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ISSN 0972-70035 Single Copy Rs. 300/- Volume 14, Number 4, August 2011, Pages 109-145 Dr KK Aggarwal Group Editor-in-Chief Dr Praveen Chandra Guest Editor Peer Review Journal www.ijcpgroup.com

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Page 1: AJCC-August 2011

ISSN 0972-70035 Single Copy Rs. 300/-

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

Dr KK AggarwalGroup Editor-in-Chief

Dr Praveen ChandraGuest Editor

Peer Review Journalwww.ijcpgroup.com

Page 2: AJCC-August 2011

From the Desk of Editor-in-Chief

Padma Shri and Dr BC Roy National AwardeeDr 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

eMedinewS is now available online on www.emedinews.in or www.emedinews.orgHead Office: E - 219, Greater Kailash, Part I, New Delhi - 48 , India. e-Mail: [email protected], Website: www.ijcpgroup.com

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 AggarwalGroup Editor-in-Chief

Fitness UpdateStartling new truth about sugarFlying 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 thermo-dynamic 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 UpdateThe Spiritual significance of Indian Flag – TirangaLage 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.

23 August 2011, Tuesday

Gastro UpdateComplimentary feeding practices between 6 and 24 monthsSupporting 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.

References1. Brown KH, Dewey KG, Allen LH. Complementary Feeding of

Young Children in Developing Countries: A Review Of CurrentScientificKnowledge.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 UpdateTotal 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 DayTemper is a weapon that we hold by the blade. James Matthew Barrie

—Dr Chandresh Jardosh

Page 3: AJCC-August 2011

An IJCP Group Publication

Dr KK AggarwalCMD, Publisher and

Group Editor-in-Chief

Dr Veena AggarwalJoint MD &

Group Executive Editor

ContentS

Dr KK AggarwalGroup Editor-in-Chief

IJCP [email protected]

Dr Praveen ChandraGuest Editor, AJCCpraveen.chandra@

medanta.org

Assistant Editor: Dr Nagendra Chouhan

ADVISoRy BoARDInternationalDr Fayoz ShanlDr Alain CribierDr Kohtian HaiDr Tanhuay CheemDr Ayman MegdeDr Alan YoungDr Gaddy GrimesDr Jung bo GegDr Rosli Mohd. AliDr S SaitoNationalDr Mansoor Hassan

Dr RK SaranDr SS SinghalDr Mohd. AhmedDr PK JainDr PK GuptaDr Naresh TrehanFACULTyDr GK Aneja Dr Ramesh ThakurDr Balram BhargavaDr HK BaliDr HM MardikarDr Sanjay MehrotraDr Vivek Menon

Dr Keyur ParikhDr Ajit MullasariDr Kirti PunamiyaDr MS HiramathDr VS NarainDr SK DwivediDr Raja Baru PanwarDr Vijay TrehanDr Rakesh VermaDr Suman BhandariDr Ravi KasliwalDr Atul AbhyankarDr Tejas PatelDr Samir Dani

AJCC SPECIALITy PANEL

Dr Sanjiv Chopra Prof. of Medicine & Faculty Dean

Harvard Medical SchoolGroup Consultant Editor

Dr Deepak ChopraChief Editorial Advisor

Anand Gopal BhatnagarEditorial Anchor

Volume 14, Number 4, August 2011

online Submission

IJCP Editorial Board

Dr Alka Kriplani, Asian Journal of obs & Gynae PracticeDr VP Sood, Asian Journal of Ear, Nose and ThroatDr Praveen Chandra, Asian Journal of Clinical CardiologyDr Swati Y Bhave, Asian Journal of Paediatric PracticeDr Vijay Viswanathan, The Asian Journal of DiabetologyDr KMK Masthan, Indian Journal of Multidisciplinary DentistryDr M Paul Anand, Dr SK Parashar, CardiologyDr CR Anand Moses, Dr Sidhartha Das, Dr Ramachandran, Dr Samith A Shetty, DiabetologyDr Ajay Kumar, GastroenterologyDr Hasmukh J Shroff, DermatologyDr Georgi Abraham, NephrologyDr Sidharth Kumar Das, RheumatologyDr V Nagarajan, NeurologyDr Thankam Verma, Dr Kamala Selvaraj, obs and Gyne

Advisory BodiesHeart Care Foundation of India

Overseas Indian Peoples Foundation

FRoM ThE DESK oF GRoUP EDIToR-IN-ChIEFOptimalMedicalTherapyforCoronaryBlockageswithReducedLeftVentricularFunction 113KK Aggarwal

REVIEw ARTICLECAD:ATruePandemicandaComprehensiveSurveillanceSystemistheNeedoftheHour 114G Kannan, NN Rajendran, JSN Murthy, GB Tharani

CASE REPoRTContinuousChangeintheDirectionofAtrialFlutterWavesonEitherSideofIsoelectricLine 121SR Mittal

PseudoElectricAlternansbyLeftPleuralEffusion 123Monika Maheshwari, Tarachand Saini

ECG FoRMULAEQTMeansSystole 125

CLINICAL ALGoRIThMInitialManagementofAtrialFibrillation 127

ExPERT oPINIoNIsthereanyRoleofLAVIinLVDiastolicFailure? 128G Devpura

PRACTICE GUIDELINESACCF/AHAReleaseGuidelineforEarlyCardiovascularRiskAssessment 129

RESEARCh REVIEwFromtheJournals... 131

EMEDINEwS SECTIoNFromeMedinewS 134

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Editorial Policies

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

Note: Asian Journal of Clinical Cardiology does not guaran-tee, 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.

Published, Printed and Edited byDr KK Aggarwal, on behalf of IJCP Publications Pvt. Ltd.

and Published at

E - 219, Greater Kailash, Part - I, New Delhi - 110 048

E-mail: [email protected]

Printed at IG Printers Pvt. Ltd., New DelhiE-mail: [email protected]

© 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.

Volume 14, Number 4, August 2011

EDIToRIAL & BUSINESS oFFICESDelhi Mumbai Kolkata Bangalore Chennai hyderabad

Dr Veena Aggarwal9811036687

E - 219, Greater Kailash, Part 1,

New Delhi - 110 048 Cont.: [email protected]@ijcp.com

[email protected]

Dinesh: [email protected]: 09831363901

[email protected]

Mr Nilesh Aggarwal9818421222

Building No. D-10 Flat No 43, 4th Floor Asmita Co-operative

Housing Society Marvey Road

Near Charkop Naka Malad (W)

Mumbai - 400 [email protected]

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111/2, Dickenson Road (Near Manipal

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Cont.: 25586337 [email protected]

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40A, Ganapathy-puram

Main Road Radhanagar Chromepet

Chennai - 600 044Cont.: 22650144 [email protected]

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9849083558H. No.

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Cont.: [email protected]

Sr.: Senior; BM: Business Manager

SITUATIoN:

© IJ

CP

Aca

dem

y

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

Lymphocyte count does not matter

you have a bad prognosis

A patient with heart failure had a total lymphocyte count (TLC) of 1,000.

Dr. Good and Dr. Bad

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

From the Desk oF Group eDitor-in-ChieFFrom the Desk oF Group eDitor-in-ChieF

Optimal Medical Therapy for Coronary Blockages with Reduced Left Ventricular Function

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

Earlier view had been that compared with medical therapy, surgical bypass of hibernating heart muscleimprovesbothsurvivalandleftheartfunction.Thisviewwasbasedonthefactthatupto50%ofpatientswithleftheartpumpingdysfunctionduetocoronaryheartblockageshaveasignificantamountofviable(hibernating)heartmuscles.

The results of Surgical Treatment for Ischemic Heart Failure (STICH), a randomized trial have shown thatcompared with optimal medical therapy alone, optimal medical therapy plus bypass surgery resulted in nosignificantimprovementintheprimaryoutcomeofall-causemortalityatamedianfollow-upof56months.

The current recommendation is that one should initiate optimal medical therapy alone rather than optimalmedicaltherapyplusbypasssurgerybecausebypasssurgeryisassociatedwithsignificantmorbidity.Bypasssurgery,however,ispreferredinpatientswithongoinganginalsymptomsdespiteoptimalmedicaltherapy.

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 AggarwalPadma Shri and Dr BC Roy National AwardeeSr.PhysicianandCardiologist,MoolchandMedcityPresident,HeartCareFoundationofIndiaGroupEditor-in-Chief,IJCPGroupandeMedinewSChairmanEthicalCommittee,DelhiMedicalCouncilDirector,IMAAKNSinhaInstitute(08-09)Hony.FinanceSecretary,IMA(07-08)Chairman,IMAAMS(06-07)President,DelhiMedicalAssociation(05-06)[email protected]://twitter.com/DrKKAggarwalKrishanKumarAggarwal(Facebook)

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

CAD: A True Pandemic and a Comprehensive Surveillance System is the Need of the HourG 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: Coronaryarterydisease,pandemic,surveillancesystem,healthstatus

*AssistantProfessorDept.ofPharmacyPractice,FacultyofPharmacySriRamachandraUniversity,Porur,Chennai**ProfessorSwamiVivekanandaCollegeofPharmacy,Erode,Chennai†ProfessorandHeadDept.ofCardiology,SriRamachandraUniversity,Porur,Chennai‡ProfessorandHeadSaveethaMedicalCollege,ThandalamAddress for correspondenceDrGKannanAssistantProfessor,Dept.ofPharmacyPractice,FacultyofPharmacySriRamachandraUniversity,Porur,Chennai-600116E-mail:[email protected]

Coronaryarterydisease(CAD)occurswhenthearteriesthatsupplybloodtotheheartmuscleharden and narrow (Bhati K, 2011; Heart

Diseases, 2011). The result is the loss of oxygen andnutrients to myocardial tissue because of diminishedcoronary blood flow (Springhouse, 2005). Thisreduction in blood flow can lead to acute coronarysyndrome (angina or myocardial infarction). CAD ison the climb and has become a true pandemic thatrespectsnoborders.

Prevalence of CAD

Global Scenario

The term ‘prevalence’ of CAD usually refers to theestimated population of people who are managingCADatanygiventime(AmericanHeartAssociation,2004). The proportion of deaths due to CAD isprojected to rise from59% in2002 to69% in2030(Mathers and Loncar, 2006). The WHO (2006)

estimatesthatatleast20millionpeoplesurviveCAD-relatedheartattacksandstrokeseveryyeararoundtheworld; many require continuing costly clinical care.By 2030, almost 23.6 million people will die fromCADs, mainly from heart disease and stroke. Theseare projected to remain the single leading causes ofdeath (WHO-Cardiovascular Disease: Prevention andControl, 2006). A recent evaluation of WHO in thecauseofdeathin2009,CADandstrokewereplacedasfirst(7,185,353deaths)andsecond(5,704,843deaths)inrankamongtotaldeaths(6,830,586,985)ofallkindofdiseases.Moreover, therateofdeath is risingmorein the under-developed countries than the developedcountries,becauseoftheirlifestyleandsocioeconomicfactors(WHO,2009).

