AJCC-August 2011

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Volume 14, Number 4, August 2011, Pages 109-145

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

23 August 2011, Tuesday Dear Colleague, In what direction would Anna’s fast end?

Most Satyagraha should end up in a win–win situation. No party should seem to look that they have won. What can happen during a Satyagraha?  The fast is broken after demands are met.  The demands are not met but the fast is broken on the promises made.  The demands are not met but the fast is broken after a committee is constituted to look into the demands.  The fast is broken on the mediation by a religious or an important person in the society.  The fast is broken after the President of the country intervenes.  The fast is broken on medical grounds.  The fast is broken by the order of a court.  The fast is broken on the intervention of local administration or the local police.  The fast is broken on the request of the followers.  Some shift from complete fast to a relay fast.

Dr KK Aggarwal Group Editor-in-Chief Fitness Update Startling new truth about sugar Flying in the face of years of scientific belief, University of Illinois researchers have demonstrated that sugar doesn’t melt, it decomposes. “This discovery is important to food scientists and candy lovers because it will give them yummier caramel flavors and more tantalizing textures. It even gives the pharmaceutical industry a way to improve excipients, the proverbial spoonful of sugar that helps your medicine go down,” said Shelly J. Schmidt, a University of Illinois professor of food chemistry.

In a presentation to the Institute of Food Technologists about the importance of the new discovery, Schmidt told the food scientists they could use the new findings to manipulate sugars and improve their products’ flavor and consistency. The scientists determined that the melting point of sugar was heating–rate dependent.

“We saw different results depending on how quickly we heated the sucrose. That led us to believe that molecules were beginning to break down as part of a kinetic process,” she said. Schmidt said a true or thermodynamic melting material, which melts at a consistent, repeatable temperature, retains its chemical identity when transitioning from the solid to the liquid state. She and Lee used high–performance liquid chromatography to see if sucrose was sucrose both before and after “melting.” It wasn’t. “As soon as we detected melting, decomposition components of sucrose started showing up,” she said.

To distinguish “melting” caused by decomposition from thermodynamic melting, the researchers have coined a new name– “apparent melting.” Schmidt and her colleagues have shown that glucose and fructose are also apparent melting materials.

Spiritual Update The Spiritual significance of Indian Flag – Tiranga Lage Rahon Anna Bhai: The science behind what makes a wave?

As we have been witnessing over the last few days, there is an ‘Anna wave’ in the country. People of all ages, from all walks of life have come out on the streets in large numbers in support of Anna. Till about few months back, Anna was a relatively unknown name to most people. Since then, he has become the biggest name in the country. A new term has been coined. Just like Gandhigiri, Annagiri is the talk of the town.

Gastro Update Complimentary feeding practices between 6 and 24 months Supporting advice for caregivers and families  Make sure children’s immunization schedules are complete by 1 year of age.  Use ORT to rehydrate children during diarrhea.  Give liquid iron supplements daily (12.5 mg/day) to infants 6 months to one year of age if daily vitamin–mineral supplements or iron–fortified foods are not being given. If the prevalence of anemia is known to be very high (≥40 %), continue supplementation until 24 months of age. For low birthweight infants, start supplementation at 2 months.  Give semi–annual, high–dose vitamin A supplements after 6 months (100,000 IU for infants and 200,000 IU for children 12 months and older) in areas where vitamin A deficiency occurs.

References 1.

Brown KH, Dewey KG, Allen LH. Complementary Feeding of Young Children in Developing Countries: A Review Of Current Scientific Knowledge. WHO/UNICEF, 1998.

2.

Dewey KG. Guiding principles for complementary feeding of the breastfed child. PAHO/WHO, 2003.

3.

WHO. Complementary feeding: family foods for breastfed children. Geneva: World Health Organization, 2000.

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

Lab Update Total Iron binding capacity (TIBC)  Increased: Acute and chronic blood loss, iron deficiency anemia, hepatitis, oral contraceptives.  Decreased: Anemia of infection and chronic diseases, cirrhosis, nephrosis, hemochromatosis —Dr Arpan Gandhi and Dr Navin Dang

Quote of the Day Temper is a weapon that we hold by the blade. James Matthew Barrie —Dr Chandresh Jardosh

Online Submission

Volume 14, Number 4, August 2011

An IJCP Group Publication

Contents From the Desk of Group Editor-in-Chief

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

IJCP Editorial Board

Optimal Medical Therapy for Coronary Blockages with Reduced Left Ventricular Function 113 KK Aggarwal

REview Article

CAD: A True Pandemic and a Comprehensive Surveillance System is the Need of the Hour G Kannan, NN Rajendran, JSN Murthy, GB Tharani

Case Report

Continuous Change in the Direction of Atrial Flutter Waves on Either Side of Isoelectric Line Pseudo Electric Alternans by Left Pleural Effusion ECG Formulae

QT Means Systole Initial Management of Atrial Fibrillation

Dr KMK Masthan, Indian Journal of Multidisciplinary Dentistry

G Devpura

Dr Ajay Kumar, Gastroenterology Dr Hasmukh J Shroff, 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

127

Expert Opinion

Dr Vijay Viswanathan, The Asian Journal of Diabetology

Dr CR Anand Moses, Dr Sidhartha Das, Dr Ramachandran, Dr Samith A Shetty, Diabetology

125

Clinical Algorithm

Is there any Role of LAVI in LV Diastolic Failure?

Dr M Paul Anand, Dr SK Parashar, Cardiology

123

Monika Maheshwari, Tarachand Saini

Dr VP Sood, Asian Journal of Ear, Nose and Throat Dr Swati Y Bhave, Asian Journal of Paediatric Practice

121

SR Mittal

Dr Alka Kriplani, Asian Journal of Obs & Gynae Practice Dr Praveen Chandra, Asian Journal of Clinical Cardiology

114

128

Practice Guidelines

ACCF/AHA Release Guideline for Early Cardiovascular Risk Assessment

129

Research Review

From the Journals ...

131

Emedinews Section

From eMedinewS

134

Volume 14, Number 4, August 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 patient with heart failure had a total

lymphocyte count (TLC) of 1,000.

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.

Lymphocyte count does not matter

You have a bad prognosis

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: In heart failure, TLC is an important prognostic factor, inversely associated with predicted mortality. Patients with low lymphocyte counts (<1,600 median count) after eight years had significantly lower survival rates than those with lymphocyte counts >1,600 (58% vs 72%, p = 0.012).

Am J Cardiol 2011;107(9):1353-6.

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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Optimal Medical Therapy for Coronary Blockages with Reduced Left Ventricular Function

F

or most patients with systolic left heart pumping (LVEF) of 35% or less and coronary artery blockages amenable to bypass surgery, one should first initiate optimal medical therapy alone rather than medical therapy plus bypass surgery.

Earlier view had been that compared with medical therapy, surgical bypass of hibernating heart muscle improves both survival and left heart function. This view was based on the fact that upto 50% of patients with left heart pumping dysfunction due to coronary heart blockages have a significant amount of viable (hibernating) heart muscles.

The results of Surgical Treatment for Ischemic Heart Failure (STICH), a randomized trial have shown that compared with optimal medical therapy alone, optimal medical therapy plus bypass surgery resulted in no significant improvement in the primary outcome of all-cause mortality at a median follow-up of 56 months.

The current recommendation is that one should initiate optimal medical therapy alone rather than optimal medical therapy plus bypass surgery because bypass surgery is associated with significant morbidity. Bypass surgery, however, is preferred in patients with ongoing anginal symptoms despite optimal medical therapy.

Source: Velazquez EJ, Lee KL, Deja MA, et al. Coronary-artery bypass surgery in patients with left ventricular dysfunction.

N Engl J Med 2011;364(17):1607-16.

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 and 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. 4, August 2011

113

Review article

CAD: A True Pandemic and a Comprehensive Surveillance System is the Need of the Hour G Kannan*, NN Rajendran**, JSN Murthy†, GB Tharani‡

Abstract Coronary artery disease (CAD) occurs when the arteries that supply blood to the heart muscle harden and narrow. According to the Global Burden of Disease Study, the developing countries contributed 3.5 million of the 6.2 million global deaths from CAD in 1990. The prevalence of CAD in India has more than doubled in the past two decades. India topped the world with 1,531,534 cardiovascular disease-related deaths in 2002, and based on WHO report, 2009, currently occupies the first place in cause of death. A comprehensive surveillance system of risk factors and CAD will be an invaluable public health research tool for monitoring population health status, guiding resource allocation and policy, identifying and prioritizing interventions for subpopulations at particular risk that would help to bring down the true pandemic which is on the climb.

Key words: Coronary artery disease, pandemic, surveillance system, health status

C

oronary artery disease (CAD) occurs when the arteries that supply blood to the heart muscle harden and narrow (Bhati K, 2011; Heart Diseases, 2011). The result is the loss of oxygen and nutrients to myocardial tissue because of diminished coronary blood flow (Springhouse, 2005). This reduction in blood flow can lead to acute coronary syndrome (angina or myocardial infarction). CAD is on the climb and has become a true pandemic that respects no borders.

Prevalence of CAD Global Scenario

The term ‘prevalence’ of CAD usually refers to the estimated population of people who are managing CAD at any given time (American Heart Association, 2004). The proportion of deaths due to CAD is projected to rise from 59% in 2002 to 69% in 2030 (Mathers and Loncar, 2006). The WHO (2006) *Assistant Professor Dept. of Pharmacy Practice, Faculty of Pharmacy Sri Ramachandra University, Porur, Chennai **Professor Swami Vivekananda College of Pharmacy, Erode, Chennai † Professor and Head Dept. of Cardiology, Sri Ramachandra University, Porur, Chennai ‡ Professor and Head Saveetha Medical College, Thandalam Address for correspondence Dr G Kannan Assistant Professor, Dept. of Pharmacy Practice, Faculty of Pharmacy Sri Ramachandra University, Porur, Chennai - 600 116 E-mail: kannagg2@yahoo.ca

114

estimates that at least 20 million people survive CADrelated heart attacks and strokes every year around the world; many require continuing costly clinical care.

By 2030, almost 23.6 million people will die from CADs, mainly from heart disease and stroke. These are projected to remain the single leading causes of death (WHO-Cardiovascular Disease: Prevention and Control, 2006). A recent evaluation of WHO in the cause of death in 2009, CAD and stroke were placed as first (7,185,353 deaths) and second (5,704,843 deaths) in rank among total deaths (6,830,586,985) of all kind of diseases. Moreover, the rate of death is rising more in the under-developed countries than the developed countries, because of their lifestyle and socioeconomic factors (WHO, 2009).

According to the Global Burden of Disease Study, the developing countries contributed 3.5 million of the 6.2 million global deaths from CAD in 1990. The projections estimate that these countries will account for 7.8 million of the 11.1 million deaths due to CAD in 2020 (Murray et al, 1996). Disability-adjusted life years (DALYs) lost can be thought of as ‘healthy years of life lost’. They indicate the total burden of a disease, as opposed to simply the resulting deaths.

