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In This Issue — A Clinical Study of 50 Cases of Cardiac Disease in Pregnancy — Gender-related Difference in Socioeconomic and Behavioral Factor in Relation to BP and Bmi of Type 2 Diabetic Workers from Match Factories and Fireworks in Sivakasi, Tamil Nadu — Dystrophin Deletion Mutation Pattern and Cardiac Involvement in 46 Cases of Dystrophinopathies — Aneurysm of Mitral Valve Complicated by Ventricular Tachycardia — Large, Dark Lesion on the Arm Present Since Birth — Updated Dietary Guidelines from the USDA and HHS

Volume 15, Number 6, October 2012 Pages 193-232

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CLINICAL CARDIOLOGY

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

Volume 15, Number 6, October 2012

Dr Deepak Chopra Chief Editorial Advisor Dr KK Aggarwal CMD, Publisher, Group Editor-in-Chief Dr Veena Aggarwal MD, Group Executive Editor Dr Praveen Chandra Guest Editor, AJCC praveen.chandra@medanta.org

from the desk of group editor-in-chief 197 Endocrine Society Issues Guidelines for Hypertriglyceridemia

KK Aggarwal

Assistant Editor: Dr Nagendra Chouhan, Dr Dharmendar Jain

AJCC Speciality Panel

Clinical Study

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

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IJCP Editorial Board

Obstetrics and Gynaecology Dr Alka Kriplani, Dr Thankam Verma, Dr Kamala Selvaraj Cardiology Dr Praveen Chandra, Dr SK Parashar Paediatrics Dr Swati Y Bhave, 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 ENT Dr Jasveer Singh Dentistry Dr KMK Masthan, Dr Rajesh Chandna Gastroenterology Dr Ajay Kumar Dermatology Dr Hasmukh J Shroff Nephrology Dr Georgi Abraham Neurology Dr V Nagarajan Journal of Applied Medicine & Surgery Dr SM Rajendran

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

198 A Clinical Study of 50 Cases of Cardiac Disease in Pregnancy

Jyoti Sidhmalswamy Ghongdemath, Shakuntala B Banale, Niranjan Nisty, L Krishna

203 Gender-related Difference in Socioeconomic and Behavioral Factor in Relation to BP and Bmi of Type 2 Diabetic Workers from Match Factories and Fireworks in Sivakasi, Tamil Nadu

V Priya, Mazher Sultana, Babuji, Kamaraj

Case Report 211 Dystrophin Deletion Mutation Pattern and Cardiac Involvement in 46 Cases of Dystrophinopathies

Suvarna Badhe, Pooja Kulkarni, Guneet Chopra Nandini Gokulchandran, Alok Sharma

215 Aneurysm of Mitral Valve Complicated by Ventricular Tachycardia

Monika Maheshwari, Nirmal Vyas, RK Gokroo

Around the globe 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

218 News and Views

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220 Large, Dark Lesion on the Arm Present Since Birth

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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 222 Updated Dietary Guidelines from the USDA and HHS

Medi Law 224 Should Doctors Prescribe Generic Medicines?

MC Gupta

lighter reading 226 Lighter Side of Medicine

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Endocrine Society Issues Guidelines for Hypertriglyceridemia 

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The Endocrine Society Guideline for the evaluation of patients with hypertriglyceridemia recommends that the diagnosis be based on fasting triglyceride levels.

Adults should be screened for hypertriglyceridemia, at least every five years as part of a lipid panel.

To facilitate assessment of cardiovascular risk, mild and moderate hypertriglyceridemia, defined as triglyceride levels of 150-999 mg/dl, should be diagnosed, as this condition may be a risk factor for cardiovascular disease.

Patients with severe and very severe hypertriglyceridemia, defined as triglyceride levels of >1,000 mg/dl, should be considered to be at risk for pancreatitis.

Patients with hypertriglyceridemia should undergo evaluation for secondary causes of hyperlipidemia, such as endocrine conditions and medications, and treatment should be focused on such secondary causes.

Patients with primary hypertriglyceridemia should be assessed for a family history of dyslipidemia and cardiovascular disease, as well as for other cardiovascular risk factors including central obesity, hypertension, abnormalities of glucose metabolism, and liver dysfunction.

For patients with moderate hypertriglyceridemia, the treatment goal should be a non-high-density lipoprotein cholesterol level in agreement with NCEP-ATP guidelines.

For patients with mild-to-moderate hypertriglyceridemia, first-line therapy should be lifestyle interventions including physical activity. A combination of diet modification and pharmacotherapy may also be considered.

For patients with moderate-to-severe hypertriglyceridemia, treatment with fibrates, niacin, and/or omega-3 fatty acids alone or in combination with statins should be considered.

A fibrate should be used as a first-line agent in patients with severe or very severe hypertriglyceridemia, in addition to reduction of dietary fat and simple carbohydrate intake.

Statins should not be used as monotherapy for severe or very severe hypertriglyceridemia, but they may be useful for the treatment of moderate hypertriglyceridemia when indicated to modify cardiovascular risk.

The guideline is published in the September 2012 issue of Journal of Clinical Endocrinology and Metabolism.

Asian Journal of Clinical Cardiology, Vol. 15, No. 6, October 2012

197

Clinical Study

A Clinical Study of 50 Cases of Cardiac Disease in Pregnancy Jyoti Sidhmalswamy Ghongdemath*, Shakuntala B Banale**, Niranjan Nisty†, L Krishna‡

Abstract Objective: To evaluate the pattern of cardiac disease in pregnancy and its impact on the maternal and fetal outcome.

Methods: A retrospective study was carried out in the Dept. of Obstetrics and Gynecology, Basaveshwar Hospital, a teaching and referral hospital, Gulbarga, Karnataka, over a period of two and a half years (January 2006 to June 2008) involving 50 pregnant women with cardiac disease. Results: The pattern of cardiac disease was as follows: 41 (82%) cases of rheumatic heart disease, five (10%) cases of cardiomyopathies and four (8%) cases congential heart diseases. Mitral stenosis (15, 36.5%) was the predominant cardiac lesion. The New York Heart Association (NYHA) Class was I/II in 40 (80%) pregnancies. Twentyeight cases were unbooked and all were illiterate. Five patients (10%) developed congestive cardiac failure. Incidence of preterm, stillbirth and maternal death in NYHA I/II was 5%, 0% and 0%, respectively, compared to 50%, 20% and 20% in NYHA Class III/IV. Conclusions: Rheumatic heart disease was the predominant type of cardiac disorder. Patients in NYHA Class I/II had a better maternal and fetal outcome than those in NYHA Class III/IV. Education, early detection and dedicated multidisciplinary approach are important in reducing the maternal and fetal morbidity and mortality.

Keywords: Pregnancy with cardiac disease, heart disease in pregnancy, cardiac disease

H

eart disease in pregnancy is not rare. The reported incidence varies from 0.4 to 4% in western population. The prevalence of rheumatic heart disease (RHD) has declined in the west, but continues to be an important cause of cardiovascular morbidity and mortality in India; constitutes 40-88% of all cardiac diseases in pregnancy.1 RHD occurs in 80% and congenital heart disease in 20%. During pregnancy, there is increase in the blood volume and pulse rate. These two factors combine to increase cardiac output by 50%, which is at its peak at 28-32 weeks. During labor, cardiac output increases intermittently because of squeezing

*Assistant Professor Dept. of Obstetrics and Gynecology PES Institute of Medical Sciences and Research Kuppam, Chittoor, Andhra Pradesh **Ex-Head, Dept. of Obstetrics and Gynecology †Professor, Dept. of Medicine MR Medical College, Gulbarga, Karnataka ‡Professor, Dept. of Obstetrics and Gynecology PES Institute of Medical Sciences and Research Kuppam, Chittoor, Andhra Pradesh Address for correspondence Dr Jyoti Sidhmalswamy Ghongdemath Dept. of Obstetrics and Gynecology PES Institute of Medical Sciences and Research Kuppam, 517 425, Chittoor, Andhra Pradesh E-mail: jyov@sify.com

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Asian Journal of Clinical Cardiology, Vol. 15, No. 6, October 2012

of blood from uterine sinuses, pain, anxiety as well as increased muscular effort.

The course of pregnancy as well as maternal and fetal morbidity and mortality are dependent on both the underlying defect and the functional maternal state.2 Delayed diagnosis and late presentation of pregnant women with heart disease may lead to fatal consequences, as the hemodynamic changes of pregnancy and peripartum period can result in rapid decompensation. The objective of the study is to evaluate the pattern of cardiac disease in pregnancy and its impact on the maternal and fetal outcome.

Material And Methods This was a retrospective study based on the review of medical records of all the pregnant women with cardiac disease at Basaveshwar Hospital, a teaching and referral hospital, attached to MR Medical College, Gulbarga, Karnataka, in the period between January 2006 and June 2008.

The following information was sought: Complete history, physical examination findings, the final diagnosis, time of diagnosis and presentation, literacy, hemogram and the final outcome. All the patients were reviewed by cardiologists on admission and echocardiography was done in all.

Clinical Study An assessment of functional grade of the heart disease was made according to the criteria of the New York Heart Association (NYHA, 1964). The patients were seen at antenatal clinic once in four weeks, upto 28 weeks; weekly thereafter, for Class I/II patients and hospitalization was advised for Class III/IV patients. Those with anemia, infections and noncompliance were also advised admission. Women on oral anticoagulants were admitted in early pregnancy (6-­12 weeks) and again in the third trimester (≼36 weeks) for switch over to heparin. Heparin was discontinued at the onset of labor. Prophylactic antibiotics were given routinely for all the patients.

The vaginal route was preferred for delivery. They were nursed in propped up position. The second stage of labor was shortened, if necessary, by the use of outlet forceps. Women who had been on anticoagulants were restarted on heparin within four hours of vaginal delivery and eight hours of cesarean.

Oral anticoagulants were resumed when prothrombin time reached 1.5-2 times the normal. Patients were discharged 5-7 days postpartum. Maternal outcome was analyzed considering these points: Congestive cardiac failure, endocarditis, mode of delivery and postpartum complications. Neonatal outcome was analyzed based on the following points: Birth weight, prematurity and birth defects.

Results Age of the patients ranged from 16 to 35 years (mean 25.5 years). The main diagnosis in these pregnancies

Table 1. Type of Cardiac Diseases Type of disease

No. of patients

Percentage (%)

Rheumatic heart disease

41

82

Congenital heart disease

05

10

Cardiomyopathy

04

08

Table 2. Type of Lesions Lesion

No. of patients

are given in Table 1 and 2. RHD was the most common cardiac disease and mitral stenosis (MS) (15, 36.5%) was the predominant cardiac lesion.

Forty patients (80%) belonged to NYHA Class I and II; 20% to class III and IV (Table 3). There was history of cardiac intervention being performed prior to pregnancy in other cardiac centers in six (12%) patients with RHD (3 mitral valve replacements, 3 mitral valvotomies). Twenty-one patients were primigavidae and 39 were multigravidae. Twentyeight patients were illiterate and all were unbooked.