According to the Global Burden of Disease Study,the developing countries contributed 3.5 millionofthe6.2millionglobaldeathsfromCADin1990.Theprojections estimate that these countries will accountfor7.8millionofthe11.1milliondeathsduetoCADin 2020 (Murray et al, 1996). Disability-adjustedlife years (DALYs) lost can be thought of as ‘healthyyears of life lost’. They indicate the total burden ofa disease, as opposed to simply the resulting deaths.Murrayetal(1996)calculatethatinIndiaandChina,aspectacularriseinthenumberofDALYsisexpectedin the coming years - from a figure of <25 millionDALYs in each country in 1990, to 30 million and35million in India andChina, respectively, in2020.

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CAD is decreasing in many developed countries, butis increasing in developing and transitional countries,partly as a result of increasing longevity,urbanizationand lifestyle changes.CAD is responsible for 10%ofDALYs lost in low and middle-income countries and18% in high-income countries (Global Burden ofCoronaryHeartDisease,2002).

CADisthemostcommoncauseofdeath(andprematuredeath)intheUK.Onein5menandonein7womendie from CAD. There are 94,000 deaths from CADin the UK each year (Greenlund et al, 2006). Withregardtoincidence,datafromtheAtherosclerosisRiskIn Communities (ARIC) and Cardiovascular HealthStudyindicatethatannually,7,85,000Americanshaveanew coronary attack and4,70,000have a recurrentattack; in addition, approximately 1,95,000 silentmyocardial infarctions occur each year. This assumesthat21%ofthe9,35,000firstandrecurrentmyocardialinfarctionsaresilent (Thometal,2001;Bolandetal,2002).Tables 1 and 2 depict the CAD prevalence inurbanandruralpopulationofdevelopedcountriesanddevelopingcountries.

Indian Scenario

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

both in the rural and urban populations, althoughit is higher in urban than in rural population, witha greaterprevalence in affluent groups (Chadha et al,1990;Enasetal,1992;Singhetal,1997).Enasetal(1996)andEnasetal (1999). It isestimatedthat9.2million productive years of life were lost in India in2000,withanexpectedincreaseto17.9millionyearsin2030.Table3depictstheCADprevalencewithrespectto age group, sample size of the study population indifferentpartsofIndia.SalientfeaturesoftheCADepidemicinIndia:

Incidence of CAD in young Indians is about12-16%, which is higher than any other ethnicgroup(Mammietal,1991).Age-standardized estimates for DALYs lost dueto CAD per 1,000 population in India are threetimes higher than in developed countries (Negusetal,1994).About5-10%ofheartattacksoccurinIndianmenand women younger than 40 years (Mackay andMensah,2004).India topped the world with 1,531,534cardiovasculardisease-relateddeaths in2002, andoccupied first place in cause of death in currentmoment based on WHO report, 2009 (Yusufetal,2004;WHO,2009).

Table 1. CAD in Urban and Rural Population of Developed CountriesAuthor year Age group Place Sample size CAD prevalence (%)Urban populationCalvet et al. 2010 45-75 France 300 50.0Arzamendi et al. 2010 20-65 Developed countries 1,260 49.0Iwasaki et al. 2011 30-70 Japan 135 9.20Icaza et al. 2009 35-74 USA General population 6.95Kivimaki et al. 2011a 30-70 UK 5,533 0.70Jain et al. 2011 35-75 London (UK) 2,369 22.0Kivimaki et al. 2011b 30-70 London (UK) 7,095 0.027Ong et al. 2011 30-70 UK 698 5.00Stansby et al. 2011 68 UK 473 30.0Ebrahim et al. 2011 20-70 UK 1,63,471 4.35Secrest et al. 2011 24-32 USA 317 2.50Rural populationOizumi et al. 2008 30-70 Japan 2,938 3.19Idris et al. 2008 30-70 UK 1,087 50.0Konishi et al. 1990 40-59 Japan 8,835 88.0

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Table 2. CAD in Urban and Rural Population of Developing Countries (Excluding India)Author year Age group Place Sample size CAD prevalence (%)Urban populationGrau 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

Rural populationOnat et al. 2010 45-74 Turkey 1,655 11.50

Pitsavos et al. 2008 30-70 Greek 2,172 1.36

Pavlović et al. 2004 37-56 Croatia 3,544 3.70

Table 3. Prevalence of CAD in Population of IndiaAuthor year Age group Place Sample size CAD prevalence (%)South IndiaGeetha et al. 2011 30-70 Chennai (Tamil Nadu) 2,350 2.93Mohan et al. 2010a 30-70 Chennai (Tamil Nadu) - 5.40Mohan et al. 2010b 30-70 Chennai (Tamil Nadu) - 11.0Kumaran et al. 2002 30-70 Mysore 435 21.75Mohan et al. 2001 20-70 Chennai (Tamil Nadu) 1,262 11.0Stein et al. 1996 Mysore 517 10.0Begom et al. 1995 25-65 South India (Urban) 506 13.9North IndiaSingh et al. 2011 <15 Chandigarh 196 0.000045Kumar et al. 2006 >35 North India (Urban + Rural) 7,169 3.96Ahmad et al. 2005 25-70 Delhi (Urban) 14,000 0.2-0.9Ahmad et al. 2005 25-70 Delhi (Rural) 14,000 0.1-0.4Singh et al. 1997 25-64 Moradabad 3575 1.5-3.0Chadha 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 61.6west IndiaLanjewar et al. 2005 25-70 Mumbai 3,871 4.20Rastogi et al. 2004 30-70 Western India 350 1.88Pinto et al. 2004 35-64 Goa 371 13.2East IndiaHazarika et al. 2002 30-70 Assam 1,015 61.0Bhattacharyya 2003 30-70 Kolkata 28 + 62 39 + 60

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Median age of first heart attack in Indians is53years(WHO,2009).1,55,88,000DALYs(WHO,2009).

Need of the Hour

Prospectivestudiesontherelativeroleandimportanceoftraditionalandnewerriskfactorsareurgentlyneededin Indians within the subcontinent as much of theknowledgeof risk factors forCADhasbeenacquiredfrom studies conducted in the Western population.It is widely believed that the association of these riskfactorswithCADindifferentsubpopulationsneedstobeascertained,andthereisspeculationthatdifferencesmightrangefromthefrequencyofpresenceofclassicalrisk factors to their total absence or irrelevance inthese populations. A cost-effective preventive strategywillneedtofocusonreducingriskfactorsbothintheindividualandinthepopulationatlarge.

Effective screening, evaluation and managementstrategiesforCADarewell-establishedinhigh-incomecountries, but these strategies have not been fullyimplemented in India which was noted by Mohanetal(2001).Akeyfactorthathampersthedevelopmentof such preventive strategies in developing countriessuchasIndiaisthemeageramount(8%)ofpublishedliterature on CAD research available from thesecountries (Mackay and Mensah, 2004). Of particularconcerntoIndiaisnotonlythehighburdenofCAD,butalsotheeffectsofthesediseasesontheproductiveworkforce aged 35-65 years. Heart diseases are risingin Asian Indians 5-10 years earlier than in otherpopulationsaround theworld.Themeanage forfirstpresentationofacutemyocardial infarction inIndiansis 53 years. CAD that manifests at a younger agecan have devastating consequences for an individual,the family and society. Prevention of these deaths inyoungpeopleisanation’smoralresponsibility(Sharmaand Ganguly, 2005). A strategy involving preventionof CADs long before their onset will be more cost-effective thanproviding interventionsat a stagewhenthediseaseiswell-established.

Therefore, it is imperative to undertake largepopulation-based, prospective studies in developingcountries such as India to identify CAD risk factors,both conventional and novel. Careful scrutiny ofavailable scientific evidence for modifiable CAD risk

factors(elevatedserumtotalandLDL-C,lowHDL-C,smoking,diabetes,hypertension, low levelofphysicalactivity and central obesity) in association withgenetically predisposing factors like Lp(a) in Indianpopulation may be helpful in formulating a moreimmediateCADpreventionstrategy.

GiventheexplosionofdiabetesandCADinIndiaandinviewof thedifferences inrace,culture,wayof life,diet, stress and strain and the myriad other factors,increasedemphasisonlifestylemodification,includingdiet,exercise,weightreductionandwheneverrelevant,stress reduction, isurgentlyneeded.A comprehensivesurveillancesystemofriskfactorsandCADwillbeaninvaluable public health research tool for monitoringpopulation health status, guiding resource allocationand policy, identifying and prioritizing interventionsfor subpopulations at particular risk, identifyingdisparities in outcomes and planning and evaluatinghealth programs. Carefully planned preventionprograms with intervention strategies by catching thevulnerable individuals at an early age could also betaken up in different parts of the country to preventthetwinepidemicofdiabetesandCAD;asbothhavecommon causative factors, and prevention strategiescould also be combined judiciously to prevent bothdisorders,asthiswouldmakeitmorecost-effective.

Resources should be directed towards applying theexistingknowledgebasetotackletheCADepidemicinpolicy, capacitybuilding and research arenas.Controlof the CAD epidemic in the Indian subcontinent istenable in the foreseeable future,provided thatpolicymakers,healthprofessionals and the laypublic in theIndiansubcontinentacknowledge itspotential impactand promptly act to address to make a major steptowardsCADfreesociety.

Suggested ReadingAhmad N, Bhopal R. Is coronary heart disease risingin India? A systematic review based on ECG definedcoronaryheartdisease.Heart2005;91(6):719-25.

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

Arzamendi D, Benito B, Tizon-Marcos H, Flores J,TanguayJF,LyH,etal.Increaseinsuddendeathfromcoronary artery disease in young adults. Am HeartJ2011;161(3):574-80.

