antihypertensive agents.23 Some beta blockers also possess intrinsic sympathomimetic activity, which can produce an increase in sympathetic activity at rest and may not effectively lower heart rate; these drugs should be avoided18 (Table 414).

Asian Journal of Clinical Cardiology, Vol. 14, No. 1, May 2011

Review Article Beta blockers are also beneficial for patients with anginal symptoms because they decrease cardiac oxygen demand.24 When being treated for angina, the patient should have a goal resting heart rate of 50 to 60 beats per minute.3 Angiotensin-converting Enzyme Inhibitors

Angiotensin-converting enzyme (ACE) inhibitors should be used in patients with CAD following MI, those who have diabetes, or those with left ventricular dysfunction. They also should be considered a treatment for hypertension in all other patients with CAD once beta-blocker therapy has been established.3 These agents block the conversion of angiotensin I to angiotensin II, reducing vasoconstriction and peripheral vascular resistance and decreasing blood pressure.14 ACE inhibitors also have cardiovascular benefits by preventing ventricular dilation that can occur in patients following MI.17 In one trial, ramipril decreased the likelihood of MI or cardiovascular death (NNT = 27 for four years) compared with placebo in patients with normal left ventricular function.25 In another study, perindopril reduced the risk of cardiovascular death or MI (NNT = 50 over four years).26 Researchers conducting a meta-analysis found that after three years of treatment with ACE inhibitors in patients following MI, cardiovascular mortality was reduced compared with placebo (NNT = 17).27 Table 4. Beta Blockers for the Treatment of Coronary Artery Disease Beta blocker

Receptors Typical dosage affected

Atenolol

β1

25 to 100 mg per day

Bisoprolol

β1

2.5 to 10 mg per day

Carvedilol

α1, β1, β2

6.25 mg to 25 mg twice per day

Labetalol

α1, β1, β2

200 to 800 mg twice per day

Metoprolol

β1

50 to 100 mg twice per day

Propranolol

β1, β2

40 to 160 mg twice per day

Timolol

β1, β2

20 to 40 mg twice per day

Note: Acebutolol and pindolol have intrinsic sympathomimetic action and should be avoided in patients with coronary artery disease.

Information from reference 14.

Asian Journal of Clinical Cardiology, Vol. 14, No. 1, May 2011

Angiotensin Receptor Blockers

Angiotensin receptor blockers (ARBs) are alternatives to ACE inhibitors. ARBs inhibit angiotensin II receptors, thereby decreasing vasoconstriction and the release of aldosterone.14 Although the likelihood of cough is somewhat lower with ARBs than with ACE inhibitors, the risk of other adverse effects is similar.14,24-26 The American Heart Association recommends using ARBs instead of ACE inhibitors only if a patient is intolerant to the latter, because no additional benefit of ARBs has been demonstrated.18 This was confirmed in several trials.18,28-30 One trial compared losartan and captopril in patients with CAD and found similar outcomes for all-cause mortality and cardiovascular death.28 In the Valsartan in Acute Myocardial Infarction (VALIANT) trial, valsartan was as effective as an ACE inhibitor in reducing mortality rates.29 In addition, the Ongoing Telmisartan Alone and in Combination with Ramipril Global Endpoint Trial (ONTARGET) showed a nonsignificant difference between telmisartan and ramipril in cardiovascular death and nonfatal MI.30 In both ONTARGET and the VALIANT trial, the combination of an ACE inhibitor and an ARB caused more renal adverse effects than an ARB or ACE inhibitor alone and conferred no mortality benefit.29,30 Calcium Channel Blockers

Calcium channel blockers are an acceptable alternative if beta blockers are not tolerated, although beta blockers more effectively alleviate anginal symptoms and improve exercise tolerance.24 The two classes of calcium channel blockers are dihydropyridines (i.e., amlodipine, nifedipine, and felodipine) and nondihydropyridines (i.e., verapamil and diltiazem). Both classes cause coronary vasodilation, reduce myocardial oxygen demand, and relieve symptoms of angina.14 One study found that short-acting nifedipine was associated with a dose-related increase in mortality and, therefore, should be avoided. Long-acting calcium channel blockers, however, have a therapeutic role in patients with CAD.31 Another study found that amlodipine reduced cardiovascular events (NNT = 16) compared with placebo, and showed similar improvements in cardiovascular events when compared with enalapril.32 Investigators comparing

Review Article Table 5. Medications for the Treatment of Stable Coronary Artery Disease Medication/medication class

Use

Comments

ACE inhibitors

All patients with hypertension, diabetes mellitus, chronic kidney disease, or left ventricular dysfunction3

Decrease mortality 21–23

Angiotensin receptor blockers

All patients with hypertension, diabetes, chronic kidney disease, or left ventricular dysfunction, and in whom ACE inhibitors are not tolerated3

No additional benefit compared with ACE inhibitors; may be considered in combination with ACE inhibitors for heart failure with left ventricular dysfunction3

Beta blockers

All patients with history of MI, acute coronary syndrome, or left ventricular dysfunction, unless contraindicated3

Decrease mortality19; avoid beta2 selective agents and agents with intrinsic sympathomimetic properties

Calcium channel blockers

Patients in whom beta blockers are not tolerated

Avoid short-acting nifedipine27

Nitrates

Patients with anginal symptoms despite use of beta blockers or calcium channel blockers

Evidence lacking on mortality benefit

Aspirin

All patients (75 to 162 mg per day), unless contraindicated3

Decreases nonfatal MI, strokes, vascular deaths32

Clopidogrel

Patients in whom aspirin is contraindicated or not tolerated3

Approved for acute coronary syndrome, recent MI, stroke, peripheral arterial disease, or coronary stent placement

Ezetimibe

Patients who have not achieved LDL goal despite statin therapy or who are intolerant of statins

Evidence lacking on mortality benefit

Fibrates

Patients with triglycerides of 200 to 499 mg per Reduction to non-HDL < 100 mg per dL (2.59 dL (2.26 to 5.64 mmol per L) and non-HDL > 130 mmol per L) reasonable3; treat if triglycerides mg per dL (3.37 mmol per L)3; triglycerides ≥ 500 ≥ 500 mg per dL to prevent pancreatitis3 mg per dL (5.65 mmol per L)

Nicotinic acid

Same as for fibrates; triglycerides of 200 to 499 mg per dL and non-HDL > 130 mg per dL3; triglycerides ≥ 500 mg per dL

Same as for fibrates; reduction to nonHDL < 100 mg per dL reasonable3; treat if triglycerides ≥ 500 mg per dL to prevent pancreatitis3

Statins

Patients with a baseline LDL ≤ 100 mg per dL3

Initiate with lifestyle measures; reduction to LDL < 70 mg per dL (1.81 mmol per L) or high-dose statin therapy reasonable3

Antihypertensive agents

Antiplatelet agents

Lipid-lowering agents

ACE = Angiotensin-converting enzyme; HDL = High-density lipoprotein; LDL = Low-density lipoprotein; MI = Myocardial infarction.

Information from references 3, 19, 21 through 23, 27, and 32.

amlodipine with valsartan found similar cardiovascular outcomes, although amlodipine significantly reduced the risk of heart failure.33 Nitrates

Nitrates can be used when a patient continues to have anginal symptoms despite using a beta blocker, calcium channel blocker, or both. Nitrates relax vascular smooth muscle and primarily cause venodilation, reducing preload and decreasing myocardial oxygen 10

demand.14 Nitrates do not play a role in the treatment of hypertension. Randomized trials evaluating the effects of nitrates on CAD outcomes have not been conducted.

Other antihypertensive drugs and drug classes, such as hydralazine, aldosterone antagonists, and diuretics, should be considered based on comorbidities such as heart failure in patients with CAD. However, these agents will not be discussed further in this article Asian Journal of Clinical Cardiology, Vol. 14, No. 1, May 2011

Review Article because they have not been found to decrease morbidity and mortality from CAD end points.

Antiplatelet Agents Antiplatelet therapy is an important component of CAD management because platelet aggregation at atherothrombotic plaque sites can produce clinically significant thrombosis and resultant MI.34 The most common antiplatelet agents used in the United States are aspirin and clopidogrel. Aspirin inhibits cyclooxygenase 1 and 2, reducing prostaglandin and thromboxaneA production and preventing platelet aggregation.14 Clopidogrel inhibits adenosine diphosphate receptors, thereby preventing platelet aggregation. Both agents irreversibly inhibit platelet activation.14 The benefit of aspirin in the secondary prevention of CAD is well defined by numerous studies and is reflected in international guidelines.3,35 In the Antithrombotic Trialists’ Collaboration Study, researchers demonstrated that patients with a history of MI who were treated with aspirin for a mean of 27 months had fewer nonfatal MIs, strokes, and vascular deaths (NNT = 35).36 A recent meta-analysis further clarified the benefit of aspirin at the dosage range currently recommended by international guidelines, finding that 30 patients needed to be treated for a mean of 33.3 months with aspirin at a dosage of 50 to 300 mg per day to prevent one cardiovascular event (nonfatal MI, nonfatal stroke, and cardiovascular death). The NNT for individual cardiovascular events was 33 for vascular death, 25 for stroke, 14 for any cause of cardiovascular death, and 12 for nonfatal MI.37 Aspirin is associated with an increased risk of hemorrhagic events.36,37 Data on adverse effects associated with aspirin therapy from long-term prevention trials involving patients with stable CAD are limited.36 In the above meta-analysis, one major hemorrhage occurred for every 111 patients with CAD who took aspirin for a mean of 33.3 months.37 Clopidogrel is approved by the U.S. Food and Drug Administration for the treatment of acute coronary syndrome, recent MI, stroke, and peripheral arterial disease. In a study of patients with a recent MI, there was no benefit of clopidogrel over aspirin in the prevention of fatal or nonfatal cardiovascular events.38 In another trial, patients deemed to be at high risk of Asian Journal of Clinical Cardiology, Vol. 14, No. 1, May 2011

atherothrombotic events were randomized to aspirin (75 to 162 mg per day) plus clopidogrel (75 mg per day) or aspirin alone. No difference in cardiovascular events was found except for a reduction in ischemic stroke, with an increased risk of bleeding in the treatment group.39 Thus, except for the significant benefit clopidogrel may provide following acute coronary syndrome or stent placement, it should not be added to aspirin therapy in patients with stable CAD to prevent future MI. Medications for the treatment of stable CAD are summarized in Table 5.3,19,21-23,27,32 References 1. Lloyd-Jones D, Adams R, Carnethon M, et al.

