AJCC march

Asian

Journal of

IJCP Group of Publications

CLINICAL CARDIOLOGY

Dr Sanjiv Chopra Prof. of Medicine & Faculty Dean Harvard Medical School Group Consultant Editor

Volume 14, Number 11, March 2012

Dr Deepak Chopra Chief Editorial Advisor Dr KK Aggarwal CMD, Publisher, Group Editor-in-Chief Dr Veena Aggarwal MD, Group Executive Editor

from the desk of group editor-in-chief 373 ` 2.84-Lakh Liver and Kidney Cancer Drug to Cost Just ` 8,880/

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

AJCC Speciality Panel Advisory Board

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

Dr SS Singhal Dr Mohd. Ahmed Dr PK Jain Dr PK Gupta Dr Naresh Trehan Faculty Dr GK Aneja Dr Ramesh Thakur Dr Balram Bhargava Dr HK Bali Dr HM Mardikar Dr Sanjay Mehrotra Dr Vivek Menon Dr Keyur Parikh

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

KK Aggarwal

clinical study 375 Glucose Tolerance in Nondiabetic Patients after First Attack of Acute Myocardial Infarction and its Outcome

Ajay S Dabhi, M Vadivelan, SR Rathava

review article 379 Omega-3 Fatty Acids and Primary and Secondary Prevention of Cardiovascular Disease

Samir Srivastava, KK Aggarwal

IJCP Editorial Board Obstetrics and Gynaecology Dr Alka Kriplani, Dr Thankam Verma, Dr Kamala Selvaraj Cardiology Dr Praveen Chandra, Dr M Paul Anand, Dr SK Parashar Paediatrics Dr Swati Y Bhave, Dr Balraj Singh Yadav, Dr Vishesh Kumar Diabetology Dr Vijay Viswanathan, Dr CR Anand Moses, Dr Sidhartha Das, Dr A Ramachandran, Dr Samith A Shetty Dentistry Dr KMK Masthan, Dr Rajesh Chandna Gastroenterology Dr Ajay Kumar Dermatology Dr Hasmukh J Shroff Nephrology Dr Georgi Abraham Neurology Dr V Nagarajan Anand Gopal Bhatnagar Editorial Anchor Advisory Bodies Heart Care Foundation of India Non-Resident Indians Chamber of Commerce & Industry World Fellowship of Religions

original study 385 Effect of Relaxation Therapy on Apolipoprotein A, B, MDA and Lipid Profile in Hypertensive Patients

Amit Tyagi, Rupal Tyagi, Ritesh Vekariya

case report 388 Idiopathic Dilated Cardiomyopathy Complicating in a Pregnancy with Uterine Fibroid

Debasmita Mandal, Pradip Kumar Saha, Chaitali Dattaray, Saroj Mandal

391 Sweet’s Syndrome with Type 2 Diabetes Mellitus: A Rare Case Presentation

RK Kotokey, Swarup Kar, Libe Nyorak, Arup Sarma, M Shebha Rupsi

medilaw

Published, Printed and Edited by Dr KK Aggarwal, on behalf of IJCP Publications Ltd. and Published at E - 219, Greater Kailash, Part - 1 New Delhi - 110 048 E-mail: editorial@ijcp.com

393 When and How Cardiologists Advertise?

Printed at IG Printers Pvt. Ltd., New Delhi E-mail: igprinter@rediffmail.com printer_ig@yahoo.com

photo quiz 394 Painless Nodules in the Fingers

© Copyright 2012 IJCP Publications Ltd. All rights reserved.

The copyright for all the editorial material contained in this journal, in the form of layout, content including images and design, is held by IJCP Publications Ltd. No part of this publication may be published in any form whatsoever without the prior written permission of the publisher.

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

Note: Asian Journal of Clinical Cardiology does not guarantee, directly or indirectly, the quality or efficacy of any product or service described in the advertisements or other material which is commercial in nature in this issue.

practice guidelines 397 AAN Releases Guideline on Magnetic Resonance Imaging for Diagnosing Acute Ischemic Stroke

expert’s opinion 398 What are the Do’s and Don’ts of Taking Blood Pressure?

HK Chopra, KK Aggarwal

around the globe 403 News and Views

lighter reading 404 Lighter Side of Medicine

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from the desk of group editor-in-chief Dr KK Aggarwal

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

` 2.84-Lakh Liver and Kidney Cancer Drug to Cost Just ` 8,880/-

T

he kidney and liver cancer drug sorafenib tosylate (Nexavar) will soon be available to patients at ` 8,880/- a pack of 120 tablets.

This has been made possible due to the ministry invoking an international trade rule allowing the generic production of an unaffordable drug that is patented. Bayer, a German multinational, holds the patent for Nexavar and sells at ` 2.84 lakh.

The Indian Controller-General of Patents, Designs and Trade Marks granted the first-ever ‘compulsory license’ in India to Natco under Section 84 of the Indian Patent Act. Sorafenib is used for the treatment of the advanced stages of kidney and liver cancer. The drug stops the growth of new blood vessels and targets other important cellular growth factors. Though it is not a life-saving drug, it is a life-extending drug. In the case of kidney cancer, it can extend the life of a patient by 4-5 years, while in the case of liver cancer it can extend life by about 6-8 months.

Under the order, Natco will also supply the drug free of cost to at least 600 needy and deserving patients every year. Natco Pharma will also have to pay a royalty to Bayer at the rate of 6% of the net sales on a quarterly basis, and the license shall be valid till the entire balance period of the patent - it was granted in 2008 and will expire in 2020.

Compulsory licensing under the Indian Patent Law The Indian Patent Law has provided for adequate powers to the Controller of Patents to issue compulsory licenses to deal with the following extreme and/or urgent situations.

A) Section 84: To prevent the abuse of patent as a monopoly and to make way for commercial exploitation of invention by an interested person.

B)

Sections 92 (1) and 92 (3): Circumstances of national emergency or extreme urgency.

C) Section 92 A: For exports of pharmaceutical products to foreign countries with public health problems.

(A) Section 84: The law provides for compulsory license under Section 84 of the Indian Patent Act, to prevent the abuse of patent as a monopoly and to make way for commercial exploitation of invention by an interested person. Under this section, any person can make an application for grant of compulsory license for a patent after three years, from the date of grant of that patent, on any of the following grounds: (a) The reasonable requirements of the public with respect to the patented invention have not been satisfied;

Asian Journal of Clinical Cardiology, Vol. 14, No. 11, March 2012

373

From the desk of group editor-in-chief (b) The patented invention is not available to the public at a reasonably affordable price.

following factors while considering the application under Section 84.

(c) The patented invention is not worked in the territory of India.

(1) The nature of the invention, the time which has elapsed since the sealing of the patent and the measures already taken by the patent or licensee to make full use of the invention;

Moreover, Section 89 specifies and explains the general purposes of granting compulsory license under Section 84 as: (i)

That the patented inventions are worked on a commercial scale in the territory of India without undue delay and to the fullest extent that is reasonably practicable;

(ii) That the interests of any person for the time being working or developing an invention in the territory of India under the protection of a patent are not unfairly prejudiced.

Further, the subsection 6 of Section 84 elaborates that the Controller shall take into account the

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(2) The ability of the applicant to work the invention to the public advantage; (3) The capacity of the applicant to undertake the risk in providing capital and working the invention, if the application were granted; (4) As to whether the applicant has made efforts to obtain a license from the patentee on reasonable terms and conditions and such efforts have not been successful within a reasonable period as the Controller may deem fit. Notably, Section 90 of the Act also empowers the controllers to settle the terms and conditions for compulsory licences.

clinical study

Glucose Tolerance in Nondiabetic Patients after First Attack of Acute Myocardial Infarction and its Outcome Ajay S Dabhi*, M Vadivelan*, SR Rathava*

Abstract Aims: To find out the incidence of impaired glucose tolerance (IGT) and frank diabetes mellitus (DM) in patients of acute myocardial infarction (AMI) and to study the natural history of IGT in relation to AMI. Study Design: A crosssectional study was done in 60 patients of AMI in whom oral glucose tolerance test (OGTT) was performed after admission.

Those with normal glucose tolerance on admission and till discharge were included in the study. Material and Methods: The study was conducted at the intensive coronary care unit (ICCU) of Shri Sayajirao General (SSG) Hospital, Vadodara, Gujarat. The study was done over a period of seven months in 60 patients of AMI. Results: The present study revealed that cardiovascular complications related to AMI were more common in patients with abnormal glucose tolerance.

Conclusion: Glucometabolic abnormalities in nondiabetic patients with acute coronary event have an influence on in-hospital and short-term cardiovascular morbidity as well as mortality.

Keywords: Impaired glucose tolerance, acute myocardial infarction

D

espite impressive strides in the diagnosis and management of myocardial infarction, it still continues to be a major public health problem worldwide. Cardiovascular disease is a major cause of death in diabetic patients.1 Although diabetes mellitus (DM) has emerged as a major risk factor for coronary artery disease (CAD)related morbidity and mortality, recently it has been suggested that impaired glucose tolerance (IGT) is also an independent risk factor.2 IGT is a dysglycemic state, which is the intermediate state between normal glycemic state and DM.3 Asymptomatic hyperglycemia is a significant public health problem and confers an increased cardiovascular risk, independent of other classical cardiovascular risk factors. In patients with IGT, cardiovascular risk is equal and in some cases, even higher than in those diagnosed to have diabetes.4

*Assistant Professor Dept. of Medicine Medical College and SSG Hospital, Vadodara Address for correspondence Dr Ajay S Dabhi 38, Alkanagar, Near Priyalaxmi Mill, Old Alembic Road Vadodara, Gujarat - 390 003 E-mail: dr_ajay_44@yahoo.co.in

AIMS OF STUDY 







To find out the incidence of IGT and frank DM in patients of acute myocardial infarction (AMI) in three months follow-up period who, after first attack of AMI, were normoglycemic on admission and till discharge.

To evaluate the relationship between plasma glucose level on admission and its outcome (in-hospital and short-term) in patients with AMI without previously known DM. To evaluate IGT as an independent cardiovascular risk factor in AMI. To study the natural history of IGT in relation to AMI and to compare the outcome in patients after three months follow-up.

MATERIAL AND METHODS In this prospective, cross-sectional study, 60 patients presenting with clinical features of AMI admitted to the intensive coronary care unit (ICCU) of Shri Sayajirao General (SSG) Hospital, Vadodara, Gujarat were taken as the study group.

Oral glucose tolerance test (OGTT) was performed in all patients and those with normal glucose tolerance on admission and till discharge were included in the study group.

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Clinical Study Inclusion Criteria Adults below the age of 65 years who presented within 24 hours of AMI for the first time and with random blood sugar (RBS) level <180 mg/dl were included in the study sample.

Exclusion Criteria Patients with DM, systemic arterial hypertension, ischemic heart disease and those with history of gestational diabetes mellitus, cerebrovascular accident, peripheral vascular disease, structural heart disease, chronic liver and kidney disease were excluded from the study.

RBS was estimated on admission and fasting blood sugar (FBS) was estimated on the second day after admission and on discharge. OGTT was carried out according to WHO guidelines under controlled conditions after an overnight fast. Impaired fasting glucose (IFG) was defined as venous plasma glucose level in the range of 110-125 mg/dl, while IGT was defined as venous plasma glucose level in the range of 140-199 mg/dl (2 hours after glucose load).

Each patient was evaluated with OGTT (FBS and PG2BS), electrocardiogram (ECG) and echocardiogram at three months follow-up.

Table 1. Age and Sex Distribution of Patients with Myocardial Infarction Age (years)

Sex

Total (%)

Male (%)

Female (%)

35-45

5 (8%)

1 (2%)

6 (10%)

46-55

9 (15%)

6 (10%)

15 (25%)

56-65

26 (44%)

13 (21%)

39 (65%)

Total

40 (67%)

20 (33%)

60 (100%)

Table 2. ECG Findings in Study Sample Patients (%) STEMI Anterior wall MI

35 (59%)

Inferior wall MI

14 (23%)

Right ventricle MI

3 (5%) 52 (87%)

Total NSTEMI Subendocardial MI

2 (3%)

ST-segment depression

4 (7%)

Fresh left bundle branch block (LBBB)

2 (3%)

Total

8 (13%)

RESULTS

Table 3. RBS and OGTT Results in Study Sample

Sixty indoor patients admitted to ICCU with AMI and satisfying the inclusion criteria were selected for the study.

Variable

The age of patients ranged from 35 to 65 years. Majority of patients were in the age group of 56-65 years (65%) indicating higher prevalence of AMI in elderly people. Out of 60 patients in the study group, 40 were males (67%) and 20 were females (33%) (Table 1).

The AMI patients were further divided into subgroups on the basis of ECG findings. ST elevation-MI (STEMI) was seen in 52 (87%) patients and non-STEMI was seen in eight (13%) patients. In cases of STEMI, 35 (59%) patients had anterior wall MI (Table 2).

