Journal of Clinical and Preventive Cardiology

: 2019  |  Volume : 8  |  Issue : 1  |  Page : 6--12

Clinical and angiographic profile of young patients with ischemic heart disease: A central India study

Sunita Dinkar Kumbhalkar1, Vikas V Bisne2,  
1 Ex-Associate Professor, Department of Cardiology, GMCH and SSH, Nagpur, Maharashtra, India
2 Senior Consultant Cardiologist, Bisne Heart Hospital, Nagpur, Maharashtra, India

Correspondence Address:
Sunita Dinkar Kumbhalkar
No. 86, Rajiv Nagar, Nagpur - 440 025, Maharashtra


Objective: The present study was undertaken in young patients of ischemic heart disease (IHD) to assess clinical, biochemical and angiographic profile, conventional and newer risk factors, and correlation of risk factors with significant and nonsignificant coronary artery disease (CAD). Materials and Methods: This was a hospital-based cross-sectional study conducted in 70 cases of young IHD (male ≤35 years and females ≤40 years). Patients were evaluated for clinical, biochemical and angiographic profiles, and conventional risk factors such as dyslipidemia, hypertension (HT), diabetes mellitus (DM), and family history of premature CAD (PCAD). Newer risk factors such as lipoprotein (a) (Lp [a]), homocysteine, and plasma fibrinogen were also assessed in some (n = 44) cases. Results: Mean age of patients was 32.97 ± 3.93 years; 11 (15.7%) were women. Various risk factors such as tobacco/gutka chewing, HT, smoking, DM, and family history of PCAD were observed in 35.7%, 22.8%, 17.1%, 11.5%, and 8.6% of patients, respectively. Nearly 77.6% of patients presented with anterior wall myocardial infarction and 61.4% were having moderate left ventricular dysfunction on echocardiography. Total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), triglycerides (TGs), and TC/high-density lipoprotein cholesterol (TC/HDL-C) were increased in 38.6%, 41.4%, 32.9%, and 25.7% patients, respectively. Newer risk factors such as Lp (a), homocysteine, and plasma fibrinogen were elevated in 61.4%, 77.3%, and 18.2% of patients, respectively. On coronary angiography, single-vessel disease was found in more than half of the patients (57.1%) followed by double-vessel disease (11.5%) and triple-vessel disease (7.1%). Coronary angiogram was normal in 24.3% of patients. Positive family history of PCAD, serum TGs, TC/HDL-C, and LDL-C/HDL-C were significantly (P < 0.05) associated with significant CAD as compared to nonsignificant CAD, whereas no such correlation was found in relation to newer risk factors. Conclusion: Indian males in South Asian population appear more prone to develop CAD; therefore, screening for risk factors should start at an earlier age. Smoking and tobacco chewing cessation, promotion of physical activities, and healthy dietary pattern have to be strongly encouraged in this vulnerable group.

How to cite this article:
Kumbhalkar SD, Bisne VV. Clinical and angiographic profile of young patients with ischemic heart disease: A central India study.J Clin Prev Cardiol 2019;8:6-12

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Kumbhalkar SD, Bisne VV. Clinical and angiographic profile of young patients with ischemic heart disease: A central India study. J Clin Prev Cardiol [serial online] 2019 [cited 2021 Jan 16 ];8:6-12
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Full Text


Coronary artery disease (CAD) is a major cause of morbidity and mortality worldwide. Earlier CAD was usually found in the older population; however, nowadays, it is often encountered by young adults. An estimated 4%–10% of individuals with documented CAD are seen to be <45 years of age.[1],[2] Numerous studies over the past 50 years, involving several generations, have consistently shown that the incidence and mortality rates for CAD are 50%–300% higher among overseas Indians compared with compatriots of other ethnicities in several countries.[3] The premature CAD (PCAD) is defined, in various studies, as having an age of onset ranging from 30 to 56 years. Asian Indians around the globe have the highest rates of PCAD, with clinical manifestations occurring about 10 years earlier than in other populations.[3],[4]

Several risk factors contribute to the increase in the prevalence of CAD in different age groups. The traditional risk factors such as hypertension (HT), diabetes mellitus (DM), high levels of triglycerides (TGs), high levels of low-density lipoprotein cholesterol (LDL-C) and low levels of high-density lipoprotein cholesterol (HDL-C), stressful, and sedentary lifestyle changes are suggested as additional risk factors for CAD.[5] Previous studies have shown that, in young individuals, smoking, HT, and dyslipidemia play an important role in the development of PCAD.[6],[7] Smoking can increase the risk of CAD by 3–5 times and a modest increase in central obesity increases the risk further.[7] Nearly 50% of young males had no risk factors and this should prompt one to evaluate for other nontraditional risk factors such as lipoprotein (a) (Lp [a]), homocysteine, and other prothrombotic conditions. There is a definite need to identify and correct the conventional risk factors for CAD at a younger age.