Heart disease and stroke statistics–2009 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee [published corrections appear in Circulation.

2009;119(3):e182, and Circulation. 2010;122(1):e11].

Circulation. 2009;119(3):e21-e181.

2. Third report of the National Cholesterol Education Program Expert Panel on detection, evaluation, and treatment of high blood cholesterol in adults (Adult Treatment Panel III). NIH Publication No. 02-5215.

September 2002.

3. Fraker TD Jr, Fihn SD, Gibbons RJ, et al. 2007 chronic angina focused update of the ACC/AHA 2002 Guidelines for the management of patients with chronic stable angina: a report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines Writing Group to develop the focused update of the 2002 Guidelines for the management of patients with chronic stable angina [published correction appears in Circulation. 2007;116(23):e558]. Circulation.

2007;116(23):2762-2772.

4. Sacks FM, Moyé LA, Davis BR, et al. Relationship between plasma LDL concentrations during treatment with pravastatin and recurrent coronary events in the Cholesterol and Recurrent Events trial. Circulation.

1998;97(15):1446-1452.

5. Heart Protection Study Collaborative Group. MRC/ BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high-risk individuals: a randomised placebo-controlled trial. Lancet. 2002;360(9326):7‑22.

6. The Long-Term Intervention with Pravastatin in Ischaemic Disease (LIPID) Study Group. Prevention of cardiovascular events and death with pravastatin in patients with coronary heart disease and a broad range of initial cholesterol levels. N Engl J Med. 1998;339(19):1349-1357.

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Review Article 7. Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S) Lancet. 1994;344(8934): 1383-1389.

8. Josan K, Majumdar SR, McAlister FA. The efficacy and safety of intensive statin therapy: a meta-analysis of randomized trials. CMAJ. 2008;178(5):576-584.

9. Secondary prevention by raising HDL cholesterol and reducing triglycerides in patients with coronary artery disease: the Bezafibrate Infarction Prevention (BIP) study Circulation. 2000;102(1):21-27.

10. Cannon CP, Braunwald E, McCabe CH, et al.; Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis in Myocardial Infarction 22 Investigators. Intensive versus moderate lipid lowering with statins after acute coronary syndromes [published correction appears in N Engl J Med. 2006;354(7): 778]. N Engl J Med. 2004;350(15):1495-1504.

11. LaRosa JC, Grundy SM, Waters DD, et al.; Treating to New Targets (TNT) Investigators. Intensive lipid lowering with atorvastatin in patients with stable coronary disease. N Engl J Med. 2005;352(14):1425-1435.

12. Baigent C, Keech A, Kearney PM, et al.; Cholesterol Treatment Trialists’ (CTT) Collaborators. Efficacy and safety of cholesterol-lowering treatment: prospective meta-analysis of data from 90,056 participants in 14 randomised trials of statins [published corrections appear in Lancet. 2005;366(9494):1358, and Lancet.

2008;371(9630):2084]. Lancet. 2005;366 (9493): 1267‑1278.

13. ACCORD Study Group. Effects of combination lipid therapy in type 2 diabetes mellitus [published correction appears in N Engl J Med. 2010; 362(18):1748]. N Engl J Med. 2010;362(17):1563-1574.

14. Lexi-Comp (Lexi-Drugs) [computer program]. Hudson, Ohio: Lexi-Comp; 2009.

15. Rubins HB, Robins SJ, Collins D, et al.; Veterans Affairs High-Density Lipoprotein Cholesterol Intervention Trial Study Group. Gemfibrozil for the secondary prevention of coronary heart disease in men with low levels of high-density lipoprotein cholesterol. N Engl J Med. 1999;341(6):410-418.

16. Kastelein JJ, Akdim F, Stroes ES, et al.; ENHANCE Investigators. Simvastatin with or without ezetimibe in familial hypercholesterolemia [published correction appears in N Engl J Med. 2008;358(18):1977]. N Engl J Med. 2008;358(14):1431-1443.

17. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. NIH Publication No. 04-5230.

August 2004.

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18. Rosendorff C, Black HR, Cannon CP, et al. Treatment of hypertension in the prevention and management of ischemic heart disease: a scientific statement from the American Heart Association Council for High Blood Pressure Research and the Councils on Clinical Cardiology and Epidemiology and Prevention [published correction appears in Circulation. 2007;116(5):e121].

Circulation. 2007;115(21):2761-2788.

19. Lewington S, Clarke R, Qizilbash N, Peto R, Collins R; Prospective Studies Collaboration. Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies [published correction appears in Lancet. 2003;361(9362):1060]. Lancet.

2002;360(9349):1903-1913.

20. Brunzell JD, Davidson M, Furberg CD, et al. Lipoprotein management in patients with cardiometabolic risk: consensus conference report from the American Diabetes Association and the American College of Cardiology Foundation. J Am Coll Cardiol.

2008;51(15):1512‑1524.

21. Salpeter SR, Ormiston TM, Salpeter EE. Cardioselective beta-blockers in patients with reactive airway disease: a meta-analysis. Ann Intern Med. 2002;137(9):715‑725.

22. Freemantle N, Cleland J, Young P, Mason J, Harrison J. Beta blockade after myocardial infarction: systematic review and meta regression analysis. BMJ. 1999;318(7200):1730-1737.

23. Law MR, Morris JK, Wald NJ. Use of blood pressure lowering drugs in the prevention of cardiovascular disease: meta-analysis of 147 randomised trials in the context of expectations from prospective epidemiological studies. BMJ. 2009;338:b1665.

24. Heidenreich PA, McDonald KM, Hastie T, et al. Metaanalysis of trials comparing beta-blockers, calcium antagonists, and nitrates for stable angina. JAMA. 1999;281(20):1927-1936.

25. Yusuf S, Sleight P, Pogue J, Bosch J, Davies R, Dagenais G; The Heart Outcomes Prevention Evaluation Study Investigators. Effects of an angiotensin-convertingenzyme inhibitor, ramipril, on cardiovascular events in high-risk patients [published corrections appear in N Engl J Med. 2000;342(10):748, and N Engl J Med. 2000;342(18):1376]. N Engl J Med. 2000;342(3):145‑153.

26. Fox KM; EURopean trial On reduction of cardiac events with Perindopril in stable coronary Artery disease Investigators. Efficacy of perindopril in reduction of cardiovascular events among patients with stable coronary artery disease: randomised, double-blind, placebo-controlled, multicentre trial (the EUROPA study). Lancet. 2003;362(9386):782-788.

Asian Journal of Clinical Cardiology, Vol. 14, No. 1, May 2011

Review Article 27. Rodrigues EJ, Eisenberg MJ, Pilote L. Effects of early and late administration of angiotensin-converting enzyme inhibitors on mortality after myocardial infarction.

Am J Med. 2003;115(6):473-479.

28. Dickstein K, Kjekshus J; Optimal Trial in Myocardial Infarction with Angiotensin II Antagonist Losartan Study Group. Effects of losartan and captopril on mortality and morbidity in high-risk patients after acute myocardial infarction: the OPTIMAAL randomised trial Lancet. 2002;360(9335):752-760.

29. Pfeffer MA, McMurray JJ, Velazquez EJ, et al.; Valsartan in Acute Myocardial Infarction Trial Investigators. Valsartan, captopril, or both in myocardial infarction complicated by heart failure, left ventricular dysfunction, or both [published correction appears in N Engl J Med. 2004;350(2):203]. N Engl J Med. 2003;349(20):1893‑1906.

30. Yusuf S, Teo KK, Pogue J, et al.; ONTARGET Investigators. Telmisartan, ramipril, or both in patients at high risk for vascular events. N Engl J Med. 2008;358(15):1547-1559.

31. Furberg CD, Psaty BM, Meyer JV. Nifedipine. Doserelated increase in mortality in patients with coronary heart disease. Circulation. 1995;92(5):1326-1331.

32. Nissen SE, Tuzcu EM, Libby P, et al.; CAMELOT Investigators. Effect of antihypertensive agents on cardiovascular events in patients with coronary disease and normal blood pressure: The CAMELOT Study: a randomized controlled trial. JAMA. 2004;292(18):2217‑2225.

33. Julius S, Kjeldsen SE, Weber M, et al.; VALUE trial group. Outcomes in hypertensive patients at high

cardiovascular risk treated with regimens based on valsartan or amlodipine: the VALUE randomised trial.

Lancet. 2004;363(9426):2022-2031.

34. Fuster V, Badimon L, Badimon JJ, Chesebro JH. The pathogenesis of coronary artery disease and the acute coronary syndromes (1). N Engl J Med. 1992;326(4): 242-250.

35. Becker RC, Meade TW, Berger PB, et al.; American College of Chest Physicians. The primary and secondary prevention of coronary artery disease: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Chest. 2008;133 (6 suppl):776S-814S. 36. Antithrombotic Trialists’ Collaboration. Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients [published correction appears in BMJ. 2002;324(7330):141]. BMJ. 2002; 324(7329):71‑86.

37. Berger JS, Brown DL, Becker RC. Low-dose aspirin in patients with stable cardiovascular disease: a metaanalysis. Am J Med. 2008;121(1):43-49.

38. CAPRIE Steering Committee. A randomised, blinded, trial of clopidogrel versus aspirin in patients at risk of ischaemic events (CAPRIE). Lancet.

1996;348(9038):1329-1339.

39. Bhatt DL, Fox KA, Hacke W, et al.; CHARISMA Investigators. Clopidogrel and aspirin versus aspirin alone for the prevention of atherothrombotic events.

N Engl J Med. 2006;354(16):1706-1717.