Murray et al (1996) calculate that in India and China, a spectacular rise in the number of DALYs is expected in the coming years - from a figure of <25 million DALYs in each country in 1990, to 30 million and 35 million in India and China, respectively, in 2020.

Asian Journal of Clinical Cardiology, Vol. 14, No. 4, August 2011

Review Article CAD is decreasing in many developed countries, but is increasing in developing and transitional countries, partly as a result of increasing longevity, urbanization and lifestyle changes. CAD is responsible for 10% of DALYs lost in low and middle-income countries and 18% in high-income countries (Global Burden of Coronary Heart Disease, 2002).

CAD is the most common cause of death (and premature death) in the UK. One in 5 men and one in 7 women die from CAD. There are 94,000 deaths from CAD in the UK each year (Greenlund et al, 2006). With regard to incidence, data from the Atherosclerosis Risk In Communities (ARIC) and Cardiovascular Health Study indicate that annually, 7,85,000 Americans have a new coronary attack and 4,70,000 have a recurrent attack; in addition, approximately 1,95,000 silent myocardial infarctions occur each year. This assumes that 21% of the 9,35,000 first and recurrent myocardial infarctions are silent (Thom et al, 2001; Boland et al, 2002). Tables 1 and 2 depict the CAD prevalence in urban and rural population of developed countries and developing countries.

Indian Scenario

The prevalence of CAD in India has more than doubled in the past two decades. This has occurred

both in the rural and urban populations, although it is higher in urban than in rural population, with a greater prevalence in affluent groups (Chadha et al, 1990; Enas et al, 1992; Singh et al, 1997). Enas et al (1996) and Enas et al (1999). It is estimated that 9.2 million productive years of life were lost in India in 2000, with an expected increase to 17.9 million years in 2030. Table 3 depicts the CAD prevalence with respect to age group, sample size of the study population in different parts of India.

Salient features of the CAD epidemic in India:  Incidence of CAD in young Indians is about 12-16%, which is higher than any other ethnic group (Mammi et al, 1991).  Age-standardized estimates for DALYs lost due to CAD per 1,000 population in India are three times higher than in developed countries (Negus et al, 1994).  About 5-10% of heart attacks occur in Indian men and women younger than 40 years (Mackay and Mensah, 2004).  India topped the world with 1,531,534 cardiovascular disease-related deaths in 2002, and occupied first place in cause of death in current moment based on WHO report, 2009 (Yusuf et al, 2004; WHO, 2009).

Table 1. CAD in Urban and Rural Population of Developed Countries Author

Year

Age group

Place

Sample size

CAD prevalence (%)

Calvet et al.

2010

45-75

France

300

50.0

Arzamendi et al.

2010

20-65

Developed countries

1,260

49.0

Iwasaki et al.

2011

30-70

Japan

135

9.20

Icaza et al.

2009

35-74

USA

General population

6.95

Kivimaki et al.

2011a

30-70

UK

5,533

0.70

Jain et al.

2011

35-75

London (UK)

2,369

22.0

Kivimaki et al.

2011b

30-70

London (UK)

7,095

0.027

Ong et al.

2011

30-70

UK

698

5.00

Stansby et al.

2011

68

UK

473

30.0

Ebrahim et al.

2011

20-70

UK

1,63,471

4.35

Secrest et al.

2011

24-32

USA

317

2.50

Oizumi et al.

2008

30-70

Japan

2,938

3.19

Idris et al.

2008

30-70

UK

1,087

50.0

Konishi et al.

1990

40-59

Japan

8,835

88.0

Urban population

Rural population

Asian Journal of Clinical Cardiology, Vol. 14, No. 4, August 2011

115

Review Article Table 2. CAD in Urban and Rural Population of Developing Countries (Excluding India) Author

Year

Age group

Place

Sample size

CAD prevalence (%)

Grau et al.

2010

30-70

France + Spain

420 + 562

0.98

Chin et al.

2009

30-70

Malaysia

2,030

10.35

Hatmi et al.

2007

20-45

Iran

3,000

25.75

Hariharan et al.

2010

30-70

Trinidad + Tobago

1,082

1.20

Sadeghi et al.

2006

35-70

Iran

6,498

29.90

Kalra et al.

2011

35-86

Nepal

142

38.00

Icaza et al.

2009

35-74

Chile

General population

1.80

Icaza et al.

2009

35-74

China

General population

0.85

Icaza et al.

2009

35-74

Spain

General population

3.70

Ozdemir et al.

2010

30-70

Turkey

24

33.33

Vaidya et al.

2009

35 - <

Eastern Nepal

-

5.70

Onat et al.

2010

45-74

Turkey

1,655

11.50

Pitsavos et al.

2008

30-70

Greek

2,172

1.36

PavloviÄ&#x2021; et al.

2004

37-56

Croatia

3,544

3.70

Urban population

Rural population

Table 3. Prevalence of CAD in Population of India Author

Year

Age group

Place

Sample size

CAD prevalence (%)

Geetha et al.

2011

30-70

Chennai (Tamil Nadu)

2,350

2.93

Mohan et al.

2010a

30-70

Chennai (Tamil Nadu)

-

5.40

Mohan et al.

2010b

30-70

Chennai (Tamil Nadu)

-

11.0

Kumaran et al.

2002

30-70

Mysore

435

21.75

Mohan et al.

2001

20-70

Chennai (Tamil Nadu)

1,262

11.0

Stein et al.

1996

Mysore

517

10.0

Begom et al.

1995

25-65

South India (Urban)

506

13.9

Singh et al.

2011

<15

Chandigarh

196

0.000045

Kumar et al.

2006

>35

North India (Urban + Rural)

7,169

3.96

Ahmad et al.

2005

25-70

Delhi (Urban)

14,000

0.2-0.9

Ahmad et al.

2005

25-70

Delhi (Rural)

14,000

0.1-0.4

Singh et al.

1997

25-64

Moradabad

3575

1.5-3.0

Chadha et al.

1997

25-64

Delhi (Urban + Rural)

13,723

96.7 (Urban) + 27.1 (Rural)

Begom et al.

1995

25-65

North India (Urban)

506

61.6

Lanjewar et al.

2005

25-70

Mumbai

3,871

4.20

Rastogi et al.

2004

30-70

Western India

350

1.88

Pinto et al.

2004

35-64

Goa

371

13.2

Hazarika et al.

2002

30-70

Assam

1,015

61.0

Bhattacharyya

2003

30-70

Kolkata

28 + 62

39 + 60

South India

North India

West India

East India

116

Asian Journal of Clinical Cardiology, Vol. 14, No. 4, August 2011

Review Article ď Ź

ď Ź

Median age of first heart attack in Indians is 53 years (WHO, 2009).

1,55,88,000 DALYs (WHO, 2009).

Need of the Hour Prospective studies on the relative role and importance of traditional and newer risk factors are urgently needed in Indians within the subcontinent as much of the knowledge of risk factors for CAD has been acquired from studies conducted in the Western population.

It is widely believed that the association of these risk factors with CAD in different subpopulations needs to be ascertained, and there is speculation that differences might range from the frequency of presence of classical risk factors to their total absence or irrelevance in these populations. A cost-effective preventive strategy will need to focus on reducing risk factors both in the individual and in the population at large.

Effective screening, evaluation and management strategies for CAD are well-established in high-income countries, but these strategies have not been fully implemented in India which was noted by Mohan et al (2001). A key factor that hampers the development of such preventive strategies in developing countries such as India is the meager amount (8%) of published literature on CAD research available from these countries (Mackay and Mensah, 2004). Of particular concern to India is not only the high burden of CAD, but also the effects of these diseases on the productive workforce aged 35-65 years. Heart diseases are rising in Asian Indians 5-10 years earlier than in other populations around the world. The mean age for first presentation of acute myocardial infarction in Indians is 53 years. CAD that manifests at a younger age can have devastating consequences for an individual, the family and society. Prevention of these deaths in young people is a nationâ&#x20AC;&#x2122;s moral responsibility (Sharma and Ganguly, 2005). A strategy involving prevention of CADs long before their onset will be more costeffective than providing interventions at a stage when the disease is well-established.

Therefore, it is imperative to undertake large population-based, prospective studies in developing countries such as India to identify CAD risk factors, both conventional and novel. Careful scrutiny of available scientific evidence for modifiable CAD risk Asian Journal of Clinical Cardiology, Vol. 14, No. 4, August 2011

factors (elevated serum total and LDL-C, low HDL-C, smoking, diabetes, hypertension, low level of physical activity and central obesity) in association with genetically predisposing factors like Lp(a) in Indian population may be helpful in formulating a more immediate CAD prevention strategy.

Given the explosion of diabetes and CAD in India and in view of the differences in race, culture, way of life, diet, stress and strain and the myriad other factors, increased emphasis on lifestyle modification, including diet, exercise, weight reduction and whenever relevant, stress reduction, is urgently needed. A comprehensive surveillance system of risk factors and CAD will be an invaluable public health research tool for monitoring population health status, guiding resource allocation and policy, identifying and prioritizing interventions for subpopulations at particular risk, identifying disparities in outcomes and planning and evaluating health programs. Carefully planned prevention programs with intervention strategies by catching the vulnerable individuals at an early age could also be taken up in different parts of the country to prevent the twin epidemic of diabetes and CAD; as both have common causative factors, and prevention strategies could also be combined judiciously to prevent both disorders, as this would make it more cost-effective.

Resources should be directed towards applying the existing knowledge base to tackle the CAD epidemic in policy, capacity building and research arenas. Control of the CAD epidemic in the Indian subcontinent is tenable in the foreseeable future, provided that policy makers, health professionals and the lay public in the Indian subcontinent acknowledge its potential impact and promptly act to address to make a major step towards CAD free society.

Suggested Reading 1. Ahmad N, Bhopal R. Is coronary heart disease rising in India? A systematic review based on ECG defined coronary heart disease. Heart 2005;91(6):719-25.

2. American Heart Association, 2004. Prevalence of Coronary heart disease. http://www.wrongdiagnosis. com/c/coronary_heart_disease/prevalence.htm.

3. Arzamendi D, Benito B, Tizon-Marcos H, Flores J, Tanguay JF, Ly H, et al. Increase in sudden death from coronary artery disease in young adults. Am Heart J 2011;161(3):574-80.

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Review Article 4. Bhattacharyya M. Coronary heart disease prevention in Kolkata, India. J R Soc Promot Health 2003;123(4): 222-8.

5. Begom R, Singh RB. Prevalence of coronary artery disease and its risk factors in the urban population of South and North India. Acta Cardiol 1995;50(3):227-40.