Since CAD is a multifactorial disease involving both genetic and environmental factors, multiprong approach for prevention is warranted since atherosclerosis has its origin in childhood, particularly in Indians; preventive strategy should begin in childhood though it is probably never too late so that younger population in their prime period of life can have better quality of life. Hence, this work was undertaken in 70 young patients of ischemic heart disease (IHD) to assess clinical, biochemical and angiographic profile, conventional and newer risk factors, and various risk factors were correlated with significant and nonsignificant CAD.

 Materials and Methods

A hospital-based cross-sectional study was done in 70 young patients (59 men and 11 women) in the Government Medical College and Superspeciality Hospital, Nagpur, in young male patients of age ≤35 years and females in premenopausal state ≤40 years of age with IHD diagnosed using criteria by European Society of Cardiology/American College of Cardiology (2000). Institutional Ethics Committee approval was obtained and written informed consent obtained from all the patients. Patient's refusal to give consent and patients in whom age could not be ascertained were excluded from the study.

All the patients were thoroughly examined clinically and relevant investigations such as electrocardiography (12 lead), two-dimensional echocardiography, and color Doppler with assessment of regional wall motion abnormality and left ventricular (LV) function (normal LV function: LV ejection fraction [LVEF] ≥50%, moderate LV dysfunction: LVEF 35%–49%, and severe LV dysfunction: LVEF <35%) were done in all patients. Waist circumference (in centimeter), fasting blood glucose level, and lipid profile (by photometric method) were done. Lp (a) (fully automated nephelometry), serum homocysteine (by photometry), and plasma fibrinogen (by clotting method) were estimated in only 44 participants due to financial constraints.

Coronary angiography (CAG) was performed by a femoral approach using modified Seldinger technique. Standardized angiographic projections were chosen for the assessment of each arterial segment. We used the coronary artery map from the Coronary Artery Surgery Study for vessel classification.[8] LV angiogram was not done to avoid the excess use of contrast material. We categorized the patients according to significant CAD (Group A – ≥70% stenosis) and nonsignificant CAD (Group B – <70% stenosis). We also categorized the patients according to lesion distribution as those having left main coronary artery (LMCA), proximal or mid-left anterior descending (LAD) coronary artery lesions, or having coronary artery lesions in other segments. The reason for choosing LMCA and proximal or mid-LAD segments for categorization was having highest severity coefficient of these lesions in Gensini CAD severity score.[9]

The case reports of all eligible patients were meticulously screened for collection of data such as age, sex, clinical presentation, and presence of conventional risk factors for CAD, namely HT, DM, dyslipidemia, smoking, tobacco/gutka chewing, family history of PCAD, and use of drugs such as oral contraceptive pills (OCPs). The coronary angiographic findings and the management strategy advised by single observer consultant cardiologist were recorded.

Statistical analysis

Continuous parameters (age and lipid profile) were presented as a mean ± standard deviation. Categorical variables were expressed in percentages. Age and lipid profile were compared between significant CAD group and nonsignificant CAD group and also compared between LAD and non-LAD lesions by applying unpaired “t” test. Categorical variables were compared with the help of Chi-square statistics. Median test was used to compare TGs, LDL, fibrinogen, homocysteine, and Lp (a) between significant CAD and nonsignificant CAD and also between LAD and non-LAD lesions. P < 0.05 was considered statistically significant. Data were analyzed on statistical software STATA version 10.0. (Stata Corp, Texas, U.S.A.)

 Observations and Results

A total of 70 participants (mean age 32.97 ± 3.93 years, range 21–40 years; 59 (84.3%) men [Figure 1] were included in this study. Majority (64.3%) of patients were in the age group of 31–35 years. The females were mostly in the age of 36–40 years (81.8%). Most of the patients (54.3%) were engaged in business and were not having a sedentary lifestyle.{Figure 1}

Major conventional risk factors were found to be tobacco/gutka chewing (35.7%), followed by HT (22.8%), smoking (17.1%), and DM (11.5%). Family history of PCAD was found in 8.6% of patients out of whom one male and one female were siblings [Figure 2]. CAD was observed in 15.7% of patients who were vegetarians. No female patient was taking OCP [Table 1].{Figure 2}{Table 1}

The common type of myocardial infarction (MI) was anterior wall MI (AWMI) (77.1%) followed by inferior wall MI (IWMI) (10%). Unstable angina and non-ST elevation MI (NSTEMI) were seen in 8.6% and 2.8% of patients, respectively [Table 2]. Treadmill test was positive in one patient. Females were having AWMI predominantly (81.8%). Majority of patients were having moderate LV dysfunction (61.4%) on echocardiography. Only 12.9% of patients were having metabolic syndrome.{Table 2}

[Table 3] shows the lipid profile of the patients. Total cholesterol (TC), LDL-C, TGs, and TC/high-density lipoprotein (TC/HDL-C) were increased in 38.6%, 41.4%, 32.9%, and 25.7% patients, respectively. HDL-C was low in 62.9% of patients. Newer risk factors such as LP (a), homocysteine, and plasma fibrinogens were elevated in 61.4%, 77.3%, and 18.2% of patients, respectively.{Table 3}