(For complete article, visit www.aafp.org)

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Clinical Study

A Study of Strength of Association of Smoking and Hypertension in Faridkot District, Punjab Sanjay Gupta*, Anita Goyal**, KS Kajal†, Parveen Kumar Gupta‡

Abstract The study has been conducted in Guru Gobind Singh Medical College, Faridkot (Punjab) with the aim to study the prevalence of hypertension among smokers and the strength of association of smoking with hypertension. A total of 261 subjects above the age of 16 years (meeting all the criteria of smokers in the study) among the OPD attendees, were selected for the study along with the controls. Criteria for smoking were taken as pack per year and smoking index. Criteria for hypertension for systolic blood pressure was taken as >139 mmHg and for diastolic it was >89 mmHg. The prevalence of hypertension among smokers was found to be 24.1% and among controls it was 15.3%. Among the different age groups in smokers, hypertension was found to be in 7.41% persons in the 26-35 years age group, 21.33% in the 36-45 years age group, 31.15% in the 46-55 years age group, 46.34% in the 56-65 years age group and 55.56% in the 66-75 years age group. Majority of the smokers were found to be either illiterate (41%) or having education only upto primary level (35%). The strength of association of smoking with hypertension has been found to be 1.75 (odds ratio). Smoking is a proven risk factor for the development of hypertension. To decrease the risk of development of hypertension and coronary artery disease, smoking cessation along with lifestyle modification should be advised as a preventive measure.

Key words: Hypertension, smoking, literacy, prevalence

T

he habit of smoking is prevalent worldwide.

Globally some 30% of adults were estimated to be smokers in 1988. It is estimated that by 2020, the number of smokers will be increased by 35% if global prevalence remains the same.1 Smoking prevalence among men is highest in the Western Pacific region and lowest in East Mediterranean region.

In Africa, 36% males and 9.4% females were smokers and in Europe 43.5% males and 23.4% females smoke tobacco.1 According to World Health Organization (WHO) study of South-east Asia region countries, prevalence of smoking in Indian males and females is 29% and 3%, respectively.1 Approximately 40% of cigarette smokers will die prematurely due to cigarette smoking unless they quit smoking.2 Cigarette smoking is a known factor for development of hypertension. *Associate Professor **DNB Student † Professor and Head Dept. of Community Medicine Guru Gobind Singh Medical College, Faridkot ‡ Private Practitioner, Faridkot Address for correspondence Dr Sanjay Gupta Associate Professor Dept. of Community Medicine Guru Gobind Singh Medical College Faridkot, Punjab - 151 203 E-mail: sanjayguptacmc@rediffmail.com

14

It contains nicotine which within seven seconds of inhalation of a cigarette, reaches the brain. This triggers various responses in the body. It signals the adrenal glands to release norepinephrine and epinephrine, which increase both diastolic and systolic blood pressure. Hypertension or high blood pressure is the most common cardiovascular disorder affecting 20% of adult population worldwide.3 A number of environmental factors have been implicated in the development of hypertension including salt intake, obesity, occupation, alcohol intake, family size and crowding. Dyslipidemia, diabetes, increased body mass index and also many known and unknown factors. The situation in India is more alarming. It was reported that of a total of 9.4 million deaths in India in 1990, cardiovascular diseases caused 2.3 million deaths of which 1.2 million deaths were due to coronary heart diseases and 0.5 million due to stroke. Hypertension is the underlying culprit for all these problems.4 The effect of smoking on blood pressure in less obese subjects, as seen in India and other developing countries are not well-studied. A very few studies has been conducted in India on the prevalence and association of smoking with hypertension. The present study is an attempt to find out the prevalence and association of smoking with hypertension.

Asian Journal of Clinical Cardiology, Vol. 14, No. 1, May 2011

Clinical Study Material and Methods The present study has been carried out in Guru Gobind Singh Medical College, Faridkot from 15 January 2008 to 14 January 2009, on patients visiting medical OPD for various ailments. Two hundred sixty-one persons above the age of 16 years were selected to participate in the study (meeting all the criteria of smokers in the study) and 261 persons of similar age and living under similar conditions but nonsmokers were taken as controls. They were subjected to detailed history and examination to collect desired information on a predesigned and pretested proforma. Criteria for smoking were taken as pack per year and smoking index. One packet of cigarettes containing 10 cigarettes has been taken as one packet (for bidi, 8 bidis means one packet). Pack year is the duration of smoking in years multiplied by number of packets of cigarettes/bidis smoking/day (for example 2 packets of cigarettes smoked/day for 20 years, Pack Year Index comes to 40). Ten pack years has been taken as minimum criteria for smoking. Smoking index, it is the number of cigarettes/bidis smoked/day multiplied by duration of years. Smoking index 100 was taken as minimum criteria for smoking. Criteria for hypertension for systolic blood pressure was taken as >139 mmHg and for diastolic it was >89 mmHg. To avoid confounding, persons already having coronary artery disease, diabetes, having body mass index (BMI) >30, positive family history for hypertension and using other forms of smoking such as chillum, cigar, pipe, hukka were excluded from the study. Data collected were tabulated and analyzed in the light of various tests of significance wherever applicable.

Results and Discussions The prevalence of hypertension among smokers has been found to be 24.1% and among controls 15.3%.

This is in accordance with the study conducted by Mahesar et al,5 which showed mean systolic pressure was higher in smokers than in nonsmokers and prevalence of hypertension was 23.5% in smokers and 16.4% in nonsmokers. Mohan et al,6 by multivariate regression analysis, showed that prevalence of hypertension was 25.6% in smokers and 18.7% in nonsmokers. A study conducted by Gupta et al7 in Jaipur, reported that mean systolic blood pressure was significantly greater in both urban and rural subject who consumed and Asian Journal of Clinical Cardiology, Vol. 14, No. 1, May 2011

smoked tobacco. In a study, in predominantly tobacco chewing urban females, the prevalence of hypertension was found to be 53.7% as compared to 28.9% in nonusers (p < 0.001).8 Many other epidemiological studies from other parts of the India have shown a significant correlation of smoking and tobacco use with hypertension prevalence, and coronary heart disease.9 In the present study, smoking has statistically significant correlation of age with hypertension (p < 0.05).

Among different age groups in smokers hypertension was found to be in 7.41% persons in the 26-35 years age group, 21.33% in the 36-45 years age group, 31.15% in the 46-55 years age group, 46.34% in the 56-65 years age group and 55.56% in the 66-75 years age group. This age-wise difference of hypertension among smokers was found to be statistically significant (Table 1). Among different age groups in control group, hypertension was found to be in 2.63% in 16-25 years of age, 5.17% in 26-35 years of age, 13.33% in 36-45 years of age, 31.9% in 46-55 years of age, 30.8% in 56-65 years of age and 17.64% in the rest (i.e. 66-75 years of age) (Table 2).

Again this age-wise difference of hypertension among controls was also found statistically significant. Study showed that in both, the study group and the control group (general population), prevalence of hypertension increases with age. This is in accordance with the meta-analysis of worldwide data for global burden of hypertension by Kearney et al.10 The prevalence of hypertension in 20-29 years of age was 8.5%, in 30-39 years of age it was 14.8%, in 40-49 year of age it was 24.8%, in 50-59 years of age it was 32.61% and in 60-69 years of age it was 39.9% and in 70 years and above it was 51.09%. There were few women smokers in our study i.e., only 1.53% but the proportion of Table 1. Hypertension among Different Age Groups in Smokers Age group 16-25

Hypertensive 0

Normotensive

Total

0%

21

100%

21

26-35

4

7.4%

50

92.6%

54

36-45

16

21.3%

59

78.7%

75

46-55

19

31.1%

42

68.9%

61

56-65

19

46.3%

22

53.7%

41

66-75

5

55.6%

4

44.4%

9

Total

63

24.1%

198

75.9%

261

X2 = 32.785; df = 5; p< 0.05

15

Clinical Study Table 2. Hypertension among Different Age Groups in Control Group Age group 16-25

Hypertensive 1

Normotensive

Total

2.6%

37

97.4%

38

26-35

3

5.2%

55

94.8%

58

36-45

10

13.3%

65

86.7%

75

46-55

15

31.9%

32

68.1%

47

56-65

8

30.8%

18

69.2%

26

66-75

3

17.6%

14

82.4%

17

Total

40

15.3%

221

84.7%

261

X2 = 24.372; df = 5; p < 0.05

hypertension in female smokers (25%) was almost same as of male (24.12%). Majority of the smokers found to be either illiterate (41%) or having education only upto primary level (35%). It showed an inverse relationship between smoking and hypertension. This is in accordance with a study conducted by Gupta et al7 in Jaipur Heart Watch 1, 2, 3 in which they observed greatest tobacco consumption among illiterate and low educational status subjects as compared to, more literate men.

In the present study, prevalence of hypertension was found to be 26.66% in rural and 23.61% in urban smokers and 16.53% in rural nonsmokers and 14.56% in urban nonsmokers. But this urban rural difference was not found to be statistically significant (>0.05).

Hypertension prevalence among cigarettes smokers was 33.33% and among Bidi smokers it was found to be 23.21%. Chi-square test revealed (>0.05) that brand did not have any statistical significance in causation of hypertension. The strength of association of smoking with hypertension was found to be 1.75 (odds ratio).

This is in accordance with the study conducted by Dochi et al11 which showed that odds ratio for smokers was 1.13 for hypertension and 1.15 for isolated hypertension.

Conclusion and Recommendations Smoking is a proven risk factor for the development of hypertension. Smoking cessation along with lifestyle modification should be advised as a preventive measure to decrease the risk of development of hypertension and coronary artery disease. Illiteracy comes in way

of knowing the effects of smoking on human health.

More illiterates take to smoking out of ignorance about ill effects on human body. There is an urgent need to create awareness regarding the harmful effects of smoking.

References 1. Corrao MA, Guindon GE, Cokkinides V, Sharma N. Building the evidence for global tobacco control.

Bull World Health Organ 2000;78(7):884-90.

2. Harrisonâ&#x20AC;&#x2122;s Principles of Internal Medicine. 16th edition, (2):2574.

3. WHO, The World Health Report. Hypertension 1997:39-45.

4. Muurray CJL, Lopez AD. Alternative projections of Mortality and Disability by Cause 1990-2020: Global Burden of Disease Study.

5. Mahesar H, Mahesar SM, Khand FD, Khand A, Seehar GM. Effect of smoking on blood pressure of inhabitants of Hyderabad vicinity. Sindh Univ Res J (Sci Ser)2009;41(1):25-30.

6. Mohan V, Deepa M, Farooq S, Datta M, Deepa R. Prevalence, awareness and control of hypertension in Chennai - The Chennai Rural Urban Epidemiology Study (CURES-52): J Assoc Physicians India 2007:55;326-32.