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BhattacharyyaM.CoronaryheartdiseasepreventioninKolkata, India. J R Soc Promot Health 2003;123(4):222-8.BegomR,SinghRB.PrevalenceofcoronaryarterydiseaseanditsriskfactorsintheurbanpopulationofSouthandNorthIndia.ActaCardiol1995;50(3):227-40.BhatiK.Causesandherbalremediesforcoronaryarterydisease or heart problem. Available at: http://www.sooperarticles.com/health-fitness-articles/heart-disease-articles/causes-herbal-remedies-coronary-artery-disease-heart-problem-368593.html, Published on 28th Mar2011.Boland LL, Folsom AR, Sorlie PD, Taylor HA,Rosamond WD, Chambless LE, et al. Occurrenceof unrecognized myocardial infarction in subjectsaged 45 to 65 years (the ARIC study). Am J Cardiol2002;90(9):927-31.Calvet D, Touzé E, Varenne O, Sablayrolles JL,Weber S, Mas JL. Prevalence of asymptomaticcoronaryarterydisease in ischemic strokepatients: thePRECORISstudy.Circulation2010;121(14):1623-9.Chadha SL, Radhakrishnan S, Ramachandran K,KaulU,GopinathN.Epidemiologicalstudyofcoronaryheart disease in urban population of Delhi. IndianJMedRes1990;92:424-30.Chin CY, Pengal S. Cardiovascular disease risk in asemirural community in Malaysia. Asia Pac J PublicHealth2009;21(4):410-20.Ebrahim S, Taylor F, Ward K, Beswick A, Burke M,Davey Smith G. Multiple risk factor interventions forprimarypreventionofcoronaryheartdisease.CochraneDatabaseSystRev2011;(1):CD001561.EnasEA,GargA,DavidsonMA,NairVM,HuetBA,Yusuf S. Coronary heart disease and its risk factors infirst-generationimmigrantAsianIndianstotheUnitedStatesofAmerica.IndianHeartJ1996;48(4):343-53.EnasEA,SalimYusuf.ThirdMeetingoftheInternationalWorkingGrouponCoronaryArteryDisease in SouthAsians.29March1998,Atlanta,USA. IndianHeart J1999;51(1):99-103.Enas EA, Yusuf S, Mehta JL. Prevalence of coronaryarterydiseaseinAsianIndians.AmJCardiol1992;70(9):945-9.GeethaL,DeepaM,AnjanaRM,MohanV.Prevalenceandclinicalprofileofmetabolicobesityandphenotypicobesity inAsianIndians. JDiabetesSciTechnol2011;5(2):439-46.Grau M, Bongard V, Fito M, Ruidavets JB, Sala J,TaraszkiewiczD,etal;REGICOR,GENESInvestigators.Prevalence of cardiovascular risk factors in men withstablecoronaryheartdisease inFranceandSpainArchCardiovascDis2010;103(2):80-9.

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HariharanS,ChenD,VialvaM,ExeterH,Billingy I,BobbKA,etal.Outcomeevaluationofcoronaryarterybypass grafting surgery applying the EuroSCORE ina Caribbean developing country. Heart Surg Forum2010;13(5):E287-91.

HatmiZN,TahvildariS,GafarzadehMotlagA,SabouriKashani A. Prevalence of coronary artery diseaserisk factors in Iran: a population based survey. BMCCardiovascDisord2007;7:32.

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Heartdiseases(2011).TheHeartandStrokeFoundation.Available at: http://www.heartandstroke.com/site/c.ikIQLcMWJtE/b.3483991/k.34A8/Statistics.htm.

IcazaG,NúñezL,MarrugatJ,MujicaV,EscobarMC,JiménezAL,etal.EstimationofcoronaryheartdiseaseriskinChileansubjectsbasedonadaptedFraminghamequations.RevMedChill2009;137(10):1273-82.

Idris I, Deepa R, Fernando DJ, Mohan V. Relationbetweenageandcoronaryheartdisease (CHD)risk inAsian Indian patients with diabetes: a cross-sectionaland prospective cohort study. Diabetes Res Clin Pract2008;81(2):243-9.

IwasakiM,KurodaS,NakayamaN,HokariM,YasudaH,SaitoH,etal.Clinicalcharacteristicsandoutcomesin carotid endarterectomy for internal carotid arterystenosisinaJapanesepopulation:10-yearmicrosurgicalexperience.JStrokeCerebrovascDis2011;20(1):55-61.

Jain P, Kooner JS, Raval U, Lahiri A. Prevalence ofcoronary artery calcium scores and silent myocardialischaemia was similar in Indian Asians and Europeanwhites in a cross-sectional study of asymptomaticsubjectsfromaUKpopulation(LOLIPOP-IPC).JNuclCardiol2011;18(3):435-42.

KivimäkiM,BattyGD,HamerM,FerrieJE,Vahtera-J,Virtanen M, et al. Using additional information onworking hours to predict coronary heart disease: acohortstudy.AnnInternMed2011b;154(7):457-63.

KivimäkiM,NybergST,BattyGD,ShipleyMJ,FerrieJE, Virtanen M, et al. Does adding information onjob strain improve risk prediction for coronary heartdiseasebeyondthestandardFraminghamriskscore?TheWhitehallIIstudy.IntJEpidemiol2011aMay9.(Epubaheadofprint)

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KonishiM,IsoH,IidaM,NaitoY,SatoS,KomachiY,etal.Trendsforcoronaryheartdiseaseanditsriskfactorsin Japan: epidemiologic and pathologic studies. JpnCircJ1990;54(4):428-35.KumarR,SinghMC,SinghMC,AhlawatSK,ThakurJS,SrivastavaA,etal.Urbanizationandcoronaryheartdisease: a study of urban-rural differences in northernIndia.IndianHeartJ2006;58(2):126-30.

Kumaran K, Fall CH, Martyn CN, Vijayakumar M,Stein CE, Shier R. Left ventricular mass and arterialcompliance: relation to coronary heart disease andits risk factors in South Indian adults. Int J Cardiol2002;83(1):1-9.

Lanjewar C, Jolly S, Mehta SR. Effects of aspirationthrombectomy on mortality in patients with acutemyocardialinfarctionundergoingprimarypercutaneouscoronaryintervention:ameta-analysisoftherandomizedtrials.IndianHeartJ2009;61(4):335-40.

Mackay J, Mensah G. The atlas of heart disease andstroke.WorldHealthOrganization,CentersforDiseaseControlandPrevention;2004.

Mammi MV, Pavithran K, Abu Rahiman P,Pisharody R, Sugathan K. Acute myocardial infarctioninnorthKerala.A20-yearhospitalbasedstudy.IndianHeartJ1991;43(2):93-6.

MathersCD,LoncarD.Projectionsofglobalmortalityandburdenofdisease from2002 to2030.PLoSMed2006;3(11):e442.

MohanV, Deepa R, Rani SS, Premalatha G; ChennaiUrbanPopulationStudy (CUPSNo. 5).Prevalence ofcoronaryarterydiseaseanditsrelationshiptolipidsinaselectedpopulationinSouthIndia:TheChennaiUrbanPopulation Study (CUPS No. 5). J Am Coll Cardiol2001;38(3):682-7.

MohanV,VassyJL,PradeepaR,DeepaM,SubashiniS.TheIndiantype2diabetesriskscorealsohelpsidentifythose at risk of macrovascular disease and neuropathy(CURES-77). J Assoc Physicians India. 2010a;58:430-3.

MohanV,VenkatramanJV,PradeepaR.Epidemiologyof cardiovascular disease in type 2 diabetes: theIndian scenario. J Diabetes Sci Technol 2010;4(1):158-70.

MurrayCJL,LopezAD.TheGlobalBurdenofDisease:AComprehensiveAssessmentofMortalityandDisabilityfrom Disease, Injuries and Risk Factors in 1990andProjectedto2020.HarvardUniversityPress:Boston,Ma;1996.OizumiT,DaimonM,JimbuY,WadaK,KamedaW,SusaS,etal.Impairedglucosetoleranceisariskfactor

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for stroke in a Japanese sample - the Funagata study.Metabolism2008;57(3):333-8.OnatA,UğurM,CiçekG,AyhanE,DoğanY,KayaH,etal.TheTurkishAdultRiskFactorsurvey2009:similarcardiovascularmortality in rural andurbanareas.TurkKardiyolDernArs2010;38(3):159-63.Ong P, Athanasiadis A, Borgulya G, Voehringer M,SechtemU.3-yearfollow-upofpatientswithcoronaryartery spasmas causeof acute coronary syndrome: theCASPAR(coronaryarteryspasminpatientswithacutecoronarysyndrome)studyfollow-up.JAmCollCardiol2011;57(2):147-52.OzdemirH,CiftçiE,TapisizA,InceE,TutarE,AtalayS,DogruU.ClinicalandepidemiologicalcharacteristicsofchildrenwithKawasakidiseaseinTurkey.JTropPediatr2010;56(4):260-2.PavlovićM,CorovićN,GomziM,SimićD,JazbecA,Tiljak MK. Smoking habits, signs of chronic diseasesandsurvival ininlandandcoastalregionsofCroatia:afollow-upstudy.CollAntropol2004;28(2):689-700.PintoRJ,BhagwatAR,LoyaYS, SharmaS.Coronaryartery disease in premenopausal Indian women:risk factors and angiographic profile. Indian Heart J1992;44(2):99-101.Pitsavos C, Kavouras SA, Panagiotakos DB, Arapi S,Anastasiou CA, Zombolos S, et al; GREECS StudyInvestigators.PhysicalactivitystatusandacutecoronarysyndromessurvivalTheGREECS(GreekStudyofAcuteCoronarySyndromes) study. JAmCollCardiol2008;27;51(21):2034-9.RastogiT,VazM,SpiegelmanD,ReddyKS,BharathiAV, Stampfer MJ, et al. Physical activity and riskof coronary heart disease in India. Int J Epidemiol2004;33(4):759-67.SecrestAM,CostacouT,GuteliusB,MillerRG,SongerTJ, Orchard TJ. Associations between socioeconomicstatus and major complications in type 1 diabetes:the pittsburgh epidemiology of diabetes complication(EDC)Study.AnnEpidemiol2011;21(5):374-81.Sharma M, Ganguly NK. Premature coronary arterydisease in Indians and its associated risk factors. VascHealthRiskManag2005;1(3):217-25.Singh RB, Rastogi SS, Rao PV, Das S, Madhu SV,DasAK,etal.Dietandlifestyleguidelinesanddesirablelevels of risk factors for the prevention of diabetesand its vascular complications in Indians: a scientificstatement of The International College of Nutrition.IndianConsensusGroupforthePreventionofDiabetes.JCardiovascRisk1997;4(3):201-8.SinghS,AulakhR,BhallaAK,SuriD,Manojkumar-R,Narula N, et al. Is Kawasaki disease incidence

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121Asian Journal of Clinical Cardiology, Vol. 14, No. 4, August 2011

Continuous Change in the Direction of Atrial Flutter Waves on Either Side of Isoelectric/LineSR 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: Atrialflutter,electrocardiogram,torsadesdepointes

ExSrProfessorandHeadDept.ofCardiologyPrincipal,JLNMedicalCollege,AjmerAddress for correspondenceDrSRMittal XI/101,BrahampuriAjmer,Rajasthan-305001E-mail:[email protected]

Case Report

A known case of hypertension and left ventricularfailure presented with deterioration of breathlessness.Electrocardiogramrevealedatrialflutterwithchangingatrioventricular conduction, left ventricular hyper-trophyandSTsegmentdepression in leadsI, II,aVLandV3-V6(Fig.1).