Twenty-six patients were known cases of cardiac disease, before the onset of index pregnancy; of these, 10 patients were unbooked. In 22 (44%) women, the diagnosis of cardiac disease was made during index pregnancy. Ten multigravida patients who presented in the first trimester, underwent medical termination of pregnancy (MTP) and tubal ligation. Thirtyseven patients continued the pregnancy beyond

Table 3. NYHA Class and Complications Class I I

II

III

IV

17

23

3

7

Anemia

5

10

3

6

PIH

0

3

0

2

CCF

0

2

0

3

Abortion

0

0

1

2

Mortality

0

0

0

2

Term

1

5

0

2

Preterm

0

2

2

3

Stillbirth

0

0

0

2

No. of patients Maternal

Fetal Low birth weight

Table 4. Type of Deliveries Vaginal deliveries at hospital

Mitral stenosis

15

Mitral stenosis with regurgitation

10

Mitral regurgitation

05

Double valve lesion

11

Atrial septal defect

01

Pulmonary stenosis

01

Pulmonary stenosis with aortic stenosis

01

MTP

10

01

Spontaneous

01

PDA with aortic regurgitation

Spontaneous

13

Assisted

10

Vaginal deliveries at home

02

Cesarean section

14

Abortions

Asian Journal of Clinical Cardiology, Vol. 15, No. 6, October 2012

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Clinical Study Table 5. Congestive Cardiac Failure Gravida Primigravida Primigravida

Diagnosis

Booking status

Time of presentation

NYHA Class

Outcome

Cardiomyopathy

Unbooked

Labor

IV

Mortality

RHD MS

Unbooked

36th week

IV

Uneventful

Para 2

Cardiomyopathy

Unbooked

Postpartum

II

Uneventful

Primigravida

Cardiomyopathy

Unbooked

Labor

IV

Mortality

Para 2

Cardiomyopathy

Unbooked

Postpartum

II

Uneventful

28 weeks. Seven patients presented in second trimester, 16 patients at third trimester, 15 in 1st stage of labor and two in postpartum period after home delivery.

Ten patients underwent instrumental vaginal (outlet forceps) delivery, 13 had spontaneous vaginal delivery at hospital and two had presented in 2nd week of postpartum after home delivery (Table 4).

There were 14 patients who required emergency cesarean section. The indications were fetal distress (6), cephalopelvic disproportion (6) and deep transverse arrest (2).

Maternal complications included anemia in 23 (46%), congestive cardiac failure (CCF) in five (10%) and pregnancy induced hypertension in five (10%) (Table 3). Among the five patients with CCF, two presented in the postpartum period, both in the 2nd week, after uneventful home delivery; two during labor and 1 in the 36th week (Table 5). One of them had RHD and rest of the four patients had peripartum cardiomyopathy. Three patients recovered with salt restriction, diuretics, digitalis and bed rest. The rest two patients with cardiomyopathy died inspite of intensive cardiac care; one after the delivery of a dead fetus and another during labor. None of the patients developed atrial fibrillation, thromboembolism or bacterial endocarditis. Nine patients presented with preterm labor and seven of them delivered at 34-36 weeks of gestation. Weight of the newborns ranged from 1.75 to 3.5 kg; 15 newborns weighed <2.5 kg, two of them aspirated meconium and were shifted to neonatal intensive care unit (NICU). None of the newborns of the three women who had received anticoagulants had any congenital malformations.

Pregnancies with NYHA III and IV were associated with higher incidence of maternal and neonatal morbidity and mortality. Incidence of preterm, stillbirth and maternal death in NYHA I and II was 5%, 0% and 0%, respectively, compared to 50%, 20% and 20% pregnancies, who were in NYHA Class III and IV.

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Asian Journal of Clinical Cardiology, Vol. 15, No. 6, October 2012

Discussion Depending on the obstetric population and profile of referral, 1-3%3 of women have a form of cardiac disease preceding or diagnosed during pregnancy.

RHD is the commonest heart disease associated with pregnancy4 and the most common lesion is MS,5,6 which leads to significant maternal and fetal morbidity and mortality. The reported incidence of RHD in pregnancy in India varies from 38 to 89%.

In our study, 82% had RHD, of whom 38.5% of patients had MS, which are comparable to that of Bhatla et al.1 The incidence of RHD was 89.5% in a study by Abdel-Hady et al.7 These patients require either balloon mitral valvuloplasty or surgical mitral commissurotomy. Both procedures are available at limited centers in India; the high cost of prosthetic valves and inadequate facilities for operative management of these patients, are hindrances to valve replacement surgery. In our study, cardiac intervention was performed prior to pregnancy in other cardiac centers, only in six (12%) patients with RHD, as majority of them were from low socioeconomic status.

Fifteen to 52% of the cardiac lesions are diagnosed for the first time during pregnancy.8 Many young women have not had thorough physical examination prior to pregnancy and are unaware of the presence of any cardiac disease. The importance of antenatal care is stressed by reports that show increased mortality among patients with no or poor antenatal care. A previous successful obstetric outcome neither excludes a significant cardiac pathology nor guarantees a successful outcome in the index pregnancy; additionally, many women may not manifest symptoms until the second or third pregnancy. In developing countries like India, negligent behavior of the patient towards their health and poor referral services lead to late diagnosis and more complications. Desai et al reported that 42% of RHD patients were diagnosed for the first

Clinical Study time during pregnancy.9 In our study, the diagnosis of cardiac disease was made during pregnancy in 22 (44%) patients and majority became symptomatic in the third trimester. Of the 26 patients in whom the diagnosis was made before the onset of pregnancy, 10 patients did not attend the ANC Clinic and presented at the end of third trimester. Majority of them were from low socioeconomic status and were illiterate.

The functional NYHA classification corresponds roughly to the morbidity and mortality in several different series of patients.1,10 Fortunately, the vast majority of the pregnant patients are in functional classes I and II; most of these patients sustain pregnancy without difficulty. In our study, majority of the patients (80%) were from Class I/II and had uneventful recovery; 20% were from Class III/IV, which was comparable to the study by Sawhney et al.5 The most common cardiac causes of death include cardiomyopathy and pulmonary hypertension.11 Two maternal deaths occurred in Class IV group, both were due to peripartum cardiomyopathy.

Peripartum cardiomyopathy is characterized by the presence of CCF developing in previously healthy women in the last month of pregnancy or in the first five months postpartum, without any etiology.12 Diagnosis is by echocardiography, which shows impairment of left ventricular systolic function.12 It occurs in 1:2,400 to 1:15,000 pregnancies.13 Risk factors include age over 30 years, multiparity, obesity, pre-eclampsia and chronic hypertension. Maternal mortality upto 50% during the first three months of puerperium has been reported.13 A case report in the Indian literature has reported uneventful recovery.14 In our study, we had four cases of cardiomyopathy, of which two patients died. Interestingly, one primigravida with age <20 years developed cardiomyopathy without any risk factors. Of the other three patients, one had preeclampsia at the time of presentation and other two were multigravidae with age >30.

The increase in demand on the heart imposed by labor requires close and continuous monitoring of mother and fetus. Vaginal delivery usually carries the lowest risk of complications, however, prolonged or difficult labor should be avoided and therefore cesarean section rates are above average (30-36%).15 The indications for the cesarean delivery are the same for the women with cardiac disease and the general population. In our study, 39% patients underwent cesarean section, which is slightly higher. Higher incidence was also reported by Chalupczak et al.16

The incidence of preterm deliveries was 14% in our study comparable with a recent study by Gelson et al.17 It was 13% as reported by Avila et al18 and 12% by Sawhney et al.5 We had a higher incidence of preterm delivery in NYHA Class III/IV than in Class I/II as was also seen in another recent study

by Liu et al.19 Antibiotic prophylaxis against endocarditis was still given despite recent recommendations that this is not required with uncomplicated cesarean or vaginal delivery.20 The occurrence of transient asymptomatic bacteremia in upto 5% of woman and the high morbidity and mortality associated with infective endocarditis, was the justification for using antibiotic prophylaxis.

Conclusion RHD was the predominant type. Maternal and perinatal outcome in patients with cardiac disease depends on the functional cardiac status of the mother at the time of presentation. The risk of maternal morbidity and mortality is greater in those patients with functional Class III/IV and unbooked cases. Perinatal outcome is also poorer in this group. School-health check-up should be strictly implemented for early detection of cardiac diseases. Education, antenatal check-up and proper intervention with dedicated multidisciplinary approach are the important steps in reducing maternal and fetal morbidity and mortality.

REFERENCES 1.

Bhatla N, Lal S, Behera G, Kriplani A, Mittal S, Agarwal N, et al. Cardiac disease in pregnancy. Int J Gynaecol Obstet 2003;82(2):153-9.

2.

Cox PB, Gogarten W, Marcus MA. Maternal cardiac disease. Curr Opin Anaesthesiol 2005;18(3):257-62.

3.

Arafeh JM, Baird SM. Cardiac disease in pregnancy. Crit Care Nurs Q 2006;29(1):32-52.

4.

Lim ST. Rheumatic heart diseases in pregnancy. Ann Acad Med Singapore 2002;31(3):340-8.

5.

Sawhney H, Aggarwal N, Suri V, Vasishta K, Sharma Y, Grover A. Maternal and perinatal outcome in rheumatic heart disease. Int J Gynaecol Obstet 2003;80(1):9-14.

6.

Ramsey PS, Ramin KD, Ramin SM. Cardiac disease in pregnancy. Am J Perinatol 2001;18(5):245-66.

7.

Abdel-Hady ES, El-Shamy M, El-Rifai AA, Goda H, Abdel-Samad A, Moussa S. Maternal and perinatal outcome of pregnancies complicated by cardiac disease.

Int J Gynaecol Obstet 2005;90(1):21-5.

8.

Mendelson MA. Congenital cardiac disease pregnancy. Clin Perinatol 1997;24(2):467-82.

and

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Desai DK, Adanlawo M, Naidoo DP, Moodley J, Kleinschmidt I. Mitral stenosis in pregnancy: a four-year experience at King Edward VIII Hospital, Durban, South Africa. BJOG 2000;107(8):953-8.

10. Sermer M, Colman J, Siu S. Pregnancy complicated by heart disease: a review of Canadian experience. J Obstet Gynaecol 2003;23(5):540-4.

11. Thorne SA. Pregnancy 2004;90(4):450-6.

in

heart

disease.

Heart

12. Hibbard JU, Lindheimer M, Lang RM. A modified definition for peripartum cardiomyopathy and prognosis based on echocardiography. Obstet Gynecol 1999;94(2): 311-6.

13. Heider AL, Kuller JA, Strauss RA, Wells SR. Peripartum cardiomyopathy: a review of the literature. Obstet Gynecol Surv 1999;54(8):526-31.

14. Baxi SR, Beenakumari R, Maya H. Peripartum cardiomyopathy. J Obstet Gynecol India 1996;1:710-1.

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15. Gei AF, Hankins GD. Cardiac disease and pregnancy.

Obstet Gynecol Clin North Am 2001;28(3):465-512.

16. Chałupczak P, Kolasińska-Kloch W, Jach R, Basta A. Pregnancy in patients with heart disease. Clin Exp Obstet Gynecol 2004;31(4):271-3.

17. Gelson E, Curry R, Gatzoulis MA, Swan L, Lupton M, Steer P, et al. Effect of maternal heart disease on fetal growth. Obstet Gynecol 2011;117(4):886-91.

18. 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.

19. Liu H, Xu JW, Zhao XD, Ye TY, Lin JH, Lin QD. Pregnancy outcomes in women with heart disease. Chin Med J (Engl) 2010;123(17):2324-30..