6. Bhati K. Causes and herbal remedies for coronary artery disease or heart problem. Available at: http://www. sooperarticles.com/health-fitness-articles/heart-diseasearticles/causes-herbal-remedies-coronary-artery-diseaseheart-problem-368593.html, Published on 28th Mar 2011.

7. Boland LL, Folsom AR, Sorlie PD, Taylor HA, Rosamond WD, Chambless LE, et al. Occurrence of unrecognized myocardial infarction in subjects aged 45 to 65 years (the ARIC study). Am J Cardiol 2002;90(9):927-31.

8. Calvet D, Touzé E, Varenne O, Sablayrolles JL, Weber S, Mas JL. Prevalence of asymptomatic coronary artery disease in ischemic stroke patients: the PRECORIS study. Circulation 2010;121(14):1623-9.

18. Hariharan S, Chen D, Vialva M, Exeter H, Billingy I, Bobb KA, et al. Outcome evaluation of coronary artery bypass grafting surgery applying the EuroSCORE in a Caribbean developing country. Heart Surg Forum 2010;13(5):E287-91.

19. Hatmi ZN, Tahvildari S, Gafarzadeh Motlag A, Sabouri Kashani A. Prevalence of coronary artery disease risk factors in Iran: a population based survey. BMC Cardiovasc Disord 2007;7:32.

20. Hazarika NC, Biswas D, Narain K, Kalita HC, Mahanta J. Hypertension and its risk factors in tea garden workers of Assam. Natl Med J India 2002;15(2):63-8.

21. Heart diseases (2011). The Heart and Stroke Foundation.

Available at: http://www.heartandstroke.com/site/c.ikI QLcMWJtE/b.3483991/k.34A8/Statistics.htm.

9. Chadha SL, Radhakrishnan S, Ramachandran K, Kaul U, Gopinath N. Epidemiological study of coronary heart disease in urban population of Delhi. Indian J Med Res 1990;92:424-30.

22. Icaza G, Núñez L, Marrugat J, Mujica V, Escobar MC, Jiménez AL, et al. Estimation of coronary heart disease risk in Chilean subjects based on adapted Framingham equations. Rev Med Chill 2009;137(10):1273-82.

10. Chin CY, Pengal S. Cardiovascular disease risk in a semirural community in Malaysia. Asia Pac J Public Health 2009;21(4):410-20.

23. Idris I, Deepa R, Fernando DJ, Mohan V. Relation between age and coronary heart disease (CHD) risk in Asian Indian patients with diabetes: a cross-sectional and prospective cohort study. Diabetes Res Clin Pract 2008;81(2):243-9.

11. Ebrahim S, Taylor F, Ward K, Beswick A, Burke M, Davey Smith G. Multiple risk factor interventions for primary prevention of coronary heart disease. Cochrane Database Syst Rev 2011;(1):CD001561.

12. Enas EA, Garg A, Davidson MA, Nair VM, Huet BA, Yusuf S. Coronary heart disease and its risk factors in first-generation immigrant Asian Indians to the United States of America. Indian Heart J 1996;48(4):343-53.

13. Enas EA, Salim Yusuf. Third Meeting of the International Working Group on Coronary Artery Disease in South Asians. 29 March 1998, Atlanta, USA. Indian Heart J 1999;51(1):99-103.

14. Enas EA, Yusuf S, Mehta JL. Prevalence of coronary artery disease in Asian Indians. Am J Cardiol 1992;70(9): 945-9.

15. Geetha L, Deepa M, Anjana RM, Mohan V. Prevalence and clinical profile of metabolic obesity and phenotypic obesity in Asian Indians. J Diabetes Sci Technol 2011; 5(2):439-46.

16. Grau M, Bongard V, Fito M, Ruidavets JB, Sala J, Taraszkiewicz D, et al; REGICOR, GENES Investigators.

Prevalence of cardiovascular risk factors in men with stable coronary heart disease in France and Spain Arch Cardiovasc Dis 2010;103(2):80-9.

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17. Greenlund KJ, Giles WH, Keenan NL, et al. Heart disease and stroke mortality in the 20th century. In: Silent Victories: The History and Practice of Public Health in 20th Century America. Ward J, Warren C (Eds.), Oxford University Press: Oxford, England; 2006.

24. Iwasaki M, Kuroda S, Nakayama N, Hokari M, Yasuda H, Saito H, et al. Clinical characteristics and outcomes in carotid endarterectomy for internal carotid artery stenosis in a Japanese population: 10-year microsurgical experience. J Stroke Cerebrovasc Dis 2011;20(1):55-61.

25. Jain P, Kooner JS, Raval U, Lahiri A. Prevalence of coronary artery calcium scores and silent myocardial ischaemia was similar in Indian Asians and European whites in a cross-sectional study of asymptomatic subjects from a UK population (LOLIPOP-IPC). J Nucl Cardiol 2011;18(3):435-42.

26. Kivimäki M, Batty GD, Hamer M, Ferrie JE, Vahtera‑J, Virtanen M, et al. Using additional information on working hours to predict coronary heart disease: a cohort study. Ann Intern Med 2011b;154(7):457-63.

27. Kivimäki M, Nyberg ST, Batty GD, Shipley MJ, Ferrie JE, Virtanen M, et al. Does adding information on job strain improve risk prediction for coronary heart disease beyond the standard Framingham risk score? The Whitehall II study. Int J Epidemiol 2011a May 9. (Epub ahead of print) Asian Journal of Clinical Cardiology, Vol. 14, No. 4, August 2011

Review Article 28. Konishi M, Iso H, Iida M, Naito Y, Sato S, Komachi Y, et al. Trends for coronary heart disease and its risk factors in Japan: epidemiologic and pathologic studies. Jpn Circ J 1990;54(4):428-35.

29. Kumar R, Singh MC, Singh MC, Ahlawat SK, Thakur JS, Srivastava A, et al. Urbanization and coronary heart disease: a study of urban-rural differences in northern India. Indian Heart J 2006;58(2):126-30.

30. Kumaran K, Fall CH, Martyn CN, Vijayakumar M, Stein CE, Shier R. Left ventricular mass and arterial compliance: relation to coronary heart disease and its risk factors in South Indian adults. Int J Cardiol 2002;83(1):1-9.

31. Lanjewar C, Jolly S, Mehta SR. Effects of aspiration thrombectomy on mortality in patients with acute myocardial infarction undergoing primary percutaneous coronary intervention: a meta-analysis of the randomized trials. Indian Heart J 2009;61(4):335-40.

32. Mackay J, Mensah G. The atlas of heart disease and stroke. World Health Organization, Centers for Disease Control and Prevention; 2004.

33. Mammi MV, Pavithran K, Abu Rahiman P, Pisharody R, Sugathan K. Acute myocardial infarction in north Kerala. A 20-year hospital based study. Indian Heart J 1991;43(2):93-6.

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

35. Mohan V, Deepa R, Rani SS, Premalatha G; Chennai Urban Population Study (CUPS No. 5). Prevalence of coronary artery disease and its relationship to lipids in a selected population in South India: The Chennai Urban Population Study (CUPS No. 5). J Am Coll Cardiol 2001;38(3):682-7.

36. Mohan V, Vassy JL, Pradeepa R, Deepa M, Subashini S. The Indian type 2 diabetes risk score also helps identify those at risk of macrovascular disease and neuropathy (CURES-77). J Assoc Physicians India. 2010a;58: 430-3.

37. Mohan V, Venkatraman JV, Pradeepa R. Epidemiology of cardiovascular disease in type 2 diabetes: the Indian scenario. J Diabetes Sci Technol 2010;4(1): 158-70.

for stroke in a Japanese sample - the Funagata study.

Metabolism 2008;57(3):333-8.

40. Onat A, Uğur M, Ciçek G, Ayhan E, Doğan Y, Kaya H, et al. The Turkish Adult Risk Factor survey 2009: similar cardiovascular mortality in rural and urban areas. Turk Kardiyol Dern Ars 2010;38(3):159-63.

41. Ong P, Athanasiadis A, Borgulya G, Voehringer M, Sechtem U. 3-year follow-up of patients with coronary artery spasm as cause of acute coronary syndrome: the CASPAR (coronary artery spasm in patients with acute coronary syndrome) study follow-up. J Am Coll Cardiol 2011;57(2):147-52.

42. Ozdemir H, Ciftçi E, Tapisiz A, Ince E, Tutar E, Atalay S, Dogru U. Clinical and epidemiological characteristics of children with Kawasaki disease in Turkey. J Trop Pediatr 2010;56(4):260-2.

43. Pavlović M, Corović N, Gomzi M, Simić D, Jazbec A, Tiljak MK. Smoking habits, signs of chronic diseases and survival in inland and coastal regions of Croatia: a follow-up study. Coll Antropol 2004;28(2):689-700.

44. Pinto RJ, Bhagwat AR, Loya YS, Sharma S. Coronary artery disease in premenopausal Indian women: risk factors and angiographic profile. Indian Heart J 1992;44(2):99-101.

45. Pitsavos C, Kavouras SA, Panagiotakos DB, Arapi S, Anastasiou CA, Zombolos S, et al; GREECS Study Investigators. Physical activity status and acute coronary syndromes survival The GREECS (Greek Study of Acute Coronary Syndromes) study. J Am Coll Cardiol 2008; 27;51(21):2034-9.

46. Rastogi T, Vaz M, Spiegelman D, Reddy KS, Bharathi AV, Stampfer MJ, et al. Physical activity and risk of coronary heart disease in India. Int J Epidemiol 2004;33(4):759‑67.

47. Secrest AM, Costacou T, Gutelius B, Miller RG, Songer TJ, Orchard TJ. Associations between socioeconomic status and major complications in type 1 diabetes: the pittsburgh epidemiology of diabetes complication (EDC) Study. Ann Epidemiol 2011;21(5):374-81.

48. Sharma M, Ganguly NK. Premature coronary artery disease in Indians and its associated risk factors. Vasc Health Risk Manag 2005;1(3):217-25.

38. Murray CJL, Lopez AD. The Global Burden of Disease: A Comprehensive Assessment of Mortality and Disability from Disease, Injuries and Risk Factors in 1990 and Projected to 2020. Harvard University Press: Boston, Ma; 1996.

49. Singh RB, Rastogi SS, Rao PV, Das S, Madhu SV, Das AK, et al. Diet and lifestyle guidelines and desirable levels of risk factors for the prevention of diabetes and its vascular complications in Indians: a scientific statement of The International College of Nutrition.

Indian Consensus Group for the Prevention of Diabetes.

J Cardiovasc Risk 1997;4(3):201-8.

39. Oizumi T, Daimon M, Jimbu Y, Wada K, Kameda W, Susa S, et al. Impaired glucose tolerance is a risk factor

50. Singh S, Aulakh R, Bhalla AK, Suri D, Manojkumar‑R, Narula N, et al. Is Kawasaki disease incidence

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Review Article rising in Chandigarh, North India? Arch Dis Child 2011;96(2):137-40.