7. Gupta R. Smoking, education status and health inequality in India. Indian J Med Res 2006;124(1): 15-22.

8. Gupta R, Gupta VP, Sarna M, Bhatnagar S, Thanvi J, Sharma V, et al. Prevalence of coronary heart disease and risk factors in an urban Indian population: Jaipur Heart Watch-2. Indian Heart J 2002;54(1):59-66.

9. Gupta R, Sharma S, Gupta VP, Gupta KD. Smoking and alcohol intake in a rural Indian population and correlation with hypertension and coronary heart disease prevalence. J Assoc Physicians India 1995;43(4): 253-8.

10. Kearney PM, Whelton M, Muntner P, Whelton PK, He J. Global burden of hypertension: analysis of worldwide data. Lancet 2005;365:217-23.

11. Dochi M, Sakata K, Oishi M, Tanaka K, Kobayashhi E, Suwazono Y. Smoking as an independent risk factor for hypertension: a 14-year longitudinal study in male Japanese workers. Tohoku J Exp Med 2009;217(1):37-43.

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Asian Journal of Clinical Cardiology, Vol. 14, No. 1, May 2011

Clinical study

Pattern of Cardiac Risk Factors in Rural Areas CI Jhala*, PC Joshi**, Bhanu Naik†

Abstract Coronary artery disease (CAD) has been often considered as ‘affluent person’s disease meaning the disease is caused by easy and sedentary lifestyle, high caloric and high fat diet which are becoming common in rural areas. CAD rates among rural Indians is about half that among urban Indians, however, one should not overlook the fact that CAD in rural areas in India, have doubled as well. This study was conducted in rural areas around Ahmedabad with the aim to study the pattern of cardiac risk factors in rural areas. A total of 1,089 subjects were studied for lipid profile and fasting blood sugar. It was found that dyslipidemia, HT, obesity and tobacco use constituted major risk factors for ischemic heart disease (IHD). In rural population this observation is alarming and clearly shows urbanization of rural areas.

Key words: Cardiac risk factors, rural areas

C

oronary risk factors have been defined as those conditions which have been demonstrated to increase the susceptibility of an individual to the morbidity and mortality from coronary atherosclerosis.1 Death of a person before his retirement is known as ‘work year loss’. This loss due to heart failure in the age group of 35-64 years in India, accounted to 92 lacks of years in the year 2000. This figure is likely to cross 1.79 crores by 2003.2 Changing lifestyle and civilization, with increasing rate of tobacco chewing and smoking in the rural areas contribute to the increasing incidences of coronary artery disease (CAD).

CAD rates among rural Indians is about half that among urban Indians, however, one should not over look the fact that CAD in rural areas in India, have doubled as well. No. of CAD in rural population has increased from 1,47,40,808 to 1,80,07,899 in five years (2000-2005.)3 Age, sex and genetic factors are nonmodifiable factors, while others are behavioral and biological factors. *Hon. Associate Director, Dept. of Research **Research co-ordinator † Microbiologist, Dept. of Pathology Address for correspondence CI Jhala Hon. Associate Director Dept. of Research Dr Jivraj Mehta Smarak Health Foundation Bakeri Medical Research Centre Ratubhai Adani Arogyadham Near Ayojan Nagar, Ahmedabad - 380 007 E-mail: info@jivrajhealthcare.org

Asian Journal of Clinical Cardiology, Vol. 14, No. 1, May 2011

Cardiovascular risk factors are; older age, (usually males over 40 and females over 50), history of tobacco chewing, smoking, altered diet habits leading to high blood levels of certain lipids (triglycerides and LDL [low-density lipoprotein]) and low levels of high-density lipoprotein (HDL), lack of exercise, sedentary habits, history of high blood pressure (BP), diabetes, previous cardiovascular disease, family history of similar diseases, obesity and chronic high stress level. Increasing use of alcohol and certain drugs like cocaine in the rural areas has also increased the incidence of CAD. CAD has been often considered as ‘affluent person’s disease’ meaning the disease is caused by easy and sedentary lifestyle, high caloric and high fat diet which are becoming common in rural areas.

Material and Methods Total 1,089 subjects in rural areas around Ahmedabad were studied for lipid profile and fasting blood sugar (10-12 hours fasting blood samples were collected and tested with standard laboratory technique). Weight and BP were recorded and resting ECG tracing was done. ST-T changes, T inversion, LBB ST-T depression with changes of left ventricular hypertrophy (LVH) were considered for ischemic heart disease (IHD).

If the values of any serum lipid level exceeded the highest value in the range of normal values of 99.9% confidence interval, it was considered as dyslipidemia.4 Accordingly, alteration from following values are considered as dyslipidemia.

17

Clinical Study Serum cholesterol: M - 173.31-193.11. F. - 184.10-207.40.

Serum HDL: M - 43.5-48.32. F. - 51.31-57.65.

Serum LDL: M - 103.58-117.64. F. - 109.51-126.53.

Serum triglyceride: M - 92.89-122.35. F. - 97.71-31.99.

All the above parameters were considered with other cardiac risk factors.

Results Out of 1,089 subjects, 625 subjects were with normal ECG and no risk factor, 269 were with normal ECG and single risk factor and 99 were with normal ECG and multiple risk factors. Thirteen subjects were with abnormal ECG without risk factor, 35 were with abnormal ECG and single risk factor and 48 were with abnormal ECG and multiple risk factors. Above mentioned data are tabulated in the Table 1.

Considering age factor, subjects above the age of 50, are more susceptible (64.59%), in comparison with subjects below 50 years (35.47%). Male are more affected (58.30%) than female (41.64%) in both age groups as mentioned in Table 2.

Out of 269 subjects with normal ECG and single risk factor, 14 were with diabetes mellitus (DM), 26 were with hypertension (HT), 21 were obese, 85 had habit of tobacco chewing or smoking and, 123 were with altered lipid profiles, as shown in Table 3.

Out of 99 subjects with normal ECG, 18 had HT/ DM/dyslipidemia, 42 had HT and dyslipidemia and 39 had HT/Obesity and dyslpidemia as tabulated in Table 4.

Out of 35 subjects with abnormal ECG and single risk factor, four were with DM, three were HT, four were obese, six were having habits of using tobacco in any form and 18 had abnormal lipid profiles. As mentioned in Table 5.

Out of 48 subjects with abnormal ECG and multiple risk factors, 18 had HT, DM and dyslipidemia, nine had HT and dyslipidemia and 21 were obese with dyslipidemia (Table 6).

Out of 464 subjects with both normal ECG and single or multiple risk factors and abnormal ECG with single 18

Table 1. General Correlation between Risk Factors Grading/Normal ECG and IHD-ECG (1,089) Grading

Normal ECG

%

IHD - ECG

%

I No risk

625

57.39%

13

1.19%

II Single risk factor

269

24.70%

35

3.21%

III Multiple risk factors

99

09.00

48

4.40%

Total

993

91.99%

96

8.81%

Table 2. Age Group - IHD Subjects Age

No

%

Male

%

Female

%

25-30

01

01.04

00

0

01

1.04

31-35

02

02.08

01

1.04

01

1.04

36-40

07

07.29

05

5.20

02

2.08

41-45

12

12.50

08

8.33

04

4.16

46-50

12

12.50

06

6.25

06

6.25

51-55

06

06.25

04

4.16

02

2.08

56-60

18

18.75

11

11.45

07

7.29

61-65

18

18.75

09

9.37

09

9.37

>65

20

20.83

12

12.50

08

8.33

Total

96

99.99

56

58.30

40

41.64

Table 3. Normal ECG with Single Risk Factor (269) Risk factors

No. of cases

%

DM

14

5.20%

HT

26

9.66%

Obesity

21

7.80%

Tobacco

85

31.59%

Dyslipidemia

123

45.72%

Total

269

99.97%

Table 4. Normal ECG and Multiple Risk Factors (99) Risk factors

No. of cases

%

DM/HT/DYSLI

18

18.18%

HT/DYSLI

42

42.42%

HT/Obesity/DYSLI

39

39.39%

Total

99

99.99%

Asian Journal of Clinical Cardiology, Vol. 14, No. 1, May 2011

Clinical Study Table 5. Abnormal ECG and Single Risk Factor IHD (35) Risk factors

IHD

%

DM

04

11.42%

HT

03

08.57%

Obesity

04

11.42%

Tobacco

06

17.01%

DYPLI

18

51.4%

Total

35

99.82%

Table 6. Multiple Risk Factors and IHD (48) Risk factors

No.

%

DM/HT/DYSLI

18

37.5%

HT/DYSLI

09

18:75%

Obesity/DYSLI

21

43:75%

Total

48

99.4%

Table 7. Dyslipidemia, Profile-wise as a Risk Factor (290) Lipids

%

tobacco than in a cigarette, bidi releases 2-3 times more tar and nicotine making bidis more dangerous health hazards).5 In patients with IHD, obesity with dyslipidemia and DM/HT/dyslipidemia are two major risk factors: 43.75% and 37.5%, respectively. Even in subjects with normal ECG, dyslipidemia (45.72%) and tobacco chewing (31.59%) constitute major single risk factors while HT/dyslipidemia constitute 42.42% and HT/obesity/dyslipidemia constitute 39.39% in multiple risk factors group. Similar swing was observed in urban population too, but in rural population this observation is alarming and clearly shows urbanization of rural areas. Simple lifestyle measures lead to prevention of CAD in first instance and/or reversal of the atherosclerotic lesions.6 So, focus should be on a comprehensive lifestyle modification, which is possible by interpersonal counseling and individual counseling as per the need. Thus, adopting prevention at an early age is an economical option than therapeutic interventions (cost of treating various cardiac risk factors in India is 3178.1 billion rupees). But if simple lifestyle of rural areas is adopted in early phase, it can reduce the burden to mere 615.7 billion rupees.

Normal ECG

%

Abnormal ECG

S. cholesterol

82

36.93

16

23.52

S. HDL

32

14.41

14

20.56

S. LDL

69

31.08

07

10.29

References

S. triglycerides

39

17.56

31

45.58

1. Sapru R, Chawdhri R. Clinical significance of cardiac risk factor. GMJ 1993:15.

or multiple risk factors with dyslipidemia are considered separately profile wise in Table 7. In subjects with normal ECG, serum cholesterol (36.93%) and serum LDL (31.08%) are main factors followed by serum triglycerides (17.56%) and serum HDL (14.41%), respectively. In subjects with abnormal ECG, serum triglycerides (45.58%) and serum cholesterol (23.52%) are main factors followed by serum HDL (20.56%) and serum LDL (10.29%), respectively.