20. Thilén U, Olsson SB. Pregnancy and heart disease: a review. Eur J Obstet Gynecol Reprod Biol 1997;75(1): 43-50.

Clinical study

Gender-related Difference in Socioeconomic and Behavioral Factor in Relation to BP and Bmi of Type 2 Diabetic Workers from Match Factories and Fireworks in Sivakasi, Tamil Nadu V Priya, Mazher Sultana, Babuji, Kamaraj

Abstract Objective: The prevalence of diabetes has been steadily increasing in workers of match factories and fire works in Sivakasi area. We investigated the differences between male and female diabetic patients on impact of socioeconomic, behavioral and other risk factors like blood pressure (BP) and body mass index (BMI). Methods: Total 112 persons (64 male and 48 female) with type 2 diabetes were selected for this study, from various hospitals situated in Sivakasi area. Socioeconomic status (SES) and other behavioral factors were ascertained by physical examination and interview. Result: There were significant difference between male and female diabetics only in certain factors. SES was found significant and inversely related to physical activity, marital status, food habit, duration and systolic BP (SBP) in female diabetics. In male, these association were weaker or absent, when education level was considered. But in income level significant differences found in SBP and detected age. Statistical significance was found between behavioral and other risk factors in both male and female diabetics. Conclusion: Physical inactivity leads to high BMI and increased SBP. Due to lack of knowledge, these diabetic patients did not avail any type of medical attention for treating diabetes till they got other complications due to untreated diabetes.

Keywords: Prevalence of diabetes, blood pressure, body mass index, socioeconomic status, physical inactivity, smoking, alcohol intake

D

iabetes prevalence is increasing in all population groups in India, but this increase seems to be greater in lower level people. The prevalence of type 2 diabetes has been reported more in fire works and match factory workers in Sivakasi area.

Socioeconomic status (SES), which plays an important role in healthcare and disease prevention, is a complex indicator of health services accessibility, knowledge of health promotion, willingness to seek treatment and lifestyle behavior (Mei Tang 2003).

Educational attainments and income adequacy are important indicators of SES. Low SES tends to be associated with a high prevalence of diabetes in developing countries (Evans et al 2000, Robbins et al 2001, Connolly et al 2000). Obesity, physical inactivity, smoking and alcohol intake are implicated in the

Presidency College, Chennai, Tamil Nadu Kani Lakshmi Clinic, Sivakasi, Tamil Nadu

development of type 2 diabetes and are also associated with low socioeconomic position (Emilie et al 2004).

Research suggests an association between low SES and high blood pressure (BP), although this association is not consistent. A study on smoking, alcohol consumption and body mass index (BMI) reveals that the lifestyle increases the risk of high BP. And it is more common among people with low SES. (Mathews et al 1997, Lynch et al 1997, Poston et al 1999, Dyer et al 1999).

Diagnostic and treatment services for high BP may be more accessible to people with high SES (Bunker et al 1995, Hoddard et al 1997).

The health impact of SES and behavioral factors may not be the same in male and female. Only a few studies have assessed sex difference in the relationship between SES and diabetes. The pathway by which SES may differently affect the development of type 2 diabetes in male and female are unclear. The impact of behavioral factors like BMI, physically inactive, smoking, alcohol consumption and family history of diabetes are closely

Asian Journal of Clinical Cardiology, Vol. 15, No. 6, October 2012

203

Clinical Study linked with insulin resistance. But, the variation of BP in SES and behavioral factors has rarely been studied.

So, the aim of the study was to assess the sex specific association of SES, behavioral factor and the difference in BP and BMI with diagnosed type 2 diabetic workers from match factories and fireworks in Sivakasi area.

Method Area: This study was carried out on workers working in match factories and fire works in Sivakasi area. Sivakasi is situated in Virudhunagar district, Tamil Nadu state, India. This place is very dry and is ideally suited for the manufacturing of fireworks, printed materials, paper and the match factories. About 3,500 match factories are situated in and around Sivakasi area. Around 30,000 persons are directly employed in these factories.

Participants: For this present study, 112 samples (64 male and 48 female) were collected from various hospitals situated in Sivakasi area. The participants were interviewed and completed questionnaires on SES and behavioral characters were collected.

Socioeconomic variables: Information on educational attainment was divided into primary (Class 5), secondary (Class 6-10) and higher (>10th class) education and income was divided in low (< ` 3,000), medium (` 3,000 - ` 5,000) and higher level (> ` 50,00).

Behavioral variables: Body weight was measured in light clothing in kilogram (kg) and height was measured in centimeters. BMI was calculated by weight in kg divided by square of height in meters. BP was measured in a sitting position for two times at the right arm after 15 minutes rest using sphygmomanometer by a well- trained nurse.

All subjects were interviewed and asked about their physical activity. It was divided into ‘active’ and ‘inactive’. Alcohol drinking habit was categorized as ‘alcoholic’ and ‘nonalcoholic’. Cigarette smoking was divided into ‘smokers’ and ‘nonsmokers’. Their family history about diabetes was analyzed and grouped into FH+ and FH–. Their age, diabetes detected age and duration were also asked during interview.

Laboratory measurement: Plasma glucose was measured using an enzymatic method by using ready made kits manufactured by Prison Diagnostic Pvt. Ltd. Mumbai.

Statistical Analysis Analysis was carried out separately for males and females using Systat 12 (2007) Statistical

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Table 1. Socioeconomic, Behavioral and Other Risk Factors Among Male and Female Factor

Male

Female

P value

Age (years) Mean SD

51.13 10.17

48.77 10.10

0.23

Diabetes detected age (years) Mean SD

47.48 9.62

44.88 9.91

0.17

Duration (years) Mean SD

3.67 2.37

3.92 2.67

0.62

SBP (mmHg) Mean SD

132.53 12.70

131.29 10.82

0.58

DBP (mmHg) Mean SD

80.03 8.09

79.23 6.84

0.57

Plasma glucose (mg/dl) Mean SD

170.02 39.78

172.83 42.61

0.72

BMI( kg/m²) Mean SD

26.59 1.99

25.38 2.60

0.0086

Marital status Married (%) Single/Widow (%)

89.06 10.94

81.25 18.75

0.24

Food habit NV (%) Veg (%)

81.25 18.75

70.83 29.17

0.196

Physically Inactive (%) Active (%)

31.25 68.75

43.75 56.25

0.174

Smoking habit Smoker (%) Nonsmoker (%)

43.75 56.25

0 100

0.000

Alcohol intake Alcoholic (%) Non alcoholic (%)

45.31 54.69

0 100

0.000

Family history of diabetes FH+ (%) FH- (%)

76.56 23.44

70.83 29.17

0.49

Education Primary (%) Secondary (%) Higher (%)

25.00 56.25 18.75

60.42 29.17 10.42

0.0008

Income Low (%) Medium (%) High (%)

28.13 37.50 34.37

54.17 25.00 20.83

0.02

FH+: Family history of diabetes present; FH–: Family history of diabetes absent; NV: Nonvegetarian; SBP: Systolic blood pressure; DBP: Diastolic blood pressure.

Clinical Study Software. Descriptive analyses were obtained for all variables and differences between males and females were assessed using t test, χ² tests and ANOVA. Sex differences in SES indicators were evaluated using linear or logistic regression models including

original SES variables. Means (standard deviation [SD]) for normal distribution and means for log normal distributed continuous variables or proportions for categorical variables were calculated among the SES groups.

Table 2(a). The Distribution of Risk Factor of Type 2 Diabetes by SES in Men Education

Factor

Income

p value

Primary

Secondary

Higher

P value

Low

Medium

High

Marital status Married (%) Single (%)

75.00 25.00

94.44 5.55

91.67 8.33

0.11

83.33 16.67

83.33 16.67

100 --

0.127

Food habit NV (%) Veg (%)

93.75 6.25

75.00 25.00

83.33 16.67

0.27

72.22 27.78

83.33 16.67

86.36 13.64

0.49

Physically Active (%) Inactive (%)

62.50 37.50

66.67 33.33

83.33 16.67

0.46

16.67 83.33

79.17 20.83

100 --

0.000

Smoking habit Smoker (%) Nonsmoker (%)

43.75 56.25

44.44 55.56

41.67 58.33

0.98

38.89 61.11

45.83 54.17

45.45 54.55

0.88

Alcohol intake Alcoholic (%) Nonalcoholic (%)

37.50 62.50

47.22 52.78

50.00 50.00

0.76

38.89 61.11

45.83 54.17

50.00 50.00

0.77

Family history of diabetes FH+ (%) FH- (%)

6.25 93.75

30.56 69.44

25.00 75.00

0.16

27.78 72.22

16.67 83.33

27.27 72.73

0.61

SBP (mmHg) Mean SD

137.00 13.06

130.39 13.19

133.00 9.67

NS

139.67 11.19

133.58 11.72

125.55 11.66

**

DBP (mmHg) Mean SD

81.75 9.18

78.94 7.61

81.00 8.16

NS

83.11 7.36

81.00 8.89

76.45 6.59

**

Plasma glucose (mg/dl) Mean SD

166.94 48.99

174.97 35.79

159.25 38.66

NS

167.61 33.39

173.33 42.59

168.36 42.88

NS

BMI kg/m² Mean SD

26.94 1.59

26.43 2.06

26.61 2.34

NS

27.70 2.24

26.73 1.73

25.23 1.52

NS

Detected age (years) Mean SD

48.94 9.46

46.44 9.67

48.67 10.11

NS

54.11 9.37

46.00 8.80

43.68 8.15

**

Duration (years) Mean SD

3.56 2.34

3.67 2.53

3.83 2.08

NS

4.39 2.64

3.63 2.64

3.14 1.69

NS

NS: No significance;**Significance p < 0.01

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Clinical Study Result Socioeconomical, behavioral and other risk factors among male and female participants are shown in Table 1. Systolic BP (SBP), diastolic BP (DBP) and BMI were higher and blood sugar was lower among males than females. Physical inactivity was more in females compared to males. Smoking and alcohol intake was found only in males. Nonvegetarians were more in males (81.25%) compared to females (70.81%). Family history of diabetes was seen more in males than females. Significant difference was

found in income (p = 0.02) and educational status (p = 0.0008) between male and female subjects. The age at which the diabetes detected was high in males (47 years) and low in females (44 years).

The distributions of various risk factors by SES are shown in Table 2a and 2b. In patients with secondary education level, more male (94.44%) members were found married than female (92.86%). In male diabetics with primary education level number of singles or widows was high. But, for female diabetics number of single or widows was high in higher education level.

Table 2(b). The Distribution of Risk Factor of Type 2 Diabetes by SES in Women Factor Marital status Married (%) Single (%) Food habit NV (%) Veg (%) Physically Active (%) Inactive (%) Smoking habit Smoker (%) Nonsmoker (%) Alcohol intake Alcoholic (%) Non alcoholic (%) Family history FH+ (%) FH- (%) SBP (mmHg) Mean SD DBP(mmHg) Mean SD Plasma glucose (mg/dl) Mean SD BMI kg/m² Mean SD Detected age (years) Mean SD Duration (years) Mean SD

Primary

Secondary

Higher

P value

Low

Medium

High

p value

82.76 17.24

92.86 7.14

40.00 60.00

0.03

76.92 23.08

83.33 16.67

90.00 10.00

0.65

68.97 31.03

78.57 21.43

60.00 40.00

0.69

84.62 15.38

58.33 41.67

50.00 50.00

0.067

37.93 62.07

78.57 21.43

100.00 --

0.004

30.46 61.54

75.00 25.00

80.00 20.00

0.025

0 100 0 100

0 100 0 100

0 100 0 100

0.0001

0 100 0 100

0 100 0 100

0 100 0 100

0.008

20.69 79.31

42.86 57.14

40.00 60.00

0.28

26.92 73.08

33.33 66.67

30.00 70.00

0.92

134.41 9.01

128.29 12.19

121.60 10.14

**

133.92 11.01

129.33 8.06

126.80 12.15

NS

80.45 7.16

78.29 6.27

74.80 5.02

**

80.27 7.41

76.33 6.14

80.00 5.58

NS

170.79 40.89

177.36 51.08

172.00 32.33

NS

178.00 38.22

161.08 49.62

173.50 46.38

NS

26.00 2.78

24.71 2.05

23.64 1.92

NS

25.68 2.99

25.39 2.26

24.58 1.84

NS

45.97 10.38

43.86 8.58

41.40 11.46

NS

46.31 11.61

42.92 9.13

43.5 7.15

NS

4.28 3.17

3.79 1.58

2.20 0.84

***

3.96 3.21

3.83 1.69

3.90 2.28

NS

NS: No significance; **Significance p < 0.01 ***p < 0.001

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0.0001

0.008

Clinical Study Table 3(a). The Relationship between Behavioral and Other Risk Factors in Male.