51. Springhouse (2005). Professional Guide to Diseases 8th Edition, Lippincott Williams and Wilkins; 2005.

52. Stansby G, Mister R, Fowkes G, Roughton M, Nugara F, Brittenden J, et al; Prospective Registry and Evaluation of Peripheral Arterial Risks, Events and Distribution Investigators. High risk of peripheral arterial disease in the United Kingdom: 2-year results of a prospective registry. Angiology 2011;62(2):111-8.

53. Stein CE, Fall CH, Kumaran K, Osmond C, Cox V, Barker DJ. Fetal growth and coronary heart disease in South India. Lancet 1996;348:1269-73.

54. Thom TJ, Kannel WB, Silbershatz H, D’Agostino RB. Cardiovascular disease in the United States and preventive approaches. In: Hurst’s The Heart, Arteries and Veins.

10th edition, Fuster V, Alexander RW, O’Rourke RA, (Eds.), McGraw-Hill: New York, NY 2001:3-7.

55. Vaidya A, Pokharel PK, Nagesh S, Karki P, Kumar S, Majhi S. Prevalence of coronary heart disease in the urban adult males of eastern Nepal: a populationbased analytical cross-sectional study. Indian Heart J 2009;61(4):341-7.

56. WHO. Cardiovascular Disease: Prevention and Control.

2006,‑http://www.who.int/mediacentre/factsheets/ fs317/en/index.html.

57. World Health Organisation. Disease and injury regional estimates for 2004. Geneva, Switzerland. Available at: http://www.who.int/healthinfo/global_burden_disease/ estimates_regional/en/index.html. Accessed 5 September 2009.

58. Yusuf S, Hawken S, Ôunpuu S, Dans T, Avezum A, Lanas F, et al; INTERHEART Study Investigators.

Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study. Lancet 2004;364:937-52.

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Case report

Continuous Change in the Direction of Atrial Flutter Waves on Either Side of Isoelectric/Line SR Mittal

Abstract A case of atrial flutter with continuous change in the direction of atrial flutter waves on either side of isoelectric line is reported.

Such a change in direction of atrial flutter waves resembles ECG appearance of QRS configuration in ventricular torsades de pointes. This finding may suggest vulnerability to atrial fibrillation.

Key words: Atrial flutter, electrocardiogram, torsades de pointes

Case Report A known case of hypertension and left ventricular failure presented with deterioration of breathlessness.

Electrocardiogram revealed atrial flutter with changing atrioventricular conduction, left ventricular hypertrophy and ST segment depression in leads I, II, aVL and V3-V6 (Fig. 1).

Figure 2. Continuous strip of lead V1 showing continuous change in the direction of atrial flutter waves on either side of isoelectric line.

Figure 1. Electrocardiogram showing atrial flutter with left ventricular hypertrophy and ST segment depression.

In lead V1, atrial flutter waves showed a continuous change in the direction from one side to the other side of isoelectric line (Fig. 2).

Discussion

Ex Sr Professor and Head Dept. of Cardiology Principal, JLN Medical College, Ajmer Address for correspondence Dr SR Mittal

XI/101, Brahampuri Ajmer, Rajasthan - 305 001 E-mail: sarweshwar_mittal@rediffmail.com

Asian Journal of Clinical Cardiology, Vol. 14, No. 4, August 2011

The term â&#x20AC;&#x2DC;Torsades de pointesâ&#x20AC;&#x2122; is used for fast ventricular tachycardia with changing amplitude and duration of QRS on either side of isoelectric line in the setting of prolonged QT interval.1,2 In our patient, regular change in the direction and amplitude of atrial 121

Case Report flutter waves on either side of isoelectric line is similar to change in QRS configuration during ‘Torsades de pointes’. This finding suggests regular change in direction of conduction in the re-entry circuit in the horizontal plane. It could also be due to more than one re-entry circuit with gradual shift from one to another. Such patients could be more prone to have atrial fibrillation.

References 1. Rho RW, Page RL. Ventricular arrhythmias. In: Hurst’s The Heart. 12th edition, Fuster V, Walsh RA, Harrington RA (Eds.), McGraw Hill, New York 2011:1006-24.

2. Olgin JE, Zipes DP. Specific arrhythmias: diagnosis and treatment. In: Braunwald’s Heart Disease. 8th edition, Libby P, Bonow RO, Mann DL, Zipes DP (Eds.), Saunders, Philadelphia 2008:863-922.

Carotid Artery Blockages Should I screen each patient for presence of carotid neck artery blockages?

The guideline says no. The potential harms include risks associated with the screening procedure itself like false positive findings leading to anxiety and the potential for unnecessary surgical procedures. Carotid angiography is associated with risk of neurological complications including stroke, with rates ranging from 0.1 to 1%.

What are the screening methods available? 

Carotid ultrasound followed by catheter angiography



Carotid ultrasound followed by MRA



Ultrasound alone

How reliable is Doppler carotid study for detecting blockages?

The reliability is variable and operator-dependent.

How risky is carotid stenting or surgery?

Both endarterectomy and carotid stenting are associated with an increased 30-day risk of stroke and death. These are in the range of 2.3-3.7% for endarterectomy.

How common is carotid artery blockage in general population?

The prevalence of carotid stenosis in general population is <1%. Screening with resultant surgical procedures causes more strokes than it can prevent. For severe (≥70%) carotid stenosis, the prevalence increases with age from approximately 0 to 3%.

At what prevalence is screening beneficial?

Only at prevalence rates of over 20% significant benefits are seen, with at best about 100 strokes prevented for every 10,000 screened. Clinical features cannot identify asymptomatic individuals likely to have carotid stenosis.

The annual risk of stroke in patients with asymptomatic carotid artery stenosis is relatively low.

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When to screen for carotid blockages?

Carotid duplex ultrasonography is not recommended for routine screening of asymptomatic patients who have no clinical manifestations of or risk factors for atherosclerosis. However, one should screen asymptomatic individuals who have: Carotid bruit  Peripheral arterial disease   Coronary disease  Aortic aneurysm  Two or more risk factors for atherosclerotic disease.

What is symptomatic carotid artery blockage?

Patients who have had a stroke or transient ischemic attack (mini paralysis) due to carotid stenosis are considered symptomatic and often benefit from carotid revascularization. Symptoms mean transient or permanent focal neurologic symptoms related to the affected artery (same side loss of vision, opposite side weakness or numbness of an extremity or the face, difficulty in speech or loss of speech). Patients with nonspecific neurologic symptoms (dizziness or syncope/near syncope) are not considered in the definition of symptomatic carotid stenosis.

What are the medical interventions for carotid blockages?

The interventions are management of hypertension, smoking cessation, use of statin drugs and low-dose aspirin.

When should one decide for carotid endarterectomy or removal of blockages with catheter?

It is indicated for selected medically stable patients with asymptomatic carotid stenosis of 60-99% who have a life expectancy of at least five years, provided the perioperative risk of stroke and death is <3%. However, long-term outcomes for patients with carotid blockages managed by intensive medical therapy may be similar to surgical management.

Asian Journal of Clinical Cardiology, Vol. 14, No. 4, August 2011

case report

Pseudo Electric Alternans by Left Pleural Effusion Monika Maheshwari*, Tarachand Saini**

Abstract We report herein a case of isolated left pleural effusion producing electric alternans in electrocardiogram without any pericardial fluid collection. Increased intracardiac pressure secondary to rapid collection of pleural fluid is the possible hypothesis for this pseudo electric alternans pattern in ECG. Thoracocentesis reverted the characteristic electrocardiographic features.

Key words: Pleural effusion, electric alternans, cardiac tamponade

E

lectric alternans in electrocardiogram (ECG) is a diagnostic hallmark of cardiac tamponade. We describe herein an interesting case of left side pleural effusion producing pseudo electric alternans pattern in ECG without any evidence of cardiac tamponade either clinically or by echocardiography.

Case Report A 32-year-old male presented in medical OPD with complaints of fever and breathlessness since past two days. On examination, his pulse was 120/min, blood pressure - 90/68 mmHg, respiratory rate - 20/min and temperature â&#x20AC;&#x201C;100.4°F. There was no cyanosis, clubbing, icterus, pallor or lymphadenopathy. Jugular venous pressure was normal. On auscultation, there was reduced air entry in left infrascapular region. Heart sounds were normal. Pulsus paradoxus was absent.

Routine laboratory investigations including renal, hepatic functions and blood biochemistry were within normal limits. X-ray chest (PA view) showed left side moderate pleural effusion (Fig. 1). ECG revealed sinus tachycardia with low voltage QRS complexes, showing electric alternans (Fig. 2). On echocardiogram, there was minimal pericardial effusion not safe for pericardiocentesis. Pleural fluid when aspirated under ultrasonographic guidance revealed 300 ml of straw *Assistant Professor

**Resident Dept. of Medicine, JLN Medical College, Ajmer Address for correspondence Dr Monika Maheshwari Naveen Niwas, 434/10 Bapu Nagar, Ajmer E-mail: opm11@rediffmail.com

Asian Journal of Clinical Cardiology, Vol. 14, No. 4, August 2011

Figure 1. X-ray chest (PA view) showing left side moderate pleural effusion.

colored pleural fluid tubercular in etiology. Patient was started antitubercular drugs and was discharged with symptomatic relief. Repeat ECG after 15 days revealed disappearance of electric alternans.

Discussion Electric alternans is a broad term that describes alternate beat variation in the direction, amplitude and duration of any component of the ECG waveform (i.e. P, PR, QRS, R-R, ST, T, U).1 Suggested mechanisms of electrical alternans include excitation of alternating populations of cells in sequential beats,2 123

Case Report I

II

III

aVR

aVL

aVF

V1

V2

V4

V5

V3

V6

results.7 But this is usually seen in massive, large pleural effusion or in bilateral pleural effusion with mediastinum getting sandwiched between increased pressure in two pleural spaces. Isolated moderate left pleural effusion causing electric alternans is not reported in literature so far to the best of our knowledge. Hence, it was worth reporting this case.

We postulate that sudden and rapid collection of fluid in pleural space in our case could result in increased intracardiac pressure sufficient to cause cardiac tamponade thereby resulting in electric alternans.

In such cases, aspiration of pleural fluid should be done immediately rather than pericardiocentesis as we did in our case.

References 1. Kalter HH, Schwartz ML. Electric alternans. NY State J Med 1948;1:1164-6.