Conclusion Out of all the cardiac risk factors mentioned earlier, dyslipidemia and tobacco use constitute major single risk factors, 51.4% and 17.01%, respectively. (Bidi being cheaper than cigarette is the most popular way of smoking among low socioeconomical group of people in rural areas. Despite containing less

2. Hon PM. Statement Gujarat Samachar. - 28th Feb., 2010.

3. Dwivedi S, Agraval R. Dept. of Medical and Preventive Cardiology, University College of Medical Sciences, New Delhi. Anna. of National. Academy of Medical Sciences 2009;45(2):97-116.

4. Jhala CI, et al. Establishment of normal Lipid reference values in healthy vegetarian population of Rural Western & Northern Gujarat and comparison with Available Similar Data of other parts of India. IMAGSB. News Bulletin/Aug. -09(4):531-3.

5. Negri E, Franzosi MG, La Vecchia C, Santoro L, Nobili A, Tognoni G. Tar yield of cigarettes and risk of acute myocardial infarction. GISSI-EFRIM. Investigators.

BMJ 1993;306:1567-70.

6. Deedwania P, Singh V. Coronary artery disease in South Asians: evolving strategies for treatment and prevention.

Indian Heart J 2005;57(6):617-31.

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case report

Concurrent First- and Second-degree Sinoatrial Block MK Jain*, SS Kabde**, AD Talele**, D Jain†

Abstract The literature is replete with reports of second-degree atrioventricular (AV) block with Wenckebach periods but occurrence of first-degree block with Wenckebach’s phenomenon at the SA node is rare. First-degree sinoatrial (SA) block theoretically cannot be diagnosed on surface ECG. However, under certain circumstances, second-degree SA block can unmask underlying first-degree SA block. We report this case of a 55-year-old man who showed rare instance of simultaneous occurrence of both types of second-degree SA block along with first-degree SA block in the same strip back-to-back.

Key words: Sinoatrial block, Wenckebach’s phenomenon, SA node dysfunction, pathologic bradycardia

T

he literature is replete with reports of seconddegree atrioventricular (AV) block with Wenckebach periods but occurrence of firstdegree block with Wenckebach’s phenomenon at the sinoatrial (SA) node is rare.1 First-degree SA block theoretically cannot be diagnosed on surface ECG.2 However, under certain circumstances, second-degree SA block can unmask underlying first-degree SA block.

The case to be described shows rare instance of simultaneous occurrence of both types of seconddegree SA block along with first-degree SA block in the same strip back-to-back.

Case Report

P-wave, PR interval, QRS, ST segment and T waves are normal.

The ECG (rhythm strip) in Figure 2 shows first four PQRS complexes (R1-R4) in lead II to have equal PP interval of 0.64 sec. This is followed by missed PQRS complex with a pause of 1.16 sec indicating type II second-degree SA block. This pause is less than twice the sinus PP interval of 1.28 second (0.64 × 2). This suggests underlying first-degree SA block. This sequence is followed by another four PQRS complexes (R5-R8) with progressive shortening of PP interval. This is again followed by a pause indicating occurrence of Wenckebach’s phenomenon at SA node. The basic sinus cycle length in Wenckebach’s phenomenon in this case can be calculated by the formula suggested by Schamroth and Dove.3

The patient was a 55-year-old man, with history of hypertension for 10 years. Physical examination revealed irregular pulse.

Serum electrolytes, blood Basic sinus cycle length = Isoconduction interval in sec. = 3.2 = 0.64 sec cell counts and serum No. of RR intervals in 4+1 +1 creatinine values were within isoconduction interval normal limits. ECG showed mild left ventricular concentric hypertrophy. His Isoconduction interval in this case starts from R5 to R9.

12-lead ECG (Fig. 1) shows progressive shortening The pause following R8 is 1.1 sec which is again less than of PP interval in lead I (with normal PR interval) twice the basic sinus cycle length of 1.28 sec (0.64 × 2) suggesting occurrence of Wenckebach’s phenomenon indicating occurrence of first-degree SA block along with at SA node. Rest of the ECG findings including second-degree type I SA block.

Discussion *Professor and Head, Dept. of Medicine **Postgraduate Student, Shyam Shah Medical College and Associated Sanjay Gandhi Memorial Hospital, Rewa † Lecturer, Dept. of Cardiology, IMS, BHU, Varanasi

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SA block has been described to be of three types (first-, second- and third-degree).3 Asian Journal of Clinical Cardiology, Vol. 14, No. 1, May 2011

Case Report In the ladder diagram B, in case of second-degree type II SA block the impulse following dropped beat should have come at D’, but due to the presence of first-degree SA block there is early resetting of the SA node. Hence the next beat comes early at position D. This has been duly demonstrated in the present case.

Figure 1. Sinus rate of 78 beats/minute, irregular, normal P-wave and PR interval (0.16 sec), normal QRS morphology with 50° axis and normal T-wave.

Second-degree SA block type I/Wenckebach’s block: This is denoted by progressively increasing SA conduction time, which is reflected on surface ECG in form of decreasing PP intervals, followed by a dropped beat (ladder diagram C). Extent of increase in conduction time goes on decreasing (decrement in increment of SA conduction time).5 This phenomenon is also clearly noticeable in both strips of ECG in Figures 1 and 2.

C 0.8 sec 0.8 sec 0.8 sec 0.8 sec 0.8 sec S

Figure 2. R1-R4 have equal PP interval of 0.64 sec, followed by a pause of 1.16 sec indicating second-degree type II SA block. R5-R8 have progressive decreasing PP intervals, followed by a pause (1.1 sec) indicating Wenckebach’s phenomenon at SA node.

First-degree SA block: There is increased SA conduction time due to delay at the SA junction which is not visible on surface ECG. This produces normal PP intervals (ladder diagram A). Hence, the diagnosis of isolated first-degree SA block cannot be made on the basis of surface ECG.4

A

0.9 sec

0.8 sec 0.7 sec

1.4 sec

Ladder diagram C.

Second-degree SA block type II: The PP interval remains constant but there is intermittent dropping of beats (all of PQRS). The pauses following are exactly twice the sinus PP intervals. This is noticeable in Figure 2 between R1-R5.

Third-degree SA block: All impulses are blocked within the SA junction and no P waves are visible on surface ECG. This results in atrial escape rhythm manifested

by P waves from an ectopic atrial pacemaker. This type of block again cannot be diagnosed on surface ECG.6

A S S-A A Ladder diagram A.

However, in presence of second-degree SA block, if the pause following PQRS is less than twice the sinus PP interval, the diagnosis of underlying first-degree SA block can be accurately made.4 B S S-A A A

S-A

B

C

Ladder diagram B.

Asian Journal of Clinical Cardiology, Vol. 14, No. 1, May 2011

D

E

In the present case, both types of second-degree SA block with underlying first-degree SA block are seen.

SA node dysfunction and AV conduction blocks are the most common causes of pathologic bradycardia.7 SA node dysfunction increases in frequency between the fifth and sixth decades of life and should be considered clinically in patients with fatigue, exercise intolerance and syncope. Idiopathic degenerative disorder of the sinus node is the most common cause for intrinsic sinus node dysfunction. This is followed by ischemic heart disease.8 Most important cause of 21

Case Report sinus node dysfunction in patients without structural abnormalities is drugs.9 These include b blockers, calcium-channel blockers, digoxin, antiarrhythmics (Class I and III) and clonidine. SA exit block is usually transient. It may be of no clinical importance except to prompt a search for the underlying cause.

In such rhythm disorders sinus arrhythmia, sinus nodal extrasystoles, atrial extrasystoles and AV block must be ruled out. Sinus arrhythmia is characterized by a phasic variation in sinus cycle length (which is related to respiration) during which maximum sinus cycle length minus the minimum sinus cycle length should be >120 msec.9 The transition from slow to rapid phase occurs gradually and this distinguishes it from SA block which manifests with sudden change in rate. Sinus nodal extrasystoles cause resetting of the SA node resulting in pauses which are equal to sinus beats and less than compensatory pauses. Such resetting does not occur in SA block. In case of SA blocks, the pauses are multiples of the basic sinus cycle length. Atrial extrasystoles can be confused with SA block especially in those cases where the premature P-wave is hidden in the preceding T-wave or if the P-wave distorts the T-wave giving a false appearance of SA block. AV block can be easily differentiated from SA block because of variable PR interval and other features of AV block.

Conclusion Calculation of basic sinus cycle length and analysis of pause in two types of second-degree SA block can unmask first-degree SA block. Wenckebach’s phenomenon can occur at any level from sinus node to bundle branch10 and its application can solve many seemingly complex rhythm disorders.

Acknowledgement We dedicate this article to Karel F Wenckebach, an astute physician, who described this phenomenon in 1899, even before the advent of clinical electrocardiography.

References 1. Lawrence RR. Sinoauricular block with Wenckebach periods, with concurrent second degree atrioventricular block with Wenckebach periods: their occurrence in a presumably healthy young adult. Dis Chest 1966;50(4):432-6.

2. Winton SS. Sino-auricular block: an analysis of eleven cases. Acta Cardiol 1948;3(2):108-20.

3. Schamroth L, Dove E. The Wenckebach phenomenon in sino-atrial block. Br Heart J 1966;28(3):350-8.

4. Rowland E, Morgado F. Sino-atrial node dysfunction, atrioventricular block and intraventricular conduction disturbances. Eur Heart J 1992;13(Suppl H):130-5.

5. Cabeen WR Jr, Roberts NK, Child JS. Recognition of the Wenckebach phenomenon. West J Med 1978;129(6):521-6.

6. Schamroth L. Sinoatrial conduction block. In: Disorders of Cardiac Rhythm. Vol. 1, 2nd edition, Blackwell Scientific Publications: Oxford 1980:331.

7. Tomaselli GF. The Bradyarrhythmias: Introduction.

In: Harrison’s Principles of Internal Medicine. Vol. 2, 7th edition, The McGraw-Hill Companies, Inc. 2008:1416.