Factor

Food Habit Non veg Veg P value

Family history FH+ (%) FH - (%) Marital status Married (%) Single (%) SBP (mmHg) Mean SD DBP (mmHg) Mean SD Plasma glucose mg/dl Mean SD BMI (kg/m²) Mean SD Detected age (years) Mean SD

Smoker No P value

Yes

Alcohol No P value

Yes

Inactive

Physically Active P value

21.15 78.85

33.33 66.67

0.37

25.00 75.00

22.22 77.78

0.79

31.03 68.97

17.14 82.86

0.19

70.00 30.00

79.55 20.45

0.40

90.38 9.62 131.8 13.22

83.33 16.67 135.5 10.06

0.48

96.43 3.57 135.0 8.83

83.33 16.67 130.6 14.88

0.09

100.0

0.01

134.0 110.1

85.00 15.00 138.9 10.53

90.91 9.09 129.6 12.64

0.48

0.15

80.00 20.00 131.2 13.98

80.08 7.74

79.83 9.85

0.94

81.07 8.70

79.22 7.61

0.38

81.59 8.20

78.74 7.88

0.16

81.30 8.81

79.45 7.78

0.43

168.7 40.36

175.5 38.36

0.59

171.8 35.02

168.5 43.57

0.74

176.7 30.08

164.4 40.83

0.21

164.3 38.19

172.6 40.65

0.43

26.43 1.93

27.29 2.18

0.22

27.23 1.36

26.09 2.26

0.01

26.72 1.80

26.48 2.15

0.63

27.79 1.87

26.05 1.81

0.001

46.50 9.69

51.75 8.38

0.07

47.36 8.17

47.58 10.73

0.92

47.24 8.83

47.69 10.35

0.85

55.05 5.19

44.05 9.22

0.000

0.29

0.37

0.004

Table 3(b). The Relationship between Behavioral and Other Risk Factors in Female Factor Family history FH+ (%) FH - (%) Marital status Married (%) Single (%) SBP (mmHg) Mean SD DBP (mmHg) Mean SD Plasma glucose mg/dl Mean SD BMI (kg/m²) Mean SD Detected age (years) Mean SD

Nonveg

Food Habit Veg

Smoker No

Alcoholic No

29.41 70.59

28.57 71.43

0.95

29.17 70.83

29.17 70.83

19.05 80.95

37.04 62.96

0.17

76.47 23.53 132.8 10.72

92.86 7.14 127.5 10.50

0.19

81.25 18.75 131.2 10.82

81.25 18.75 131.2 10.82

76.19 23.81 136.5 8.42

85.19 14.82 127.1 10.82

0.43

79.38 6.77

78.86 7.26

0.82

79.23 6.84

79.23 6.84

79.86 7.21

78.74 6.64

0.58

170.2 41.56

179.2 46.01

0.53

172.8 42.61

172.8 42.61

168.48 38.72

176.2 45.83

0.53

25.49 2.80

25.12 1.93

0.61

25.38 2.60

25.38 2.60

26.46 2.86

24.54 2.07

0.01

44.44 11.33

45.93 5.21

0.54

44.88 9.91

44.88 9.91

51.33 5.33

39.85 9.78

0.000

P value

0.13

Physically Inactive Active

P value

0.001

Asian Journal of Clinical Cardiology, Vol. 15, No. 6, October 2012

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Clinical Study There was significant difference in education level and marital status among female diabetics (p = 0.03).

Most of the male nonvegetarians were found in primary education group. But female nonvegetarians were more in secondary education group. While comparing income levels, there was no significant difference noticed in male food habits. But, in females there was a significant difference (p = 0.06).

Physical inactivity was high in primary education level and low income group in both males and females.

But, there was significant difference in education level (p = 0.004) and income level (p = 0.02) in females.

In males, smoking habit was high in secondary education level with medium income. And there was no smoking habit among female of any education and income level.

Alcohol intake was high in higher education level and high income level male.

Family history of diabetes was reported high among both male (30.56%) and female (42.86%) with secondary education and no significant association found in income groups.

SBP was more in primary educated (137 mmHg) and lower income level (139 mmHg) males. Also similar trend found in female diabetics. There was statistical significance found in diastolic pressure in males at income level and female at education levels.

Plasma glucose level was high in both male (174.9 mg/ dl) and female (177.3 mg/dl) subjects with secondary education level. Male (173.3 mg/dl) diabetics with medium income and female (178 mg/dl) diabetics in lower income level had high glucose level.

Male diabetics in lower income level had high BMI 27.7 kg/m². But female diabetics with primary education level had high BMI 26.9 kg/m².

Diabetes detected age was high among male diabetics (54 years) and low among female diabetics (46 years) who were in low income level. And diabetes was detected very early in both the males and females in high income level.

Table 3a and 3b shows the relation between behavioral factors and other risk factors. Among male diabetics, significant association found between marital status and smoking habit (p = 0.09). Systolic pressure in male diabetics was more in vegetarians (135.5 mmHg), smokers (135 mmHg), alcoholic (134 mmHg) and physically inactive (138.9 mmHg). But, there was statistical significance found only in physical activity and SBP (p = 0.003). In male diabetics, plasma glucose

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was more in vegetarians (175.58 mg/dl), smokers (171.86 mg/dl) and alcoholic (176. mg/dl). BMI was also more in vegetarians (27.2 kg/m²), smokers (27.23 kg/m²) and physically inactive (27.79 kg/m²) males. But, BMI showed statistical significance between smokers and nonsmokers (p = 0.015) and physically active and inactive (p = 0.01) males.

In female diabetics, SBP was high in non-vegetarians (132.8 mmHg) and physically inactive (136.57 mmHg).

Statistical significance (p = 0.01) was found between physical activity and SBP in females. Plasma glucose was found more in vegetarians (179.21 mg/dl) and physically active (176.22 mg/dl) females. In female diabetics, BMI showed significance (p = 0.01) with physical activity, it was more (26.46 kg/m²) in case of physically inactive females. Duration of diabetes shows significant difference between physically active and inactive females (p = 0.02).

Discussion This study shows that there is significant difference between male and female diabetics only in certain factors. In the third National Health and Nutrition Examination Survey (2001), SES was significantly associated with type 2 diabetes in both AfricanAmerican and white women. But, no relationship was found for men. Rathmann et al (2005) found that patients with long-standing diabetes along with severe disabling diabetic complication and poor health may result in low SES. According to Tang et al (2003) in the National Population Health Survey in Canada, low income and education remained significantly associated with selfreported diabetes after controlling for BMI and physical activity in women. In men, the association was weaker and did not persist after controlling for risk factors.

In the present study, there was significant difference in male only in few factors and SES. But, female showed significant inverse association with SES. This study reveals BMI was more among low income level male diabetics. Poor diet, lack of physical activity and smoking habit had lead to increase in BMI of these diabetic cases. Female diabetics in primary education level have more BMI. Lack of knowledge, consumption of junk food and sedentary lifestyle has increased the BMI of female diabetics. The association between SES and obesity was found in several studies, obesity being stronger in women than in men. Rathman et al (2005) analyzed that an inverse association of BMI and SES was found only in women. Ramachandran et al (2002) found that obesity is common in Indians and the adverse effect of central obesity is manifested

Clinical Study in increasing tertiles of BMI both in men and women.

BMI was found more in Indian women.

Physical inactivity is another major behavioral risk factor of type 2 diabetes. Lantz et al (1998) found in US adult that physical activity was less in low SES groups. Ford et al found women with higher SES were more physically active than women with low SES; whereas this social gradient may be less pronounced in men. Rathman et al (2005) in KORA survey proved that physical inactivity was reported more in men and women in low SES. In the present study, physical inactivity is high among both male and female diabetics who were in low income level. Physically inactive female were more in low education level. Normally, well-educated and those who earn more are more likely to engage in high physical activity.

Mathews et al (1997) identified people with high occupational status and in particular high education attainments were less likely to smoke and drink excess alcohol. Study conducted in Canada showed that lower income was inversely associated with smoking and diet intake. But, in this present study there was no difference in smoking habit between education level and income level in males. Alcohol intake was more in higher income group. Because of more work, stress, body pain and work tension they may resort to alcohol.

Kivimaki et al (2004) identified that there was a weak inverse relationship between SES and BP. Higher education attainment was associated with lower SBP. But association involving occupational status and DBP did not reach statistical significance. Stronger links with lifestyle and risk factors may partially explain the greater BP differences between educational levels and occupational status.

Marmot et al (2001) in the Whitehall study found difference in SBP was no more than 3-5 mmHg between the highest and lowest employment grade. INTER-SALT study, Stamler (1992) proved an inverse association between years of education and BP. He found that, for men 28 out of 47 populations and for women 38 of 47 populations, this inverse association was seen. The US Hanes III study showed no association between SES and BP. In this present study SBP was more in primary education and low income level in both males and females. Tension, worry about the uncertainty in life, work pressure and poor diet regulation may increase the BMI. Previous researches consistently showed a positive relationship between body weight and BP. Increased BMI was the predictor of higher BP.

Hoskins et al found that a family history of diabetes was a risk factor for diabetes in Melanesians and Indians living in Fiji. Ramachandran et al (1988) reported a high prevalence of diabetes among Indian children who had one or two diabetic parents. But, in the present study, there was no significant difference in family history of diabetes and SES between males and females.

This study shows low income male diabetics had longer duration of diabetes and diabetes detected age was also higher. Even in female diabetics primary education group had diabetes over long duration and the detected age was high. Due to poverty and lack of knowledge these diabetic patients were not aware of the free healthcare facilities and never tried to avail any type of medical attention for treating diabetes, till they got complication due to prolonged untreated diabetes.

In conclusion, in female diabetics, SES was found to be significantly and inversely related to physical activity, marital status, food habit, duration and SBP. In male, these associations were weaker or absent when education level was considered. But, in income level significant differences found were in SBP and detected age. Significant differences found in both male and female behavioral characters and other risk factors like SBP and BMI. Physical inactivity leads to high BMI and it increases SBP. But, the differences between male and female diabetic patients needs to be further investigated.

Acknowledgment We thank Mr. Ramadas, Mr Navaneethan and Mrs. Asha for the help they extended while collecting the samples.

Also we thank Mr Ponmurugan for the statistical and secretarial help.

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Case Report

Dystrophin Deletion Mutation Pattern and Cardiac Involvement in 46 Cases of Dystrophinopathies Suvarna Badhe*, Pooja Kulkarni**, Guneet Chopra*, Nandini Gokulchandran*, Alok Sharma*

Abstract Dystrophinopathies are X-linked recessive disorders which includes Duchenne muscular dystrophy and Becker muscular dystrophy. Forty-six cases were included in our study. Our main aim was to identify the exon deletions in these cases, determine the extent of cardiac involvement by two dimensional echocardiography and whether a correlation exists between the two.

It was found that the cases having left ventricular ejection fraction â&#x2030;¤40% majorly showed deletions in the proximal exons as compared to the distal exons.