Table 3 shows that glucose tolerance in all patients of study sample was normal till discharge.

On second day of admission

At the end of three months follow-up, 40 patients (67%) in Group A had normal glucose tolerance, while 14 patients (23%) in Group B1 had IGT and six patients (10%) in Group B2 had frank DM (Table 4). Table 5 shows segment motion abnormality in AMI on 2-D Echo done at the time of admission and on follow-up.

Worsening of involved segment was noticed more in

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Values

On admission RBS (mg/dl)

121 ± 57

FBS (mg/dl)

97 ± 8

PG2BS (mg/dl)

117 ± 18

On discharge FBS (mg/dl)

93 ± 12

PG2BS (mg/dl)

104 ± 8

In study, cut-off value of RBS <180 mg/dl.

Table 4. Division of Study Sample-based on Glucose Tolerance at the End of 3-months Follow-up Group

Patients (%)

Result

A

40 (67%)

NGT

B1

14 (23%)

IGT

B2

6 (10%)

Frank DM

Total NGT = Normal glucose tolerance.

60 (100%)

Table 5. Comparison of Segment Motion Abnormality in Both Groups Segment motion abnormality

Group A (%)

Group B (%)

Total (%)

Normokinesia

10 (25%)

6 (30%)

16 (27%)

Hypokinesia

21 (53%)

8 (40%)

29 (48%)

Akinesia

5 (12%)

3 (15%)

8 (13%)

Paradoxical movement

4 (10%)

3 (15%)

7 (12%)

On admission

Percentage of involved patients

Clinical Study 60 50 40

1 (5%)

7 (12%)

15 (38%)

8 (40%)

23 (38%)

20 10 0

Akinesia

10 (25%)

5 (25%)

15 (25%)

Paradoxical movement

9 (22%)

6 (30%)

15 (25%)

Table 6. Comparison of Left Ventricle Ejection Fraction in Both Groups LVEF (%)

Group A (%)

Group B (%)

Total (%)

>50 (normal)

10 (25%)

6 (30%)

16 (27%)

41-50

21 (53%)

8 (40%)

29 (48%)

31-40

5 (12%)

3 (15%)

8 (13%)

<30

4 (10%)

3 (15%)

7 (12%)

>50 (normal)

6 (15%)

1 (5%)

7 (12%)

41-50

15 (38%)

8 (40%)

23 (38%)

31-40

10 (25%)

5 (25%)

15 (25%)

<30

9 (22%)

6 (30%)

15 (25%)

On admission

On follow-up

Table 7. Comparison of Both Groups for Complicated MI Acute MI

Group A (%)

Group B (%)

Total (%)

Complicated

17 (43%)

19 (95%)

36 (60%)

Uncomplicated

23 (57%)

1 (5%)

24 (40%)

Total

40 (100%)

20 (100%)

60 (100%)

Table 8. Comparison of Both Groups for MI-related Mortality Acute MI

Group A (%)

Group B (%)

Total (%)

Alive

39 (98%)

16 (80%)

55 (91%)

Death

1 (2%)

4 (20%)

5 (9%)

Total

40 (100%)

20 (100%)

60 (100%)

>50% 41-50% 31-40% <30% LVEF (%) On follow-up

Percentage of involved patients

6 (15%)

Hypokinesia

Group A Group B

30

On follow-up Normokinesia

On admission

40 35 30 25 Group A Group B

20 15 10 5 0

>50% 41-50% 31-40% <30% LVEF (%)

Figure 1. Comparison of left ventricle ejection fraction in both groups.

Group B as compared to Group A on 2-D Echo. Table 6 shows progression to poor cardiac pump function in Group B as compared to Group A on 2-D Echo at three months follow-up. Out of 36 patients who developed cardiovascular complications related to AMI, 95% patients had abnormal glucose tolerance (IGT and frank DM). Among complications, patients developed congestive heart failure (CHF), cardiogenic shock and arrhythmias (Fig. 1 and Table 7).

Table 8 shows that death due to cardiac cause was more in Group B than Group A. Cause of death was CHF in all patients.

DISCUSSION Acute myocardial infarction is the commonest cause of cardiovascular disability in developed countries and the leading cause of morbidity and mortality in developing countries.5 Cardiovascular relative risk increases 2-4 folds in patients with diabetes as compared to the nondiabetic population.6 Stress hyperglycemia is usually associated with AMI and quite a large number of patients Contâ&#x20AC;&#x2122;d on page 384...

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review article

Omega-3 Fatty Acids and Primary and Secondary Prevention of Cardiovascular Disease Samir Srivastava*, KK aggarwal**

Abstract The prevalence of cardiovascular disease (CVD) is increasing dramatically especially in developing countries like India.

CVD is a leading cause of morbidity and mortality. There has been a growing awareness of the role of nutrients in the prevention of CVD. One specific recommendation in the battle against CVD is the increased intake of omega-3 fatty acids, which are polyunsaturated fatty acids. Studies have reported inverse associations of CVD with dietary intake of omega-3 fatty acids, suggesting that omega-3 fatty acids supplementation might exert protective effects on CVD. They exert their cardioprotective effect through multiple mechanisms. Omega-3 fatty acid therapy has shown promise as a useful tool in the primary and secondary prevention of CVD. This review briefly summarizes the effects of omega-3 fatty acids in primary and secondary prevention of CVD.

Keywords: Cardiovascular disease, polyunsaturated fatty acids, omega-3 fatty acids

Nutrition and cardiovascular disease Recent years have witnessed greater emphasis on prevention of chronic diseases with focus on societal lifestyles, cultural attitudes toward health, and dietary influences on health conditions.1 The major cardiovascular diseases (CVD) affecting the developed world have at their core atherosclerosis and hypertension, both of which are profoundly affected by diet and can be approached, at least in part, from a nutritional point of view.2 Studies have shown that cardioprotective nutrients, if routinely incorporated in a healthy diet, would markedly reduce the population risk of coronary heart disease (CHD).3 Therapeutic lifestyle changes, effected through a cardiac rehabilitation program comprising regular exercise and the intake of a combination of dietary nutrients (eicosapentaenoic acid [EPA], docosahexaenoic acid [DHA], oleic acid, folic acid and vitamins A, B6, D and E), reduced various risk factors in myocardial infarction (MI) patients, which supports the rationale for nutritional programs in the secondary prevention of CHD.4 Vitamins have antioxidant effects and thus have favorable effects. Although beneficial to the heart, they do not provide the all round cardioprotection that is required. Interest in omega-3 fatty acids has grown

Cardioceuticals: A New Category Cardioceuticals contain all essential nutrients including vitamins, minerals, omega-3-fatty acids and other antioxidants like a-lipoic acid and coenzyme Q10 in an appropriate proportion and provides all round cardioprotection. Cardioceuticals improve different parameters that contribute to a healthy heart such as increasing oxygenation, protection of artery walls, clot prevention antioxidant effect, maintaining healthy rhythm of the heart and cholesterol lowering. By virtue of these effects, they reduce the risk factors of the heart and subsequently cost of treatment in the high-risk patients by reducing need for re-hospitalization, improve the quality of living and reduce the mortality rates in the high-risk population. steadily since the observation that Greenland Eskimos have a low incidence of CVD in the setting of a diet rich in fatty fish. Recent research has highlighted their effects, including potential clinical advantages.1 In this review, we briefly discuss the evidence demonstrating the effects of omega-3 fatty acids in the primary and secondary prevention of CVD.5 Omega-3 fatty acids

*Associate Director Dept. of Cardiology Fortis Escorts Heart Institute, New Delhi **Senior Physician and Cardiologist Moolchand Medcity, New Delhi

Omega-3 fatty acids are long chain polyunsaturated fatty acids (PUFAs). The major dietary sources of omega-3 fatty acids are fish containing EPA and DHA, as well as nuts, seeds and vegetable oils containing

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review article α-linolenic acid (ALA). Omega-3 fatty acids, especially those derived from marine sources, may be a useful tool for the primary and secondary prevention of CVD.1 As the only dietary source of omega-3 PUFA, ALA is considered to be inadequate because humans convert typically <5% of ALA to EPA and even less to DHA.6 Mechanism of action: Omega-3s exert their cardioprotective effects through multiple mechanisms, including reducing arrhythmias and altering production of prostaglandins, which reduces inflammation and improves platelet and endothelial function. To date, no serious adverse effects of omega-3s have been identified, despite extensive study.1 In addition, there appear to be additional benefits to the use of fish oil, including lowering significantly elevated triglyceride levels, preventing atrial fibrillation (AF), reducing mortality rates in congestive heart failure patients and perhaps stabilizing atherosclerotic plaques.7 The American Heart Association (AHA) recommends the use of omega-3 PUFA at a dose of approximately 1 g/day of combined DHA and EPA, either in the form of fatty fish or fish oil supplements (in capsules or liquid form) in patients with documented CHD,6 and at least 500 mg/day for individuals without disease.5 Omega-3 PUFA therapy has shown great promise in primary and, particularly in secondary prevention of CVD. Primary prevention of CVD The evidence for the role of omega-3 PUFA in the primary prevention of CVD is limited by the lack of randomized controlled trials (RCTs). Most of the evidence for the use of omega-3 PUFA comes from case-control studies and prospective cohort studies, with not all studies showing benefit.8 A study that investigated the relation between fish consumption and CHD in 852 middle-aged men without CHD in the town of Zutphen, The Netherlands showed that consumption of as little as one or two fish dishes per week may be of preventive value in relation to CHD. The study found an inverse dose-response relation between fish consumption in 1960 and death from CHD during 20 years of follow-up. Mortality from CHD was >50% lower among those who consumed at least 30 g of fish per day than among those who did not eat fish.9 Three large prospective cohort studies have shown differing results as to any possible benefits of omega-3 PUFA intake.

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Asian Journal of Clinical Cardiology, Vol. 14, No. 11, March 2012



The Health Professional Study included 44,895 male healthcare professionals aged 40-75 years, free of CVD, who completed dietary questionnaires and were followed up for six years showed no significant reduction in the risk of CVD even with 5-6 servings of fish per week.9,10

The two large prospective cohort studies which did show some cardiovascular benefit were the Physicians’ Health Study and the Nurses’ Health Study.9 



The Physicians’ Health Study studied the effects of weekly fish consumption (at least one fish meal per week) on 21,185 healthy male physicians aged 40-85 years followed up for 11 years. Eating fish once a week, compared to fish consumption less than once a month, decreased the risk of sudden cardiac death (SCD) and all-cause mortality. There was however, no risk reduction for MIs or total cardiac mortality.9,11 The Nurses’ Health Study was conducted in 84,688 healthy female nurses aged 34-59 years who were followed up for 16 years. A higher consumption of fish and omega-3 fatty acids was associated with a lower risk of CHD, and deaths due to CHD.9,12

Further epidemiological evidence has been obtained from the analysis of the Multiple Risk Factor Intervention Trial (MRFIT) database. MRFIT was a multifactorial risk factor intervention study, which randomized 12,866 middle-aged men at high-risk of CHD in the USA to either an intervention group or usual care group, and followed them up for 10.5 years. Study of the ‘usual care’ group demonstrated no association between dietary intake of ALA (the predominant dietary PUFA) and risk of CHD deaths.

A reduction in 10-year mortality rates was observed with increased intake of PUFAs.9,13 Similar positive effects of fish consumption on cardiovascular (CV) outcomes were noticed in the Honolulu Heart Program, where heavy smokers with high fish consumption were at lower risk for CHD mortality than those who smoked heavily and had low fish consumption. The Honolulu Heart Program began in 1965 to follow a cohort of 8,006 Japanese-American men aged 45-65 years who lived on Oahu, Hawaii, in 1965.5,14 The Japan EPA Lipid Intervention Study (JELIS), a primary (n = 14,981) and secondary (n = 3,664) prevention trial concluded that EPA is a promising treatment for prevention of major coronary events, and especially nonfatal coronary events, in Japanese hypercholesterolemic (total cholesterol ≥6.5 mmol/l)

review article patients. In patients with no history of coronary artery disease, EPA treatment reduced major coronary events by 18%.5,15 Secondary prevention OF CVD

Coronary Artery Disease The GISSI (Gruppo Italiano per lo Studio della Sopravvivenza nell’ Infarto Miocardico)-Prevenzione study randomized 11,323 post-MI patients to receive a fish oil supplement (1 g daily containing 850 mg of concentrated EPA and DHA) versus no supplement, 300 mg of a vitamin E supplement versus no supplement and both supplements versus no supplements.