Figure 2. Electrocardiogram with low voltage QRS complexes, showing electric alternans.

alternation of the AP waveform3 and global movement of the heart within the chest.4 Electrocardiographic alternans was first described in 1908 by Hering.5 Shortly thereafter, Lewis6 recognized that cardiac alternans could occur in normal hearts as a result of marked acceleration of heart rate and also in the impaired or intoxicated myocardium. Pleural effusion in presence of an otherwise insignificant pericardial effusion can increase intrapericardial pressure to such a degree that cardiac tamponade

2. Brody JG, Rossman PL. Electric alternans: report of two additional cases. JAMA 1937;108(10):799-802.

3. Boyyet MR, Jewell BR. Analysis of the effects of changes in rate and rhythm upon electrical activity in the heart.

Prog Biophys Mol Biol 1980;36(1):1-52.

4. Colvin J. Electrical alternans: case report and comments on the literature. Am Heart J 1958;55(4):513-7.

5. Hering HE Das Wesen des Herzalternans. Munchen Med Wochenshr 1908;4:1417-21.

6. Lewis T. Notes upon alternation of the heart. Q J Med 1911;os4(2):141-4.

7. Yaska K, Wann SL, Sagaer K. Pleural effusion as a cause of right ventricular diastolic collapse. Circulation 1992;86:609-17.

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ECG Formulae

QT Means Systole

QT interval (QTc ≤0.40 second)

QT Interval

Bazett’s formula: QTc = (QT)/Sq - root RR (in seconds)

QT interval is measured from beginning of QRS to end of T-wave in the frontal plane 

Poor Man’s Guide to upper limits of QT: For HR = 70 bpm, QT ≤0.40 second; for every 10 bpm increase above 70 subtract 0.02 second, and for every 10 bpm decrease below 70 add 0.02 second.

For example:



QT ≤0.38 @ 80 bpm QT ≤0.42 @ 60 bpm



QT Prolongation Drugs

Type 1A anti-arrhythmic agents (i.e., quinidine, procainamide, disopyramide) and tricyclic anti- depressants/phenothiazines



Normal: Heart rate dependent (corrected QT = QTc = measured QT ÷ Sq-root RR in seconds; upper limit for QTc = 0.44 second) Long QT syndrome: “LQTS” (based on upper limits for heart rate; QTc ≥0.47 second for males and ≥0.48 second in females is diagnostic for hereditary LQTS in absence of other causes of increased QT) This abnormality may have important clinical implications since it usually indicates a state of increased vulnerability to malignant ventricular arrhythmias, syncope and sudden death. The prototype arrhythmia of the LQTS is torsade de pointes, a polymorphic ventricular tachycardia characterized by varying QRS morphology and amplitude around the isoelectric baseline Causes of LQTS include the following: n

“Lytes”

Hypokalemia, hypocalcemia or hypomagnesemia CNS

Catastrophes such as stroke, seizure, coma,

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intracerebral or brainstem bleeding Several other conditions (i.e. bundle branch block, infarction and ischemia) may also cause QT prolongation.

n

Drugs (many anti-arrhythmics, tricyclics, phenothiazines and others) Electrolyte abnormalities (↓ K+, ↓ Ca++, ↓ Mg++) CNS disease (especially subarachnoid hemorrhage, stroke trauma) Hereditary LQTS (e.g. Romano-Ward syndrome) Coronary heart disease (some post-MI patients)

Rule: Prolonged QT = Systolic dysfunction

Source: AJCC’s Electrocardiography Formulae in Clinical Practice, pg:39-41.

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ECG Formulae The QT Interval - Key Points 

The QT interval is measured from the onset on the Q-wave (or the onset of the R-wave if there is no Q) until the termination of the T-wave.



Select that lead in which the QT interval appears to be longest.



Precise measurement of the QT interval is usually not necessary. Practically speaking one only cares if the QT interval is normal or prolonged.



Hypercalcemia produces QT shortening but this is very difficult to recognize clinically.



Determination of the QT interval means little when the heart rate is rapid (faster than about 90-100/min).

RR Interval - Heart Rate RR interval is the duration of ventricular cardiac cycle (an indicator of ventricular rate) QT = Should be less than half of RR

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Clinical Algorithm

Initial Management of Atrial Fibrillation

Patient with diagnosis of atrial fibrillation Hemodynamically stable (no angina, no hypotension, etc.)?

Yes

No

Control ventricular rate (goal = <100 beats per minute): administer diltiazem, 15 mg IV over 2 minutes, then 5 to 15 mg per hour by continuous IV infusion or administer other rate-control drug.

Electrical cardioversion: sedate, then shock (100 J, 200 J, 300 J, 360 J) until sinus rhythm returns.

Spontaneous conversion to sinus rhythm?

Yes Assess cause of atrial fibrillation; hospital discharge, follow-up

No Contraindications to cardioversion?

Yes Consider long-term anticoagulation.

No Consider cardioversion, if indicated (see text): Start heparin IV; then chooseâ&#x20AC;&#x201D; Atrial fibrillation <48 hours: immediate medical or electrical cardioversion

Atrial fibrillation >48 hours or unknown duration: Later elective cardioversion (electrical cardioversion with or without medical cardioversion) after 3 weeks of warfarin

Early TEEâ&#x20AC;&#x201C;guided cardioversion (electrical cardioversion with or without medical cardioversion) Yes

Consider long-term anticoagulation.

No Assess cause of atrial fibrillation; hospital discharge, follow-up

IV = Intravenous; J = Joule; TEE = Transesophageal echocardiography.

Source: Adapted from Am Fam Physician. 2002;66(2):249-236.

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Expert Opinion

Is there any Role of LAVI in LV Diastolic Failure?

G Devpura

L

eft atrial volume index (LAVI) is increasingly being recognized as a relatively load-independent marker of left ventricular (LV) filling pressure.

LAVI on resting echocardiography, specifically in patients with suspected heart failure (HF) and normal LV systolic function is a powerful independent predictor of LV diastolic dysfunction as predicted by serum N-terminal pro-B-type natriuretic peptide (NT-proBNP). In a population with a high suspicion of diastolic HF, LAVI may significantly contribute to diagnostic precision.

Lim and his colleagues from the Dept. of Cardiovascular Medicine, Northwick Park Hospital, Middlesex, UK assessed the capacity of LAVI to predict LV diastolic dysfunction in comparison with NT-proBNP in patients with suspected HF and a normal ejection fraction (EF).1 They did echocardiography studies in 137 patients with suspected HF and calculated both LAVI and NT-proBNP estimations. Raised LAVI and reduced LV systolic function were defined as >26 ml/m2 and LVEF <50%, respectively. Of 137 patients, 21 were excluded (two with significant mitral valve disease and 19 with AF). Of the remaining 116 subjects, 92 showed normal LV systolic function. The univariate predictors of serum log NT-proBNP were age (p < 0.001), LA dimension (p = 0.001), LAVI (p < 0.001), A-wave (p = 0.001), E:A (p = 0.07) and septal wall thickness (p = 0.004).

However, on multivariate analysis, LAVI was found to be the most consistent and significant predictor of NT-proBNP.

patients with LV hypertrophy (LVH). In patients with LVH, the mitral L-wave appears to be a marker of pseudonormal LV filling and predictor of future HF events.

Lam and his colleagues from the Division of Cardiology, Dept. of Medicine, National University of Singapore, examined the relationship of the mitral L-wave with echocardiographic indexes of diastolic function and HF events in patients with LVH.2 Of 177 patients, the L-wave was present in 35 (20%) (Group I) and absent in 142 (Group II).

Patients in Group I had higher early (E) to late (A) transmitral flow velocity (E/A) ratio (1.2 vs 0.8), shorter mitral E-wave deceleration time (201 vs 225 msec), lower pulmonary venous systolic/diastolic velocity ratio (1.1 vs 1.6), shorter LV isovolumic relaxation time (83 vs 94 msec), larger left atrial volume (36 vs 23 ml/m2), and higher E to early mitral annular velocity (E/E’) ratio (septal E/E’, 12.2 vs 9.1; lateral annular E/E’, 10.9 vs 7.8) compared with Group II (all p < 0.05). The difference between pulmonary venous atrial reversal and mitral A-wave durations was ≥30 msec in more patients of Group I (70% vs 6%, p < 0.001). During a mean follow-up of 12.0 months, 11 patients were hospitalized for HF. The L-wave was associated with a hazard ratio (HR) of 4.7 (p = 0.011) for incident HF, and remained a significant predictor (HR 4.2, p = 0.026) after adjustment for cardiovascular risk factors.

Thus, L-wave has significance in AF and other LA disorders.

Is there any significance of mitral L-wave?

References

L-wave, represents mid-diastolic transmitral flow. It is of unknown clinical and prognostic significance in

2. Lam CS, et al. J Am Soc Echocardiogr 2005;18(4): 336-41.

1. Lim TK, et al. Eur J Heart Fail 2006;8(1):38-45.

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Associate Professor, Dept. of Medicine Senior Cardiologist, SMS Medical College and Hospital, Jaipur

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Practice Guidelines

ACCF/AHA Release Guideline for Early Cardiovascular Risk Assessment

A

therosclerotic cardiovascular disease is the leading cause of death among adults in the United States. Because coronary heart disease (CHD) has a long asymptomatic latent period, there is an opportunity for early preventive measures.

The American College of Cardiology Foundation (ACCF) and the American Heart Association (AHA) have created a guideline to assist physicians with the early cardiovascular risk assessment of asymptomatic adults. The goal of this assessment is to guide targeted preventive efforts based on the patientâ&#x20AC;&#x2122;s individual risk. Initial evaluation includes broadly categorizing patients by risk. Further intervention is based on these risk assessments.

C-Reactive Protein. Measurement of C-reactive protein levels can be useful in selecting candidates for statin therapy in the following patients: men 50 years and older and women 60 years and older with a low-density lipoprotein cholesterol level less than 130 mg per dL (3.37 mmol per L) who are not on lipid-lowering medications, hormone therapy, or immunosuppressant therapy and do not have clinical CHD, diabetes mellitus, chronic kidney disease, severe inflammatory conditions, or contraindications to statins. Measurement of C-reactive protein levels may be reasonable in younger patients with intermediate cardiovascular risk, but is not recommended for high-risk patients.

Recommendations

A1C. Measurement of A1C levels may be reasonable in patients without diabetes to assess cardiovascular risk.

Global Risk Scoring

Microalbuminuria. Urinalysis to detect microalbuminuria is reasonable in patients with hypertension or diabetes, and may be reasonable in intermediate-risk patients without these conditions.

Global risk scores (e.g., Framingham Risk Score) that include multiple traditional cardiovascular risk factors effectively combine individual risk factor measurements into a single quantitative estimate of risk. These scores should be used in all cardiac risk assessment evaluations to guide the initiation of targeted preventive measures.

Lipoprotein-Associated Phospholipase A2. Measurement of lipoprotein-associated phospholipase A2 levels may be reasonable in intermediate-risk patients.

Family History and Genomic Testing

Imaging and Other Testing

Family history of atherothrombotic cardiovascular disease should be obtained, although genotype testing is not recommended.