Keywords: Dystrophinopathy, Duchenne muscular dystrophy, Becker muscular dystrophy, cardiac

D

ystrophinopathies are X-linked recessive disorders caused by mutations in the duchenne muscular dystrophy (DMD) gene, encoding the dystrophin protein. The dystrophin gene consists of 79 exons over 2.2 Mb of genomic DNA, which encodes a huge 427 kDa membrane-associated protein found in some neurons and all muscle cells.1 Becker muscular dystrophies (BMD)/DMD are collectively termed as dystrophinopathy and are estimated to occur in 1:12,000 and 1:3,500 male births, respectively.

The majority of mutations in dystrophin are exonic or multiexonic deletions (around 60% in DMD and 80% in BMD); less frequent are duplications (around 10%), and the remaining mutations are single nucleotide changes generating nonsense (DMD) or missense mutations (BMD). There are two mutational hotspots: 30% of mutations occur at the proximal hotspot (exons 3-7) and 60% distally (exons 44-55).

Mutations in DMD usually disrupt the open reading frame, whereas mutations in BMD retain the open reading frame, generating an internally truncated

*Dept. of Medical Services and Clinical Research *Dept. of Research and Development NeuroGen Brain and Spine Institute, Surana Sethia Hospital and Research Centre, Suman Nagar, Chembur, Mumbai Address for correspondence Ms. Pooja Kulkarni Clinical Research Associate NeuroGen Brain and Spine Institute, Surana Sethia Hospital and Research Centre, Suman Nagar, Sion - Trombay Road, Chembur, Mumbai - 400 071 E-mail: poojakul28@gmail.com, publications@neurogen.in

dystrophin molecule with sufficient biological activity. Hence, patients with BMD exhibit milder progression with ambulation maintained into the teenage and adult years. On the other hand, patients with DMD tend to lose independent ambulation by 10-15 years of age depending on their gene deletion and succumb to death by the end of the second decade usually due to cardiorespiratory compromise.2 Cardiac involvement in DMD and BMD includes cardiomyopathy and arrhythmias. The incidence of cardiomyopathy increases with age in DMD patients.

Cardiomyopathy can be evident at 10 years of age and is nearly universal in DMD patients over the age of 20.

Approximately 70% of boys with BMD have cardiac involvement by age 20.

To study the deletion patterns and the cardiac conditions in dystrophinopathy, we hereby present 46 cases of the same.

Material and Method A total of 46 male cases of dystrophinopathy were included in the study, which comprised of 43 DMD cases and 3 BMD cases. The age of the DMD cases ranged from 4.5 to 19 years with an average of 11.5 years, while the age range of the BMD cases was from 24 to 33 years with an average of 26.5 years. Except for 1 BMD case all the other cases were sporadic with no family history. Their gene deletions and duplications were recorded and their cardiac function was found using two dimensional echocardiography (Table 1).

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case report Table 1. Showing the Gene Deletions and LVEF in 46 Cases of Dystrophinopathy Age (years)

13 13 11 9 9 17 10 8.5 6 12 10 11 10 13 4.5 8.5 10 11 33 17 11 8 11 13 13 9 13 11 13 18 7 11 14 18 10 10 10 10 11 30 23 24 19 7 8 17

212

Gene deletion

45-49 21 8-19 51 and 52 8-13, 17,19 No deletions No deletions No deletions 48-50 Promotor gene No deletions 8-11 8-44 46-51.

49-52 49-51 49-50 48-50 12 Nonsense mutation No deletions 46-47 No deletions 47 and 50 53-55 49-50 53 45-50 49-50 5 -13 45-52 8-13, 17, 19, 20, 21, 43, 45, 46, 47 48-50 3-7

LVEF (%)

60 75 45 55 55 50 60 60 60 74 60 40 55 60 72 55 60 55 40 55 60 65 55 60 55 65 33 60 60 40 60 55

50 50 44 6, 8, 12, 13, 17, 19 49 and 50 45-48 57-61 No exon del 3, 4, 8, 12, 17 No deletion 46-51 51

73 67 65 70 46 50 55 45 60 55 60 30

60 30

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Results Thirty-eight out of 46 (82.6%) cases showed deletions in one or more exons while, in the other eight cases no deletion was detected. Duplication of the exons 5761 was detected in only one out 46 cases (2.1%). The majority (25 out of 46 i.e. 54.3%) had deletions in the distal rod domain between exons 45-55. Eight out 46 (17.3%) showed deletions in the proximal rod domain between exons 3-21. Two out of 46 (4.3%) showed large deletions spanning both the regions from exon 3-55. One case (2.1%) showed nonsense mutation and promoter gene deletion was also detected in only (2.1%) case out of the total 46 cases.

On studying the ejection fractions of the 46 cases, it was found that four cases had left ventricular ejection fraction LVEF ≤40% while 42 cases had LVEF ≥41%.

Our analysis showed that the cases having LVEF ≤40% majorly showed deletions in the proximal exons as compared to the distal exons.

Discussion Dystrophinopathies are due to mutations in the dystrophin gene on chromosome Xp21.1 and comprise the allelic entities DMD, BMD and X-linked dilative cardiomyopathy (XLDCM). These are X-linked disorders affecting the synthesis of dystrophin, a large, sarcolemmal protein that is absent in DMD3 and reduced in amount or abnormal in size in BMD patients.4 Dystrophin provides the connection between a large, multimeric complex of glycoproteins in the muscle cell membrane and intracellular actin filaments, thereby transmitting forces generated by sarcomere contraction to the extracellular matrix.5,6 Dystrophin has an important role in stabilizing the cell membrane of both skeletal and cardiac myocytes7,8 and its absence produces sarcolemmal fragility, muscle cell degeneration and leads to conformational changes in stretch-activated calcium channels, resulting in pathologic leakage of calcium in the muscle cytosol.9 Intracellular calcium accumulation then leads to protease activation, increased reactive oxygen species production, and cell death.10,11 Finally, impaired vasoregulation occurs via marked reduction in membrane-associated neuronal nitric oxide synthase in both cardiac and skeletal muscle.12 Without dystrophin, neuronal nitric oxide (NO) synthase mislocalizes to the cytosol, this greater distance between neuronal nitric oxide synthase and the sarcolemma may impair NO diffusion through the myocyte membrane to the microvasculature. As a consequence, insufficient NO

case report release follows muscle contraction, resulting in muscle ischemia.13 Unopposed vasoconstriction may, therefore, explain the necrosis observed in skeletal and cardiac muscle of dystrophinopathy patients. Microvasculature abnormalities have also been shown to result primarily from the absence of dystrophin or sarcoglycan components of the dystrophin-glycoprotein complex in cardiomyocytes.14,15 Subclinical or clinical cardiac injury is present in about 90% of the DMD/BMD patients but is the cause of death in only 20% of the DMD and 50% of the BMD patients.16 Correlations between dystrophin mutations and the onset of cardiomyopathy have been noted.

Rita Wen Kaspar et al have analyzed 78 BMD and XLDCM patients with common deletion mutations predicted to alter the dystrophin protein and correlated their mutations to cardiomyopathy age of onset. They observed that deletions affecting the amino-terminal domain are associated with early-onset dilated cardiomyopathy (DCM; mid-20s), whereas deletions removing part of the rod domain and hinge 3 have a later-onset (DCM; mid-40s).17 Some mutations result in only cardiomyopathy without skeletal myopathy.

X-chromosome inactivation, the random process by which 1 of the 2X chromosomes in female cells becomes transcriptionally inactive, may result in cardiomyocytes with an active X chromosome with the abnormal dystrophin gene. The X chromosome containing the normal dystrophin gene may become inactivated in cardiac muscle to a greater degree than in skeletal muscle, causing female carriers to develop dystrophinopathic cardiomyopathy. The exact prevalence and severity in the carrier population are uncertain.18-21 Almost all DMD patients who survive to the third decade of life display cardiomyopathy.22 Recognition may be delayed by relative physical inactivity obscuring symptomatology and also because, in most cases, the patient presents at an early stage of the disease. BMD patients, whose skeletal myopathy occurs later and progresses more slowly, experience worse cardiomyopathy than do DMD patients: Upto 70% have left ventricular (LV) dysfunction on echocardiography.

Perhaps because of less skeletal muscle weakness, these patients can perform more strenuous exercise with dystrophin-deficient myocardial muscle fibers and have earlier manifestations of myocardial disease.23 Most cardiac magnetic resonance imaging (CMR) data in MDs currently exist for patients with DMD and BMD. The pathology of cardiomyopathy in patients with dystrophinopathy classically produces subepicardial

fibrosis of the inferolateral wall,24 remarkably similar to the pattern observed in some patients with viral myocarditis. Cardiac screening has been recommended for female DMD/BMD mutation carriers, particularly beginning after the teenage years, as these individuals are known to be at risk for developing cardiomyopathy.25 Interestingly, CMR has revealed a pattern of myocardial fibrosis in mutation carriers similar to that seen in DMD patients.26 Because myocardial damage in carriers has been observed even in the absence of clinically apparent muscular weakness, cardiac screening should be considered in female relatives of DMD/BMD patients. In patients predisposed to cardiomyopathies because of dystrophinopathy, occult regional cardiac dysfunction can be diagnosed with CMR tagging. This method of strain imaging analysis may offer a sensitive approach for delineating the presence and progression of cardiovascular disease and for assessing therapies designed to modulate the onset and course of heart failure.27,28 Our aim was to identify the exons, which are most commonly affected in cases of DMD/BMD, to determine the extent of cardiac involvement in these cases and to identify if a correlation exists between the exons affected and the cardiac involvement in these patients.

In conclusion, LVEF â&#x2030;¤ 40% in dystrophinopathy patients can be correlated to the deletions in the proximal exons.

Cardiac involvement, though present in most cases might be difficult to detect solely based on LVEF, and hence continued monitoring of these patients is essential.

Newer imaging techniques like CMR may help to detect the cardiac abnormalities earlier and in the follow-up of these patients. Although, the accurate diagnosis of DMD/BMD by DNA methods represents a considerable challenge because of the unusual characteristics of this gene and its mutations; genetic counseling, carrier detection and DNA analysis will dramatically improve the early detection and prevention of these disorders.

References 1.

Milasin J, Muntoni F, Severini GM, Bartoloni L, Vatta M, Krajinovic M, et al. A point mutation in the 5â&#x20AC;&#x2122; splice site of the dystrophin gene first intron responsible for X-linked dilated cardiomyopathy. Hum Mol Genet 1996;5(1):73-9.

2.

Aartsma-Rus A, Van Deutekom JC, Fokkema IF, Van Ommen GJ, Den Dunnen JT. Entries in the Leiden Duchenne muscular dystrophy mutation database: an overview of mutation types and paradoxical cases that confirm the reading-frame rule. Muscle Nerve 2006;34(2):135-44.

3.

Feng J, Yan JY, Buzin CH, Sommer SS, Towbin JA. Comprehensive mutation scanning of the dystrophin

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case report gene in patients with nonsyndromic X-linked dilated cardiomyopathy. J Am Coll Cardiol 2002;40(6):1120-4.

4.

Hoffman EP, Brown RH, Kunkel LM. Dystrophin: the protein product of the Duchene muscular dystrophy locus. 1987. Biotechnology 1992;24:457-66.

5.

Monaco AP, Bertelson CJ, Liechti-Gallati S, Moser H, Kunkel LM. An explanation for the phenotypic differences between patients bearing partial deletions of the DMD locus. Genomics 1988;2(1):90-5.

6.

Rafael JA, Cox GA, Corrado K, Jung D, Campbell KP, Chamberlain JS. Forced expression of dystrophin deletion constructs reveals structure-function correlations. J Cell Biol 1996;134(1):93-102.