In lead V1, atrial flutter waves showed a continuouschangeinthedirectionfromonesidetotheothersideofisoelectricline(Fig.2).

Discussion

The term ‘Torsades de pointes’ is used for fastventricular tachycardia with changing amplitude andduration of QRS on either side of isoelectric line inthesettingofprolongedQTinterval.1,2Inourpatient,regularchangeinthedirectionandamplitudeofatrial

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.

CAse report

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

flutterwavesoneithersideofisoelectriclineissimilarto change in QRS configuration during ‘Torsadesde pointes’. This finding suggests regular change indirection of conduction in the re-entry circuit in thehorizontal plane. It could also be due to more thanone re-entry circuit with gradual shift from one toanother. Such patients could be more prone to haveatrialfibrillation.

ReferencesRhoRW,PageRL.Ventriculararrhythmias.In:Hurst’sTheHeart.12thedition,FusterV,WalshRA,HarringtonRA(Eds.),McGrawHill,NewYork2011:1006-24.

OlginJE,ZipesDP.Specificarrhythmias:diagnosisandtreatment. In: Braunwald’s Heart Disease. 8th edition,Libby P, Bonow RO, Mann DL, Zipes DP (Eds.),Saunders,Philadelphia2008:863-922.

1.

2.

Should I screen each patient for presence of carotid neck artery blockages? The guideline says no. The potential harms include risksassociated with the screening procedure itself like falsepositive findings leading to anxiety and the potential forunnecessary surgical procedures. Carotid angiographyis associated with risk of neurological complicationsincludingstroke,withratesrangingfrom0.1to1%.

what are the screening methods available?CarotidultrasoundfollowedbycatheterangiographyCarotidultrasoundfollowedbyMRAUltrasoundalone

how reliable is Doppler carotid study for detecting blockages? Thereliabilityisvariableandoperator-dependent.

how risky is carotid stenting or surgery? Both endarterectomy and carotid stenting are associatedwith an increased30-day riskof stroke anddeath.Theseareintherangeof2.3-3.7%forendarterectomy.

how common is carotid artery blockage in general population?Theprevalenceofcarotidstenosisingeneralpopulationis<1%. Screening with resultant surgical procedures causesmore strokes than it can prevent. For severe (≥70%)carotid stenosis, the prevalence increases with age fromapproximately0to3%.

At what prevalence is screening beneficial?Only at prevalence rates of over 20% significant benefitsare seen, with at best about 100 strokes prevented forevery 10,000 screened. Clinical features cannot identifyasymptomatic individuals likely to have carotid stenosis.The annual risk of stroke in patients with asymptomaticcarotidarterystenosisisrelativelylow.

when to screen for carotid blockages?Carotidduplexultrasonography isnotrecommendedforroutine screening of asymptomatic patients who haveno clinical manifestations of or risk factors for athero-sclerosis. However, one should screen asymptomaticindividualswhohave:

CarotidbruitPeripheralarterialdiseaseCoronarydiseaseAorticaneurysmTwoormoreriskfactorsforatheroscleroticdisease.

what is symptomatic carotid artery blockage?Patients who have had a stroke or transient ischemicattack (mini paralysis) due to carotid stenosis areconsidered symptomatic and often benefit from carotidrevascularization. Symptoms mean transient or permanentfocal neurologic symptoms related to the affected artery(samesidelossofvision,oppositesideweaknessornumbnessof an extremity or the face, difficulty in speech or loss ofspeech). Patients with nonspecific neurologic symptoms(dizziness or syncope/near syncope) are not considered inthedefinitionofsymptomaticcarotidstenosis.

what are the medical interventions for carotid blockages?The interventions are management of hypertension,smoking cessation, use of statin drugs and low-doseaspirin.

when should one decide for carotid endarterectomy or removal of blockages with catheter?It is indicated for selected medically stable patients withasymptomatic carotid stenosis of 60-99% who have a lifeexpectancyofatleastfiveyears,providedtheperioperativeriskofstrokeanddeathis<3%.However,long-termoutcomesforpatientswithcarotidblockagesmanagedbyintensivemedicaltherapymaybesimilartosurgicalmanagement.

Carotid Artery Blockages

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Electric alternans in electrocardiogram(ECG) isadiagnostichallmarkofcardiactamponade.Wedescribe herein an interesting case of left side

pleural effusion producing pseudo electric alternanspattern in ECG without any evidence of cardiactamponadeeitherclinicallyorbyechocardiography.

Case Report

A 32-year-old male presented in medical OPD withcomplaints of fever and breathlessness since past twodays. On examination, his pulse was 120/min, bloodpressure - 90/68 mmHg, respiratory rate - 20/minand temperature –100.4°F. There was no cyanosis,clubbing, icterus, pallor or lymphadenopathy. Jugularvenous pressure was normal. On auscultation, therewasreducedairentryinleftinfrascapularregion.Heartsoundswerenormal.Pulsusparadoxuswasabsent.

Routine laboratory investigations including renal,hepaticfunctionsandbloodbiochemistrywerewithinnormal limits.X-raychest (PAview) showed left sidemoderatepleuraleffusion(Fig.1).ECGrevealedsinustachycardiawithlowvoltageQRScomplexes,showingelectric alternans (Fig. 2). On echocardiogram,there was minimal pericardial effusion not safe forpericardiocentesis. Pleural fluid when aspirated underultrasonographic guidance revealed 300 ml of straw

AbstrACt

We report herein a case of isolated left pleural effusion producing electric alternans in electrocardiogram without any peri-cardial 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: Pleuraleffusion,electricalternans,cardiactamponade

Pseudo Electric Alternans by Left Pleural Effusion

Monika Maheshwari*, Tarachand Saini**

*AssistantProfessor **ResidentDept.ofMedicine,JLNMedicalCollege,AjmerAddress for correspondenceDrMonikaMaheshwariNaveenNiwas,434/10BapuNagar,AjmerE-mail: [email protected]

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

coloredpleuralfluidtubercularinetiology.Patientwasstarted antitubercular drugs and was discharged withsymptomaticrelief.RepeatECGafter15daysrevealeddisappearanceofelectricalternans.

Discussion

Electric alternans is a broad term that describesalternate beat variation in the direction, amplitudeanddurationofanycomponentoftheECGwaveform(i.e. P, PR, QRS, R-R, ST, T, U).1 Suggestedmechanisms of electrical alternans include excitationofalternatingpopulationsofcellsinsequentialbeats,2

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

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

alternationoftheAPwaveform3andglobalmovementof the heart within the chest.4 Electrocardiographicalternans was first described in 1908 by Hering.5Shortly thereafter, Lewis6 recognized that cardiacalternans could occur in normal hearts as a resultof marked acceleration of heart rate and also inthe impaired or intoxicated myocardium. Pleuraleffusion in presence of an otherwise insignificantpericardial effusion can increase intrapericardialpressure to such a degree that cardiac tamponade

results.7 But this is usually seen in massive, largepleural effusion or in bilateral pleural effusionwith mediastinum getting sandwiched betweenincreased pressure in two pleural spaces. Isolatedmoderateleftpleuraleffusioncausingelectricalternansis not reported in literature so far to the best of ourknowledge. Hence, it was worth reporting this case.Wepostulatethatsuddenandrapidcollectionoffluidin pleural space in our case could result in increasedintracardiac pressure sufficient to cause cardiactamponade thereby resulting in electric alternans.In such cases, aspiration of pleural fluid shouldbe done immediately rather than pericardiocentesisaswedidinourcase.

ReferencesKalterHH,SchwartzML.Electricalternans.NYStateJMed1948;1:1164-6.BrodyJG,RossmanPL.Electricalternans:reportoftwoadditionalcases.JAMA1937;108(10):799-802.BoyyetMR,JewellBR.Analysisoftheeffectsofchangesinrateandrhythmuponelectricalactivityintheheart.ProgBiophysMolBiol1980;36(1):1-52.ColvinJ.Electricalalternans:casereportandcommentsontheliterature.AmHeartJ1958;55(4):513-7.Hering HE Das Wesen des Herzalternans. MunchenMedWochenshr1908;4:1417-21.LewisT.Notesuponalternationoftheheart.QJMed1911;os4(2):141-4.Yaska K, Wann SL, Sagaer K. Pleural effusion as acauseofrightventriculardiastoliccollapse.Circulation1992;86:609-17.

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I II III

aVR aVL aVF

V1 V2 V3

V4V5 V6

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125Asian Journal of Clinical Cardiology, Vol. 14, No. 4, August 2011

QT Means SystoleeCG FormulAe

Source: AJCC’sElectrocardiographyFormulaeinClinicalPractice,pg:39-41.

QT interval (QTc ≤0.40 second)

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

Poor Man’s Guide to upper limits of QT: ForHR=70bpm,QT≤0.40second;forevery10bpmincrease above 70 subtract 0.02 second, and forevery10bpmdecreasebelow70add0.02 second.Forexample:

QT≤0.38@80bpm

QT≤0.42@60bpm

QT Prolongation

Drugs

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

“Lytes”

Hypokalemia,hypocalcemiaorhypomagnesemia

CNS

Catastrophes such as stroke, seizure, coma,intracerebralorbrainstembleeding

Severalotherconditions (i.e.bundlebranchblock,infarction and ischemia) may also cause QTprolongation.