The primary combined efficacy endpoint was death, nonfatal MI and stroke. At the end of 1-year of follow-up, patients taking the fish oil supplement had a 15% reduction in the primary endpoint, including 21% and 30% reductions in total and CV mortality, respectively.16 The major factor in the mortality reduction by omega-3 PUFAs was shown to be a striking 45% reduction in SCDs, which had not been a stated primary endpoint for the GISSI-Prevenzione trial.17 Assessment of the time course of the benefit of omega-3 PUFAs in postMI patients showed that the reduction in risk of sudden death was specifically relevant and statistically significant already at four months. A similarly significant, although delayed, pattern after 6-8 months of treatment was observed for cardiovascular, cardiac and coronary deaths.18 In a subgroup analysis of findings from the GISSI trial, Macchia et al found that the magnitude of reduction in mortality due to SCD increased with progressively worsening left ventricular (LV) systolic function. The effect of omega-3 PUFA treatment on SCD was related to the degree of systolic dysfunction, with the benefit on SCD reduction in patients with ejection fraction (EF) ≤40% being 4-fold higher than in those with EF >50%.19 The secondary prevention arm of the JELIS trial, suggested that the reduction of nonfatal CHD events may require higher doses (2-3 g/day of DHA + EPA) and/or a longer duration of treatment (3-5 years).15 The Diet and Reinfarction Trial (DART) was the first RCT of dietary fish intake in secondary cardiovascular prevention of MI in 2,033 men who recovered from a recent MI.5,20 These patients were allocated to three different dietary advice groups: 

Fat advice group, in which participants were advised to reduce dietary fat intake to 30% of total energy and to increase the polyunsaturated/ saturated (P/S) ratio to 1.





Fiber advice group, in which participants were advised to increase their intake of cereal fiber to 18 g daily.

Fish advice group, in which participants were instructed to either eat at least two weekly portions (200-400 g) of fatty fish or to take a daily fish oil supplement.

At two years, there was a reduction of 29% in allcause mortality after MI among men that followed a high fish intake diet and 16% reduction in the risk of ischemic heart disease events compared to the remaining two groups. The reduction in CV events was particularly impressive in the subgroup that took the fish oil supplement as opposed to simply increasing dietary fish consumption. The benefit of the high fish intake group started to manifest early and persisted throughout study duration.5,21 The Indian Study on Infarct Survival also demonstrated a significant effect of omega-3 fatty acid therapy on mortality in patients who had an MI. In this study, 360 Indian patients were randomized within 24 hours following an MI into three groups: a) Fish oil capsules (providing 1.8 g of EPA + 0.72 g/d of DHA daily), b) a mustard oil group 20 g/day (providing 2.9 g ALA daily) and c) a placebo group. At 1-year follow-up, there were significant reductions in total CHD events and nonfatal MI and a 50% reduction in SCD in the fish oil and mustard oil groups when compared with the placebo group. The fish oil and mustard oil groups also showed significant reductions in total cardiac arrhythmias, LV enlargement and angina pectoris compared with the placebo group. Total cardiac deaths showed no significant reduction in the mustard oil group; however, the fish oil group had significantly less cardiac deaths compared with the placebo group (11.4% vs 22.0%). The study population significantly differed from those in other published studies in that they were enrolled within 24 hours of MI and were predominantly vegetarian. Also, they received no aggressive treatment typical of modern post-MI therapies.22 The Lyon Diet Heart Study also demonstrated a decline in the nonfatal MIs and cardiac deaths with Mediterranean diet at an extended follow-up (with a mean of 46 months per patient). Also, the protective effect of a Mediterranean dietary pattern was maintained upto four years after the first infarction.23 The randomized, double-blind Study on Prevention of Coronary Atherosclerosis by Intervention with Marine Omega-3 fatty acids (SCIMO) in 223 patients with angiographically-proven coronary artery disease found

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review article that dietary intake of omega-3 fatty acids modestly decreases the course of coronary atherosclerosis in humans. Comparison of baseline versus post-treatment angiograms showed that coronary segments in the fish oil group showed less progression and more regression than segments in the placebo group.24

Arrhythmias It has been shown that for individuals at high-risk of fatal ventricular arrhythmias, regular daily ingestion of fish oil fatty acids may significantly reduce potentially fatal ventricular arrhythmias.25 Anand et al also suggest that any patient with documented CHD and those with risk factors for SCD, such as LV dysfunction, LV hypertrophy, prior MI or high-grade ventricular dysrhythmias, should consider fish oil supplementation.26

Hypertension A meta-analysis of 31 placebo-controlled trials on 1,356 subjects demonstrated a dose-response effect of fish oil on blood pressure (BP), of -0.66/-0.35 mmHg/g omega-3 fatty acids. The hypotensive effect may be strongest in hypertensive subjects and those with clinical atherosclerotic disease or hypercholesterolemia.27 Results of another meta-analysis of controlled clinical trials suggest that diet supplementation with a relatively high dose of omega-3 PUFA (≥3 g/day) can lead to clinically relevant BP reductions in individuals with untreated hypertension. In the six studies that enrolled untreated hypertensives (n = 291), significant reductions of systolic BP and diastolic BP were present in two and four trials, respectively.28 INTERMAP observational data on food omega-3 PUFA and BP noted that omega-3 fatty acids from foods such as fish, nuts, seeds and vegetable oils have a small but important antihypertensive effect. INTERMAP was an international cross-sectional epidemiologic study conducted in almost 5,000 men and women in China, Japan, the United Kingdom and the United States.

In the study, omega-3 PUFA intake related inversely to BP, including in nonhypertensive persons. Food omega-3 PUFA may thus contribute to prevention and control of adverse BP levels.29

Atrial Fibrillation Omega-3 fatty acids can be used to prevent AF post bypass particularly in patients with contraindications to sotalol or b-blockers (i.e., chronic obstructive lung disease or bradycardia).5 Calò et al investigated the effect of preoperative and postoperative

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treatment with omega-3 fatty acids in preventing the occurrence of AF after bypass surgery in 160 patients with no prior history of AF. They demonstrated that omega-3 fatty acids supplementation during hospitalization in patients undergoing coronary artery bypass graft substantially reduced the incidence of postoperative AF and was associated with a shorter hospital stay. New-onset postoperative AF was noticed in 33.3% of the control group and in 15.2% of the omega-3 fatty acids group.30 Conclusion 













Heart disease is the leading cause of death worldwide and a major public health problem.

Data now support the contention that appropriate nutritional interventions may have an important effect in preventing or delaying the appearance of CVD. One specific recommendation in the battle against CVD is the increased intake of omega-3 fatty acids, which are PUFAs. The nutritionally essential omega-3 fatty acids are ALA, EPA and DHA. The omega-3 PUFAs of particular interest for the prevention of CVD include EPA and DHA, found predominantly in fish and fish oils.

The association between fish consumption and risk of CVD has been extensively studied and there is abundant evidence for the cardioprotective nature of omega-3 fatty acids.

Several mechanisms explaining the cardioprotective effect of omega-3 PUFAs have been suggested, including antiarrhythmic, hypolipidemic and antithrombotic roles.

The AHA currently recommends consumption of 1 g/day of a DHA and EPA combination in patients with established CHD. In patients without CHD, at least 500 mg/day of EPA plus DHA is recommended; this goal can be met by eating two fish meals per week, with an emphasis on fatty fish.

References 1.

Defilippis AP, Blaha MJ, Jacobson TA. Omega-3 fatty acids for cardiovascular disease prevention. Curr Treat Options Cardiovasc Med 2010;12(4):365-80.

2.

Getz GS, Reardon CA. Nutrition and cardiovascular disease. Arterioscler Thromb Vasc Biol 2007;27(12): 2499-506.

3.

Kris-Etherton PM, Hu FB, Ros E, Sabaté J. The role of tree nuts and peanuts in the prevention of coronary heart disease: multiple potential mechanisms. J Nutr 2008;138(9):1746S-1751S.

review article 4.

Carrero JJ, Fonollá J, Marti JL, Jiménez J, Boza JJ, López-Huertas E. Intake of fish oil, oleic acid, folic acid, and vitamins B-6 and E for 1 year decreases plasma C-reactive protein and reduces coronary heart disease risk factors in male patients in a cardiac rehabilitation program. J Nutr 2007;137(2):384-90.

5.

Artham SM, Lavie CJ, Milani RV, Anand RG, O’Keefe JH, Ventura HO. Fish oil in primary and secondary cardiovascular prevention. Ochsner J 2008;8(2):49-60.

6.

Lavie CJ, Milani RV, Mehra MR, Ventura HO. Omega-3 polyunsaturated fatty acids and cardiovascular diseases.

J Am Coll Cardiol 2009;54(7):585-94.

7.

Roth EM, Harris WS. Fish oil for primary and secondary prevention of coronary heart disease. Curr Atheroscler Rep 2010;12(1):66-72.

8.

Kandasamy N, Joseph F, Goenka N. The role of omega-3 fatty acids in cardiovascular disease, hypertriglyceridaemia and diabetes mellitus. Br J Diab Vasc Dis 2008;8(3):121-8.

9.

Kromhout D, Bosschieter EB, de Lezenne Coulander C. The inverse relation between fish consumption and 20-year mortality from coronary heart disease. N Engl J Med 1985;312(19):1205-9.

10. Ascherio A, Rimm EB, Stampfer MJ, Giovannucci EL, Willett WC. Dietary intake of marine n-3 fatty acids, fish intake, and the risk of coronary disease among men.

N Engl J Med 1995;332(15):977-82.

11. Morris MC, Manson JE, Rosner B, Buring JE, Willett WC, Hennekens CH. Fish consumption and cardiovascular disease in the physicians’ health study: a prospective study. Am J Epidemiol 1995;142(2):166-75.

12. Hu FB, Bronner L, Willett WC, Rexrode KM, Albert CM, Hunter D, et al. Fish and omega-3 fatty acid intake and risk of coronary heart disease in women. JAMA 2002;287(14):1815-21.

13. Dolecek TA. Epidemiological evidence of relationships between dietary polyunsaturated fatty acids and mortality in the multiple risk factor intervention trial. Proc Soc Exp Biol Med 1992;200(2):177-82.

14. Rodriguez BL, Sharp DS, Abbott RD, Burchfiel CM, Masaki K, Chyou PH, et al. Fish intake may limit the increase in risk of coronary heart disease morbidity and mortality among heavy smokers. The Honolulu Heart Program. Circulation 1996;94(5):952-6.

15. Yokoyama M, Origasa H, Matsuzaki M, Matsuzawa Y, Saito Y, Ishikawa Y, et al; Japan EPA Lipid Intervention Study (JELIS) Investigators. Effects of eicosapentaenoic acid on major coronary events in hyper-cholesterolaemic patients (JELIS): a randomised open-label, blinded endpoint analysis. Lancet 2007;369(9567):1090-8.

16. GISSI-Prevention Investigators (Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto miocardico).

Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarction: results of the GISSI-prevention trial. Lancet 1999;354(9177):447-55.

17. Leaf A. On the reanalysis of the GISSI-Prevenzione.

Circulation 2002;105(16):1874-5.

18. Marchioli R, Barzi F, Bomba E, Chieffo C, Di Gregorio D, Di Mascio R, et al; GISSI-Prevenzione Investigators. Early protection against sudden death by n-3 polyunsaturated

fatty acids after myocardial infarction: time-course analysis of the results of the Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico (GISSI)Prevenzione. Circulation 2002;105(16):1897-903.

19. Macchia A, Levantesi G, Franzosi MG, Geraci E, Maggioni AP, Marfisi R, et al; GISSI-Prevenzione Investigators. Left ventricular systolic dysfunction, total mortality, and sudden death in patients with myocardial infarction treated with n-3 polyunsaturated fatty acids.

Eur J Heart Fail 2005;7(5):904-9.

20. Burr ML, Fehily AM, Gilbert JF, Rogers S, Holliday RM, Sweetnam PM, et al. Effects of changes in fat, fish, and fibre intakes on death and myocardial reinfarction: Diet and Reinfarction Trial (DART). Lancet 1989;2(8666): 757-61.

21. Patel JV, Tracey I, Hughes EA, Lip GY. Omega-3 polyunsaturated fatty acids: a necessity for a comprehensive secondary prevention strategy. Vasc Health Risk Manag 2009;5:801-10.

22. Singh RB, Niaz MA, Sharma JP, Kumar R, Rastogi V, Moshiri M. Randomized, double-blind, placebo-controlled trial of fish oil and mustard oil in patients with suspected acute myocardial infarction: the Indian experiment of infarct survival-4. Cardiovasc Drugs Ther 1997;11(3): 485-91.

23. de Lorgeril M, Salen P, Martin JL, Monjaud I, Delaye J, Mamelle N. Mediterranean diet, traditional risk factors, and the rate of cardiovascular complications after myocardial infarction: final report of the Lyon Diet Heart Study. Circulation 1999;99(6):779-85.

24. von Schacky C, Angerer P, Kothny W, Theisen K, Mudra H. The effect of dietary omega-3 fatty acids on coronary atherosclerosis. A randomized, double-blind, placebo-controlled trial. Ann Intern Med 1999;130(7): 554-62.