7.

Corrado K, Rafael JA, Mills PL, Cole NM, Faulkner JA, Wang K, Chamberlain JS. Transgenic mdx mice expressing dystrophin with a deletion in the actin-binding domain display a “mild Becker” phenotype. J Cell Biol 1996;134(4):873-84.

8.

9.

Menke A, Jockusch H. Extent of shock-induced membrane leakage in human and mouse myotubes depends on dystrophin. J Cell Sci 1995;108 ( Pt 2):727-33.

Pasternak C, Wong S, Elson EL. Mechanical function of dystrophin in muscle cells. J Cell Biol 1995;128(3):355-61.

10. Franco-Obregón A Jr, Lansman JB. Mechanosensitive ion channels in skeletal muscle from normal and dystrophic mice. J Physiol 1994;481 ( Pt 2):299-309.

11. Fong PY, Turner PR, Denetclaw WF, Steinhardt RA. Increased activity of calcium leak channels in myotubes of Duchenne human and mdx mouse origin. Science 1990;250(4981):673-6.

12. Jung C, Martins AS, Niggli E, Shirokova N. Dystrophic cardiomyopathy: amplification of cellular damage by Ca2+ signalling and reactive oxygen species-generating pathways. Cardiovasc Res 2008;77(4):766-73.

13. Bia BL, Cassidy PJ, Young ME, Rafael JA, Leighton B, Davies KE, et al. Decreased myocardial nNOS, increased iNOS and abnormal ECGs in mouse models of Duchenne muscular dystrophy. J Mol Cell Cardiol 1999;31(10): 1857-62.

14. Sander M, Chavoshan B, Harris SA, Iannaccone ST, Stull JT, Thomas GD, et al. Functional muscle ischemia in neuronal nitric oxide synthase-deficient skeletal muscle of children with Duchenne muscular dystrophy. Proc Natl Acad Sci U S A 2000;97(25):13818-23.

15. Wheeler MT, Allikian MJ, Heydemann A, Hadhazy M, Zarnegar S, McNally EM. Smooth muscle cell-extrinsic vascular spasm arises from cardiomyocyte degeneration in sarcoglycan-deficient cardiomyopathy. J Clin Invest 2004;113(5):668-75.

16. Finsterer J, Stöllberger C. The heart in human dystrophinopathies. Cardiology 2003;99(1):1-19.

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17. Kaspar RW, Allen HD, Ray WC, Alvarez CE, Kissel JT, Pestronk A, et al. Analysis of dystrophin deletion mutations predicts age of cardiomyopathy onset in becker muscular dystrophy. Circ Cardiovasc Genet 2009;2(6): 544-51.

18. Hainsey TA, Senapati S, Kuhn DE, Rafael JA. Cardiomyopathic features associated with muscular dystrophy are independent of dystrophin absence in cardiovasculature. Neuromuscul Disord 2003;13(4): 294-302.

19. Verhaert D, Richards K, Rafael-Fortney JA, Raman SV. Cardiac involvement in patients with muscular dystrophies: magnetic resonance imaging phenotype and genotypic considerations. Circ Cardiovasc Imaging 2011;4(1):67-76.

20. Grain L, Cortina-Borja M, Forfar C, Hilton-Jones D, Hopkin J, Burch M. Cardiac abnormalities and skeletal muscle weakness in carriers of Duchenne and Becker muscular dystrophies and controls. Neuromuscul Disord 2001;11(2):186-91.

21. Hoogerwaard EM, van der Wouw PA, Wilde AA, Bakker E, Ippel PF, Oosterwijk JC, et al. Cardiac involvement in carriers of Duchenne and Becker muscular dystrophy.

Neuromuscul Disord 1999;9(5):347-51.

22. Nolan MA, Jones OD, Pedersen RL, Johnston HM. Cardiac assessment in childhood carriers of Duchenne and Becker muscular dystrophies. Neuromuscul Disord 2003;13(2):129-32.

23. Politano L, Nigro V, Nigro G, Petretta VR, Passamano L, Papparella S, et al. Development of cardiomyopathy in female carriers of Duchenne and Becker muscular dystrophies. JAMA 1996;275(17):1335-8.

24. McNally EM. New approaches in the therapy of cardiomyopathy in muscular dystrophy. Annu Rev Med 2007;58:75-88.

25. Melacini P, Fanin M, Danieli GA, Villanova C, Martinello F, Miorin M, et al. Myocardial involvement is very frequent among patients affected with subclinical Becker’s muscular dystrophy. Circulation 1996;94(12):3168-75.

26. Frankel KA, Rosser RJ. The pathology of the heart in progressive muscular dystrophy: epimyocardial fibrosis.

Hum Pathol 1976;7(4):375-86.

27. Yilmaz A, Gdynia HJ, Ludolph AC, Klingel K, Kandolf R, Sechtem U. Images in cardiovascular medicine.

Cardiomyopathy in a Duchenne muscular dystrophy carrier and her diseased son: similar pattern revealed by cardiovascular MRI. Circulation 2010;121(10):e237-9.

28. Ashford MW Jr, Liu W, Lin SJ, Abraszewski P, Caruthers SD, Connolly AM, et al. Occult cardiac contractile dysfunction in dystrophin-deficient children revealed by cardiac magnetic resonance strain imaging. Circulation 2005;112(16):2462-7.

Case report

Aneurysm of Mitral Valve Complicated by Ventricular Tachycardia MONIKA MAHESHWARI*, NIRMAL VYAS, RK GOKROO

Abstract An interesting case of mitral valve aneurysm secondary to myxomatous valvular degeneration presenting with ventricular tachycardia in emergency department is described herein.

Keywords: Mitral valve aneurysm, myxomatous valvular degeneration, ventricular tachycardia

A

neurysm is an echolucent space that is contiguous with the cavity of origin and is completely bounded by a thin layer of tissue extending from the cavity of origin.1 Aneurysms of cardiac valves are usually secondary to infective endocarditis.2 Rarely, such aneurysms can occur without any evidence of infection, in the presence of connective tissue disorders, Marfanâ&#x20AC;&#x2122;s syndrome, pseudoxanthoma elasticum or myxomatous valvular degeneration.3 We report herein one such case of noninfective mitral valve aneurysm complicated by ventricular tachycardia.

Case Report A 28-year-old female presented in emergency department with complaints of sudden-onset of palpitation and breathlessness. On examination, her systolic blood pressure was 70 mmHg, with pulse rate of 160/minute regular, temperature 98°F and respiratory rate - 30/minute. Jugular venous pressure was raised upto the angle with cold and sweaty extremities. There was pallor but no cyanosis, icterus, pedal edema or lymphadenopathy. Electrocardiogram showed regular wide QRS ventricular tachycardia (Fig. 1). Echocardiography demonstrated small

*DM(Cardio) 2nd Year Resident Dept. of Cardiology JLN Medical College, Ajmer, Rajasthan Address for correspondence Dr Monika Maheswari Navin Niwas, 434/10, Bapu Nagar, Ajmer - 305 001, Rajasthan E-mail: opm11@rediffmail.com

Figure 1. Electrocardiogram showing ventricular tachycardia.

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case report

Figure 2. Echocardiograph (parasternal long-axis view) demonstrating localized saccular bulge of the anterior mitral leaflet.

Figure 4. Right coronary angiogram showing normal right coronary artery.

On Doppler color flow mapping presence of eccentric mitral regurgitation jet further supported the etiology of mitral valve prolapse.

The ventricular tachycardia (VT) was reverted to normal sinus rhythm with 100 Joules of synchronized direct current (DC) shock. Following reversion to sinus rhythm coronary angiogram was performed, which revealed normal coronary vessels (Figs. 3 and 4) and ruled out ischemic cause of VT. For definitive treatment and further management, we advised the patient surgical excision of the aneurysm followed by mitral valve repair. However, she did not give consent and was discharged on b-blockers and antiarrhythmics.

DISCUSSION

Figure 3. Left coronary angiogram showing normal left anterior descending and left circumflex artery.

fluttering echoes on the mitral valve and a localized saccular bulge of the anterior mitral leaflet protruding into the left ventricle during systole measuring 2.2 x 3.1 cm (Fig. 2) suggestive of mitral valve aneurysm secondary to myxomatous degeneration of mitral valve.

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Aneurysms of the mitral valve are rare complications of aortic valve endocarditis. The cause of the aneurysm is most likely a combination of occult infection of the mitral valve leaflets by migration via the intervalvular fibrosa1 or by seeding of the anterior mitral valve leaflet from the aortic valve regurgitation jet in combination with leaflet weakening due to the high velocity regurgitant jet.4 Rarely aneurysms of the mitral valve can occur in association with connective tissue disorders.3 Mitral valve aneurysms can be confused with several abnormalities including flail mitral leaflets, papillofibroelastomas or myxomas involving the mitral

case report valve, and nonendothelialized cysts of the mitral valve.5 Although TTE may occasionally identify subtle valvular abnormalities, the better resolution provided by TEE yields a more definitive identification. Color flow Doppler distinguishes the aneurysm from these other abnormalities by demonstrating direct communication between the aneurysm and the left ventricle.6 Early detection and prompt intervention are important to prevent the complications of valvular aneurysms, which include rupture, embolism and endocarditis.

Aneurysmectomy with mitral valve repair is the procedure of choice; replacement should be reserved for those cases where repair would compromise valvular function.7

2.

Lee CH, Tsai LM. Transesophageal echocardiographic recognition of mitral valve aneurysm. J Ultrasound Med 2005;24(8):1141-4.

3.

Chua SO, Chiang CW, Lee YS, Chang CH, Hung JS. Perforated aneurysm of the anterior mitral valve. A Doppler and two-dimensional echocardiographic report.

Chest 1990;97(3):753-4.

4.

Rachko M, Safi AM, Yeshou D, Salciccioli L, Stein RA. Anterior mitral valve aneurysm: a subaortic complication of aortic valve endocarditis: a case report and review of literature. Heart Dis 2001;3(3):145-7.

5.

Mollod M, Felner KJ, Felner JM. Mitral and tricuspid valve aneurysms evaluated by transesophageal echocardiography. Am J Cardiol 1997;79(9):1269-72.

6.

Changlani M, Lieb D, Kaczkowski D, Moss S. The role of color flow Doppler in the echocardiographic diagnosis of mitral valve aneurysm. J Am Soc Echocardiogr 1993;6(6):610-2.

7.

Ruparelia N, Lawrence D, Elkington A. Bicuspid aortic valve endocarditis complicated by mitral valve aneurysm.

J Card Surg 2011;26(3):284-6.

REFERENCES 1.

Sachdev M, Peterson GE, Jollis JG. Imaging techniques for diagnosis of infective endocarditis. Infect Dis Clin North Am 2002;16(2):319-37, ix.

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Around the globe

News and Views

Kolkata tops metros in heart disease risk Kolkata: On World Heart Day this year, Kolkatans will have to pledge to take better care of their hearts by growing more healthy food habits and leading a disciplined lifestyle. A recent study showed that 74% of respondents from the city had the risk of developing cardiovascular diseases (CVDs), highest among the metros. The all-India figure stands at 72%, according to Saffolalife Heart Study 2012. Kolkata also emerged the ‘smoking capital’ with 19% of the respondents being smokers, the all-India figure being about 16%.

According to doctors, smoking is known to increase blood pressure and release free radicals.”Though medical science has advanced now with effective drugs and devices like stents and pacemakers being easily available in the market, there is no substitute for prevention. A healthy lifestyle, including a proper diet and briskly walking 4-5 km daily are effective ways of preventing heart ailments,” said Dr D Kahali, senior consultant cardiologist at BM Birla Heart Research Centre.