Resting Electrocardiography (ECG). Resting ECG is reasonable in patients with hypertension or diabetes, and may be considered in patients without these conditions.

Laboratory Testing

Lipoprotein and Apolipoprotein. Lipid measurements, including lipoprotein levels, apolipoprotein levels, and particle size/density, beyond the standard lipid profile are not recommended.

Transthoracic Echocardiography. Echocardiography to detect left ventricular hypertrophy may be considered in patients with hypertension, but is not recommended in those without hypertension.

Natriuretic Peptide. Measurement of natriuretic peptide levels is not recommended.

Carotid Intima-Media Thickness. Measurement of carotid intima-media thickness is reasonable in intermediate-risk patients; however, high-quality results are dependent on properly performing the test.

Source: Adapted from Am Fam Physician. 2011;84(2):234-235.

Brachial/Peripheral Flowâ&#x20AC;&#x201C;Mediated Dilation. Peripheral arterial flowâ&#x20AC;&#x201C;mediated dilation is not recommended.

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practice guidelines Arterial Stiffness. Measurement of arterial stiffness is not recommended outside of research settings.

Ankle-Brachial Index. Measurement of ankle-brachial index is reasonable for intermediate-risk patients.

Exercise and Stress ECG. Exercise ECG may be considered in intermediate-risk patients (including sedentary adults who are considering a vigorous exercise program), particularly if non-ECG markers, such as exercise capacity, are noted.

Stress Echocardiography. Stress echocardiography is not recommended in low- or intermediate-risk patients. It is used mainly in the advanced cardiac evaluation of symptomatic patients to estimate prognosis in those with known coronary artery disease and to assess those with known or suspected valvular heart disease.

Myocardial Perfusion Imaging. Stress myocardial perfusion imaging may be considered in patients with diabetes or a strong family history of CHD, or if a previous risk assessment suggested high risk of

CHD. It is not indicated for patients with low or intermediate risk, and is used mainly in the advanced cardiac evaluation of symptomatic patients and to estimate prognosis in patients with known coronary artery disease.

Calcium Scoring Methods. Measurement of cardiac calcium levels is reasonable in patients with intermediate risk (10 to 20 percent 10-year risk), may be reasonable in those with low to intermediate risk (6 to 10 percent 10-year risk), and is not recommended in patients with low risk (less than 6 percent 10-year risk). Measurement of cardiac calcium levels is reasonable in patients 40 years and older with diabetes.

Coronary Computed Tomography Angiography. Coronary computed tomography angiography is not recommended.

Magnetic Resonance Imaging. Magnetic resonance imaging for detection of vascular plaque is not recommended. n

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Research Review

From the Journals ...

Is Compression-Only CPR More Effective Than Standard CPR? Background: There has been increasing interest in cardiopulmonary resuscitation (CPR) using compressions alone over compressions plus rescue breathing. Besides theoretically improving cerebral perfusion, chest compressions may be preferable to rescue breathing among bystanders performing CPR. Animal models and a previous randomized human trial have found some clinical benefit in persons who received only chest compressions, compared with a traditional approach of compressions plus rescue breathing. Rea and colleagues conducted a randomized controlled trial of CPR compressions with or without rescue breathing among patients with potential cardiac arrest to determine which method is more effective.

The Study: Participants were identified from 911 system calls. Eligibility was determined if the 911 dispatcher concluded that the person was unconscious and not breathing normally, and if the caller was willing to perform CPR with the dispatcherâ&#x20AC;&#x2122;s assistance. Callers were randomized to be instructed to give chest compressions alone, or chest compressions plus rescue breathing in a 15:2 ratio, until the arrival of emergency medical services (EMS) personnel. The primary outcome was survival to hospital discharge, with a secondary outcome of favorable neurologic status at the time of hospital discharge (defined as no worse than moderate cerebral disability). Patients with cardiac arrest attributed to trauma, drowning, or asphyxiation (e.g., choking), who were younger than 18 years, and who were already receiving CPR were excluded. Patients also were excluded retrospectively if they were later determined by EMS personnel to not have been in cardiac arrest.

Results: A total of 1,941 participants were included in the study, with an average EMS response time of 6.5 minutes from dispatch to arrival at the scene. No significant differences were seen between groups regarding survival to hospital discharge (12.5 percent for compressions alone versus 11.0 percent Asian Journal of Clinical Cardiology, Vol. 14, No. 4, August 2011

for compressions plus rescue breathing), or in the likelihood of survivors having favorable neurologic status (14.4 versus 11.5 percent, respectively). Among patients who were determined to have had a cardiac cause of arrest, compression-only CPR was associated with better neurologic status at discharge (18.9 percent for compressions alone versus 13.5 percent with compressions plus rescue breathing), although overall survival rates remained similar (5.0 versus 7.2 percent, respectively).

Conclusion: The authors conclude that giving bystanders CPR instructions to use chest compressions alone does not increase overall survival compared with instructions to use chest compressions plus rescue breathing, although in this study it did somewhat improve neurologic outcomes in patients who had a cardiac cause of arrest. These results support a strategy for laypersons that emphasizes chest compressions and minimizes rescue breathing.

Source: Am Fam Physician. 2011;84(1):120-122.

Patterns and Intensity of Medical Therapy in Patients Undergoing Percutaneous Coronary Intervention Context: The Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation (COURAGE) study, which provided optimal medical therapy (OMT) to all patients and demonstrated no incremental advantage of percutaneous coronary intervention (PCI) on outcomes other than anginarelated quality of life in stable coronary artery disease (CAD), suggests that a trial of OMT is warranted before PCI. It is unknown to what degree OMT is applied before PCI in routine practice or whether its use increased after the COURAGE trial.

Objective: To examine the use of OMT in patients with stable angina undergoing PCI before and after the publication of the COURAGE trial.

Design, Setting and Participants: An observational study of patients with stable CAD undergoing PCI in the National Cardiovascular Data Registry between 131

Research Review September 1, 2005, and June 30, 2009. Analysis compared use of OMT, both before PCI and at the time of discharge, before and after the publication of the COURAGE trial. Optimal medical therapy was defined as either being prescribed or having a documented contraindication to all medicines (antiplatelet agent, β-blocker and statin).

Main Outcome Measures: Rates of OMT before PCI and at discharge (following PCI) between the two study periods.

Results: Among all 4,67,211 patients (1,73,416 before [37.1%] and 2,93,795 after [62.9%] the COURAGE trial) meeting study criteria, OMT was used in 2,06,569 patients (44.2%; 95% confidence interval [CI], 44.1-44.4%) before PCI and in 3,03,864 patients (65.0%; 95% CI, 64.9-65.2%) at discharge following PCI (p < 0.001). Before PCI, OMT was applied in 75,381 patients (43.5%; 95% CI, 43.2-43.7%) before the COURAGE trial and in 1,31,188 patients (44.7%; 95% CI, 44.5-44.8%) after the COURAGE trial (p < 0.001). The use of OMT at discharge following PCI before and after the COURAGE trial was 63.5% (95% CI, 63.3-63.7%) and 66.0% (95% CI, 65.8-66.1%), respectively (p < 0.001).

Results: Overall 30-day mortality was 18%. Causes of death were right ventricular dysfunction (two patients), carcinoid crises (one patient) and pneumonia (one patient). Four patients required permanent pacemaker for complete heart block. Of those that survived initial surgery, median follow-up was 26 months (interquartile range 8-42); 1- and 2-year survival rates were 56% and 44%, respectively. There was no significant difference in survival between those patients in the New York Heart Association (NYHA) Class I/II, mild/moderate right ventricular dilatation or N-terminal brain natriuretic peptide (NT-proBNP) <1,245 pg/ml-1 compared with those in NYHA class III/IV, severe right ventricular enlargement or NT-proBNP >1,245 pg/ml-1, respectively.

Long-term causes of death were related to advanced metastatic carcinoid tumor. No patient required re-operation for bioprosthetic degeneration.

Conclusion: Among patients with stable CAD undergoing PCI, less than half were receiving OMT before PCI and approximately two-thirds were receiving OMT at discharge following PCI, with relatively little change in these practice patterns after publication of the COURAGE trial.

Conclusion: Valve surgery for carcinoid heart disease is of higher risk compared with most other forms of valvular surgery. However, in those that survive the operation significant improvement in functional class occurs. Most long-term complications were related to the tumor itself rather than cardiac complications.

Source: Borden WB, Redberg RF, Mushlin AI, et al.

JAMA 2011;305(18):1882-9.

Source: Bhattacharyya S, Raja SG, Toumpanakis C, et al.

Eur J Cardiothorac Surg 2011;40(1):168-72.

Outcomes, Risks and Complications of Cardiac Surgery for Carcinoid Heart Disease

Treatment Strategies in Severe Symptomatic Carotid and Coronary Artery Disease

Objective: The development of carcinoid heart disease causes significant valvular dysfunction, eventually leading to symptomatic right heart failure and impaired survival. Data regarding cardiovascular surgery are limited. We sought to identify outcomes, risks and complications of valve surgery for carcinoid heart disease.

Coexistent carotid artery stenosis (CS) and multivessel coronary artery disease (CAD) is not infrequent. One in 5 patients with multivessel CAD has a severe CS, and CAD incidence reaches 80% in those referred for carotid revascularization. We reviewed treatment strategies for concomitant severe CS and CAD. We performed a literature search (MEDLINE) with terms including carotid artery stenting (CAS), coronary artery bypass grafting (CABG), carotid endarterectomy (CEA), stroke and myocardial infarction (MI). The

Methods: Twenty-two patients with carcinoid heart disease underwent cardiac valve surgery between 2006 and 2010. Patients were considered for surgery 132

if (1) they had stable carcinoid tumor, (2) they had severe valvular dysfunction and (3) were symptomatic and (4) they had no other significant comorbidities.

Three patients underwent tricuspid valve replacement alone, 15 patients underwent tricuspid and pulmonary valve replacement, two patients underwent tricuspid, pulmonary and mitral valve replacement and two patients underwent quadruple valve replacement.

Asian Journal of Clinical Cardiology, Vol. 14, No. 4, August 2011

Research Review main therapeutic option for CS-CAD has been (simultaneous or staged) CEA-CABG. This, however, is associated with a high risk of MI (in those with CEA prior to CABG) or stroke (CABG prior to CEA), and the cumulative major adverse event rate (MAE - death, stroke or MI) reaches 10-12%. With increasing adoption of CAS, a sequential strategy of CAS followed by CABG has emerged. Registries (usually single-center) indicate an MAE rate of ≈7% for CAS followed by CABG (frequently after >30 days, due to double antiplatelet therapy). Recently, 1-stage CAS-CABG has been introduced. This involves different antiplatelet regimens and, in some centers, preferred off-pump CABG, with a cumulative MAE of 1.4-4.5%. No randomized trial comparing different treatment strategies in CS-CAD has been conducted, and thus far reported series are prone to selection/ reporting bias. In addition to the established surgical treatment (CEA-CABG, sequential/simultaneous), hybrid revascularization (CAS-CABG) is emerging as a viable therapeutic option. Larger, preferably multicenter, studies are required before this can become widely applied.