25. Leaf A, Albert CM, Josephson M, Steinhaus D, Kluger J, Kang JX, et al; Fatty Acid Antiarrhythmia Trial Investigators. Prevention of fatal arrhythmias in highrisk subjects by fish oil n-3 fatty acid intake. Circulation 2005;112(18):2762-8.

26. Anand RG, Alkadri M, Lavie CJ, Milani RV. The role of fish oil in arrhythmia prevention. J Cardiopulm Rehabil Prev 2008;28(2):92-8.

27. Morris MC, Sacks F, Rosner B. Does fish oil lower blood pressure? A meta-analysis of controlled trials.

Circulation 1993;88(2):523-33.

28. Appel LJ, Miller ER 3rd, Seidler AJ, Whelton PK. Does supplementation of diet with ‘fish oil’ reduce blood pressure? A meta-analysis of controlled clinical trials.

Arch Intern Med 1993;153(12):1429-38.

29. Ueshima H, Stamler J, Elliott P, Chan Q, Brown IJ, Carnethon MR, et al; INTERMAP Research Group. Food omega-3 fatty acid intake of individuals (total, linolenic acid, long-chain) and their blood pressure: INTERMAP study. Hypertension 2007;50(2):313-9.

30. Calò L, Bianconi L, Colivicchi F, Lamberti F, Loricchio ML, de Ruvo E, et al. N-3 fatty acids for the prevention of atrial fibrillation after coronary artery bypass surgery: a randomized, controlled trial.

J Am Coll Cardiol 2005;45(10):1723-8.

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Clinical Study ...Cont’d from page 377

developed IGT or frank DM in due course after AMI.7 The risk of CHF is also increased in patients with stress hyperglycemia. Elevated glycosylated hemoglobin (HbA1C) in nondiabetic patients is a risk factor for one year mortality after AMI. Hyperglycemia in AMI is a transient phenomenon that is induced by acute stress, which increases the levels of cortisol and catecholamines in blood. HbA1C is the most powerful indicator of high blood glucose on admission. It is a marker of acute stress and also reflects the prevailing disturbed glucometabolic state.8 Patients with AMI with IGT and frank DM are at increased risk of in-hospital and short-term morbidity as well as mortality. Few possible mechanisms may explain this observation.9 





Hyperglycemia is a reflection of relative insulin deficiency which is associated with increased lipolysis and excess circulating free fatty acids.

This effect is exaggerated in cases of acute stress such as MI. Free-fatty acids are toxic to ischemic myocardium and may lead to damaged cardiac cell membranes, calcium overload and arrhythmias. High concentration of free-fatty acids during myocardial ischemia increases myocardial contractility. Insulin deficiency also limits the ability of cardiac muscle to take up glucose for anerobic metabolism.

Hyperglycemia may precipitate an osmotic diuresis, resulting in volume depletion that may interfere with Frank-Starling mechanism which is an important compensatory mechanism, for the failing left ventricle. Reflex adaptation to hemodynamic stress secondary to infarction may be impaired by autonomic dysfunction which is common in diabetics. Also, diabetics have extensive CAD that limits the availability of collateral blood flow to the infarct zone.10 IGT may be a marker of more extensive cardiac damage in AMI, which may lead to greater rise in stress hormones (promoting glycogenolysis and hyperglycemia) and may also increase the risk of CHF and mortality.

LIMITATIONS 



384

This cross-sectional, comparative study was conducted with only 60 patients of AMI and hence, information regarding boundaries of abnormal glucose tolerance could not be derived. Larger samples are needed to decide the cut-off values of abnormal glucose tolerance.

In our study, three months follow-up was done, but long-term follow-up studies are needed to find out future development of overt DM in patients with IGT as well as long-term prognosis.

Asian Journal of Clinical Cardiology, Vol. 14, No. 11, March 2012



Measurement of stress markers like circulating catecholamines and cortisol would be needed to exclude influence of stress hyperglycemia in glucometabolic abnormalities, which was not done in our study.

CONCLUSION Patients with AMI who were found to have IGT and frank DM on screening with OGTT on follow-up had a high incidence of cardiovascular morbidity especially dyskinesia of involved segment, pump failure, arrhythmias and recurrent cardiac events as well as mortality. Thus, glucometabolic abnormalities in nondiabetic patients with acute coronary event have an influence on cardiovascular morbidity (in-hospital and short-term) as well as mortality. IGT confers an increased cardiovascular risk in acute ischemic event, even in the absence of other classic coronary risk factors. Hence, OGTT should be included in the armamentarium in patients with AMI to detect at high cardiovascular risk individuals.

REFERENCES 1.

Jovon GE. Cause of death in 1144 patients with diabetes mellitus. CMAJ 1986;134(7):754-64.

2.

Capes SE, Hunt D, Malmberg K, Gerstein HC. Stress hyperglycemia and increased risk of death after myocardial infarction in patients with and without diabetes: a systematic review. Lancet 2000;355(9206):773-8.

3.

American Diabetes Association. Consensus Development Conference on Insulin Resistance. 5-6 November 1997.

Diabetes Care 1998;21(2):310-4.

4.

Norhammar AM, Rydèn L, Malmberg K. Admission plasma glucose. Independent risk factor for long-term prognosis after myocardial infarction, even in nondiabetic patients. Diabetes Care 1999;22(11):1827-31.

5.

Stubbs PJ, Allghband-Zadeh J, Laycock JF, Collinson PO, Carter GD, Noble MI. Significance of an index of insulin resistance on admission in non-diabetic patients with acute coronary syndromes. Heart 1999;82(4):443-7.

6.

Antman EM, Braunwald E. Acute myocardial infarction.

Braunwald’s Heart Disease. 8th edition, P. Libby et al (Eds.), Saunders, Philadelphia, 2008.

7.

Mizock BA. Alteration in carbohydrate metabolism during stress: a review of the literature. Am J Med 1995;98(1):75-84.

8.

Oswald GA, Smith CC, Betteridge DJ, Yudkin JS. Determinants and importance of stress hyperglycemia in non-diabetic patients with myocardial infarction.

Br Med J (Clin Res Ed) 1986;293(6552):917-22.

9.

Fuller JH, Shipley MJ, Rose G, Jarrett RJ, Keen H. Coronaryheart-disease risk and impaired glucose tolerance.

The Whitehall study. Lancet 1980;1(8183):1373-6.

10. Tavani A, Bertuzzi M, Gallus S, Negri E, La Vecchia C. Diabetes mellitus as a contributor to risk of acute myocardial infarction. J Clin Epidemiol 2002;55(11):1082-7.

original study

Effect of Relaxation Therapy on Apolipoprotein A, B, MDA and Lipid Profile in Hypertensive Patients Amit Tyagi*, Rupal Tyagi*, Ritesh Vekariya**

Abstract We conducted a controlled study on the effect of selected yoga practice in the control and management of 40 cases of essential hypertension and equal number of healthy (nonhypertensive) controls. Free radical cellular damage is considered to be the underlying common biological factor in essential hypertension. We, therefore, investigated lipid profile, lipid peroxidation and apolipoprotein A and B levels of subjects with essential hypertension. The specific yoga training protocol not only helped to decrease blood pressure but also to retard the progression of cellular damage due to free radicals.

Keywords: Essential hypertension, yoga, free radicals

T

he modern way of life has resulted in increase in stress to everybody, whether he is an overworked executive or a school going child. The increased stress along with a lack of physical activity has increase the prevalence of hypertension and cardiovascular disease manifold.1 In recent years, yoga has been advocated as panacea for stress-induced and psychosomatic disorders2 and there has been strong claim that yoga can help to control hypertension.3 However, most of these reports are based on empirical observations without elucidating the rationale and mechanisms underlying this cure of hypertension by yoga. This study provides a rational explanation on the possible action of yoga practice in control of blood pressure (BP).

Aims To investigate serum lipid, lipid peroxidation and apolipoprotein A and B (apo A and B) levels in patients with essential hypertension, before and after specific yoga training.

*Associate Professor Dept. of Biochemistry **Postgraduate Student Dept. of Medicine CU Shah Medical College, Surendranagar, Gujarat Address for correspondence Dr Amit Tyagi Dept. of Biochemistry CU Shah Medical College, Dudhraj Road Surendranagar, Gujarat - 363 001 E-mail: ami_tyagi2001@yahoo.com

Material and Methods Forty patients with essential hypertension and without evidence of any renal, cardiac or respiratory disease were selected. Forty healthy age- and sex-matched normotensive subjects who did not exhibit hypertension even on a specific physical test were also selected as controls. After physical and medical check-up and basal measurement, patients were given a progressive yogic muscular relaxation training for one hour daily for 30 days.

Blood samples were collected in plain bulb before the relaxation therapy and after one month of the relaxation therapy. Serum apo A, apo B, total cholesterol, triglyceride and high-density lipoprotein (HDL)cholesterol were all estimated by kit method. Serum MDA (malondialdehyde) was estimated by Buege et al method.4 Discussion Hypertension is considered as a condition of increase in BP without any organic illness. This may not be true. Recent studies indicate that free radical oxidative damage to cellular integrity is a common factor in hypertension.3 Hypertension places patients at high-risk for target organ damage including retina, brain, heart, kidney, etc. Regular practice of yoga reduces BP to the tune of 10-15 mmHg. The chronic stress-induced sustained muscular contraction reduces lumen diameter of blood vessels in the muscles. This in turn increases BP. Stretching of muscles and relaxing the same as done in yogic exercise reverts this effect.

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Original Study

The present study confirmed the positive effects of yogic muscular relaxation therapy on biochemical and oxidative stress in hypertension. Hypertensive patients engaged in yogic muscular relaxation therapy demonstrated lower apo A, MDA, serum total cholesterol, triglyceride and low-density lipoprotein cholesterol (LDL-C).

Oxidative stress generally causes damage to the membrane polyunsaturated fatty acids leading to the generation of lipid peroxidation product i.e. MDA, which is known to be toxic to cellular components.6 Apo A is the major component of HDL and apo B is the major component of LDL and very LDL (VLDL).

Function of apo A is to activate the lecithin cholesterol acyltransferase (LCAT) enzyme and transport cholesterol from peripheral tissue to liver for degradation. An apo B function is as a cholesterol carrier to tissue.7

1.2 1

g/l

0.4

0

0.93

0.68

0.59

Controls

Patients Patients (before therapy) (after therapy)

Figure 1. Comparative levels of serum apo A in normotensive controls and hypertensive patients before and after therapy.

1.4 1.2 1

0.38

0.8

0.51

0.27

0.6 0.4

0.93 0.59

0.2 0

Controls

0.75

Patients Patients (before therapy) (after therapy)

Figure 2. Comparative levels of serum apo B in normotensive controls and hypertensive patients before and after therapy.

p value

Serum apo A (g/l)

0.93 ± 0.22

0.68 ± 0.28

<0.001

14

Serum apo B (g/l)

0.93 ± 0.38

0.59 ± 0.51

<0.01

12

Serum MDA (nM/l)

6.44 ± 1.6

12.3 ± 2.3

<0.001

10

Serum total cholesterol (mg/dl)

180 ± 41

220 ± 45

<0.001

Serum triglyceride (mg/dl)

105 ± 42

128 ± 53

>0.05

Serum HDLcholesterol (mg/dl)

43 ± 12

45 ± 15

>0.05

Serum VLDLcholesterol (mg/dl)

21 ± 8

26 ± 11

>0.05

Serum LDLcholesterol (mg/dl)

113 ± 43

147 ± 45

<0.01

Asian Journal of Clinical Cardiology, Vol. 14, No. 11, March 2012

0.22

0.2

Controls Patients (mean ± SD) (before therapy) (mean ± SD)

386

0.28

0.6

The present study shows that levels of apo A and apo B were decreased significantly and MDA, total cholesterol, triglycerides and LDL-C were increased Table 1. Comparative Levels of Serum Apo A, Apo B, MDA and Lipid Profile in Normotensive Healthy Controls and Hypertensive Patients before Therapy

0.22

0.8

g/l

Sustained muscular contraction sends hostile signals to the brain, alerting it to impending danger. This does secrete stress hormones and neurotransmitters associated with stress and high BP. This possibly may be reverted by constant practice of yoga. Regular yoga may reduces stress hormones ‘aldosterone’, and ‘vasopressin’, which are potent vasoconstrictors.5

nM/l

16

8

2.3

1.6

6

12.3

4 2 0

2.14

6.44 3.5

Controls

Patients (before therapy)

Patients (after therapy)

Figure 3. Comparative levels of serum MDA in normotensive controls and hypertensive patients before and after therapy.

Original Study

300

250 45 46

mg/dl

200

41 45

150

41

53 180

220

100

43

51

42 189

12

50 105

128

103

43

113

15

Triglycerides

128

10

45

40

0 Total cholesterol

147

8 21

HDL-cholesterol

11 26

10 21

VLDL-cholesterol

LDL-cholesterol

Figure 4. Comparative levels of serum lipid profile in normotensive controls and hypertensive patients before and after therapy.