QT Interval

QTintervalismeasuredfrombeginningofQRStoendofT-waveinthefrontalplane

Normal:Heartratedependent(correctedQT=QTc=measuredQT÷Sq-rootRRinseconds;upperlimitforQTc=0.44second)

Long QT syndrome:“LQTS”(basedonupperlimits for heart rate; QTc ≥0.47 second formalesand≥0.48secondinfemalesisdiagnosticforhereditaryLQTSinabsenceofothercausesofincreasedQT)

This abnormality may have important clinicalimplicationssinceitusuallyindicatesastateofincreasedvulnerabilitytomalignantventriculararrhythmias, syncope and sudden death. TheprototypearrhythmiaoftheLQTSistorsadedepointes, a polymorphic ventricular tachycardiacharacterizedbyvaryingQRSmorphologyandamplitudearoundtheisoelectricbaseline

CausesofLQTSincludethefollowing:

Drugs (many anti-arrhythmics, tricyclics,phenothiazinesandothers)

Electrolyte abnormalities (↓ K+, ↓ Ca++,↓Mg++)

CNS disease (especially subarachnoidhemorrhage,stroketrauma)

Hereditary LQTS (e.g. Romano-Wardsyndrome)

Coronary heart disease (some post-MIpatients)

Rule:ProlongedQT=Systolicdysfunction

n

n

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The QT Interval - Key Points

TheQTintervalismeasuredfromtheonsetontheQ-wave(ortheonsetoftheR-waveifthereisnoQ)

untiltheterminationoftheT-wave.

SelectthatleadinwhichtheQTintervalappearstobelongest.

PrecisemeasurementoftheQTintervalisusuallynotnecessary.Practicallyspeakingoneonlycaresifthe

QTintervalisnormalorprolonged.

HypercalcemiaproducesQTshorteningbutthisisverydifficulttorecognizeclinically.

Determination of the QT interval means little when the heart rate is rapid (faster than about

90-100/min).

RR Interval - Heart Rate

RRintervalisthedurationofventricularcardiaccycle(anindicatorofventricularrate)

QT=ShouldbelessthanhalfofRR

eCG FormulAe

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127Asian Journal of Clinical Cardiology, Vol. 14, No. 4, August 2011

Initial Management of Atrial Fibrillation

Source: AdaptedfromAmFamPhysician.2002;66(2):249-236.

Patientwithdiagnosisofatrialfibrillation

Hemodynamicallystable(noangina,nohypotension,etc.)?

Considerlong-termanticoagulation.

Assesscauseofatrialfibrillation;hospitaldischarge,follow-up

NoYes

Assesscauseofatrialfibrillation;hospitaldischarge,follow-up

Yes

Electricalcardioversion:sedate,thenshock(100J,200J,300J,360J)untilsinusrhythmreturns.

Control ventricular rate (goal = <100beats per minute): administer diltiazem,15mg IVover2minutes, then5 to15mg per hour by continuous IV infusionoradministerotherrate-controldrug.

Spontaneousconversiontosinusrhythm?

Considerlong-termanticoagulation.

Considercardioversion,ifindicated(seetext):StartheparinIV;thenchoose— Atrialfibrillation<48hours:immediatemedical orelectricalcardioversion Atrialfibrillation>48hoursorunknown duration: Laterelectivecardioversion(electrical cardioversionwithorwithoutmedical cardioversion)after3weeksofwarfarin EarlyTEE–guidedcardioversion(electrical cardioversionwithorwithoutmedical cardioversion)

Contraindicationstocardioversion?

Yes No

No

NoYes

IV=Intravenous;J=Joule;TEE=Transesophagealechocardiography.

CliniCAl AlGorithm

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Is there any Role of LAVI in LV Diastolic Failure?

G Devpura

Left atrial volume index (LAVI) is increasinglybeingrecognizedasarelativelyload-independentmarker of left ventricular (LV) filling pressure.

LAVI on resting echocardiography, specifically inpatientswithsuspectedheartfailure(HF)andnormalLV systolic function is a powerful independentpredictor of LV diastolic dysfunction as predictedby serum N-terminal pro-B-type natriuretic peptide(NT-proBNP). Inapopulationwithahigh suspicionof diastolic HF, LAVI may significantly contribute todiagnosticprecision.

LimandhiscolleaguesfromtheDept.ofCardiovascularMedicine, Northwick Park Hospital, Middlesex, UKassessed the capacity of LAVI to predict LV diastolicdysfunction in comparison with NT-proBNP inpatients with suspected HF and a normal ejectionfraction(EF).1

They did echocardiography studies in 137 patientswith suspected HF and calculated both LAVI andNT-proBNP estimations. Raised LAVI and reducedLV systolic function were defined as >26 ml/m2and LVEF <50%, respectively. Of 137 patients, 21were excluded (two with significant mitral valvedisease and 19 with AF). Of the remaining 116subjects,92showednormalLVsystolic function.Theunivariate predictors of serum log NT-proBNP wereage (p < 0.001), LA dimension (p = 0.001), LAVI(p<0.001),A-wave (p=0.001),E:A(p=0.07)andseptalwallthickness(p=0.004).

However, on multivariate analysis, LAVI was foundtobe themost consistent and significantpredictorofNT-proBNP.

Is there any significance of mitral L-wave?

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

patientswithLVhypertrophy(LVH).InpatientswithLVH, the mitral L-wave appears to be a marker ofpseudonormal LV filling and predictor of future HFevents.

Lam and his colleagues from the Division ofCardiology, Dept. of Medicine, National Universityof Singapore, examined the relationship of the mitralL-wave with echocardiographic indexes of diastolicfunctionandHFeventsinpatientswithLVH.2

Of177patients,theL-wavewaspresentin35(20%)(GroupI)andabsentin142(GroupII).

Patients in Group I had higher early (E) to late (A)transmitralflowvelocity(E/A)ratio(1.2vs0.8),shortermitral E-wave deceleration time (201 vs 225 msec),lower pulmonary venous systolic/diastolic velocityratio (1.1 vs 1.6), shorter LV isovolumic relaxationtime (83 vs 94 msec), larger left atrial volume (36vs 23 ml/m2), and higher E to early mitral annularvelocity (E/E’) ratio (septal E/E’, 12.2 vs 9.1; lateralannular E/E’, 10.9 vs 7.8) compared with Group II(all p < 0.05). The difference between pulmonaryvenousatrialreversalandmitralA-wavedurationswas≥30msecinmorepatientsofGroupI(70%vs6%,p< 0.001). During a mean follow-up of 12.0 months,11patientswerehospitalizedforHF.

The L-wave was associated with a hazard ratio (HR)of 4.7 (p = 0.011) for incident HF, and remaineda significant predictor (HR 4.2, p = 0.026) afteradjustmentforcardiovascularriskfactors.

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

ReferencesLimTK,etal.EurJHeartFail2006;8(1):38-45.Lam CS, et al. J Am Soc Echocardiogr 2005;18(4):336-41.

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1.2.

expert opinion

AssociateProfessor,Dept.ofMedicineSeniorCardiologist,SMSMedicalCollegeandHospital,Jaipur

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ACCF/AHA Release Guideline for Early Cardiovascular Risk Assessment

prACtiCe GuiDelines

Atherosclerotic cardiovascular disease is theleading cause of death among adults in the United States. Because coronary heart

disease(CHD)hasalongasymptomaticlatentperiod,there is anopportunity for earlypreventivemeasures.The American College of Cardiology Foundation(ACCF) and the American Heart Association (AHA)have created a guideline to assist physicians with theearly cardiovascular risk assessment of asymptomaticadults.Thegoalofthisassessmentistoguidetargetedpreventive efforts based on the patient’s individualrisk. Initial evaluation includes broadly categorizingpatientsbyrisk.Furtherinterventionisbasedontheseriskassessments.

Recommendations

Global Risk Scoring

Global risk scores (e.g.,FraminghamRiskScore) thatincludemultiple traditional cardiovascular risk factorseffectivelycombineindividualriskfactormeasurementsinto a single quantitative estimate of risk. Thesescores should be used in all cardiac risk assessmentevaluationstoguidetheinitiationoftargetedpreventivemeasures.

Family history and Genomic Testing

Family history of atherothrombotic cardiovasculardiseaseshouldbeobtained,althoughgenotypetestingisnotrecommended.

Laboratory Testing

Lipoprotein and Apolipoprotein. Lipid measurements,includinglipoproteinlevels,apolipoproteinlevels,andparticle size/density,beyond the standard lipidprofilearenotrecommended.

Natriuretic Peptide.Measurementofnatriureticpeptidelevelsisnotrecommended.

C-Reactive Protein. Measurement of C-reactiveprotein levels can be useful in selecting candidatesfor statin therapy in the following patients: men50 years and older and women 60 years and olderwith a low-density lipoprotein cholesterol level lessthan130mgperdL (3.37mmolperL)whoarenoton lipid-lowering medications, hormone therapy, orimmunosuppressant therapy and do not have clinicalCHD,diabetesmellitus,chronickidneydisease,severeinflammatory conditions, or contraindications tostatins.MeasurementofC-reactiveprotein levelsmaybe reasonable in younger patients with intermediatecardiovascular risk, but is not recommended forhigh-riskpatients.

A1C.MeasurementofA1Clevelsmaybereasonableinpatientswithoutdiabetestoassesscardiovascularrisk.

Microalbuminuria. Urinalysis to detect micro-albuminuriaisreasonableinpatientswithhypertensionordiabetes,andmaybereasonableinintermediate-riskpatientswithouttheseconditions.

Lipoprotein-Associated Phospholipase A2. Measurementof lipoprotein-associatedphospholipaseA2 levelsmaybereasonableinintermediate-riskpatients.

Imaging and other Testing

Resting Electrocardiography (ECG). Resting ECG isreasonable in patients with hypertension or diabetes,and may be considered in patients without theseconditions.

Transthoracic Echocardiography. Echocardiography todetect left ventricularhypertrophymaybe consideredinpatientswithhypertension,butisnotrecommendedinthosewithouthypertension.

Carotid Intima-Media Thickness. Measurement ofcarotid intima-media thickness is reasonable inintermediate-riskpatients;however,high-qualityresultsaredependentonproperlyperformingthetest.

Brachial/Peripheral Flow–Mediated Dilation.Peripheralarterialflow–mediateddilationisnotrecommended.Source: AdaptedfromAmFamPhysician.2011;84(2):234-235.

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Arterial Stiffness. Measurement of arterial stiffness isnotrecommendedoutsideofresearchsettings.

Ankle-Brachial Index. Measurement of ankle-brachialindexisreasonableforintermediate-riskpatients.

Exercise and Stress ECG. Exercise ECG may beconsidered in intermediate-risk patients (includingsedentary adults who are considering a vigorousexercise program), particularly if non-ECG markers,suchasexercisecapacity,arenoted.

Stress Echocardiography.Stress echocardiography isnotrecommendedinlow-orintermediate-riskpatients.Itis used mainly in the advanced cardiac evaluation ofsymptomatic patients to estimate prognosis in thosewith known coronary artery disease and to assessthosewithknownorsuspectedvalvularheartdisease.