Source: Dzierwa K, Pieniazek P, Musialek P, et al. Med Sci Monit 2011;17(8):RA191-7.

Cone Reconstruction in Ebstein’s Anomaly repair: Early and Long-term Results Background: The main Ebstein anomaly (EA) repairs are based on the monocusp reconstruction of the tricuspid valve and are limited by the frequent need for replacement or the high recurrence of valve

regurgitation. Objective: To evaluate the feasibility and effects of anatomical repair of Ebstein’s anomaly using the cone reconstruction technique on patients’ clinical evaluation, tricuspid valve function and right ventricular morphology. Methods: We compared the clinical, echocardiographic and radiological data of 52 consecutive patients, with a mean age of 18.5 ± 13.8 years, submitted to the cone reconstruction technique, obtained in the preoperative, early postoperative (EPO) and long-term (LPO) periods. Results: There were two in-hospital deaths (3.8%) and two more during the follow-up. Mean functional class of preoperative heart failure improved from 2.2 to 1.2 after 57 months of mean follow-up of 97% of patients (p < 0.001). The mean degree of preoperative tricuspid regurgitation decreased from 3.6 to 1.6 in the EPO (p < 0.001), remaining at 1.9 in LPO period (p > 0.05).

The indexed RV functional area increased from 8.53 ± 7.02 cm2/m2 preoperatively to 21.01 ± 6.87 cm2/m2 in the EPO (p < 0.001) and remained unchanged at 20.28 ± 5.26 cm2/m2 in LPO period (p > 0.05). The mean cardiothoracic ratio was decreased from 0.66 ± 0.09 to 0.54 ± 0.06 (p <0.001) in the long-term.

Conclusion: The cone technique showed low inhospital mortality, resulting in an effective and longlasting repair of tricuspid regurgitation, restoring the functional area of the right ventricle and allowing reverse remodeling of the heart and clinical improvement in most patients in the long-term.

Source: Silva JP, Silva LD, Moreira LF, et al. Arq Bras Cardiol 2011 Aug 5. [Epub ahead of print]

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Emedinews Section

From eMedinewS

South Asians More Vulnerable to Diabetes, Coronary Artery Disease A new study led by an Indian-origin scientist has revealed that South Asians are more likely to add dangerous organ-hugging fat that can lead to diabetes and coronary artery disease. The team at McMaster University led by Dr Sonia Anand found that these ethnic groups tend to add dangerous fat onto their internal organs like their liver when they gain weight, while others just add it to their waistline. “The new study showed South Asians have less space to store fat below the skin than white Caucasians,” said Dr Anand, a professor of medicine and epidemiology at McMaster University. “Their excess fat, therefore, overflows to ectopic compartments, in the abdomen and liver where it may affect function,” she said. This visceral fat, she added, is associated with metabolic problems such as elevated glucose and abnormal lipids, which are risk factors that ultimately lead to coronary artery disease. (Source: http://www.newstrackindia.com/ newsdetails/232949, 31 July, 2011) Afib Hospital Days Reduced with Dronedarone Cardiovascular hospitalization and length of stay declined significantly in patients with paroxysmal or persistent atrial fibrillation or flutter treated with dronedarone (Multaq), a post-hoc analysis of a large randomized trial showed. First cardiovascular hospitalization occurred in 26% fewer patients treated with dronedarone versus placebo, and the rate of hospitalization for Afib was almost 40% lower with dronedarone. The total number of hospital days associated with Afib was reduced by about one-third, including a significant reduction in the number of ICU/CCU days. (Source: Medpage Today) Local Practice Patterns Drive Diagnostic Angios There is wide variation among US institutions in the rate of positive findings of obstructive coronary artery disease (CAD) when patients undergo 134

diagnostic angiography, a retrospective study found.

Among hospitals, the rate of positive findings (≥50% obstruction) varied from 23 to 100%, reported Pamela S Douglas, MD, from Duke University Medical Center in Durham, NC, and colleagues.

Hospitals with lower rates of obstructive CAD findings performed coronary angiography more often in younger patients, women, blacks and outpatients (all p < 0.001), researchers reported in the August 16 Journal of the American College of Cardiology. (Source: Medpage Today) Absolute Blood Flow Better Predictor of Cardiac Events Using data on absolute myocardial blood flow reserve gained through rubidium-82 PET imaging is prognostic of death, myocardial infarction (MI) and other major cardiovascular events, a single-center study found. Patients with impaired myocardial flow reserve had higher incidences of MI and cardiac death, even when their summed stress scores (SSS) were within the normal range, reported Maria C Ziadi, MD, from the University of Ottawa Heart Institute in Ontario, and colleagues. All cardiac deaths occurred in patients with a severely impaired myocardial flow reserve (<1.5) - 1% in the group with normal SSS, and 6.5% in the group with abnormal SSS, according to the study published online in the Journal of the American College of Cardiology. (Source: Medpage Today) Sweetened Drinks Boost Heart Disease Risk Beverages sweetened with fructose or high-fructose corn syrup can worsen cardiovascular risk factors, even in the young and healthy, researchers have found.

When these types of drinks accounted for at least a quarter of a person’s daily calories over two weeks, there were significant increases in triglycerides, LDL cholesterol and apolipoprotein B (apoB) concentrations that weren’t seen with glucose, Kimber Stanhope, PhD, of the University of California Davis and colleagues reported online in the Journal of Clinical Endocrinology and Metabolism.

Asian Journal of Clinical Cardiology, Vol. 14, No. 4, August 2011

eMedinewS Section Fitness Update

Lab Update

What’s the best exercise for heart health?

Metabolic Panel (14), Comprehensive

A combination of weight training and aerobic exercise might be the best prescription for overweight people at risk for diabetes and heart disease, a new study suggests. People doing only aerobic exercise dropped weight and inches off their waistlines - so an aerobic-only program is also a good (and less time-consuming) option, researchers said.

Those in the study who just lifted weights saw very little benefit in terms of heart health, although they did gain strength. ‘Aerobic plus resistance is clearly the optimal program,’ said Dr Timothy Church, who studies exercise and disease at Louisiana State University’s Pennington Biomedical Research Center in Baton Rouge.

Test includes: Alanine aminotransferase (ALT/ SGPT); albumin:globulin (A:G) ratio; albumin, serum; alkaline phosphatase, serum; aspartate aminotransferase (AST/SGOT); bilirubin, total; BUN; BUN:creatinine ratio; calcium, serum; carbon dioxide, total; chloride, serum; creatinine, serum; globulin, total; glucose, serum; potassium, serum; protein, total, serum; sodium, serum.

A Rich New Source of Heart-healthy Food Ingredients - Seaweed

In an article, that may bring smiles to the faces of vegetarians who consume no dairy products and vegans, who consume no animal-based foods, scientists have identified seaweed as a rich new potential source of heart-healthy food ingredients.

Seaweed and other ‘macroalgae’ could rival milk products as sources of these so-called ‘bioactive peptides,’ they conclude in an article in ACS’s Journal of Agricultural and Food Chemistry. Maria Hayes and colleagues Ciarán Fitzgerald, Eimear Gallagher and Deniz Tasdemir note increased interest in using bioactive peptides, now obtained mainly from milk products, as ingredients in socalled functional foods. Those foods not only provide nutrition, but have a medicine-like effect in treating or preventing certain diseases.

Seaweeds are a rich but neglected alternative source, they state, noting that people in East Asian and other cultures have eaten seaweed for centuries: Nori in Japan, dulse in coastal Europe, and limu palahalaha in native Hawaiian cuisine.

—Rajat Bhatnagar, International Sports & Fitness Distribution, LLC, http://www.isfdistribution.com

Asian Journal of Clinical Cardiology, Vol. 14, No. 4, August 2011

The Comprehensive Metabolic Panel (CMP) is a frequently ordered panel of tests that gives your doctor important information about the current status of your kidneys, liver and electrolyte and acid/base balance as well as of your blood sugar and blood proteins. Abnormal results, and especially combinations of abnormal results, can indicate a problem that needs to be addressed.

—Dr Arpan Gandhi and Dr Navin Dang

How safe is angiography radiation?

The mean duration of fluoroscopy in electrophysiologic cardiac interventional procedures ranges from 15 to 67 minutes. The radiation dose from one hour of fluoroscopy during electrophysiologic ablation procedures can result in 0.7-1.4 excess fatal malignancies/1,000 women and 1.0-2.6/1,000 men as per two studies published in American Journal of Cardiology (1998) and Circulation (2004).

At what prevalence is screening for stroke beneficial?

Only at prevalence rates of over 20% significant benefits are seen with at best about 100 strokes prevented for every 10,000 screened at 20% prevalence.

Clinical features cannot identify asymptomatic individuals likely to have carotid stenosis. The annual risk of stroke in patients with asymptomatic carotid artery stenosis is relatively low.

—Dr KK Aggarwal, Group Editor-in-Chief, IJCP Group of Publications and eMedinewS

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eMedinewS Section Sudden Cardiac Death How is sudden cardiac death different from sudden cardiac arrest?

Sudden cardiac arrest is cessation of cardiac activity, which can be revived after resuscitation. On the other hand, sudden cardiac death (SCD) is unsuccessful sudden cardiac arrest.

How common is sudden cardiac death?

About 4-5,00,000 people in US, 7,00,000 in Europe and 2 million in India die every year directly due to SCD. In India, majority of them die before reaching the hospital; about 75% of them can be revived if chest compression cardiac resuscitation (CCCR) is taught to all.

What are the three clinical phases after a sudden cardiac arrest? 



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Clinical phase: Lasts 0-5 minutes; ventricular fibrillation is the main electrical activity and the treatment of choice is defibrillation followed by CCCR. Hemodynamic phase: Lasts 5-10 minutes; ventricular fibrillation persists and the patient, in addition, has hemodynamic instability. These patients require effective two minutes of CCCR before defibrillation is attempted followed by two minutes of CCCR again.

Metabolic phase: Phase beyond 10 minutes. Only hypothermia system can work here.

How is cardiac arrest treated in the first five minutes?

The first five minutes after cardiac arrest is the clinical phase. In this phase, ventricular fibrillation is the main electrical activity. The treatment of choice is defibrillation followed by CCCR. How is cardiac arrest that presents between 5-10 minutes of the arrest managed?

The second 5-10 minutes of cardiac arrest is the hemodynamic phase. Ventricular fibrillation persists and the patient, in addition, has hemodynamic instability. These patients require effective two minutes of CCCR before defibrillation is attempted followed by two minutes of CCCR again.