8. Olgin JE, Zipes DP. Diagnosis of specific arrhythmias.

In: Braunwald’s Heart Disease ‘A Textbook of Cardiovascular Medicine’. 8th edition, Saunders Elsevier.

2008:896.

9. Victor L. Bradyarrhythmias and Pacemakers. In: Hurst’s The Heart. Vol. 1, 12th edition, The McGraw-Hill Companies, Inc. 2008:991.

10. Upshaw CB Jr, Silverman ME. The Wenckebach phenomenon: a salute and comment on the centennial of its original description. Ann Intern Med 1999;130(1): 58-63.

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Asian Journal of Clinical Cardiology, Vol. 14, No. 1, May 2011

Expert opinion

What is the Role of Primary Percutaneous Coronary Intervention in the Management of Acute MI? Shrenik Shah

395 patients. Re-perfusion success was 97%.

Ninety-four percent Thrombolysis in Myocardial Infarction Grade 3 (TIMI-3) flow was seen within 60 minutes in angioplasty group. No significant improvement in LV function during rest/exertion at six weeks follow-up was seen. There was significant reduction of in-hospital mortality in combined death/re-infarction, intracranial hemorrhage, in high risk group.

T

he management of acute myocardial infarction (MI) has undergone considerable changes in last two decades. In patients with ST elevation myocardial infarction (STEMI), primary angioplasty is becoming first choice of therapy. However, because of low availability of such treatment even in developed countries, most patients with STEMI are re-perfused with intravenous thrombolysis. Many patients do not receive a re-perfusion therapy at all.

Data from large clinical trials indicate that after successful thrombolysis, >50% of patients have significant stenosis and around 30% have spontaneous inducible ischemia, where re-occlusion of an infarctrelated artery is a potential treat. Therefore, early risk assessment is of great importance in patients who are thrombolyzed and are not thrombolyzed. Because recurrent events are mainly due to presence of an unstable residual stenosis of the infarct-related coronary artery, an effective therapy should include an invasive procedure like angioplasty.

Angioplasty is generally preferred in acute MI if (ACC/ AHA Guidelines 2004) 1. Skilled percutaneous coronary intervention (PCI) laboratory is available with surgical back-up. Doorto-balloon time/door-to-needle time is <1 hour and medical contact to balloon/door-to-balloon is <90 minutes.

2. High risk from STEMI; cardiogenic shock Killip Class >3.

3. Contraindication to fibrinolysis including increased risk of bleeding and ICH. 4. Late presentation - symptoms onset >3 hours ago.

5. Diagnosis of STEMI is in doubt.

Randomized Trials Comparing Primary Angioplasty with Thrombolysis  PAMI (Primary Angioplasty in Myocardial Infarction) trial: It was the largest trial with

Interventional Cardiologist Sterling Hospital, Ahmedabad

Asian Journal of Clinical Cardiology, Vol. 14, No. 1, May 2011









Mayo Clinic Trial (PAMI vs t-PA) trial: Number of patients was 108. Assessed myocardial salvage by technitium-99m sestamibi tomographic imaging showed no significant difference in salvage.

Netherlands (Zwolle) trial (PAMI vs STK): Number of patients was 142. There was significant reduction in re-infarction with higher pre discharge left ventricular ejection fraction.

GUSTO-IIb (Global Use of Strategies To Open occluded coronary arteries in acute coronary syndrome): Angioplasty substudy; largest trial comparing primary balloon angioplasty with thrombolysis (t-PA). Showed significant reduction in incidence of primary endpoints (death, nonfatal re-MI/disabling stroke at 30 days). No significant advantage was noted at six months.

PCAT (Primary Coronary Angioplasty Trial): Meta-analysis of 10 randomized trial like Dewood, PAMI-1, Zijlstra, Mayo, Zijlstra, Ribeiro, Grinfeld, Ribichini, Garciam GUSTO IIb. (Conducted between 1989-1996) showed significant decrease in 30-day mortality, combination of death and re-MI, in total stroke and hemorrhagic stroke.

Follow-up study revealed that 26 lives were saved per 1,000 patients treated with primary angioplasty strategy. This beneficial effect persisted at six months.

Trials of Thrombolysis Versus Transfer for Primary Angioplasty PRAGUE I and II: Primary angioplasty in patients transferred from general community hospitals to 23

Expert Opinion specialized Percutaneous Transluminal Coronary Angioplasty (PTCA) units without emergency thrombolysis; AIR-PAMI (Air Primary Angioplasty in MI) and DANAMI (DANish trial in Acute MI).

All these trials demonstrated more favorable outcomes for patients treated with primary angioplasty despite the intrinsic transportation delay. Pooled analysis of comparative inter-hospital transportation trials (n = 1,242) revealed a significant reduction in 30-day mortality.

Advantages of Primary Angioplasty (Pci) Strategy 



 

Superior restoration of flow: Myocardial salvage and survival is directly related to TIMI flow.

GUSTO-I trial verified relationship between TIMI-3 flow and survival for primary angioplasty (~93-98%).

Treatment of the inciting pathobiology in acute MI: In stent-PAMI trial, stenting decreases the risk of re-occlusion and re-stenosis.

Anatomical definition and risk stratification.

Reduction in complications (mechanical complications of MI): GUSTO-I and PAMI I and II trials demonstrated in combined meta-analysis, a 86% decrease in risk of mechanical complications like MR, VSD and free wall rupture.

Challenging Groups of Patients for PCI (PAMI)  Elderly patients: In pooled analysis of PAMI, Netherlands (Zwolle) and Mayo Clinic randomized trials revealed significant reduction in mortality for elderly (>70 years) subgroup treated with angioplasty (3.5% vs 16%; p = 0.02).  Prior CABG: Increased mortality with prior coronary artery bypass graft (CABG) and acute MI due to co-existent factors like advanced age, prior MI, multi-vessel disease, diabetes mellitus, impaired LV function. In GUSTO-I trial, TIMI-3 flow was seen in less number of patients with bypass graft. In PAMI trials (n = 93), vein graft primary balloon angioplasty is associated with higher rates of TIMI-3 flow versus thrombolysis.  Patient with contraindications to thrombolytic treatment: In MITRA registry, there was significant decrease in mortality in patient with primary angioplasty as compared to conservative treatment.  Cardiogenic shock: SHOCK trial (Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock) verified a rate for revascularization in cardiogenic shock (n = 302). A significant survival advantage for revascularization was noted at six months and 1-year but not at 30-day primary endpoint. Clearly, rapid re-perfusion is critical to success in patient with cardiogenic shock. n

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Asian Journal of Clinical Cardiology, Vol. 14, No. 1, May 2011

Research Review

From the Journals ...

Effects of Intensive Blood Pressure Control in Patients with Diabetes Mellitus Background: The risk of cardiovascular disease rises as systolic blood pressure increases in patients with type 2 diabetes mellitus. Current guidelines from the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure advise lowering systolic blood pressure to less than 130 mm Hg in patients with diabetes; however, there is little evidence to indicate that this improves clinical outcomes. The Action to Control Cardiovascular Risk in Diabetes (ACCORD) Study Group evaluated the effects of intensive blood pressure control on cardiovascular events in patients with diabetes.

The Study: A total of 4,733 patients with type 2 diabetes were randomized to one of two blood pressure control groups: intensive therapy (target systolic blood pressure of less than 120 mm Hg) or a control group (target systolic blood pressure of less than 140 mm Hg). Patients were followed for an average of 4.7 years. Blood pressure was managed using standard antihypertensive agents, but no specific strategy was enforced. The primary outcome was a composite of the first occurrence of a major fatal or nonfatal cardiovascular event (i.e., myocardial infarction or stroke). Various secondary outcomes (i.e., separate assessments for myocardial infarction, stroke, congestive heart failure, and all-cause mortality) also were evaluated.

Results: Baseline traits between groups were similar, including initial blood pressure and incidence of previous cardiovascular events. No significant difference in the primary outcome was noted between groups, despite the intensive treatment group maintaining significantly lower blood pressure than the control group (mean blood pressures: 119.3/64.4 mm Hg versus 133.5/70.5 mm Hg, respectively). Most secondary outcomes showed no differences between groups, including all-cause or cardiovascular-related mortality, congestive heart failure, or myocardial infarction. However, the Asian Journal of Clinical Cardiology, Vol. 14, No. 1, May 2011

intensive therapy group had a lower incidence of total strokes than did the control group (0.32 versus 0.53 percent per year, respectively; hazard ratio = 0.59; P = .01) and nonfatal strokes (0.30 versus 0.47 percent per year, respectively; hazard ratio = 0.63; P = .03).

Conclusion: The authors conclude that a more stringent blood pressure goal for patients with type 2 diabetes does not significantly reduce the primary cardiovascular outcome or most secondary outcomes compared with standard blood pressure goals. In this study, the number of total and nonfatal strokes was lower in the intensive therapy group, although the clinical benefit was limited (number needed to treat = 89 for five years to prevent one stroke).

Am Fam Physician. 2011;83(5):612-613.

Electrocardiographic Changes and Arrhythmias Following Percutaneous Atrial Septal Defect and Patent Foramen Ovale Device Closure Objectives: To compare pre- and post-procedure electrocardiograms (ECGs) in a large cohort of patients after percutaneous closure of atrial septal defect (ASD) and patent foramen ovale (PFO).

Background: Percutaneous device closure of ASD or PFO is commonplace. Conduction and rhythm anomalies associated with percutaneous device placement have been reported.

Methods: We reviewed records for all patients who underwent percutaneous device closure of ASD or PFO at our institution from 1999 to 2008. Preprocedure ECG and Holter studies were compared to available short-term (<2 months after placement) and intermediate follow-up (>2 months) ECG or Holter.

Results: Pre- and post-procedural ECGs were available in 610 patients (305 females, average age 50 Âą 18.1 years, range 1-91 years, 384 PFO, 184 ASD, 42 with multiple defects, mean device size 16 mm, range 5-38 mm). We report an incidence of 5.2% (32/610) of arrhythmias in the 4 months 25

Research Review following device placement, including 29 patients with atrial tachyarrhythmias (ATs, 22 fibrillation, 7 flutter), 1 with junctional tachycardia, and 2 with heart block.