Table 2. Comparative Levels of Serum Apo A, Apo B, MDA and Lipid Profile in Normotensive Healthy Controls and Hypertensive Patients after Therapy Control (mean ± SD)

Patients (after therapy) (mean ± SD)

p value

Serum apo A (g/l)

0.93 ± 0.22

0.59 ± 0.22

<0.001

Serum apo B (g/l)

0.93 ± 0.38

0.75 ± 0.27

>0.05

Serum MDA (nM/l)

6.44 ± 1.6

3.5 ± 2.14

<0.001

Serum total cholesterol (mg/dl)

180 ± 41

189 ± 46

>0.05

Serum triglyceride (mg/dl)

105 ± 42

103 ± 51

>0.05

Serum HDL-cholesterol (mg/dl)

43 ± 12

40 ± 10

>0.05

Serum VLDL-cholesterol (mg/dl)

21 ± 8

21 ± 10

>0.05

Serum LDL-cholesterol (mg/dl)

113 ± 43

128 ± 41

>0.05

significantly in hypertensive patients (before therapy) compared to normotensive healthy controls (Table 1 and Figs. 1-4).

almost comparable to normotensive healthy control (Table 2, Figs. 1, 3 and 4).

Progressive yogic muscular relaxation therapy exercise significantly decreased levels of apo A, MDA, total cholesterol, triglycerides and LDL-C. The level is

The specific yoga training protocol not only helped to decrease BP but also to retard the progression of cellular damage due to free radicals.

Conclusion

Cont’d on page 390...

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case report

Idiopathic Dilated Cardiomyopathy Complicating in a Pregnancy with Uterine Fibroid DEBASMITA MANDAL*, PRADIP KUMAR SAHA**, CHAITALI DATTARAY†, SAROJ MANDAL‡

Abstract Idiopathic dilated cardiomyopathy (DCM) during gestation is a rare coincidence. These patients can experience hazardous complications like cardiac failure and even death during pregnancy due to physiologically increased in vascular volume and cardiac output. A previously diagnosed case of idiopathic dilated cardiomyopathy (ejection fraction [EF] 32% and severe left ventricular systolic dysfunction in Echo Doppler, NYHA functional Class IV) who also had a big uterine fibroid was admitted to our antenatal ward at 33 weeks four days of gestation with signs of left ventricular failure. She required intensive coronary care unit (ICCU) care and was treated with digoxin, inotrops and diuretics, etc. She was managed expectantly upto 36 weeks and cesarean section was done due to intrauterine growth restriction (IUGR). Postpartum period was also eventful with another episode of cardiac failure, which needed ventilator support as well as ICCU back-up. She was followed up with regular echocardiography and ECG and showed improvement at sixth month with EF of 42%. Adequate counseling prenatally and antenatally and good multidisciplinary support may lead to successful pregnancy outcome in patients with idiopathic DCM.

Keywords: Idiopathic dilated cardiomyopathy, pregnancy, fibroid, left ventricular failure

D

ilated cardiomyopathy (DCM) is defined as dilatation of one or both ventricles with reduced left ventricular ejection fraction (LVEF) in the absence of coronary, valvular, congenital or any systemic diseases known to cause myocardial dysfunction.1 The predominant features are evidenced by increased myocardial mass, cardiomegaly with dilatation and enlargement of one or both ventricles with improper contractility and impairment of systolic function.2 It has been observed that young nonpregnant women with DCM have poor prognosis and survival than women with peripartum cardiomyopathy.3 It is only very rare that DCM is well-documented before pregnancy.4 During gestation, the physiologic hemodynamic alteration and procoagulant state of pregnancy can destabilize the cardiac disease as well as the pregnancy outcome itself. Authors have documented a negative impact of pregnancy on clinical course of women with DCM and have also shown an increased incidence of neonatal complications in mothers with DCM.5 *Assistant Professor **RMO cum Clinical Tutor †Associate Professor Dept. of Obestetrics and Gynecology ‡Final Year Post Doctoral Trainee, Dept. of Cardiology IPGME & R, SSKM Hospital, Kolkata Adress for correspondence Dr Debasmita Mandal Qr. No. C/11, SSKM Hospital Campus 242, AJC Bose Road, Kolkata, West Bengal - 700 020 E-mail: drdebasmitamondal@yahoo.com

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In this case report, we present the clinical sequel of a young woman with DCM and a big fundal fibroid during antenatal period and subsequent successful pregnancy outcome at 36 weeks gestation.

Case report A 24-year-old primigravida at 33 weeks four days of gestation was referred with chief complaints of acute exacerbation of breathlessness and palpitation for four days. Previously, she required admission at eight weeks gestation at a local health center for severe orthopnea.

Ultrasonography (USG) done then corroborated the gestationl age and revealed a big fundal fibroid (14.2 x 13.6 x 13.2 cm3) in USG. Echo Doppler diagnosed DCM with severe left ventricular systolic dysfunction, ejection fraction (EF) of 32%, moderate mitral regurgitation and moderate pulmonary arterial hypertension.

Later, on admission in our antenatal ward she was found to be moderately anemic, afebrile and normotensive. All other peripheral signs like cyanosis, jaundice, clubbing and edema were absent. Uterine height corresponded to 32 weeks gestation. She had dyspnea at rest (New York Heart Association [NYHA] functional Class IV), tachycardia, raised jugular venous pressure (JVP) and left ventricular failure while investigations revealed hemoglobin level of 9.2 g/dl with 29% packed cell volume; liver function test, renal function test and coagulation profile were within normal range. Previously, USG done at showed

case report Table 1. Overview of Literatures on Idiopathic DCM in Pregnancy (All Case Reports and Study that could be Found Searching MEDLINE from 1980-2010) Authors

No. of pregnancies

Complications during pregnancy

Mode of termination

Gestational age at delivery

Neonatal outcome

Mazor et al2 (1994)

1

Slow progress of labor

LSCS

36 weeks

No morbidity

Chan et al9 (1999)

1

Thromboembolic stroke

LSCS

31 weeks

1.6 kg baby IUGR

PIH

2 by forceps 1 therapeutic abortion

34 Âą 5.9 weeks

2 normal 1 (multiple cardiac anomalies)

20 weeks

Stillbirth

Berstein et

al7

(2001) 3

Yacoub et al6 (2002)

1

LVF

Therapeutic abortion

Avila et al8 (2003)

18

CCF, angina, arrhythmia, thromboembolism abortion, maternal death

Majority by NVD

Grewal et al5 (2010)

27

PPH, pre-eclampsia LVF

Majority by NVD

Stillbirth, prematurity

38 weeks

Prematurity, fetal, death, IUGR

LSCS = Lower segment cesarean section; IUGR = Intrauterine growth restriction; PIH = Pregnancy-induced hypertension; LVF = Left ventricular failure; CCF = Congestive cardiac failure; PPH = Postpartum hemorrhage; NVD = Normal vaginal delivery.

adequate fetal growth and excluded the absence of congenital anomaly. Chest X-ray on admission revealed a dilated heart with pulmonary venous congestion.

ECG revealed sinus tachycardia and echocardiography showed dilated left atrium and ventricle with global hypokinesia of left ventricle and LVEF was 24%. She was shifted to intensive coronary care unit (ICCU) for better management and treated conservatively with digoxin, diuretics, potassium supplements and heparin and inotrops. After stabilization of heart failure by regular echocardiographies monitoring was continued.

EF of left ventricle was found to vary between 25% and 32% with medical treatment.

Simultaneous USG fetal monitoring and iron and calcium supplementation were continued. At 36 weeks five days, pregnancy was terminated by elective lower segment cesarean section for intrauterine growth restriction (IUGR) and oligohydramnious undergraded epidural anesthesia. A 2.49 kg girl baby was delivered with Apgar score of 9 and 8 at 1 and 5 minutes, respectively.

Postoperatively patient again developed left ventricular failure and cardiogenic shock, which required ICCU admission and multidisciplinary support. She was discharged after two weeks and asked to be on followup. Neonate did not show any congenital affection.

Follow-up echocardiography at sixth month showed relatively improved left ventricular systolic function with EF of 42%. For contraception, she was advised progesterone-only pill.

Discussion While the incidence of DCM (idiopathic and secondary) is observed to be 5-8 cases per 1,00,000 population per year,5 occurrence of idiopathic DCM during gestation is rare.2,4,6 Yacoub et al while reporting such case conducted a MEDLINE search from 1980 to 2000 and found only two pregnant cases with idiopathic or primary DCM.6 From 2001 to 2010, few authors shared their experience and total number of pregnancies reported were 48.5,7,8 Very limited supporting data are available for management guidelines during pregnancy.

Pregnancy outcome of 51 pregnancies showed increased rate of therapeutic abortions and maternal complications included pregnancy-induced hypertension, preterm labor, low birth weight, intrauterine death and ventricular tachycardia, arrhythmia, thromboembolism, infective endocarditis and heart failure, etc.

Grewal et al studied 36 pregnancies with DCM, which included 27 women with idiopathic DCM and observed cesarean deliveries in seven pregnancies for obstetric indications only; no operative interference was present for cardiac indications and preferred method of anesthesia was epidural.5 They observed poor neonatal outcome in women with severe DCM (moderate/ severe LV systolic dysfunction and NYHA functional Class III/IV) if concomitant obstetric risk factors were present.

The present case had severe left ventricular systolic dysfunction with EF of 32% (severe DCM) in first trimester. Adding to this, the presence of big fundal fibroid also increased the obstetric risk. The mode of

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case report delivery was cesarean section under graded epidural anesthesia for an obstetric indication not due to heart disease per se. Maternal morbidity included heart failure twice (33 weeks and immediate postpartum period), oligohydramnious and IUGR. We also concur with other authors regarding the fact that pregnancy is a major determinant for deterioration of DCM cases.5,9 Many have advised against conception with DCM and poor left ventricular systolic function with EF <30-50%.10 But, there is minimal evidence-based data to recommend it. Simultaneously repeated pregnancies should be discouraged in these patients.

Class IV) with big fundal fibroid to have a successful pregnancy outcome at term.

Routine administration of anticoagulant is required throughout the pregnancy to avoid thromboembolism.

Though, the present case was managed successfully due to optimal obstetric, ICCU and NICU coordination, undertaking pregnancy in these woman is hazardous and becomes a cause of concern for the family and attending physicians. In our experience, counseling plays a vital role preconceptionally and antenatally.

Conclusion In DCM, prepregnant hemodynamically stable status, good left ventricular function may result in favorable outcome. To avoid such potentially fatal situations of severe DCM in pregnancy like ours, whenever an antenatal patient complains of effort intolerance, dyspnea and palpitation, ECG and Echo Doppler should ideally be recommended.

In a properly monitored environment pregnancy may be allowed to extend to term provided patient is clinically and hemodynamically stable. This is one of the rare case of severe DCM (severe left ventricular systolic dysfunction, EF [32%] and clinically NYHA

References 1.

Elliott P. Cardiomyopathy. Diagnosis and management of dilated cardiomyopathy. Heart 2000;84(1):106-12.

2.

Mazor M, Levitas E, Gussarsky Y, Friedman S, Leiberman JR. Idiopathic dilated cardiomyopathy in pregnancy. Arch Gynecol Obstet 1994;255(1):51-3.

3.

van Hoven KH, Kitsis RN, Katz SD, Factor SM. Peripartum versus idiopathic dilated cardiomyopathy in young women: a comparison of clinical, pathologic and prognostic features. Int J Cardiol 1993;40(1):57-65.

4.

Oakley C, Child A, Jung B, Presbitero P, Tornos P, Klien W, et al. Task Force on the Management of Cardiovascular Diseases During Pregnancy of the European Society of Cardiology. Expert consensus document on management of cardiovascular diseases during pregnancy. Eur Heart J 2003;24(8):761-81.

5.

Grewal J, Siu SC, Ross HJ, Mason J, Balint OH, Sermer M, et al. Pregnancy outcomes in women with dilated cardiomyopathy. J Am Coll Cardiol 2010;55:45-52.

6.

Yacoub A, Martel MJ. Pregnancy with primary dilated cardiomyopathy. Obstet Gynecol 2002;99(5 Pt 2):928-30.

7.

Berstein PS, Magriples U. Cardiomyopathy in pregnancy: a retrospective study. Am J Perinatol 2001;18(3):163-8.

8.

Avila WS, Rossi EG, Ramires JA, Grinberg M, Bortolotto MR, Zugaib M, et al. Pregnancy in patients with heart disease: experience with 1,000 cases. Clin Cardiol 2003;26(3):135-42.

9.

Chan F, Kee WD. Idiopathic dilated cardiomyopathy presenting in pregnancy. Can J Anaesth 1999;46(12): 1146-9.