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What is the management of cardiac arrest that presents after 10 minutes of the arrest?

The patient, after 10 minutes of arrest, is in the metabolic phase. Only hypothermia system can work here.

What is chest compression cardiac resuscitation?

CCCR involves compressing the chest with a speed of 100/minute. The mantra is to push as hard and as fast as possible. Each compression should lower the sternum by 1.5-2 inches, should be continuous and allow full recoil of the sternum. One person can effectively carry out chest compression for only 1-2 minutes. After that fatigue will invariably set in. Therefore, it is important to switch resuscitations between available bystanders.

Is CCCR effective in children?

CCCR is more effective in adults. In children, and in conditions like unwitnessed cardiac arrest and noncardiac arrests, one may have to do complete cardiac pulmonary resuscitation (CPR) involving breathing and chest compression cycles.

How to defibrillate in sudden cardiac arrest?

While defibrillating, use the maximum Jules available in the machine. After defibrillation, one should not wait to watch for the rhythm but continue CCCR uninterrupted for the next two minutes.

How long should one wait before starting CCCR?

Do not waste more than 10 seconds to check pulse or breathing before starting CCCR. Even a second’s delay matters. Therefore, CCCR should be started without delay.

What is the role of soda bicarb in CCCR?

In basic cardiac resuscitation, injection adrenaline, atropine, endotracheal tube, soda bicarb, etc. have no role.

Who should lead the CCCR?

When multiple rescuers are available, the person highest trained should become the leader, direct and take over the first two minutes of the resuscitation cycle.

Asian Journal of Clinical Cardiology, Vol. 14, No. 4, August 2011

eMedinewS Section What should be the compression to breathing ratio in CPR?

When giving CPR involving breathing-chest compression cycles, the ratio should be 30 compressions: Two breaths. This ratio should not be more than five cycles in two minutes.

How effective should be breathing in CPR?

One should not push more than 50% of the tidal volume in each breath. Don’t push air into the stomach as it will impair hemodynamics. If the respiratory rate is more, it will also impair hemodynamics.

What is the significance of gasping respiration in CPR or CCCR?

Medicolegal Update Sudden Death-autopsy-four Cases Found Dead in Toilet During Daily Pursuits

Left ventricular hypertrophy is the second leading cause of sudden cardiac death in adults in India. 

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Agonal/gasping respiration is ineffective respiration and should be an indication for cardiac resuscitation.

In fact, gasping is the sign that your resuscitation is likely to be successful. 

Criteria Improve Transesophageal Echo Rate Prescreening patients who are set to have transesophageal echocardiography (TEE) reduces inappropriate scans, researchers said. In a singlecenter study, 16% of scans were canceled after prescreening with appropriate use criteria, James Kirkpatrick, MD, of the University of Pennsylvania, and colleagues reported in the Journal Echocardiography. The cancellation rate was just 2% when patients were not prescreened. (Source: Medpage Today) Coronary Calcium better than CRP to Stratify Risk Among asymptomatic individuals with normal LDL cholesterol levels and elevated high-sensitivity C-reactive protein (hsCRP), measuring the burden of calcium in the coronary arteries with cardiac CT appears to stratify the risk of cardiovascular disease, researchers found. (Source: Medpage Today)

Asian Journal of Clinical Cardiology, Vol. 14, No. 4, August 2011



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The long-standing raised high blood pressure which causes secondary damage to the wall of the main pumping chamber of the heart, the left ventricle, leading to hypertrophy which is associated with cardiac arrhythmias.

The mechanism of death in a majority of patients dying of sudden cardiac death is ventricular fibrillation and as a consequence there may be no prodromal symptoms associated with the death.

These patients may be going about their daily business and suddenly collapse without the typical features of myocardial infarction such as chest pain and shortness of breath. There are a number of cases in which patients feel the effect of myocardial ischemia. Myocardial ischemia is associated with referred pain, classically to the front of the chest, the left arm and the jaw.

Patients may feel generally unwell, with nausea, dizziness and vomiting.

These symptoms may precede the death for any length of time ranging from a few minutes to several hours.

I had conducted the postmortem examination of four cases found dead in toilet during daily pursuits; the cases of left ventricular hypertrophy leading to sudden cardiac death.

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

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lighter reading

Lighter Reading

An Inspirational Story

Spiritual Update

Building your House

Anger, Hostility, Aggression: Risk Factors for Heart Attack

The contractor was sorry to see his good worker go and asked if he could build just one more house as a personal favor. The carpenter said yes, but over time it was easy to see that his heart was not in his work. He resorted to shoddy workmanship and used inferior materials. It was an unfortunate way to end a dedicated career.

When the carpenter finished his work, his employer came to inspect the house. Then he handed the front-door key to the carpenter and said, “This is your house… my gift to you.”

The carpenter was shocked!

What a shame! If he had only known he was building his own house, he would have done it all so differently.

So it is with us. We build our lives, a day at a time, often putting less than our best into the building.

Then, with a shock, we realize we have to live in the house we have built. If we could do it over, we’d do it much differently.

But, you cannot go back. You are the carpenter, and every day you hammer a nail, place a board, or erect a wall.

Someone once said, ‘Life is a do-it-yourself project.’

Your attitude, and the choices you make today, help build the ‘house’ you will live in tomorrow.

Build-wisely!

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Anger, hostility and aggression are three risk factors for heart attack with the fulcrum at the level of anger. A thought arises from the thoughtless state of mind called consciousness, which is then analyzed by the intellect and converted into an action, which is either egocentric or ego-fugal. All actions lead to memory and memory leads to desire. If the desire can be fulfilled, it will end up into action again and the cycle of action, memory and desire continues leading to habit or an addiction…

Laugh a While Building Rome

Marilyn, the teacher, asked her 5th grade history class, ‘When was Rome built?’ and called on Timothy to answer first. ‘Rome was built at night.’ was his answer. ‘At night?’ asked Mrs. Taylor, holding her ruler firmly in her boney-knuckled hands. ‘How ever did you get such an idea?’

‘Well,’ gulped the student, hoping his answer would satisfy her, ‘everyone knows Rome wasn’t built in a day’.

Mind Teaser In which of the following locations is carcinoid tumor most common?

1. Esophagus 2. Stomach 3. Small bowel 4. Appendix

Answer: 4. Appendix

An elderly carpenter was ready to retire. He told his employer-contractor of his plans to leave the house-building business to live a more leisurely life with his wife and enjoy his extended family. He would miss the paycheck each week, but he wanted to retire. They could get by.

Asian Journal of Clinical Cardiology, Vol. 14, No. 4, August 2011

Conference Calendar

Conference Calendar

Cardiovascular and Interventional Radiological Society of Europe (CIRSE 2011) September 10-14, 2011 Venue: ICM - Internationales Congress Center Messegelände, Munich, Alemania Website: http://www.cirse.org/ Annual Scientific Meeting of the British Hypertension Society September 12-14, 2011 Venue: Queens’ College, Silver St, Cambridge, Reino Unido Website: http://www.bhsoc.org/ High Blood Pressure Research 2011 Scientific Sessions September 20-24, 2011 Venue: Walt Disney World Dolphin Resort Orlando, Florida, Estados Unidos Website: http://my.americanheart.org/professional/Sessions/ HBPR/HBPR_UCM_316905_SubHomePage.jsp 22nd Annual Coronary Interventions September 21-23, 2011 Venue: Hilton La Jolla Torrey Pines, San Diego, California, United States Website: http://www.scripps.org/assets/documents/sudden_ cardiac_arrest_brochue2011.pdf Issues of Congenital Heart Disease September 23, 2011 Venue: Congress Hall, Kiev, Ukraine Website: http://www.nbscience.com/23.html 16th Annual Meeting of the European Council for Cardiovascular Research September 30 to October 2, 2011 Venue: La Colle sur Loup, Nice, France Website: http://www.eccr.org Worldcon 2011 – XVI World Congress of Cardiology, Echocardiography and Allied Imaging Techniques September 30th to October 2, 2011 Venue: The Leela Kempinski, Gurgaon, India Website: http://www.worldcon2011.org

Asian Journal of Clinical Cardiology, Vol. 14, No. 4, August 2011

Heart Rhythm Congress 2011 October 02-05, 2011 Venue: Hilton Birmingham Metropole Hotel, Birmingham, UK Website: http://www.heartrhythmcongress.com/ Cardio/Pulmonary for Primary Care Physicians October 02-06, 2011 Venue: Disney’s Boardwalk Resort Orlando, Florida, Estados Unidos Website: http://www.mer.org/schedule/conference/123 Eurothrombosis Summit 2011 October 07-08, 2011 Venue: Sheraton Porto Hotel and Spa, Rua Tenente Valadim, Portugal Website: http://www.eurothrombosis-summit2011.org/ 30th National Congress of Cardiology: 50 Años Viviendo Con La Cardiología October 12-14, 2011 Venue: Hotel Barcelo Guatemala City, Guatemala Website: http://www.medical-events.com/congress/30thnational-congress-of-cardiology-4134 2011 Cardiometabolic Health Congress October 19-22, 2011 Venue: Sheraton Boston Hotel, Boston MA Website: http://www.cardiometabolichealth.org/index.asp 2nd Annual Emirates Cardiac Society Congress October 20-22, 2011 Venue: Grand Hyatt Dubai, Dubai, UAE Website: http://www.ecsc.ae/ Canadian Cardiovascular Congress October 22-26, 2011 Venue: Convention Centre, Vancouver, BC, Canada Website: http://www.cardiocongress.org Evolving Challenges in Promoting Cardiovascular Health 2011 October 21-22, 2011 Venue: CosmoLaxia, Barcelona, Spain Website: http://www.nyas.org/Events/Detail. aspx?cid=116dc806-0b05-4ba2-9046-ad1c2fa52cd6

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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).

140

-

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

-

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

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

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

A subtitle can be added if necessary.

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

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

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

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

- It should not contain abbreviations, footnotes or references.

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

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

- Ethical guidelines followed by the investigations should be described.

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

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

- Method of allocating the subjects into different groups.

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

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

-

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

-

Confidence intervals for the measurements should be provided wherever appropriate.

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

Asian Journal of Clinical Cardiology, Vol. 14, No. 4, August 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

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

- All photomicrographs should indicate the magnification of the print.

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

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

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

-

Do not use clips/staples on photographs and artwork.

-

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

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

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

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

2. Total number of pages ________________________

Books

6. Suggestions for reviewers (name and postal address)

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

Indian 1.____________Foreign 1._ _______________

2.____________

2._ _______________

Articles in Books

3.____________

3._ _______________

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

4.____________

4._ _______________

Tables -

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

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

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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. 4, August 2011

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

7. All authors’ signatures________________________ 8. Corresponding author’s name, current postal and e-mail address and telephone and fax numbers __________________________________________

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

Dr KK Aggarwal

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

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