Around 72% of respondents from the city had very low good cholesterol (HDL) level. A whopping 78% said they consumed less than two helpings of healthy whole grams per day while 67% exercise less than four times a week. “Controlling of obesity, regular exercises along with dietary modification - low-calorie, nutrient-rich food, more fresh vegetables and whole grain cerealshelp maintain a healthy life by preventing CVD,” said Ipshita Chakravarty, chief dietician at Fortis Hospital.

Chakravarty was part of the team that conducted the study.

More alarmingly, the young population is at high-risk of developing heart ailments, showed the study. Around 75% of the male population in the age group of 30-44 stood the risk of CVD while the corresponding figure for the female population was 57%. “Now we get very young patients with heart ailments. I recently treated a 22-year-old youth for blockage in the main artery,” said Kahali. The study conducted across 12 cities had covered more than 1.12 lakh people in the age group of 30-80 years. According to experts, the projected number

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of CVD-related deaths in India by 2020 will be more than double the number in 1990, which was 11.75 lakh.

Majority of them could in the productive working age group of 30-44. (Source: TOI, Sept. 27, 2012) Nine small meals a day may help you shed kilos London: Instead of three square meals a day, eating little and often is healthier, and one should have as many as nine meals every day, experts have claimed.

Consuming little food at intervals may help lower BP and cholesterol, and even encourage weight loss, the Daily Mail reported. In a recent study, scientists from the Imperial College, London, compared the diets of more than 2,000 people from the UK, Japan, China and the US. While they all had the same calorie intake and food, half the participants ate fewer than six times a day, while the remainder ate more than six times. The study found that the first group had a significantly higher systolic BP - the pressure that blood exerts on vessels while the heart is beating - compared with the more frequent eaters. They were also significantly heavier.

Researchers are now planning a larger trial involving 50 patients with high BP who will eat either three or nine meals a day to assess the effects of the different regimens. As well as their BP, patients will have their insulin level, glucose and fatty acids recorded.

(Source: TOI) Pause for a cause as Parikrama lends its voice to World Heart Fest 2012 Cardiological Society of India is organizing “World Heart Fest 2012” a daylong extravaganza event dedicated to the prevention of heart diseases at the NSIC Grounds, Kalkaji in New Delhi on 30th September, 2012 after the World Heart Day. The event would witness country’s one of the most celebrated rock bands - ‘Parikrama’, who are known for their passionate love for music. The event will witness history by a major Guinness World Records TM achievement with attempt for hoisting 25,000 heart shaped balloons and create the biggest human heart logo ever.

Around the globe There will be various activities aimed to drive awareness about prevention of heart diseases such as free cholesterol, cardiac check-ups, healthy heart tips, expert talks, etc. It would be graced by the presence of political figures, celebrities and corporate leaders.

The corporate and medical fraternity has extended its support by partnering with the event. The event will also be inaugurated by Hon’ble Chief Minister of Delhi Smt. Sheila Dikshit along with Shri. Sandeep Dikshit, MP. Dr Ashok Seth, Chairman Cardiac Sciences - Fortis Escorts Heart Institute, New Delhi is elated to witness so many people extensively joining this initiative. We feel that with the increase of heart attacks, India will be the highest capital in Cardiac diseases among all countries in the world by 2020. In reverse to this we are happy to organize this event preventing heart diseases among Indians, he said.

Weight gain after bypass not affected by diet Lifestyle factors - including dietary intake, physical activity levels, and treadmill time - were not predictive of weight regain from 2 to 6 years after Roux-en-Y gastric bypass, researchers found. (Source: Medpage Today) For universal health coverage, Plan Panel to train quacks New Delhi: The Planning Commission has proposed to train registered medical practitioners, commonly referred to as quacks, to ensure universal health coverage reaches even the remote populations. “Affordability, accessibility and quality are three pillars of universal health coverage (UHC). The challenge is to fill the gaps especially in rural areas where there is a problem of trained manpower. We would like to train traditional midwives and registered medical practitioners (RMPs) - some people call them jholawala doctors or quacks - to be used because they have been providing services in remote areas all these years. It is important to respect and use what we have. The XIIth plan document talks about this need,” Syeda Hameed, a member of the commission, told. The Indian Express. India, according to the commission, had 26,329 doctors in the public sector in March 2011 against a requirement of 1,09,484, a massive shortage of nearly 76% despite the fact that every year some 43,740 students are awarded MBBS. A Health Ministry plan to train rural healthcare workers

as “half-way doctors” through a course prescribed and managed by the Medical Council of India had raised hackles of the doctor lobby which claimed it would amount to leaving the rural population in the hands of semi-doctors.

Now, the ministry has renewed efforts to push it through with a different name. Sources said the idea of using quacks as first-line health workers wasn’t received with much enthusiasm in the Plan Panel’s meetings. It was, in fact, seen as a move that would derail states’ efforts to crack down on quackery. Hameed admitted that the idea was greeted with a certain amount of “professional arrogance” by the Health Ministry and anticipates stiff resistance from doctors as well. She, however, added: “Supplementing the public sector is important and since they themselves will not go and work in boondocks, we need to weigh all options.”

Hameed said there is a proposal to make states institute a special cadre of officers to deal solely with public health, and added that there is a need to use cheap technological innovations to make healthcare more accessible and affordable. States, she added, would be required to invest in a management information system so that health data is easily accessed. “Though we tried to give states greater flexibility in the XIIth plan... there is a need to evolve a formula where laggard states like Bihar and Uttar Pradesh get extra funds. Right now the system is such that states like Tamil Nadu and Kerala, which have good healthcare systems in place, get most of the money,” she said.

(Source: Indian Express, Oct 3, 2012) Upping physical activity slashes CV events, deaths in type 2 diabetics Not surprisingly, higher levels of leisure-time physical activity cut the risk of cardiovascular and all-cause mortality in people with type 2 diabetes, a new analysis from the Swedish National Diabetes Register (NDR) shows. But, in an important additional finding, researchers report that among diabetics who did little or no exercise at baseline, those who managed to substantially increase their leisure-time physicalactivity levels over approximately five years cut their risk of death by almost two-thirds. Dr Björn Zethelius (Uppsala University, Sweden) presented the study findings here at the European Association for the Study of Diabetes (EASD) 2012 Meeting. (Source: Medscape)

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Photo Quiz

Large, Dark Lesion on the Arm Present Since Birth

A

n otherwise healthy 16-year-old boy presented with an asymptomatic, black to brown plaque on his right proximal forearm. The lesion was present at birth, but was flatter and lighter in color. Physical examination revealed a discrete, ovalshaped plaque that measured 7 Ă&#x2014; 3 cm. The lesion had a cobblestone pattern with prominent hair growth (see accompanying figure).

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

A.

Acquired melanocytic nevus.

B.

Becker nevus.

Source: Adapted from Am Fam Physician. 2011;84(11):1287-1288.

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C.

Congenital melanocytic nevus.

D.

Melanoma.

E.

Plexiform neurofibroma.

See the following page for discussion.

photo quiz Discussion The answer is C: congenital melanocytic nevus.

Congenital melanocytic nevi are generally present at birth or appear within the first few months of life.1 The incidence ranges from 1 to 2 percent for any size of congenital melanocytic nevi to approximately one in 20,000 for giant nevi.2 Most congenital melanocytic nevi are intradermal or compound in nature.3 They are classified according to their expected diameter in adulthood as small (less than 1.5 cm), medium or intermediate (1.5 to 19.9 cm), and large or giant (20 cm or greater).2,4,5 Small and medium nevi are usually round or oval and symmetric. At birth, these lesions are flat or mildy palpable and tan in color, but over time they become raised and darken. They may have a verrucous or cobblestone surface.5 Hypertrichosis may become prominent.

Giant congenital melanocytic nevi can have irregular color patterns and are often accompanied by multiple smaller “satellite” nevi. Although nevi are usually benign, some, particularly giant nevi, may be associated with the development of malignant melanoma.1 Congenital melanocytic nevi, especially those occurring in the posterior trunk, may rarely involve the central nervous system. The usual treatment for small and medium congenital melanocytic nevi is observation.4 The decision to remove a lesion is based on the malignant potential and its cosmetic outcome.4 Prophylactic excision is performed for giant congenital melanocytic nevi to lower the risk of melanoma. Other treatments include superficial excision, laser treatment, curettage, chemical peel, and dermabrasions with regular follow-up. A conservative approach with serial photography of the nevus and close follow-up has also been recommended.2 All patients with congenital melanocytic nevi should be instructed on sun protection.1,4 Acquired melanocytic nevi are small (less than 8 mm in diameter), well circumscribed, and round or ovoid with a homogenous surface and even pigmentation.

Compared with the congenital type, acquired melanocytic nevi are smaller, are more uniform in architecture and morphology, and occur in greater numbers. Becker nevi are more common in males. They typically appear at 10 to 20 years of age as a brownish, circumscribed macule or patch that gradually enlarges in an irregular fashion, similar to a geographic configuration.6 Hypertrichosis may develop a few years after the pigmentation. The lesion is asymptomatic and unilateral with a predilection for the upper torso, often the shoulder. Melanoma is a malignant tumor that can present as an enlarging, asymmetric, variegated lesion with an irregular border. It is rare in childhood and

Summary Table Condition

Characteristics

Acquired melanocytic nevus

Small, well-circumscribed, round or ovoid lesion with a homogenous surface and even pigmentation; multiple nevi present

Becker nevus

Asymptomatic, brownish, circumscribed macule or patch that gradually enlarges in an irregular fashion; usually occurs on one shoulder; hypertrichosis may be present

Congenital melanocytic nevus

Flat to mildly palpable, tan-colored lesion present at birth or soon after; tends to become raised and darken over time; hypertrichosis may be present

Melanoma

Malignant tumor that can present as an enlarging, asymmetric, variegated lesion with irregular border

Plexiform neurofibroma

Subcutaneous manifestation of type 1 neurofibromatosis; tender, firm nodules; early lesions may appear as hyperpigmentation and hypertrichosis

typically does not have hypertrichosis. Melanoma can be diagnosed with a biopsy.

Plexiform neurofibromas are a subcutaneous manifestation of type 1 neurofibromatosis.7 They are often present at birth and result from diffuse thickening of nerve trunks.7 Although most are associated with tender, firm nodules, early lesions may appear as hyperpigmentation and hypertrichosis.

REFERENCES 1.

Yan AC, Smolinski KN. Melanocytic nevi: challenging clinical situations in pediatric dermatology. Adv Dermatol.

2005;21:65-80.

2.

Kinsler V, Bulstrode N. The role of surgery in the management of congenital melanocytic naevi in children: a perspective from Great Ormond Street Hospital. J Plast Reconstr Aesthet Surg. 2009;62(5):595-601.

3.

McLaughlin MR, O’Connor NR, Ham P. Newborn skin: part II. Birthmarks. Am Fam Physician. 2008;77(1):56-60.

4.

Marghoob AA, Borrego JP, Halpern AC. Congenital melanocytic nevi: treatment modalities and management options. Semin Cutan Med Surg. 2007;26(4):231-240.

5.

Schaffer JV. Pigmented lesions in children: when to worry.

Curr Opin Pediatr. 2007;19(4):430-440.

6.

Leung AK, Kong AY. What’s your diagnosis? Hairy hyperpigmented lesion on a teenager’s back. Consultant.

2010;50(9):395-396.

7.

Leung AK, Robson WL. Case in point: a young girl with café au lait spots. Consultant Pediatricians. 2006;5(4): 229-232.