10. Thorne SA, Nelson-Piercy C, MacGregor A, Gibbs S, Crowhurst J, Panay N, et al. Pregnancy and contraception in heart disease and pulmonary arterial hypertension.

J Fam Plann Reprod Health Care 2006;32(2):75-81.

...Contâ&#x20AC;&#x2122;d from page 387

in patients of essential hypertension. Indian J Clin Biochem 1996;11(2):129-33.

References 1.

Leon AS. Physical activity levels and coronary heart disease. Analysis of epidemiologic and supporting studies. Med Clin North Am 1985;69(2):3-20.

2.

Selvamurthy W. Yoga for every one: a physiologistâ&#x20AC;&#x2122;s view. Souvenir, Second Congress of Asian and Oceanian Physiological Societies. New Delhi 1990:p.10-26.

3.

Talukdar B, Verma S, Jain SC, Majumdar M. Effect of yoga training on plasma lipid profile, RBC membrane lipid peroxidation and Na+-K+ ATPase activity

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4.

Buege et al. Methods of enzymology; 1975.

5.

Sujit chandratreya; Hypertension and yoga. Internet: http://www.yogapoint.com: An official site of Yoga Vidya Dham.

6.

Del Maestro RF. An approach to free radicals in medicine and biology. Acta Physiol Scand Suppl 1980;492:153-68.

7.

In: Textbook of Medical Biochemistry. Chatterjee MN, Shinde R, 5th edition, Jaypee Publications, New Delhi, 2002.

case report

Sweet’s Syndrome with Type 2 Diabetes Mellitus: A Rare Case Presentation RK Kotokey*, Swarup Kar**, Libe Nyorak**, Arup Sarma**, M Shebha Rupsi**

Abstract Sweet’s syndrome is an acute febrile neutrophilic dermatosis, which is associated with erysipelas, disseminated erythema nodosum, internal malignancies, inflammatory bowel disease, etc. But, Sweet’s syndrome associated with type 2 diabetes mellitus has not been reported in the literature. In this article, we describe a patient of type 2 diabetes mellitus who has Sweet’s syndrome.

Keywords: Sweet’s syndrome, type 2 diabetes mellitus

S

weet’s syndrome, which was described by RD Sweet in 1964, is characterized by sudden onset of fever, leukocytosis and cutaneous eruption.

The eruption consists of tender, erythematous, welldemarcated papules and plaques, which show dense neutrophilic infiltrates microscopically. The lesions may appear anywhere, but favor the upper body including the face.1 Arthralgias or arthritis, alveolitis, sterile osteomeylitis, renal, hepatic and central nervous system (CNS) involvement have been reported.2 The condition is more common in women and the mean age of onset is the mid-to-late fifties. Sweet’s syndrome may last from one week to more than four years.

The etiology of Sweet’s syndrome is unknown, though it is presumed to be a type of hypersensitivity reaction, which leads to stimulation of a cascade of cytokines that precipitate neutrophil activation and infiltration.3,4 T-cell-mediated immune response has been 5 postulated.

CASE REPORT A 35-year-old female presented with type 2 diabetes mellitus and skin lesions over the face, dorsum of the hands anterior aspects of the legs and back (Figs. 1 and 2).

On examination, the skin lesions were well-demarcated, erythematous papules with plaques, which were tender. The skin was discolored as shown in the

*Head **Postgraduate Trainee, Dept. of Medicine Assam Medical College, Dibrugarh, Assam

Figure 1.

Figure 2.

accompanying picture. Pulse rate was 70/min, regular, of normal volume and character, with no radio-radial or radiofemoral delay; BP was 130/80 mmHg. There was no cyanosis, clubbing or anemia.

Systemic examination: Cardiovascular system, CNS and respiratory systems were normal. Abdominal examination revealed hepatomegaly, which was soft in consistency and nontender.

Investigations Hb: 7 g/dl; TLC: 10,200/mm3; DLC: N75L20E1M4B0; ESR: 40 mm/1st hour; FBS: 134 mg/dl; PPBS: 290 mg/dl; HbA1C: 10.2%; Rh factor, ASO titer, CRP: Negative; dsDNA: Negative.

Histopathological examination showed diffuse inflammatory infiltrates in dermis, band-like infiltrates in papillary dermis with dermal edema.

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case report DISCUSSION

Conclusion

Sweet’s syndrome, or acute febrile neutrophilic dermatosis, is a condition characterized by sudden onset of fever, leukocytosis and tender, erythematous, well-demarcated papules and plaques, which show dense neutrophilic infiltrates on histological examination.

Peculiarity of the present case is that in this case Sweet’s syndrome is associated with type 2 diabetes mellitus and this association has not yet been reported in literature. Moreover, as consistent with literature, our patient is a female, though the age of presentation was a bit early i.e. 35 years.

The condition is more common in women and the mean age of onset is mid-to-late fifties. In fact, it was originally described in women with elevated WBC counts. Ironically this disease now is usually seen in neutropenic patients with cancer, most often in association with acute leukemia but also in association with a variety of other malignancies.6 The lesions may appear anywhere, but favor the upper body including the face.1 The individual lesions are often described as pseudovesicular or pseudopustular, but may be frankly pustular, bullous or ulcerative.

Acknowledgment

Oral and eye involvement (conjunctivitis or episcleritis) have been frequently reported. Arthralgias or arthritis are present in 33-62%.3 Alveolitis, sterile osteomyelitis, renal, hepatic and CNS involvement have been reported.2 Sweet’s syndrome may last from one week to more than four years. Recurrence is common (25-37%).2,3 Although, it may occur in the absence of other known diseases, Sweet’s syndrome is often associated with other diseases like hematologic (including leukemia), and immunologic (rheumatoid arthritis, inflammatory bowel disease).

A genetic association has been suggested. Human leukocyte antigen (HLA) analysis has given variable results. Mizoguchi described an increase in the frequency of HLA Bw54 in Japanese patients with Sweet’s syndrome.7 However, recently in a series of 41 European, Caucasian patients, no significant HLA associations were found.8

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We are thankful to the Principal and Chief Superintendent, Assam Medical College and Hospital, Dibrugarh for kindly allowing us to publish the hospital records.

REFERENCES 1.

Wilson DB, Lynch PJ. Sweet’s Syndrome and Related Disorders. In: Principles and Practice of Dermatology.

Sams WM, Lynch PJ (Eds.), NY, 1996.

2.

Fett DL, Gibson LE, Su WP. Sweet’s syndrome: systemic signs and symptoms and associated disorders. Mayo Clin Proc 1995;70(3):234-40.

3.

von den Driesch P. Sweet’s syndrome (acute febrile neutrophilic dermatosis). J Am Acad Dermatol 1994;31(4):535-56; quiz 557-60.

4.

Barnhill RL, Busam KJ. Vascular Diseases in Histopathology of the Skin. Elder D, (Ed.), NY 1997:204-6.

5.

von den Driesch P, Grushwitz M, Hornstein OP. Adhesion molecule modulation in Sweet’s syndrome compared to erythema multiforme. Eur J Dermatol 1993;3:393-7.

6.

Finberg R. Infections in patients with cancer. Chapter 82.

In: Harrison’s Principles of Internal Medicine. 17th edition 2008:p. 535.

7.

Mizoguchi M, Matsuki M, Mochizuki M, Watanabe R, Ogawa K, Harada S, et al. Human leukocyte antigen in Sweet’s syndrome and its relationship to Behcet’s syndrome. Arch Dermatol 1988;124(7):1069-73.

8.

von den Driesch P, Simon M Jr, Djawari D, Wassmuth R. Analysis of HLA antigens in Caucasian patients with acute febrile neutrophilic dermatosis (Sweet’s syndrome). J Am Acad Dermatol 1997;37(2 Pt 1): 276-8.

medilaw

When and How Cardiologists Advertise?

MCI Regulations, 2002 1: 6.1 Advertising: 6.1.1 Soliciting of patients directly or indirectly, by a physician, by a group of physicians or by institutions or organizations is unethical.

A physician shall not make use of him/her (or his/her name) as subject of any form or manner of advertising or publicity through any mode either alone or in conjunction with others which is of such a character as to invite attention to him or to his professional position, skill, qualification, achievements, attainments, specialities, appointments, associations, affiliations or honors and/or of such character as would ordinarily result in his self-aggrandizement. A physician shall not give to any person, whether for compensation or otherwise, any approval, recommendation, endorsement, certificate, report or statement with respect of any drug, medicine, nostrum remedy, surgical or therapeutic article, apparatus or appliance or any commercial product or article with respect of any property, quality or use thereof or any test, demonstration or trial thereof, for use in connection with his name, signature or photograph in any form or manner of advertising through any mode nor shall he boast of cases, operations, cures or remedies or permit the publication of report thereof through any mode. A medical practitioner is however, permitted to make a formal announcement in press regarding the following: 1. On starting practice.

2. On change of type of practice.

3. On changing address.

4. On temporary absence from duty.

5. On resumption of another practice.

6. On succeeding to another practice.

7. Public declaration of charges.

6.1.2 Printing of self-photograph, or any such material of publicity in the letter head or on sign-board of the consulting room or any such clinical establishment shall be regarded as acts of self-advertisement and unethical conduct on the part of the physician.

However, printing of sketches, diagrams, picture of human system shall not be treated as unethical.

7.12 An institution run by a physician for a particular purpose such as a maternity home, nursing home, private hospital, rehabilitation center or any type of training institution, etc. may be advertised in the lay press, but such advertisements should not contain anything more than the name of the institution, type of patients admitted, type of training and other facilities offered and the fees.

7.13 It is improper for a physician to use an unusually large sign-board and write on it anything other than his name, qualifications obtained from a University or a statutory body, titles and name of his speciality, registration number including the name of the State Medical Council under which registered. The same should be the contents of his prescription papers. It is improper to affix a sign-board on a chemistâ&#x20AC;&#x2122;s shop or in places where he does not reside or work.â&#x20AC;?

7.19 A physician shall not use touts or agents for procuring patients.

Other regulations The advertisement should not violate Drugs and Magic Remedies (Objectionable Advertisement) Act, 1954, Consumer Protection Act, 1986, PNDT Act, 1994, Clinical establishment act (draft), etc.

The advertisement should not be false, misleading or indecent.

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photo quiz

Painless Nodules in the Fingers

A

61-year-old woman presented with a history of chronic pain and stiffness in multiple joints.

She had morning stiffness in her hands, hips, and knees that gradually improved with activity. She did not report any foot pain or stiffness, fever, or rash.

On examination she had swelling around the distal interphalangeal joints in multiple fingers with relative sparing of the proximal and metacarpophalangeal joints (Figure 1). The joints were not warm or tender to palpation.

Laboratory studies showed normal values of rheumatoid factor and anticyclic citrullinated peptide, and a normal white blood cell count. Hand radiography was ordered (Figure 2).

Figure 1.

Question Based on the patientâ&#x20AC;&#x2122;s history, physical examination, and radiographic findings, which one of the following is the most likely diagnosis?

A. Gouty arthritis.

B. Osteoarthritis.

C. Psoriatic arthritis.

Figure 2.

D. Rheumatoid arthritis.

See the following page for discussion.

Source: Adapted from Am Fam Physician. 2011;83(10):1203-1205.

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photo quiz Discussion The correct answer is B: osteoarthritis.

Heberden nodes (hard or bony swellings in the distal interphalangeal joints) along with a deviated distal finger are a classic finding in osteoarthritis. The patient has a variant form of the condition known as erosive osteoarthritis that is common in postmenopausal women. The radiograph of her hands shows subchondral sclerosis and the “gull wing” deformity in the distal interphalangeal joint of the left middle finger (Figure 3). The gull wing deformity is indicative of this variant form.1 Swelling and erosive changes of the proximal interphalangeal joints (Bouchard nodes) often occur in patients with osteoarthritis, but were not present in this patient.

Osteoarthritis is the most common cause of progressive, arthritic disease.2 It affects millions of Americans and is the most common cause of disability in the United States. The erosive form of osteoarthritis is more common in women, with an estimated female-to-male ratio of 12:1, whereas the generalized form has a femaleto-male ratio of 10:1.3,4 Patients with osteoarthritis have a decrease in chondrocyte response to growth factors that stimulate joint repair after repetitive joint stress.5 The acute phase is characterized by inflamed, tender joints and osteophyte formation around the joint margins.6 As the patient progresses into the chronic phase, inflammatory changes subside and the joints become painless to palpation. Bony outgrowths continue to form, resulting in the development of Heberden nodes.

Gouty arthritis is an intermittent, inflammatory arthritis that usually presents acutely as a red, swollen, warm, and painful joint. The metatarsophalangeal joint is most commonly affected (podagra).7 Monosodium urate monohydrate crystal deposition leads to stiffness, swelling, and periarticular subcutaneous nodules (tophi). Radiographic findings include erosive, sclerotic margins with lytic “rat bite” lesions. Laboratory work may show elevated uric acid levels during an acute attack, but the diagnosis is made by identifying crystals in joint fluid with negative birefringence under polarized light.