Myocardial Perfusion Imaging. Stress myocardialperfusion imaging may be considered in patientswith diabetes or a strong family history of CHD, orif a previous risk assessment suggested high risk of

CHD. It is not indicated for patients with low orintermediaterisk,and isusedmainly in theadvancedcardiac evaluation of symptomatic patients and toestimate prognosis in patients with known coronaryarterydisease.

Calcium Scoring Methods. Measurement of cardiaccalciumlevelsisreasonableinpatientswithintermediaterisk(10to20percent10-yearrisk),maybereasonableinthosewithlowtointermediaterisk(6to10percent10-yearrisk),andisnotrecommendedinpatientswithlowrisk(lessthan6percent10-yearrisk).Measurementof cardiac calcium levels is reasonable in patients40yearsandolderwithdiabetes.

Coronary Computed Tomography Angiography. Coro-nary computed tomography angiography is notrecommended.

Magnetic Resonance Imaging. Magnetic resonanceimaging for detection of vascular plaque is notrecommended.

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From the Journals ...reseArCh review

Is Compression-Only CPR More Effective Than Standard CPR?

Background: There has been increasing interestin cardiopulmonary resuscitation (CPR) usingcompressions alone over compressions plus rescuebreathing. Besides theoretically improving cerebralperfusion, chest compressions may be preferable torescue breathing among bystanders performing CPR.Animal models and a previous randomized humantrial have found some clinical benefit inpersonswhoreceived only chest compressions, compared witha traditional approach of compressions plus rescuebreathing.ReaandcolleaguesconductedarandomizedcontrolledtrialofCPRcompressionswithorwithoutrescuebreathingamongpatientswithpotentialcardiacarresttodeterminewhichmethodismoreeffective.

The Study: Participants were identified from 911system calls. Eligibility was determined if the 911dispatcherconcludedthatthepersonwasunconsciousand not breathing normally, and if the caller waswilling to perform CPR with the dispatcher’sassistance.Callerswererandomizedtobeinstructedtogive chest compressions alone, or chest compressionsplus rescuebreathing ina15:2 ratio,until thearrivalof emergency medical services (EMS) personnel. Theprimary outcome was survival to hospital discharge,with a secondary outcome of favorable neurologicstatus at the time of hospital discharge (defined asno worse than moderate cerebral disability). Patientswithcardiacarrestattributedtotrauma,drowning,orasphyxiation (e.g., choking), who were younger than18 years, and who were already receiving CPR wereexcluded.Patientsalsowereexcludedretrospectivelyiftheywere later determinedbyEMSpersonnel tonothavebeenincardiacarrest.

Results: A total of 1,941 participants were includedin the study, with an average EMS response timeof 6.5 minutes from dispatch to arrival at thescene. No significant differences were seen betweengroups regarding survival to hospital discharge (12.5percent for compressions alone versus 11.0 percent

for compressions plus rescue breathing), or in thelikelihood of survivors having favorable neurologicstatus(14.4versus11.5percent,respectively).Amongpatients who were determined to have had a cardiaccauseof arrest, compression-onlyCPRwas associatedwithbetterneurologicstatusatdischarge(18.9percentfor compressions alone versus 13.5 percent withcompressions plus rescue breathing), although overallsurvivalratesremainedsimilar(5.0versus7.2percent,respectively).

Conclusion: The authors conclude that givingbystandersCPRinstructionstousechestcompressionsalonedoesnotincreaseoverallsurvivalcomparedwithinstructions to use chest compressions plus rescuebreathing, although in this study it did somewhatimprove neurologic outcomes in patients who had acardiaccauseofarrest.Theseresultssupportastrategyforlaypersonsthatemphasizeschestcompressionsandminimizesrescuebreathing.

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 Re-vascularization and Aggressive Drug Evaluation(COURAGE) study,whichprovidedoptimalmedicaltherapy (OMT) to all patients and demonstratedno incremental advantage of percutaneous coronaryintervention (PCI) on outcomes other than angina-relatedqualityof life in stablecoronaryarterydisease(CAD), suggests that a trial of OMT is warrantedbefore PCI. It is unknown to what degree OMT isapplied before PCI in routine practice or whether itsuseincreasedaftertheCOURAGEtrial.

Objective: To examine the use of OMT in patientswithstableanginaundergoingPCIbeforeandafterthepublicationoftheCOURAGEtrial.

Design, Setting and Participants: An observationalstudy of patients with stable CAD undergoing PCIintheNationalCardiovascularDataRegistrybetween

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reseArCh review

September 1, 2005, and June 30, 2009. Analysiscompared use of OMT, both before PCI and at thetime of discharge, before and after the publicationof the COURAGE trial. Optimal medical therapywas defined as either being prescribed or havinga documented contraindication to all medicines(antiplateletagent,β-blockerandstatin).

Main Outcome Measures: RatesofOMTbeforePCIand at discharge (following PCI) between the twostudyperiods.

Results: Among all 4,67,211 patients (1,73,416before [37.1%] and 2,93,795 after [62.9%] theCOURAGE trial) meeting study criteria, OMT wasused in 2,06,569 patients (44.2%; 95% confidenceinterval[CI],44.1-44.4%)beforePCIandin3,03,864patients (65.0%; 95% CI, 64.9-65.2%) at dischargefollowing PCI (p < 0.001). Before PCI, OMTwas applied in 75,381 patients (43.5%; 95% CI,43.2-43.7%) before the COURAGE trial and in1,31,188 patients (44.7%; 95% CI, 44.5-44.8%)after the COURAGE trial (p < 0.001). The use ofOMTatdischargefollowingPCIbeforeandaftertheCOURAGE trial was 63.5% (95% CI, 63.3-63.7%)and 66.0% (95% CI, 65.8-66.1%), respectively(p<0.001).

Conclusion: Among patients with stable CADundergoing PCI, less than half were receiving OMTbeforePCIandapproximatelytwo-thirdswerereceivingOMT at discharge following PCI, with relativelylittlechangeinthesepracticepatternsafterpublicationoftheCOURAGEtrial.

Source: Borden WB, Redberg RF, Mushlin AI, et al. JAMA 2011;305(18):1882-9.

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

Objective:Thedevelopmentofcarcinoidheartdiseasecauses significant valvular dysfunction, eventuallyleading to symptomatic right heart failure andimpaired survival. Data regarding cardiovascularsurgery are limited. We sought to identify outcomes,risks and complicationsof valve surgery for carcinoidheartdisease.

Methods: Twenty-two patients with carcinoid heartdisease underwent cardiac valve surgery between2006 and 2010. Patients were considered for surgery

if (1) they had stable carcinoid tumor, (2) they hadseverevalvulardysfunctionand(3)were symptomaticand (4) they had no other significant comorbidities.Three patients underwent tricuspid valve replacementalone,15patientsunderwenttricuspidandpulmonaryvalve replacement, two patients underwent tricuspid,pulmonary and mitral valve replacement and twopatientsunderwentquadruplevalvereplacement.

Results: Overall30-daymortalitywas18%.Causesofdeathwererightventriculardysfunction(twopatients),carcinoid crises (one patient) and pneumonia (onepatient).Fourpatientsrequiredpermanentpacemakerforcompleteheartblock.Ofthosethatsurvivedinitialsurgery,medianfollow-upwas26months(interquartilerange8-42);1-and2-yearsurvivalrateswere56%and44%,respectively.TherewasnosignificantdifferenceinsurvivalbetweenthosepatientsintheNewYorkHeartAssociation (NYHA) Class I/II, mild/moderate rightventricular dilatation or N-terminal brain natriureticpeptide (NT-proBNP)<1,245pg/ml-1comparedwiththose in NYHA class III/IV, severe right ventricularenlargementorNT-proBNP>1,245pg/ml-1,respectively.Long-term causes of death were related to advancedmetastatic carcinoid tumor. No patient requiredre-operationforbioprostheticdegeneration.

Conclusion: Valve surgery for carcinoidheart diseaseis of higher risk compared with most other forms ofvalvular surgery. However, in those that survive theoperation significant improvement in functional classoccurs.Most long-termcomplicationswere related tothetumoritselfratherthancardiaccomplications.

Source: Bhattacharyya S, Raja SG, Toumpanakis C, et al. Eur J Cardiothorac Surg 2011;40(1):168-72.

Treatment Strategies in Severe Symptomatic Carotid and Coronary Artery Disease

Coexistentcarotidarterystenosis(CS)andmultivesselcoronaryarterydisease(CAD)isnot infrequent.Onein 5 patients with multivessel CAD has a severe CS,and CAD incidence reaches 80% in those referredfor carotid revascularization. We reviewed treatmentstrategies for concomitant severe CS and CAD. Weperformedaliteraturesearch(MEDLINE)withtermsincluding carotid artery stenting (CAS), coronaryarterybypassgrafting(CABG),carotidendarterectomy(CEA), stroke and myocardial infarction (MI). The

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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 withCEA prior to CABG) or stroke (CABG prior toCEA), and the cumulative major adverse event rate(MAE - death, stroke or MI) reaches 10-12%. Withincreasing adoption of CAS, a sequential strategyof CAS followed by CABG has emerged. Registries(usually single-center) indicate an MAE rate of ≈7%for CAS followed by CABG (frequently after >30days, due to double antiplatelet therapy). Recently,1-stageCAS-CABGhasbeenintroduced.Thisinvolvesdifferent antiplatelet regimens and, in some centers,preferredoff-pumpCABG,withacumulativeMAEof1.4-4.5%. No randomized trial comparing differenttreatment strategies in CS-CAD has been conducted,and thus far reported series are prone to selection/reporting bias. In addition to the established surgicaltreatment (CEA-CABG, sequential/simultaneous),hybrid revascularization (CAS-CABG) is emerging asa viable therapeutic option. Larger, preferably multi-center, studies are required before this can becomewidelyapplied.