Among other findings, the average P-wave duration was increased on intermediate follow-up as compared to early follow-up (p < 0.001). Development of newonset 1st degree AV Block after the procedure was associated with an increased risk of ATs post-procedure (p < 0.0001).

Conclusion: We report a low risk of clinically significant post-procedure arrhythmias after device placement.

Clinically significant heart block occurred in only two patients (0.3%). Changes in several markers of atrial conduction were found, suggesting an effect of device closure on intra-atrial conduction.

Johnson JN, Marquardt ML, Ackerman MJ, et al. Catheter Cardiovasc Interv. 2011 May 11. [Epub ahead of print]

Predictors of Infarct-related Artery Patency Following Combined Lytic Therapy in Patients with ST-segment Elevation Myocardial Infarction Treated with Immediate Percutaneous Coronary Intervention Background and aim: Patency of infarct-related artery (IRA) before percutaneous coronary intervention (PCI) for ST-elevation myocardial infarction (STEMI) is associated with better outcomes. Little is known of the clinical or angiographic predictors of IRA recanalization after administration of combined fibrinolytic therapy before PCI. Methods: A total of 225 STEMI patients, admitted to remote hospitals with anticipated transfer time to cathlab >90 minutes were enrolled. All patients received a half dose of alteplase and a full dose of abciximab at the remote hospital and were immediately transferred for angiography. In angiographic analysis, the culprit lesion (CL) was defined as the minimal lumen diameter (MLD) point in IRA (CLMLD) (in group with occluded IRA, measurement was done after the first pass of the guidewire).

Results: Occluded IRA (TIMI 0+1) was found in 14.2% of patients (n = 32) and patent IRA (TIMI 2+3) in 85.8% (n = 193) at baseline angiography.

Baseline and angiographic characteristics were similar in both groups, except for a higher rate of smoking

in the TIMI 2+3 group (73.1% vs 50%; p = 0.009) and longer distance from CLMLD point to the nearest proximal side branch in the TIMI 0+1 group (21.2 Âą 10.3 mm vs 13.8 Âą 11.2 mm; p = 0.002).

In multivariate analysis, smoking and distance from CLMLD to the nearest proximal side branch were independent predictors of IRA patency at baseline.

Conclusions: Angiographic (anatomical) IRA parameter as distance from CLMLD point to nearest proximal side branch may influence the efficacy of combined fibrinolytic therapy before PCI despite the similar clinical characteristics and time delay to angiography. Smoking has a paradoxical beneficial effect on combined thrombolytic therapy effectiveness.

Rakowski T, Dziewierz A, Siudak Z, et al.

Kardiol Pol 2011;69(5):452-7.

Platelet Activity and Cardiovascular Risk in Apparently Healthy Individuals: A Review of the Data Cardiovascular disease is a major cause of morbidity and mortality. Numerous risk scores exist to identify healthy individuals at increased risk of developing cardiovascular disease. Although platelets are a key mediator in the pathogenesis of cardiovascular disease, the role of platelet activity measurements and the incidence of cardiovascular disease are uncertain.

Platelet aggregometry, the most well-studied method of platelet function testing, is associated with risk factors for cardiovascular disease. However, data supporting platelet aggregation and incident cardiovascular disease is conflicting. Plasma markers of platelet activation are promising candidates. Soluble CD40L and P-selectin are easily measured with a standardized ELISA, and there is some data to suggest an association with cardiovascular disease, but further studies are required.

While mean platelet volume is a promising candidate, platelet count and bleeding time are not specific for platelet activity nor are they associated with cardiovascular disease in a healthy population. For this field to progress, we recommend large-scale, prospective studies that measure a battery of these platelet function tests in individuals without cardiovascular disease to better understand the associations, if any, between platelet activity and cardiovascular disease.

Sharma G, Berger JS. J Thromb Thrombolysis 2011 May 12.

[Epub ahead of print]

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Emedinews Section

From eMedinewS Consensus Document Advises Treating Hypertension in those Age 80 or Older Major medical organizations last week released an expert consensus document to manage older patients with or at risk for hypertension. While 64% of men and 78% of women older than age 80 years have high blood pressure, only one in three men and one in four women have adequate control of their blood pressure. (http://content.onlinejacc.org/cgi/content/ full/j.jacc.2011.01.008) Results from the Hypertension in the Very Elderly Trial (HYVET) in 2008 showed clear benefits for using antihypertensive therapy in people age 80 years and older, including a 30% reduction in stroke, 23% reduction in cardiac death, 64% reduction in heart failure and 21% reduction in all-cause mortality.  Target blood pressure <140/90 mmHg in persons age 65-79 years and a maximum systolic blood pressure between 140 and 145 mmHg in persons 80 years and older (if tolerated)  Angiotensin-converting enzyme (ACE) inhibitors, b-blockers, angiotensin-receptor blockers (ARB), diuretics and calcium-channel blockers (CCB) are all effective in lowering blood pressure and reducing cardiovascular events among the elderly.

The choice between drugs should be based on efficacy, tolerability, comorbidities and cost.  Antihypertensive drugs should generally be started at the lowest dose, then increased in gradual increments as tolerated. If the first drug reaches its maximum dose, then a second should be added - a diuretic if it wasn’t the first drug. If the antihypertensive response is inadequate after reaching full doses of two classes of drugs, a third drug from another class should be added.  When blood pressure is >20/10 mmHg above goal, therapy should be initiated with two antihypertensive drugs.  One should check blood pressure measures in the standing position also.  Lifestyle changes may be all that are needed for milder hypertension (physical activity, restriction of salt, weight control, smoking cessation and avoidance of excessive alcohol intake-more than two drinks for men and one drink for women daily).

Asian Journal of Clinical Cardiology, Vol. 14, No. 1, May 2011

Recommendations on Initial Choice of Antihypertensive Drug Class (ABCD Rule) as per NICE Guidelines  In patients aged >55 years or in black (African or Afro-Caribbean descent) patients of any age, the first choice for initial treatment should be either a C (calcium-channel blocker) or a D (thiazide-type diuretic) drug.  In patients aged <55 years, the first choice for initial treatment should be an A drug (ACE inhibitor or an ARB if an ACE inhibitor is not tolerated).  If initial treatment was with a C or D drug and a second drug is needed, add an A drug (ACE inhibitor or an ARB if an ACE inhibitor is not tolerated).  If treatment was started with an A drug, add a C or D drug.  If treatment with three drugs is needed, the combination of A, C and D drugs should be used.  B drugs (b-blockers) should be reserved for patients for whom there is a separate indication additional to hypertension, and for combination therapy.

(Source: BMJ, April 16)

Prehypertension, Hypertension Link to Diabetes Stronger in Whites than in African Americans Prehypertension and hypertension are independently associated with increased risk for type 2 diabetes in people of White ethnicity, according to a study in the journal Diabetes Care.

Aldosterone Antagonist in Mild Heart Failure: New Evidence Aldosterone antagonist therapy reduces mortality in patients with moderate-to-severe heart failure. The EMPHASIS-HF trial demonstrated the efficacy of eplerenone in reducing mortality as well as risk of hospitalization in patients with systolic heart failure and mild symptoms.

One should use aldosterone antagonist therapy to treat heart failure in patients with NYHA functional 27

eMedinewS Section Class II HF and LVEF â&#x2030;¤30%, or NYHA functional Class III-IV HF and LVEF <35%, if they can be carefully monitored for serum potassium and renal function.

Cilostazol for Prevention of Ischemic Stroke The antiplatelet agent cilostazol is a phosphodiesterase 3 inhibitor that is used mainly to treat intermittent claudication in patients with peripheral artery disease.

Several controlled trials in Asia have found that cilostazol is effective for the secondary prevention of cerebral infarction.

Young children who spend too much time watching TV or playing computer games have narrower eye arteries than kids who are more physically active, according to a study published online in Arteriosclerosis, Thrombosis and Vascular Biology: Journal of the American Heart Association.

Young Indian Adults Developing more Risk Factors for Heart Disease

In the largest such trial (CSPS II), cilostazol (100 mg twice-daily) was not inferior to aspirin (81 mg daily) in preventing recurrent stroke (infarction or hemorrhage) at a mean follow-up of 29 months in 2,757 patients in Japan with a recent noncardioembolic cerebral infarction.

Increasingly, young adults residing in urban areas of India are developing hypertension, obesity and diabetes, which suggests that the country may soon experience an increase in heart disease rates, according to a study published in the Journal of the American College of Cardiology.

Newer Antiplatelet Quells Reactivity after PCI

Cath Lab has Role in Treatment of Heart Defects

Platelet reactivity after percutaneous coronary intervention (PCI) reached significantly lower levels with prasugrel compared with high-dose clopidogrel.

High on-treatment platelet reactivity occurred in five times as many patients treated with clopidogrel as with prasugrel. Carriers and noncarriers of the loss-of-function allele CYP2C19*2 had significantly lower platelet reactivity values when treated with prasugrel, Greek researchers reported in the April issue of the Journal of the American College of Cardiology: Cardiovascular Interventions.

Duration, Quality of Sleep may be Linked to CVD Risk People who sleep badly, and not for long, have a 65% increased risk of cardiovascular disease and an even greater risk of coronary heart disease, compared with normal sleepers, according to new research presented at the EuroPRevent 2011 meeting.

Medicare to Pay for MRIs in Patients with Pacemakers The Centers for Medicare and Medicaid Services (CMS) has determined that the evidence is strong enough to reimburse for magnetic-resonance imaging (MRI) exams in Medicare patients who have permanent pacemakers.

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Too much Television may Increase Future Cardiovascular Risk for Children

Cardiac catheterization, used predominantly as a diagnostic method, should be added to the toolbox for treating heart defects in children, according to the American Heart Association (AHA). The AHA offered a laundry list of 22 catheter-based treatment scenarios that should be considered for pediatric heart defects in a statement appearing online in Circulation: Journal of the American Heart Association.

Women may be More Likely than Men to Sustain Kidney Damage after Coronary Angiography Women are much more likely than men to sustain kidney damage after undergoing a common heart imaging test called coronary angiography, according to a study presented at a National Kidney Foundation meeting.