Psoriatic arthritis presents as painful, red, swollen joints in the fingers, but in conjunction with psoriasis of the skin or scalp.4 The joint swelling is secondary to inflammation of the ligaments and tendons, not skeletal changes. Men and women are equally affected, and patients may be positive for human leukocyte

Figure 3. Radiograph of patient with erosive osteoarthritis showing “gull wing” deformity in the distal interphalangeal joint of the left middle finger (arrow).

Summary Table Condition

Characteristics

Gouty arthritis

Monoarticular involvement, most commonly the metatarsophalangeal joint (podagra) with subcutaneous, periarticular nodules (tophi); red, swollen, warm, painful joint in acute attack; erosive, sclerotic margins with lytic “rat bite” lesions on radiography

Osteoarthritis

Polyarticular involvement with joint stiffness and swelling at the proximal interphalangeal joints (Bouchard nodes) and distal interphalangeal joints (Heberden nodes); radial deviation in the chronic phase; osteophyte formation with “gull wing” deformity on radiography

Psoriatic arthritis

Associated with psoriasis; inflammation of the tendons and ligaments leads to painful, red, swollen joints; joint erosion, spurs, and pencil-in-cup deformity on radiography

Rheumatoid arthritis

Symmetric stiffness in multiple joints in the morning that lasts at least 45 minutes; boggy, warm, tender joints, primarily involving the proximal interphalangeal and metacarpophalangeal joints; “swan neck” deformity in chronic cases; erosive margins and joint-space narrowing on radiography

antigen-B27. Radiography shows joint erosion, spurs, and pencil-in-cup deformity.

Rheumatoid arthritis is an erosive, inflammatory arthritis that affects women three times more often than men.8 Patients present with symmetric stiffness in multiple joints, most often occurring in the morning, that lasts at least 45 minutes before subsiding.9 Joints are boggy, warm, and tender to palpation as in osteoarthritis, but lack erythema and rarely involve the distal interphalangeal joint. Elevated titers of

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photo quiz rheumatoid factor and anticyclic citrullinated peptide antibodies, as well as erosive margins and joint-space narrowing on radiography, also help to differentiate rheumatoid arthritis from osteoarthritis. A “swan neck” deformity is present in chronic cases.

progressive systemic sclerosis. Radiol Clin North Am. 1988;26(6):1195-1212.

5.

Felson DT, Zhang Y. An update on the epidemiology of knee and hip osteoarthritis with a view to prevention.

Arthritis Rheum. 1998;41(8):1343-1355.

6.

Kellgren JH, Moore R. Generalized osteoarthritis and Heberden’s nodes. Br Med J. 1952;1(4751):181-187.

7.

Klippel J, Dieppe P, Ferri F. Regional pain and monoarticular disorder. In: Harris ED, Genovese MC, eds. Primary Care Rheumatology. Philadelphia, Pa.: W.B. Saunders; 2000:117-124.

8.

Gottlieb A, Korman NJ, Gordon KB, et al. Guidelines of care for the management of psoriasis and psoriatic arthritis: Section 2. Psoriatic arthritis: overview and guidelines of care for treatment with an emphasis on the biologics. J Am Acad Dermatol. 2008;58(5):851-864.

9.

Rindfleisch JA, Muller D. Diagnosis and management of rheumatoid arthritis. Am Fam Physician. 2005;72(6): 1037-1047.

REFERENCES 1.

Swagerty DL Jr, Hellinger D. Radiographic assessment of osteoarthritis. Am Fam Physician. 2001;64(2):279-286.

2.

Sinkov V, Cymet T. Osteoarthritis: understanding the pathophysiology, genetics, and treatments. J Natl Med Assoc. 2003;95(6):475-482.

3.

Greenspan A. Erosive osteoarthritis. Semin Musculoskelet Radiol. 2003;7(2):155-159.

4.

Gold RH, Bassett LW, Seeger LL. The other arthritides.

Roentgenologic features of osteoarthritis, erosive osteoarthritis, ankylosing spondylitis, psoriatic arthritis, Reiter’s disease, multicentric reticulohistiocytosis, and

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practice guidelines

AAN Releases Guideline on Magnetic Resonance Imaging for Diagnosing Acute Ischemic Stroke

C

omputed tomography (CT) is the diagnostic standard for acute stroke even though its accuracy has not been formally established.

The sensitivity of CT, which is estimated to be 12 to 92 percent, depends on the imaging features of infarction, time from onset to examination, and study populations, among other factors. Its sensitivity for diagnosing ischemic stroke in the initial hours is limited; therefore, improved accuracy is needed to develop and provide optimal stroke treatment.

Diffusion- and perfusion-weighted imaging, which are newer magnetic resonance imaging techniques, may improve diagnostic yield. Diffusion-weighted imaging measures the net movement of water in tissue due to random molecular motion, also known as brownian motion. It shows hyperintense ischemic tissue changes within minutes to hours after arterial occlusion caused by a reduced diffusion capacity within the affected tissues. Perfusion-weighted imaging allows the measurement of capillary perfusion. The American Academy of Neurology (AAN) evaluated the evidence for the use of magnetic resonance imaging in the diagnosis of acute ischemic stroke.

Clinical Questions and Recommendations Diffusion- and perfusion-weighted imaging were assessed to determine their sensitivity specificity compared with other imaging modalities, and volume of diffusion- and perfusion-weighted imaging abnormality was evaluated to determine if it predicts initial clinical severity, final infarct size, and late clinical outcomes.

The AAN determined that diffusion-weighted imaging is superior to noncontrast CT for the diagnosis of acute ischemic stroke within 12 hours of symptom onset; however, there is insufficient evidence regarding the accuracy of perfusion-weighted imaging. Baseline diffusion-weighted imaging volume is probably useful in predicting baseline clinical stroke severity and final

Source: Adapted from Am Fam Physician. 2011;83(4):483-484.

lesion volume in patients with anterior circulation stroke syndromes. It may also be useful in predicting clinical outcomes as measured by the National Institutes of Health Stroke Scale and Barthel Index. However, it may not be useful in predicting baseline National Institutes of Health Stroke Scale score in patients with posterior circulation stroke syndromes. Baseline perfusionweighted imaging volume may be useful in predicting baseline clinical stroke severity.

Clinical Context Noncontrast CT can be used to assess for infarct and to exclude hemorrhage and other structural lesions that can mimic stroke in patients with acute neurologic impairment. Diffusion-weighted imaging is superior to CT in the diagnosis of acute ischemic stroke within 12 hours of symptom onset relative to clinical and imaging outcomes. In clinical practice, however, cost, availability, and medical management requirements must be considered when making decisions about which imaging modality to use.

The sensitivity of diffusion-weighted imaging is estimated to be 80 to 90 percent in the emergency evaluation of patients with possible stroke. Case series and small comparative studies have reported that diffusion-weighted imaging had almost 100 percent sensitivity for diagnosing stroke in the hyperacute stage; however, cases of diffusion-weighted imagingâ&#x20AC;&#x201C;negative stroke were increasingly reported. False-negative diffusion-weighted imaging may be attributable to mild strokes, brainstem location, and earlier time from onset. False-negative results may become less common as imaging improves.

Positive diffusion-weighted imaging in patients with transient ischemic attacks is common. Acute ischemic lesions on diffusion-weighted imaging are found in approximately 40 percent of patients with transient ischemic attack; this finding correlates with symptom duration. A recent study determined that diagnoses based on diffusion-weighted imaging could result in increased annual incidence of stroke and reduced annual incidence of transient ischemic attack.

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expert’s opinion

What are the Do’s and Don’ts of Taking Blood Pressure?

HK Chopra, KK Aggarwal

C

orrect measurement of the blood pressure (BP) is essential in the diagnosis and management of hypertension.

mercury manometer should be visible but does not have to be at the level of the heart.4 

For diagnosis, take multiple readings at various times throughout the waking hours of the patient.



Avoid extraneous variables that can influence the BP in the 60 minutes prior to evaluation like food intake, strenuous exercise (can lower the BP), smoking and the ingestion of caffeine.1



Do’s 



















Smoking transiently raises the BP. The office BP may be underestimated in a heavy smoker, who has not smoked for more than 30 minutes before the measurement is made. Check BP both before and after the smoking.

Take BP in a normal room temperature. Taking BP in cool room (12°C or 54°F) or while the patient is talking can raise the measured value by 8-15 mmHg. As of now, mercury BP instruments provide the most accurate measurement of BP. Aneroid apparatus should be checked against a mercury device since the air gauge may be in error.2 Use proper-sized cuff.3 A too small cuff can lead to overestimation of the systolic pressure by 10-50 mmHg in obese patients.











Use proper length of BP cuff bladder. The length should be 80%, and the width at least 40% of the circumference of the upper arm.3,4



Take the BP in the sitting position with the back supported.5



heart.2

Support the arm at the level of the If the arm is allowed to hang down when the patient is sitting or standing the measured BP will be elevated by 10-12 mmHg due to the added hydrostatic pressure-induced by gravity.6 The opposite is true if the arm is above the level of the heart. The





Source: Essential Questions in Hypertension Volume 2, 2011.

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Make the patient sit quietly for five minutes before the BP is measured.2 Twenty to 30% of patients with hypertension in the physician’s office are normotensive outside of the office.7 White coat or isolated office hypertension, should be suspected in a person with hypertension in the absence of end-organ damage or with normal ambulatory BP taken at work or at home.1,2 Place the BP cuff with the bladder midline over the brachial artery pulsation, with the arm without restrictive clothing (the patient’s sleeve should not be rolled up as this may act as a tourniquet).3 The lower end of the BP cuff should be 2-3 cm above the antecubital fossa to minimize noise related to the stethoscope touching the cuff.

Inflate the cuff to 30 mmHg higher than systolic, as estimated from the disappearance of the pulse in the brachial artery by palpation.2 Measure the initial systolic pressure by palpation to avoid potential problems with an auscultatory gap.6 During measurement neither the patient nor the observer should talk.3 Stethoscope should be placed lightly over the brachial artery. Use of excessive pressure can increase turbulence and delay the disappearance of sound and the diastolic pressure reading may be reduced by upto 10-15 mmHg.6 Deflate the cuff slowly at a rate of 2-3 mmHg per heartbeat.8 The diastolic pressure is equal to phase V. The point of muffling should be used in those patients in whom there is more than a 10 mmHg difference between phases IV and V.4,9 This can occur in children, and in high-output states such as thyrotoxicosis, anemia and aortic regurgitation.

The BP should be measured initially in both arms.10 If there is a disparity due to a unilateral arterial lesion, the arm with higher pressure should be used.

expert’s opinion 











The mean interarm diastolic and systolic BP differences can be 3 and 5 mmHg, respectively.

Take BP at least twice on each visit, with the measurements separated by 1-2 minutes. If the second value is more than 5 mmHg different from the first, continued measurements should be made until a stable value is attained. The recorded value on the patient’s chart should be the average of the last two measurements.9



Measure the leg BP also at the first sitting. The systolic pressure in the leg in normal subjects is usually 10-20% higher than that in the brachial artery.



Measure BP at the wrist in obese people, since wrist diameter is not significantly affected.















Wrist cuffs are smaller and easier to handle.1 Systolic BP rises and diastolic BP falls in more distal arteries. Keep the wrist at the level of the heart.

Measure the BP at roughly the same time each day and the relation to meals and medications should be noted.

Don’ts 

no sounds will be heard until 140 mmHg; as a result, the latter value will be mistakenly considered to be the systolic pressure. The auscultatory gap is seen in increased arterial stiffness and carotid atherosclerosis.7

Do not measure the BP after antihypertensive drugs are taken. If the BP is taken soon after drug ingestion, the BP may be normal or even below normal and then will gradually increase to potentially hypertensive levels until the next dose is taken (Trough or nadir effect).

Do not check BP immediately after taking coffee as it can raise the BP acutely in nonhabitual coffee drinkers.

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Do not forget to measure the BP in the legs in suspected coarctation of the aorta.

Do not take arm BP in women with breast cancer who have undergone bilateral axillary lymph node dissection.

If there has been unilateral axillary node dissection, BP should always be taken in the contralateral arm.

Tourniquet effect may damage the lymphatics and exacerbate the arm edema.

Do not miss cuff inflation hypertension. The muscular activity used to inflate the cuff can acutely raise the BP by as much as 12/9 mmHg, an effect called cuff inflation hypertension that dissipates within 5-20 seconds (average 7 seconds in one study).16,17 Inflate the cuff to at least 30 mmHg above systolic and then allow the sphygmomanometer to fall no more than 2-3 mmHg/heartbeat.16 In the absence of end-organ damage, the diagnosis of mild hypertension should not be made until the BP has been measured on at least two additional visits, spaced over a period of one week or more.18,19 BP drops by an average of 10-15 mmHg between the first and third visits in newly diagnosed patients.19,20 It stabilizes by six visits in most cases.19

References

Do not rely on automated oscillometric BP devices.