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:ThemainEbstein anomaly (EA) repairsare based on the monocusp reconstruction of thetricuspid valve and are limited by the frequent needfor replacement or the high recurrence of valve

regurgitation. Objective: To evaluate the feasibilityand effects of anatomical repair of Ebstein’s anomalyusing the cone reconstruction technique on patients’clinical evaluation, tricuspid valve function and rightventricular morphology. Methods: We compared theclinical,echocardiographicandradiologicaldataof52consecutivepatients,with amean ageof18.5±13.8years,submittedtotheconereconstructiontechnique,obtained in the preoperative, early postoperative(EPO) and long-term (LPO) periods. Results: Therewere two in-hospital deaths (3.8%) and two moreduring the follow-up. Mean functional class ofpreoperative heart failure improved from 2.2 to 1.2after57monthsofmeanfollow-upof97%ofpatients(p<0.001).Themeandegreeofpreoperativetricuspidregurgitation decreased from 3.6 to 1.6 in the EPO(p<0.001),remainingat1.9inLPOperiod(p>0.05).The indexed RV functional area increased from 8.53±7.02cm2/m2preoperativelyto21.01±6.87cm2/m2in the EPO (p < 0.001) and remained unchanged at20.28±5.26cm2/m2 inLPOperiod (p>0.05).Themean 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 in-hospital mortality, resulting in an effective and long-lasting repair of tricuspid regurgitation, restoring thefunctionalareaoftherightventricleandallowingreverseremodeling of the heart and clinical improvement inmostpatientsinthelong-term.

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

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From eMedinewSemeDinews seCtion

South Asians More Vulnerable to Diabetes, Coronary Artery Disease

A new study led by an Indian-origin scientist hasrevealed that South Asians are more likely to adddangerousorgan-huggingfat thatcan leadtodiabetesand coronary artery disease. The team at McMasterUniversity led by Dr Sonia Anand found that theseethnic groups tend to add dangerous fat onto theirinternalorgans liketheir liverwhentheygainweight,while others just add it to their waistline. “The newstudy showed South Asians have less space to storefat below the skin than white Caucasians,” saidDr Anand, a professor of medicine and epidemiologyat McMaster University. “Their excess fat, therefore,overflows to ectopic compartments, in the abdomenand liverwhere itmayaffect function,” shesaid.Thisvisceral fat, she added, is associated with metabolicproblemssuchaselevatedglucoseandabnormallipids,whichareriskfactorsthatultimatelyleadtocoronaryartery disease. (Source: http://www.newstrackindia.com/newsdetails/232949, 31 July, 2011)

Afib Hospital Days Reduced with Dronedarone

Cardiovascular hospitalization and length of staydeclined significantly in patients with paroxysmalor persistent atrial fibrillation or flutter treated withdronedarone (Multaq), a post-hoc analysis of alarge randomized trial showed. First cardiovascularhospitalizationoccurredin26%fewerpatientstreatedwith dronedarone versus placebo, and the rate ofhospitalization for Afib was almost 40% lower withdronedarone. The total number of hospital daysassociatedwithAfibwas reducedby about one-third,including a significant reduction in the number ofICU/CCUdays.(Source: Medpage Today)

Local Practice Patterns Drive Diagnostic Angios

There is wide variation among US institutions in therate of positive findings of obstructive coronaryartery disease (CAD) when patients undergo

diagnostic angiography, a retrospective study found.Among hospitals, the rate of positive findings(≥50%obstruction)variedfrom23to100%,reportedPamela S Douglas, MD, from Duke UniversityMedical Center in Durham, NC, and colleagues.Hospitals with lower rates of obstructive CADfindings performed coronary angiography more oftenin younger patients, women, blacks and outpatients(allp<0.001), researchers reported in theAugust16Journal of the American College of Cardiology. (Source: Medpage Today)

Absolute Blood Flow Better Predictor of Cardiac Events

Using data on absolute myocardial blood flowreserve gained through rubidium-82 PET imaging isprognostic of death, myocardial infarction (MI) andothermajorcardiovascularevents,asingle-centerstudyfound.Patientswithimpairedmyocardialflowreservehad higher incidences of MI and cardiac death, evenwhentheirsummedstressscores(SSS)werewithinthenormalrange,reportedMariaCZiadi,MD,fromtheUniversity ofOttawaHeart Institute inOntario, andcolleagues.Allcardiacdeathsoccurredinpatientswithaseverelyimpairedmyocardialflowreserve(<1.5)-1%inthegroupwithnormalSSS,and6.5%inthegroupwithabnormalSSS, according to the studypublishedonline in the Journal of the American College of Cardiology.(Source: Medpage Today)

Sweetened Drinks Boost Heart Disease Risk

Beverages sweetened with fructose or high-fructosecorn syrup can worsen cardiovascular risk factors,evenintheyoungandhealthy,researchershavefound.When these types of drinks accounted for at least aquarter of a person’s daily calories over two weeks,there were significant increases in triglycerides, LDLcholesterolandapolipoproteinB(apoB)concentrationsthatweren’tseenwithglucose,KimberStanhope,PhD,of the University of California Davis and colleaguesreportedonlineinthe Journal of Clinical Endocrinology and Metabolism.

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Fitness Update

what’s the best exercise for heart health?

A combination of weight training and aerobicexercise might be the best prescription for over-weightpeopleatriskfordiabetesandheartdisease,a new study suggests. People doing only aerobicexercise dropped weight and inches off theirwaistlines-soanaerobic-onlyprogramisalsoagood(and less time-consuming)option,researcherssaid.Thoseinthestudywhojustliftedweightssawverylittlebenefitintermsofhearthealth,althoughtheydidgainstrength. ‘Aerobicplusresistance isclearlythe optimal program,’ said Dr Timothy Church,who studies exercise anddisease atLouisianaStateUniversity’sPenningtonBiomedicalResearchCenterinBatonRouge.

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

Inanarticle,thatmaybringsmilestothefacesofvegetarianswhoconsumenodairyproductsandvegans, who consume no animal-based foods,scientists have identified seaweed as a rich newpotentialsourceofheart-healthyfoodingredients.Seaweedandother ‘macroalgae’ could rivalmilkproducts as sources of these so-called ‘bioactivepeptides,’ they conclude in an article in ACS’s Journal of Agricultural and Food Chemistry.MariaHayes and colleagues Ciarán Fitzgerald, EimearGallagher and Deniz Tasdemir note increasedinterestinusingbioactivepeptides,nowobtainedmainlyfrommilkproducts,asingredientsinso-called functional foods. Those foods not onlyprovide nutrition, but have a medicine-likeeffect in treating or preventing certain diseases.Seaweeds are a rich but neglected alternativesource, they state, noting that people in EastAsian andother cultureshave eaten seaweed forcenturies:NoriinJapan,dulseincoastalEurope,andlimupalahalahainnativeHawaiiancuisine.

—Rajat Bhatnagar, International Sports & Fitness Distribution, LLC,

http://www.isfdistribution.com

Lab Update

Metabolic Panel (14), Comprehensive

Test includes: Alanine aminotransferase (ALT/SGPT); albumin:globulin (A:G) ratio; albumin,serum; alkaline phosphatase, serum; aspartateaminotransferase (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.

The Comprehensive Metabolic Panel (CMP) is afrequently ordered panel of tests that gives yourdoctor important information about the currentstatus of your kidneys, liver and electrolyte andacid/basebalanceaswellasofyourbloodsugarandblood proteins. Abnormal results, and especiallycombinations of abnormal results, can indicate aproblemthatneedstobeaddressed.

—Dr Arpan Gandhi and Dr Navin Dang

How safe is angiography radiation?

The mean duration of fluoroscopy in electro-physiologiccardiacinterventionalproceduresrangesfrom 15 to 67 minutes. The radiation dose fromone hour of fluoroscopy during electrophysiologicablationprocedurescanresultin0.7-1.4excessfatalmalignancies/1,000womenand1.0-2.6/1,000menaspertwostudiespublishedinAmerican Journal of Cardiology (1998)andCirculation (2004).

At what prevalence is screening for stroke beneficial?

Only at prevalence rates of over 20% significantbenefits are seen with at best about 100 strokespreventedforevery10,000screenedat20%prevalence.Clinical features cannot identify asymptomaticindividualslikelytohavecarotidstenosis.Theannualriskof stroke inpatientswithasymptomaticcarotidarterystenosisisrelativelylow.

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

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Sudden Cardiac Death

how is sudden cardiac death different from sudden cardiac arrest?

Sudden cardiac arrest is cessation of cardiac activity,whichcanberevivedafterresuscitation.Ontheotherhand, sudden cardiac death (SCD) is unsuccessfulsuddencardiacarrest.

how common is sudden cardiac death?

About4-5,00,000peopleinUS,7,00,000inEuropeand2millioninIndiadieeveryyeardirectlyduetoSCD.In India, majority of them die before reaching thehospital; about 75% of them can be revived if chestcompressioncardiacresuscitation(CCCR)istaughttoall.

what are the three clinical phases after a sudden cardiac arrest?

Clinical phase: Lasts 0-5 minutes; ventricularfibrillation is the main electrical activity and thetreatment of choice is defibrillation followed byCCCR.Hemodynamic phase: Lasts 5-10 minutes;ventricular fibrillation persists and the patient,in addition, has hemodynamic instability. Thesepatients require effective two minutes of CCCRbeforedefibrillation isattemptedfollowedbytwominutesofCCCRagain.Metabolic phase: Phasebeyond10minutes.Onlyhypothermiasystemcanworkhere.

How is cardiac arrest treated in the first five minutes?

Thefirstfiveminutesaftercardiacarrestistheclinicalphase. In this phase, ventricular fibrillation is themain electrical activity. The treatment of choice isdefibrillationfollowedbyCCCR.

how is cardiac arrest that presents between 5-10 minutes of the arrest managed?

The second 5-10 minutes of cardiac arrest is thehemodynamic phase. Ventricular fibrillation persistsand the patient, in addition, has hemodynamicinstability.Thesepatientsrequireeffectivetwominutesof CCCR before defibrillation is attempted followedbytwominutesofCCCRagain.

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

The patient, after 10 minutes of arrest, is in themetabolic phase. Only hypothermia system can workhere.

what is chest compression cardiac resuscitation?

CCCRinvolvescompressingthechestwithaspeedof100/minute.Themantraistopushashardandasfastaspossible.Eachcompressionshouldlowerthesternumby 1.5-2 inches, should be continuous and allow fullrecoilofthesternum.Onepersoncaneffectivelycarryoutchestcompressionforonly1-2minutes.Afterthatfatiguewillinvariablysetin.Therefore,itisimportanttoswitchresuscitationsbetweenavailablebystanders.

Is CCCR effective in children?

CCCR is more effective in adults. In children, andin conditions like unwitnessed cardiac arrest andnoncardiacarrests,onemayhavetodocompletecardiacpulmonaryresuscitation(CPR)involvingbreathingandchestcompressioncycles.

How to defibrillate in sudden cardiac arrest?

Whiledefibrillating,use themaximumJules availablein the machine. After defibrillation, one should notwait to watch for the rhythm but continue CCCRuninterruptedforthenexttwominutes.

how long should one wait before starting CCCR?