Vitamin D may Explain Racial BP Disparities Levels of serum 25-hydroxyvitamin D (25(OH)D) appear to explain at least part of the differences in blood pressure typically seen between blacks and whites, a cross-sectional study showed. After adjustment for numerous sociodemographic characteristics, health and healthcare-related factors, behavioral risk factors and biomarkers, blacks had an average systolic blood pressure that was 4 mmHg higher than Asian Journal of Clinical Cardiology, Vol. 14, No. 1, May 2011

eMedinewS Section whites, according to Kevin Fiscella, MD, MPH, of the University of Rochester in N.Y., and colleagues.

Further adjustment for serum 25(OH)D, however, cut that difference by about a quarter, to 2.9 mmHg, the researchers reported online in the Journal of General Internal Medicine.

argued, the findings do not support “the current recommendations of a generalized and indiscriminate reduction of salt intake at the population level.”

To explore the issue, they analyzed data from the National Health and Nutrition Examination Survey (NHANES) for 2001-2006. The analysis included 1,984 non-Hispanic blacks and 5,156 non-Hispanic whites 20 and older.

According to a study published in the journal Circulation, black patients may be experiencing worse outcomes after heart transplants than patients of other racial backgrounds.

Black participants were more likely to have low 25(OH)D levels; 61% of blacks and 11% of whites had levels of 2-15 ng/ml. At the upper end of the scale, 2.3% of blacks and 25.5% of whites had levels of 31-80 ng/ml. Average systolic blood pressure was 124.1 mmHg in blacks and 120.8 mmHg in whites.

After adjusting for age and sex, the average difference was 5.2 mmHg. That was reduced to 4 mmHg in a fully adjusted model that excluded 25(OH)D levels.

Adding serum 25(OH)D levels reduced the average difference in systolic blood pressure by 26% (7-46%).

In an analysis that excluded participants who were taking antihypertensives, that figure rose to 39%.

FDA Concerned about Potential Heart Risks among Some Patients who Add Fibrate to Statin FDA said it was concerned about trial data suggesting that adding a fibrate drug to a statin increased the risk of cardiac events in women and will convene an advisory committee meeting next month to review the findings.

Salt Study Discounts Link to Hypertension In a study that seems likely to re-energize the debate over dietary salt, European researchers found that the changes in the amount of sodium excreted in the urine were related to changes in systolic blood pressure. But they were not linked to diastolic pressure or the risk of developing hypertension, according to Jan Staessen, MD, PhD, of the University of Leuven in Leuven, Belgium, and colleagues. And levels of urinary sodium excretion were inversely related to the risk of dying of cardiovascular causes, Staessen and colleagues reported in the May 4 issue of the Journal of the American Medical Association. Taken together, Staessen and colleagues Asian Journal of Clinical Cardiology, Vol. 14, No. 1, May 2011

Black Patients may be Experiencing Worse Outcomes after Heart Transplants

Age may be Used as Effectively as Medical Tests to Predict Risk of Heart Disease A person’s age can be used as effectively as medical tests to predict the risk of heart disease or stroke, according to a new study published in the journal PLoS ONE. Rheumatoid Arthritis with Carotid Plaque at Risk of CAD Patients with rheumatoid arthritis (RA) found to have atherosclerosis as evidenced by the presence of carotid plaque are at high-risk for acute coronary events. Among RA patients with no carotid plaque and no history of coronary events, the incidence of new acute events was 1.1 (95% CI 0.6-1.7) per 100 person-years, according to Inmaculada del Rincón, MD, of the University of Texas at San Antonio, and colleagues.

Secondhand Tobacco Smoke associated with Higher Blood Pressure Exposure to secondhand tobacco smoke appears to be associated with higher blood pressure in boys, researchers found. Among boys ages 8-17, those who lived with a smoker had an average systolic blood pressure that was 1.6 mmHg higher than in those who did not live with a smoker (p < 0.001), according to Jill Baumgartner, PhD, a research fellow at the University of Minnesota’s Institute on the Environment in St. Paul.

Waist Size is a Better Predictor of Health, Especially in Heart Patients Research studies and health experts have long predicted that waist size is a better way to estimate heart disease and mortality risk than boy mass index (BMI). Now a new review article published in the Journal of the American College of Cardiology adds to the list of evidence in favor of measuring waist size. The article, 29

eMedinewS Section which reviews and analyzes results from several major studies, declares that waist size provides a far more accurate way to predict a heart patient’s chances of dying at an early age from a heart attack or other causes. Researchers from the Mayo Clinic analyzed data from just under 16,000 heart patients who had participated in previous studies. More than onethird of the patients died during the studies, which lasted from six months to eight years. The researchers found that heart patients with a high ratio of waist-tohip circumference or a large waist size (greater than 35 inches for women or greater than 40 inches for men) were 70% more likely to die during the study period than those with smaller waists. The combination of a large waist and a high BMI upped the risk of death even more, indicating that overall body weight does play a part, although it’s to a lesser extent. In order to keep your waistline down, aim to exercise or be active on most days of the week.

Research Suggests Landmark Heart Study has had Little Impact The number of people getting optimal medical therapy hasn’t changed significantly since 2007, when a landmark study found that the right combination of drugs prevents heart attacks and deaths as effectively as procedures to restore cardiac blood flow. Most heart disease patients fail to get the best mix of life-saving medications before they land in the hospital needing intervention for clogged arteries, and one-third aren’t given the proper drugs after, according to a study published in the Journal of the American Medical Association.

Medicolegal Update The Majority of Fatal Stab Wounds are on the Chest

Death due to sharp force violence is the most common cause of homicide in India including many other parts of Europe, as well as in Africa and Asia.

It also accounts for 30% of fatal and non-fatal family assaults in the USA. In the year 2010, I conducted medicolegal postmortems on 29 cases (from south Delhi) of death due to stab wounds. 

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Medifinance Update Goals of the Mutual Fund

Many funds are designed to invest in companies that meet specific investor goals, like growth, value, dividend or income to name a few. Only companies that meet certain criteria will be included in the fund.

For example, a growth fund looks for companies with significant, untapped growth potential, whereas a value fund will look for companies that are undervalued by the market as a way to increase investor returns. Both of these types of funds are designed for long-term capital appreciation.

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

A stab wound is produced as a result of penetration of long narrow instruments with blunt or pointed ends such as knife, dagger, nail, needle, spear, arrow, screwdriver, etc. into the depths of the body, penetrating the skin and the underlying tissues that is deeper than its length and width on skin.

It can be caused by driving the object into the body or from the body’s pressing or falling against the object. The object penetrates into the body due to its momentum.

The wound is called punctured wound when it enters a body cavity only one way. But, when the weapon enters the body on one side and comes out through the other side, it is called a perforating wound.

The wound of entry is larger and the wound of exit is smaller due to tapering of the blade in stab wound which is contrary to firearm missile entry and exit wounds.

The doctor conducting the postmortem examination must keep in mind that the shape and size of the wound suggests the width and type of weapon whether it is single edged or otherwise, the depth of the wound will indicate the length of weapon, the directions and dimensions of the wound indicate the relative position of the assailant and the victim, and the position, direction and number of wound may indicate manner of production, i.e., suicide, accident or homicide.

The doctor must preserve a broken fragment of weapon, if found, for the police. It may help to identify the weapon or connect the accused person with the crime.

—Dr Sudhir Gupta, Additional Professor, Forensic Medicine & Toxicology, AIIMS

Asian Journal of Clinical Cardiology, Vol. 14, No. 1, May 2011

lighter reading

Lighting Reading

An Inspirational Story Courtesy

A wonderful story comes from 19th century England.

According to the account, Queen Victoria was once at a diplomatic reception in London. The guest of honor was an African chieftain. All went well during the meal until, at the end, finger bowls were served. The guest of honor had never seen a British finger bowl, and no one had thought to brief him beforehand about its purpose. So he took the bowl in his two hands, lifted it to his mouth and drank its contents down!

For an instant there was breathless silence among the British privilege guests, and then they began to whisper to one another. All that stopped; however, when Queen Victoria silently took her finger bowl in her two hands, lifted it, and drank its contents! A moment later, 500 surprised British ladies and gentlemen simultaneously drank the contents of their own finger bowls.

It was the queen’s uncommon courtesy that guarded her guest from certain embarrassment.

Success Principles

“Knowledge, ability, experience are of little avail in reaching high success if courtesy be lacking, “Courtesy is the one passport that will be accepted without question in every land, in every office, in every home, in every heart in the world. For nothing commends itself so well as kindles; and courtesy is kindness.”

As the doctor approached the school boy to give him an injection, the boy yelled out loud with pain.

“What’s the matter?” said the doctor crossly. “I haven’t touched you yet.”

“You’re standing on my foot!” answered the boy.

make sure

During Medical Practice A patient with dilated cardiomyopathy developed sudden cardiac arrest.

Oh my God! Why was ICD (implantable cardioverter defibrillator) not given?

© IJCP ACADEMY

Quotes Humility makes great men twice honorable.

—Benjamin Franklin

If you wonder where your child left his roller skates, try walking around the house in the dark.

—Leopold Fechtner

Asian Journal of Clinical Cardiology, Vol. 14, No. 1, May 2011

Make sure that all patients with less than 35 years of age are considered for ICD therapy.

Dr KK Aggarwal

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

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

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

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

Covering letter -

- -

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

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

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

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

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-

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

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

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

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

A subtitle can be added if necessary.

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

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

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

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

- It should not contain abbreviations, footnotes or references.

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

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

- Ethical guidelines followed by the investigations should be described.

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

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

- Method of allocating the subjects into different groups.

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

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

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

-

Confidence intervals for the measurements should be provided wherever appropriate.

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

Asian Journal of Clinical Cardiology, Vol. 14, No. 1, May 2011

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 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.

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

- All photomicrographs should indicate the magnification of the print.

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

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

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

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Do not use clips/staples on photographs and artwork.

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

Please complete the following checklist and attach to the manuscript: 1. Classification (e.g. original article, review, selected summary, etc.)_______________________________ 2. Total number of pages ________________________ 3. Number of tables ____________________________ 4. Number of figures ___________________________ 5. Special requests _____________________________

Books

6. Suggestions for reviewers (name and postal address)

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

Indian 1.____________Foreign 1._ _______________

2.____________

2._ _______________

Articles in Books

3.____________

3._ _______________

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

4.____________

4._ _______________

Tables -

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

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

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

Asian Journal of Clinical Cardiology, Vol. 14, No. 1, May 2011

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 Website: www.ijcpgroup.com

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