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Practice guidelines

Updated Dietary Guidelines from the USDA and HHS

T

he U.S. Department of Agriculture (USDA) and the U.S. Department of Health and Human Services (HHS) jointly created the updated version of the Dietary Guidelines for Americans, 2010. The Dietary Guidelines for Americans are reviewed every five years, by law.

Previous versions of the guidelines stated that the recommendations were meant for healthy Americans older than two years, whereas the 2010 update changed this wording to specify that the recommendations apply not only to those who are healthy, but also to those who are at increased risk of chronic disease.

Table 1. Overview of Key Recommendations from the Dietary Guidelines for Americans, 2010

The updated guidelines are based on two main concepts: focusing on balancing caloric intake over time to reach and maintain a healthy body weight; and consuming more nutrientdense foods and beverages in place of those high in sodium, saturated fats, added sugars, and refined grains.

The key recommendations from the guidelines specifically address how to balance caloric intake for weight management; reduce consumption of less healthy foods; increase overall intake of healthier foods and nutrients; and develop healthy eating patterns (Table 1). The guidelines emphasize that most personsâ&#x20AC;&#x2122; nutritional needs are best met solely by consuming foods, but that fortified foods and dietary supplements may be helpful in some cases.

Limit alcohol consumption to no more than one drink per day in women and two drinks per day in men

The guidelines cover additional dietary recommendations specific to certain population groups, including persons 50 years and older, and women who are pregnant or breastfeeding, or who are capable of becoming pregnant. For

Account for all foods and beverages consumed to assess overall healthy eating pattern goals

Balance caloric intake for weight management Control total caloric intake to manage body weight Increase physical activity and reduce time spent doing sedentary activities Maintain appropriate caloric balance during childhood, adolescence, adulthood, pregnancy and breastfeeding, and older age Prevent or reduce overweight and obesity by improving eating and physical activity behaviors Reduce intake of less healthy foods Get less than 10 percent of calories from saturated fatty acids; avoid consuming trans fatty acids

Limit consumption of foods with refined grains Reduce daily sodium intake to <2,300 mg; or < 1,500 mg in persons who are black, older than 50 years, or who have hypertension, diabetes mellitus, or chronic kidney disease Reduce intake of calories from solid fats and added sugars Increase intake of healthier foods and nutrients Choose a variety of protein foods; replace those higher in solid fats with proteins lower in solid fats Choose foods that provide more potassium, fiber, calcium, and vitamin D Consume at least one-half of grains as whole grains Increase intake of vegetables, fruits, and fat-free or low-fat dairy products; eat a variety of vegetables Increase the amount and variety of seafood in diet Use oils in place of solid fats, when possible Build healthy eating patterns

Follow food safety recommendations Make sure eating pattern meets appropriate nutrient and caloric needs

Source: Adapted from Am Fam Physician. 2011;84(3):333-334.

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practice guidelines older persons, recommendations involve consuming foods fortified with vitamin B12 (e.g., fortified cereals) or taking dietary supplements to ensure adequate vitamin levels. Women who are pregnant or breastfeeding are advised to consume 8 to 12 oz of seafood per week, but to limit consumption of white (albacore) tuna to 6 oz per week and to avoid consuming tilefish, shark, swordfish, and king mackerel. Pregnant women are advised to take an iron supplement. For women capable of becoming pregnant, the guidelines address iron intake by recommending that this population choose foods that

include heme iron, provide additional iron sources, and are high in nutrients that enhance iron absorption (e.g., vitamin C). These women also are advised to consume 400 mcg of synthetic folic acid per day.

Also included in the guidelines are basic food safety principles to help reduce the risk of foodborne illness, and a section about helping Americans make healthy choices to improve overall nutrition and physical activity in the United States. The updated guidelines also noted and took into consideration that almost 15 percent of households recently have been unable to obtain sufficient food to meet dietary needs.

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Medi Law

Should Doctors Prescribe Generic Medicines? mC Gupta

prescribe or supply drugs, remedies or appliances as long as there is no exploitation of the patient.

Drugs prescribed by a physician or brought from the market for a patient should explicitly state the proprietary formulae as well as generic name of the drug.”

What are your comments about the news that the health ministry plans to bring in a legislation to make it mandatory for doctors to prescribe generic medicines?

Ans. My comments are as follows: 





The news item, briefly, is as follows: “A bill is already being drafted to push low-cost medicine, along with an ambitious plan to provide free medicine to all. The out-of-pocket expense on healthcare is too high. Generic medicine will ensure that it is affordable. The bill will make sure that a list of generic medicines and combination drugs are available in all districts, and it is prescribed by doctors. The government has a list of nearly 350 medicines for which generic varieties will be made available. The out-of-pocket expenditure for healthcare is 78% of total expenditure on healthcare.

Generic medicine would reduce the burden on the common man.”





This is what happens when doctors fail to selfregulate themselves. Neither the MCI nor the IMA have ever done anything in this regard.

The MCI Regulations, 2002, clearly as follows: “Every physician should, as far as possible, prescribe drugs with generic names and he/she shall ensure that there is a rational prescription and use of drugs.”---Regulation 1.5 “Drugs prescribed by a physician or brought from the market for a patient should explicitly state the proprietary formulae as well as generic name of the drug.”—Regulation 6.3.

The two regulations are reproduced below: “1.5 Use of Generic names of drugs: Every physician should, as far as possible, prescribe drugs with generic names and he/she shall ensure that there is a rational prescription and use of drugs.”

“6.3 Running an open shop (Dispensing of Drugs and Appliances by Physicians): A physician should not run an open shop for sale of medicine for dispensing prescriptions prescribed by doctors other than himself or for sale of medical or surgical appliances. It is not unethical for a physician to

Advocate and Medicolegal Consultant

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

Asian Journal of Clinical Cardiology, Vol. 15, No. 6, October 2012



The MCI or the State Medical Councils have never punished till date a physician for violating the above regulations. I have complained against physicians quoting Regulation 1.5. Medical councils have always ignored such complaint. I do not know of any IMA initiative in encouraging or helping the doctors to follow these regulations.

When doctors do not follow a mild law, it is natural that tougher laws may be proposed even though the medical community is likely to protest that the government is trying to place restrictions upon their professional freedom.

It is an irony that even though India is one of the world’s largest exporters of generic drugs, its domestic market for generic drugs is small. It may be mentioned that India exports to over 200 countries, including the highly regulated markets of the US, Europe, Japan and Australia.

The reasons why domestic market for generic drugs is small in India are as follows:  There is no punishment for using brand names in place of generic names. Likewise, there is no reward for prescribing by generic names.  Prescribing by brand names is an effortless job.

Brand names are brief, catchy, though often misleading. They need not be remembered.

Sales agents drum them into the physicians’ ears constantly.  Prescribing by brand names carries rewards from the pharma companies in various forms.  It is easy to confuse a patient into thinking that a new and better medicine is being prescribed when, in fact, only the brand is changed.  Generic drugs are cheaper and hence their use is less beneficial for all concerned (the physician; the retailing chemist; the manufacturing pharma company, etc.), except for the patient who has to make the payment.  Even the government/politicians gain from

Medi Law brand drugs. Firstly, the DCGI stands to gain by having the power to grant permission for a brand name; Secondly, the government stands to gain by way of fees for granting permission; Thirdly, the political party in power stands to gain in donations from the pharma companies concerned. 



Generic drugs are cheaper than branded drugs. For example, common medicines like paracetamol costs ` 10 per strip of 10 tablets when branded, while the generic variety costs around ` 2.45 per strip. One of the reasons for lesser cost of generic drugs is that there are no R&D costs (Research and development costs). After the patent of the original company expires, any company can manufacture and sell the drug under a generic name. An example is ibuprofen.

The disadvantages of prescribing by brand names are as follows:  Brand drugs are more costly. For example, in October 2010, generic simvastatin (20 mg)

cost £1.12 for a pack of 28, compared with approximately £30 for a pack of 28 of the branded version. 





Brand drugs produced by shady companies are likely to be spurious or of low quality but yet some doctors are prone to prescribe them for ulterior motives.

Brand names can be similar and confusing.

It is not uncommon for the same generic drug to have 30, 40 or even 100 brand names from different companies. Confusion can lead to prescription errors (wrong drug being prescribed or supplied by the chemist or the dispenser). Prescription errors are a wellknown cause of risk to patient.

Brand drugs are often undesirable combinations of two or more generic drugs. It is a safer and better medical practice to minimize the use of combination drugs.

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lighter reading

Face Difficulties Positively

This parable is told of a farmer who owned an old mule. The mule fell into the farmer’s well.

The farmer heard the mule praying or whatever mules do when they fall into wells. After carefully assessing the situation, the farmer sympathized with the mule, but decided that neither the mule nor the well was worth the trouble of saving.

Instead, he called his neighbors together, told them what had happened, and enlisted them to help haul dirt to bury the old mule in the well and put him out of his misery.

Where there is determination there is success

QUOTE

An Inspirational Story

Lighter Side of Medicine

— BK Sapna

Initially the old mule was hysterical! But as the farmer and his neighbors continued shoveling and the dirt hit his back, a thought struck him. It suddenly dawned on him that every time a shovel load of dirt landed on his back, HE WOULD SHAKE IT OFF AND STEP UP!

It wasn’t long before the old mule, battered and exhausted, stepped triumphantly over the wall of that well! What seemed like it would bury him actually helped him… all because of the manner in which he handled his adversity.

That’s life! If we face our problems and respond to them positively, and refuse to give in to panic, bitterness, or self–pity… the adversities that come along to bury us usually have within them the potential to benefit and bless us!

Eye Laugh Cassie was taking two of her grandsons on their very first train ride, from Dayton, Ohio, to Washington, DC.

laugh a while

This he did, blow after blow. “Shake it off and step up…shake it off and step up…shake it off and step up!” He repeated to encourage himself. No matter how painful the blows, or how distressing the situation seemed, the old mule fought panic and just kept right on SHAKING IT OFF AND STEPPING UP!

Think of all that you wanted to achieve in the past few days. Now check if you have achieved it or are still trying for it. Check if you have left anything midway. Pick out one of the things that you wanted to achieve or create an aim for yourself and think, “I am the one who is victorious and I will achieve whatever I set out to. I will not leave any task unfinished.”

A vendor came down the corridor selling Pop Rocks, something neither had ever seen before.

Cassie bought each grandson a bag.

The first one eagerly tore open the bag and popped one into his mouth just as the train went into a tunnel. When the train emerged from the tunnel, he looked across to his brother and said: “I wouldn’t eat that if I were you.”

“Why not?” replied the curious brother “I took one bite and went blind for half a minute.”

Dr. Good and Dr. Bad Situation: A heart patient wanted to know if he could

meditate under a pyramid

226

Although aortic valve replacement is usually the treatment of choice for acute or chronic severe aortic regurgitation, aortic valve repair is sometimes possible in aortic regurgitation due to endocarditis and valve-sparing operations are a major consideration in patients with aortic dissection — Experts: Dr Ganesh K Mani, Dr Yugal Mishra, Dr Deepak Khurana, Dr Rajesh Kaushish, Dr K S Rathor, Dr Sandeep Singh and Dr KK Aggarwal).

Asian Journal of Clinical Cardiology, Vol. 15, No. 6, October 2012

You cannot do it

Go ahead

©IJCP Academy

Valvular Heart Disease Update

Aortic regurgitation in the elderly

Lesson: The effect of meditation under a pyramid as twice

as strong as meditating outside the pyramid.

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 -

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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.

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A subtitle can be added if necessary.

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- 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).

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

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

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

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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.

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- 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.

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

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

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._ _______________

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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 _____________________________

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

Dr KK Aggarwal

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