Donotwastemorethan10secondstocheckpulseorbreathingbeforestartingCCCR.Evenasecond’sdelaymatters. Therefore, CCCR should be started withoutdelay.

what is the role of soda bicarb in CCCR?

In basic cardiac resuscitation, injection adrenaline,atropine, endotracheal tube, sodabicarb, etc.havenorole.

who should lead the CCCR?

Whenmultiplerescuersareavailable,thepersonhighesttrainedshouldbecometheleader,directandtakeoverthefirsttwominutesoftheresuscitationcycle.

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Medicolegal Update

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

Left ventricular hypertrophy is the second leadingcauseofsuddencardiacdeathinadultsinIndia.

The long-standing raised high blood pressurewhich causes secondary damage to the wall ofthe main pumping chamber of the heart, theleft ventricle, leading to hypertrophy which isassociatedwithcardiacarrhythmias.

The mechanism of death in a majority ofpatients dying of sudden cardiac death isventricular fibrillation and as a consequencethere may be no prodromal symptoms asso-ciatedwiththedeath.

These patients may be going about their dailybusiness and suddenly collapse without thetypicalfeaturesofmyocardialinfarctionsuchaschestpainandshortnessofbreath.Thereareanumberofcasesinwhichpatientsfeeltheeffectofmyocardialischemia.Myocardialischemiaisassociated with referred pain, classically to thefront of the chest, the left arm and the jaw.Patientsmayfeelgenerallyunwell,withnausea,dizzinessandvomiting.

Thesesymptomsmayprecedethedeathforanylength of time ranging from a few minutes toseveralhours.

I had conducted the postmortem examinationof fourcases founddead in toiletduringdailypursuits;thecasesofleftventricularhypertrophyleadingtosuddencardiacdeath.

—Dr Sudhir Gupta, Additional Professor, Forensic Medicine &

Toxicology, AIIMS

what should be the compression to breathing ratio in CPR?

When giving CPR involving breathing-chestcompressioncycles,theratioshouldbe30compressions:Twobreaths.This ratio shouldnotbemore thanfivecyclesintwominutes.

how effective should be breathing in CPR?

One should not push more than 50% of the tidalvolumeineachbreath.Don’tpushairintothestomachasitwillimpairhemodynamics.Iftherespiratoryrateismore,itwillalsoimpairhemodynamics.

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

Agonal/gasping respiration is ineffective respirationand shouldbe an indication for cardiac resuscitation.In fact, gasping is the sign that your resuscitation islikelytobesuccessful.

Criteria Improve Transesophageal Echo Rate

Prescreening patients who are set to havetransesophageal echocardiography (TEE) reducesinappropriate scans, researchers said. In a single-center study, 16% of scans were canceled afterprescreening with appropriate use criteria,James Kirkpatrick, MD, of the University ofPennsylvania,andcolleaguesreportedintheJournal Echocardiography. The cancellation rate was just2% when patients were not prescreened. (Source: Medpage Today)

Coronary Calcium better than CRP to Stratify Risk

Among asymptomatic individuals with normalLDLcholesterollevelsandelevatedhigh-sensitivityC-reactiveprotein (hsCRP),measuring theburdenofcalciuminthecoronaryarterieswithcardiacCTappearstostratifytheriskofcardiovasculardisease,researchersfound.(Source: Medpage Today)

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

liGhter reADinG

Lighter Reading

An Inspirational Story

Building your house

An elderly carpenter was ready to retire. He toldhis employer-contractor of his plans to leave thehouse-buildingbusinesstoliveamoreleisurelylifewith his wife and enjoy his extended family. Hewouldmissthepaycheckeachweek,buthewantedtoretire.Theycouldgetby.

Thecontractorwassorrytoseehisgoodworkergoandaskedifhecouldbuildjustonemorehouseasa personal favor. The carpenter said yes, but overtime it was easy to see that his heart was not inhiswork.Heresortedtoshoddyworkmanshipandused inferiormaterials. Itwasanunfortunatewaytoendadedicatedcareer.

Whenthecarpenterfinishedhiswork,hisemployercame to inspect the house. Then he handed thefront-door key to the carpenter and said, “This isyourhouse…mygifttoyou.”

Thecarpenterwasshocked!

What a shame! If he had only known he wasbuildinghisownhouse,hewouldhavedoneitallsodifferently.

Soitiswithus.Webuildourlives,adayatatime,oftenputting less thanourbest intothebuilding.Then, with a shock, we realize we have to live inthe house we have built. If we could do it over,we’ddoitmuchdifferently.

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

Someoneoncesaid,‘Lifeisado-it-yourselfproject.’Your attitude, and the choices you make today,helpbuildthe‘house’youwillliveintomorrow.

Build-wisely!

Laugh a While

Building Rome

Marilyn, the teacher, asked her 5th grade historyclass, ‘When was Rome built?’ and called onTimothytoanswerfirst.‘Romewasbuiltatnight.’was his answer. ‘At night?’ asked Mrs. Taylor,holding her ruler firmly in her boney-knuckledhands.‘Howeverdidyougetsuchanidea?’

‘Well,’ gulped the student, hoping his answerwould satisfy her, ‘everyone knows Rome wasn’tbuiltinaday’.

Mind Teaser

In which of the following locations is carcinoidtumormostcommon?

1.Esophagus

2.Stomach

3.Smallbowel

4.Appendix

Spiritual Update

Anger, hostility, Aggression: Risk Factors for heart Attack

Anger,hostilityandaggressionarethreeriskfactorsfor heart attack with the fulcrum at the level ofanger.Athoughtarisesfromthethoughtlessstateofmind called consciousness, which is then analyzedbytheintellectandconvertedintoanaction,whichiseitheregocentricorego-fugal.Allactionsleadtomemory and memory leads to desire. If the desirecanbefulfilled,itwillendupintoactionagainandthe cycle of action, memory and desire continuesleadingtohabitoranaddiction…

Answer:4.Appendix

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139Asian Journal of Clinical Cardiology, Vol. 14, No. 4, August 2011

Conference CalendarConFerenCe CAlenDAr

Cardiovascular and Interventional Radiological Society of Europe (CIRSE 2011)September10-14,2011Venue:ICM-InternationalesCongressCenterMessegelände,Munich,AlemaniaWebsite:http://www.cirse.org/

Annual Scientific Meeting of the British Hypertension SocietySeptember12-14,2011Venue:Queens’College,SilverSt,Cambridge,ReinoUnidoWebsite:http://www.bhsoc.org/

High Blood Pressure Research 2011 Scientific SessionsSeptember20-24,2011Venue:WaltDisneyWorldDolphinResortOrlando,Florida,EstadosUnidosWebsite:http://my.americanheart.org/professional/Sessions/HBPR/HBPR_UCM_316905_SubHomePage.jsp

22nd Annual Coronary InterventionsSeptember21-23,2011Venue:HiltonLaJollaTorreyPines,SanDiego,California,UnitedStatesWebsite:http://www.scripps.org/assets/documents/sudden_cardiac_arrest_brochue2011.pdf

Issues of Congenital Heart DiseaseSeptember23,2011Venue:CongressHall,Kiev,UkraineWebsite:http://www.nbscience.com/23.html

16th Annual Meeting of the European Council for Cardiovascular ResearchSeptember30toOctober2,2011Venue:LaCollesurLoup,Nice,FranceWebsite:http://www.eccr.org

Worldcon 2011 – XVI World Congress of Cardiology, Echocardiography and Allied Imaging TechniquesSeptember30thtoOctober2,2011Venue:TheLeelaKempinski,Gurgaon,IndiaWebsite:http://www.worldcon2011.org

Heart Rhythm Congress 2011October02-05,2011Venue:HiltonBirminghamMetropoleHotel,Birmingham,UKWebsite:http://www.heartrhythmcongress.com/

Cardio/Pulmonary for Primary Care PhysiciansOctober02-06,2011Venue:Disney’sBoardwalkResortOrlando,Florida,EstadosUnidosWebsite:http://www.mer.org/schedule/conference/123

Eurothrombosis Summit 2011October07-08,2011Venue:SheratonPortoHotelandSpa,RuaTenenteValadim,PortugalWebsite:http://www.eurothrombosis-summit2011.org/

30th National Congress of Cardiology: 50 Años Viviendo Con La CardiologíaOctober12-14,2011Venue:HotelBarceloGuatemalaCity,GuatemalaWebsite:http://www.medical-events.com/congress/30th-national-congress-of-cardiology-4134

2011 Cardiometabolic Health CongressOctober19-22,2011Venue:SheratonBostonHotel,BostonMAWebsite:http://www.cardiometabolichealth.org/index.asp

2nd Annual Emirates Cardiac Society CongressOctober20-22,2011Venue:GrandHyattDubai,Dubai,UAEWebsite:http://www.ecsc.ae/

Canadian Cardiovascular CongressOctober22-26,2011Venue:ConventionCentre,Vancouver,BC,CanadaWebsite:http://www.cardiocongress.org

Evolving Challenges in Promoting Cardiovascular Health 2011October21-22,2011Venue:CosmoLaxia,Barcelona,SpainWebsite:http://www.nyas.org/Events/Detail.aspx?cid=116dc806-0b05-4ba2-9046-ad1c2fa52cd6

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

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

Covering letter

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

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

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

Manuscript- Three complete sets of the manuscript should be

submitted and preferably with a CD; typed double spaced throughout (including references, tables and legends to figures).

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

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

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

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.

StatisticsThe 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.

- 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.

Information for Authors

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141Asian 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.

ReferencesThese 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:

ArticlesPaintal 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.

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

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

Tables- These should be typed double spaced on separate

sheets with the table number (in Roman Arabic numerals) and title above the table and explanatory notes below the table.

Legends- These should be typed double spaces on a separate

sheet and figure numbers (in Arabic numerals) corresponding with the order in which the figures are presented in the text.

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

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

summary, etc.)_______________________________2. Total number of pages ________________________3. Number of tables ____________________________4. Number of figures ___________________________5. Special requests _____________________________6. Suggestions for reviewers (name and postal address) Indian 1. ___________Foreign 1. _______________ 2. ___________ 2. _______________ 3. ___________ 3. _______________ 4. ___________ 4. _______________7. All authors’ signatures________________________8. Corresponding author’s name, current postal and

e-mail address and telephone and fax numbers __________________________________________

For Editorial Correspondence Dr KK AggarwalGroup Editor-in-Chief

Asian Journal of Clinical CardiologyE - 219, Greater Kailash, Part - 1,

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