The readings are typically lower and the method11 has some greater inherent error.

1.

Do not miss pseudohypertension, which is characterized by systolic and diastolic pressures estimated from the sphygmomanometer that are ≥10 mmHg above the directly measured intraarterial or oscillometric pressure.12,13

Beevers G, Lip GY, O’Brien E. ABC of hypertension: blood pressure measurement. Part II-conventional sphygmomanometry: technique of auscultatory blood pressure measurement. BMJ 2001;322:1043-7.

2.

O’Brien E, Asmar R, Beilin L, Imai Y, Mancia G, Mengden T, et al. Practice guidelines of the European Society of Hypertension for clinic, ambulatory and self blood pressure measurement. J Hypertens 2005;23(4): 697-701.

Do not forget to measure supine and standing measurements in the elderly to detect postural hypotension.14

3.

Beevers G, Lip GY, O’Brien E. ABC of hypertension. Blood pressure measurement. Part I-sphygmomanometry: factors common to all techniques. BMJ 2001;322:981-8.

4.

Pickering TG, Hall JE, Appel LJ, Falkner BE, Graves J, Hill MN, et al. Recommendations for blood pressure measurement in humans and experimental animals: part 1: blood pressure measurement in humans: a statement for professionals from the Subcommittee of Professional and Public Education of the American Heart Association Council on High Blood Pressure Research.

Circulation 2005;111(5):697-716.

Do not miss the silent gap. In some patients, the Korotkoff sounds transiently disappear as the cuff is deflated. As an example, the Korotkoff sounds in a patient with a systolic pressure of 190 mmHg may be first heard at 190 mmHg, disappear at 155 mmHg and then be re-heard at 140 mmHg. If the cuff is only inflated to a pressure of 160 mmHg,

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expert’s opinion 5.

Jamieson MJ, Webster J, Philips S, Jeffers TA, Scott AK, Robbo J, et al. The measurement of blood pressure: sitting or supine, once or twice? J Hypertens 1990;8(7):635-40.

6.

O’Brien E. Ambulatory blood pressure measurement is indispensible to good clinical practice. J Hypertens Suppl 2003;21(2):S11-8.

7.

Pickering TG, James GD, Boddie C, Harshfield GA, Blank S, Laragh JH. How common is white coat hypertension? JAMA 1988;259(2):225-8.

8.

Tholl U, Forstner K, Anlauf M. Measuring blood pressure: pitfalls and recommendations. Nephrol Dial Transplant 2004;19(7):766.

9.

Bailey RH, Bauer JH. A review of common errors in the indirect measurement of blood pressure.

Sphygmomanometry. Arch Intern Med 1993;153(24): 2741-8.

10. Gosse P. Blood pressure should be measured in both arms on the first consultation. J Hypertens 2002;20(6):1045-6.

11. Landgraf J, Wishner SH, Kloner RA. Comparison of automated oscillometric versus auscultatory blood pressure measurement. Am J Cardiol 2010;106(3):386-8.

12. Zweifler AJ, Shahab ST. Pseudohypertension: a new assessment. J Hypertens 1993;11(1):1-6.

13. Hla KM, Feussner JR. Screening for pseudohypertension.

A quantitative, noninvasive approach. Arch Intern Med 1988;148(3):673-6.

14. Mancia G, De Backer G, Dominiczak A, Cifkova R, Fagard R, Germano G, et al. Management of Arterial Hypertension of the European Society of Hypertension;

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European Society of Cardiology. 2007 Guidelines for the Management of Arterial Hypertension: The Task Force for the Management of Arterial Hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). J Hypertens 2007;25(6):1105-87.

15. Cavallini MC, Roman MJ, Blank SG, Pini R, Pickering TG, Devereux RB. Association of the auscultatory gap with vascular disease in hypertensive patients. Ann Intern Med 1996;124(10):877-83.

16. Veerman DP, van Montfrans GA, Wieling W. Effects of cuff inflation on self-recorded blood pressure. Lancet 1990;335:451-3.

17. Mejia AD, Egan BM, Schork NJ, Zweifler AJ. Artefacts in measurement of blood pressure and lack oftarget organ involvement in the assessment of patients with treatmentresistant hypertension. Ann Intern Med 1990;112(4): 270-7.

18. U.S. Preventive Services Task Force. Screening for high blood pressure: U.S. Preventive Services Task Force reaffirmation recommendation statement. Ann Intern Med 2007;147(11):783-6.

19. Hartley RM, Velez R, Morris RW, D’Souza MF, Heller RF. Confirming the diagnosis of mild hypertension. Br Med J (Clin Res Ed) 1983;286:287-9.

20. Watson RD, Lumb R, Young MA, Stallard TJ, Davies P, Litter WA. Variation in cuff blood pressure in untreated outpatients with mild hypertension - implications for initiating antihypertensive treatment. J Hypertens 1987;5(2):207-11.

around the globe

News and Views

Obese People Have Lower Levels Of Antinuclear Antibodies A study to be published in Arthritis and Rheumatism finding antinuclear antibodies in roughly 14% of the study subjects. Such antibodies are common and frequently used as a marker for autoimmune diseases and researchers found that the autoantibodies were less common in overweight and obese individuals than in people of normal weight.

FDA Adds New Safety Warnings To Statins The warnings will include the side effects of memory loss, confusion, a rise in blood sugar, which can lead to diabetes, and drug interaction causing muscle damage.

New Troponin Threshold For Periprocedural MI The currently recommended troponin cut-off to define periprocedural myocardial infarction (MI) identifies almost a quarter of patients as having had such an MI. Dr Victor Novack (Harvard) used recommended definitions of periprocedural MI - namely, measure of the biomarkers troponin and creatinine kinase-MB (CK-MB) of more than three times the 99th percentile of the upper reference limit-and found that just 7% of patients would have had a procedural MI using the CK-MB criteria, compared with 24.3% using troponin.

Their report is published online February 27, 2012 in the Archives of Internal Medicine.

Trimetazidine for Heart Failure An old antianginal drug, the fatty-acid-oxidation inhibitor trimetazidine (flavedon), may have potential as a heart-failure treatment, according to a metaanalysis that concluded that the drug improved left ventricular ejection fraction (LVEF), functional capacity, and ventricular dimensions in 884 HF patients across 16 randomized trials.

The current analysis is published in the March 6, 2012 issue of the Journal of the American College of Cardiology.

It improve LVEF by 6.46 points, total exercise time by

64 seconds, NYHA functional class by 0.57%, LV endsystolic diameter by 6.67 mm, LV end-diastolic diameter by 6.05 mm and B-type natriuretic-peptide levels by 203.40 pg/ml.

Large Quantities of Selenium Supplements May Raise Risk for Type 2 Diabetes Supplements of selenium, a trace mineral that may help prevent some cancers, might increase the risk of type 2 diabetes if taken in large quantities, according to a review of existing studies published online Feb. 29 in The Lancet.

Professor Margaret Rayman, of the UK’s University of Surrey, said that to help prevent raising the chance of developing diabetes, people with selenium levels ≥122 µg/l in their blood shouldn’t take selenium supplements. Higher-than-normal levels of selenium may contribute to the development of…hair loss and certain cancers.

The average daily intake recommendations for selenium are 60 mg/day for men and 53 mg/day for women. The US Institute of Medicine has set a tolerable upper limit for selenium at 400 mg/day. Too much selenium can cause a condition called selenosis, which includes symptoms, such as gastrointestinal upset, hair loss, white blotchy nails, garlic breath odor, fatigue, irritability and mild nerve damage.

AKI Biomarkers Following Cardiac Surgery Several biomarkers predicted the severity of acute kidney injury (AKI) after cardiac surgery more quickly than did serum creatinine, according to a study published online March 1 in the Journal of the American Society of Nephrology. Elevated levels of urinary and plasma neutrophil gelatinase-associated lipocalin (NGAL) - a biomarker of structural renal tubular injury - conferred more than a seven-fold likelihood of severe injury after heart surgery.

Patients with high levels of interleukin-18 or an elevated urinary albumin-to-creatinine ratio were 3 times more likely to have severe injury than patients who had low levels of the biomarkers.

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lighter reading

This story is about a beautiful, expensively dressed lady who complained to her psychiatrist that she felt that her whole life was empty; it had no meaning.

So the counselor called over the old lady who cleaned the office floors, and then said to the rich lady, “I’m going to ask Mary here to tell you how she found happiness. All I want you to do is listen.”

So the old lady put down her broom and sat on a chair and told her story: “Well, my husband died of malaria and three months later my only son was killed by a car. I had nobody… I had nothing left. I couldn’t sleep; I couldn’t eat; I never smiled at anyone, I even thought of taking my own life. Then one evening a little kitten followed me home from work. Somehow I felt sorry for that kitten. It was cold outside, so I decided to let the kitten in. I got it some milk, and it licked the plate clean.

Then it purred and rubbed against my leg, and for the first time in months, I smiled. Then I stopped to think; if helping a little kitten could make me smile, maybe doing something for people could make me happy. So the next day I baked some biscuits and took them to a neighbor who was sick in bed. Every day I tried to do something nice for someone. It made me so happy to see them happy. Today, I don’t know of anybody who sleeps and eats better than I do. I’ve found happiness, by giving it to others.”

When she heard that, the rich lady cried. She had everything that money could buy, but she had lost the things which money cannot buy. Source: http://www. heartnsouls.com/str_compassion.shtml) –Ms Ritu Sinha

Quote

Happiness comes from giving

Laugh a While

An Inspirational Story

Lighter Side of Medicine “Your chances of success in any undertaking can always be measured by your belief in yourself.” −Robert Collier

Science Lesson Miss Jones had been giving her second-grade students a lesson on science. She had explained about magnets and showed how they would pick up nails and other bits of iron. Now it was question time, and she asked, “My name begins with the letter ‘M’ and I pick up things. What am I?”

A little boy on the front row proudly said, “You’re a mother!”

Funny Insults Height of humiliation plus insult……

A grammar freak girlfriend to her boyfriend U R as useless as an ‘ay’ in ‘okay’…

−Dr GM Singh

Dr. Good and Dr. Bad Situation: A hypertensive patient on b-blockers when evaluated for his leg pains, was found to have an ankle brachial index of 0.4.

Give him pentoxifylline

stop b-blockers and start other anti-BP drugs

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To help monitor your diabetes over time, especially if it is not possible to monitor using the A1C test To help determine the effectiveness of changes to your diabetic treatment plan. −Dr Arpan Gandhi and Dr Navin Dang

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©IJCP Academy

Lab update

Fructosamine

Lesson: Ankle brachial index of <0.5 indicates severe peripheral

vascular disease. b-blockers due to their a-receptor action can worsen the peripheral vascular disease.

Dr KK Aggarwal

Asian

Journal of

CLINICAL CARDIOLOGY

Information for Authors

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

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

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

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

Covering letter -

- -

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

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

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

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

-

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

-

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

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

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

A subtitle can be added if necessary.

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

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

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

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

- It should not contain abbreviations, footnotes or references.

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

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

- Ethical guidelines followed by the investigations should be described.

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

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

- Method of allocating the subjects into different groups.

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

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

-

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

-

Confidence intervals for the measurements should be provided wherever appropriate.

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

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Discussion -

This should consist of a review of the literature and relate the major findings of the article to other publications on the subject. The particular relevance of the results to healthcare in India should be stressed, e.g. practicality and cost.

References These should conform to the Vancouver style. References should be numbered in the order in which they appear in the texts and these numbers should be inserted above the lines on each occasion the author is cited (Sinha12 confirmed other reports13,14...). References cited only in tables or in legends to figures should be numbered in the text of the particular table or illustration. Include among the references papers accepted but not yet published; designate the journal and add ‘in press’ (in parentheses). Information from manuscripts submitted but not yet accepted should be cited in the text as ‘unpublished observations’ (in parentheses).

At the end of the article the full list of references should include the names of all authors if there are fewer than seven or if there are more, the first six followed by et al., the full title of the journal article or book chapters; the title of journals abbreviated according to the style of the Index Medicus and the first and final page numbers of the article or chapter. The authors should check that the references are accurate. If they are not this may result in the rejection of an otherwise adequate contribution.

Examples of common forms of references are: Articles

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

- All photomicrographs should indicate the magnification of the print.

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

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

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

-

Do not use clips/staples on photographs and artwork.

-

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

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

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

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

2. Total number of pages ________________________

Books

6. Suggestions for reviewers (name and postal address)

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

Indian 1.____________Foreign 1._ _______________

2.____________

2._ _______________

Articles in Books

3.____________

3._ _______________

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

4.____________

4._ _______________

Tables -

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

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

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

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

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

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

Dr KK Aggarwal

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