On CAG, single-vessel disease (SVD) was found in 57.1% of patients followed by double-vessel disease (DVD) (11.5%), and triple-vessel Disease (TVD) (7.1%). CAG was normal in 17 (24.3%) patients out of which 14 had AWMI followed by unstable angina and NSTEMI in 2 patients and 1 patient, respectively [Figure 3]. Almost 46.1% of patients with normal CAG were having a habit of tobacco chewing in the form of gutka. Thrombus and dissection on CAG were observed in 4.2% patients each.{Figure 3}

LAD was most common vessel involved in 82.5% of patients followed by right coronary artery (RCA) (12.5%) and left circumflex artery (LCX) (5%). Most of the females had LAD involvement as SVD. LMCA involvement was not seen in our study. In subgroup analysis, positive family history of PCAD, serum TGs, TC/HDL-C, and LDL-C/HDL-C was significantly (P < 0.05) associated with group of patients having significant CAD as compared to nonsignificant CAD [Table 4], whereas no such correlation was found in relation to newer risk factors such as Lp (a), homocysteine, and plasma fibrinogen [Table 5].{Table 4}{Table 5}

The positive history of PCAD, history of tobacco intake, and ratio of LDL-C/HDL-C were significantly (P < 0.05) associated with proximal or mid-LAD lesions as compared to non-LAD lesions [Table 6]. No significant correlation was found between LAD and non-LAD vessel involvement in relation to newer risk markers such as Lp (a), homocysteine, and plasma fibrinogen [Table 7].{Table 6}{Table 7}


Manifest CAD in a young person can have devastating consequences for the patient and the family.[10] Many studies include patients age <40 years while choosing young patients with CAD.[11],[12],[13] Patient subgroups <35 years are at times referred to as very young.[12] The CAD among Indians is usually more aggressive at the time of presentation compared with Caucasians or East Asians. Various factors that are thought to contribute to this rising epidemic include urbanization of rural areas, large-scale migration of rural population to urban areas, increase in sedentary lifestyle, abdominal obesity, metabolic syndrome, DM, inadequate consumption of fruits and vegetables, increased use of fried, processed and fast foods, tobacco abuse, poor awareness, and control of CAD risk factors, unique dyslipidemia (high TGs and low HDL-C levels), and possible genetic predisposition due to Lp (a) excess.[3] The incidence of CAD in younger age group has been rising in India, especially in the males.[14] The disease is associated with considerable morbidity, psychological changes, and financial burden for the individual and the family, especially when it affects the young individual. Male sex is more prone to CAD when compared to their premenopausal female counterparts. It was observed in the INTERHEART study that South Asian men encountering AMI were 5.6 years younger than women.[15]

There are no universal definition/criteria for young CAD. Further, there are no guidelines to describe the cutoff age. Various workers[16],[17],[18] studied young CAD patients in varied age groups and whose mean age was similar to our study participants. Gender differences in CAD risk are also important.[19] Middle-aged men have a 2–5 times higher risk than women. However, risk ratio differs between populations.[20] There was a clear male preponderance (84.3%) in our study, which was in agreement with previous studies, suggesting that CAD is predominantly a disease of men.[21],[22],[23] Female represented only 15.7% of our patients. This was a much higher frequency compared with data from India (5%).[24] In our study, 84.3% of patients were taking mixed diet and 15.7% were vegetarians. Majority (54.3%) were businessmen and physically active.

Abnormal lipids, smoking, HT, DM, abdominal obesity, psychosocial factors, consumption of fruits, vegetables, alcohol, and regular physical activity account for most of the risk of MI worldwide in both sexes and at all ages in all regions. Positive family history of PCAD was observed in 8.6%, of whom one male and one female were siblings. Gutka (containing tobacco) chewing was a major risk factor in young IHD patients (37.7%). Systemic HT was associated with IHD in 22.8% of patients; this was in closed agreement with Chandrakasu et al.[14] Smoking and DM were associated with IHD in 17.1% and 11.5% patients, respectively, whereas other workers have reported a higher percentage.[14],[25],[26] There was a decrease in HDL-C and increase in TC, LDL-C, TC/HDL-C ratio; this was correlated with previous studies.[16],[25] Hypertriglyceridemia was seen in 32.9% which was corresponding with Kasliwal et al.[26] Majority of patients suffered from acute MI predominantly AWMI (74.6%) followed by IWMI (10%). About 8.6% of patients had unstable angina. It was specifically noted that females were predominantly presented with AWMI (81.8%). Our findings were similar to findings of other workers.[14],[16],[18]

We found no significant difference in homocysteine level between significant and nonsignificant CAD groups as well as no difference observed in homocysteine level of females with or without CAD. Logistic regression analysis for evaluating independent CAD risk factor showed hyperhomocysteinemia as an independent risk factor for PCAD in male and study for the underlined causes of hyperhomocystneimia showed that male gender and Vitamin B12 deficiency had a significant influence on the incidence of hyperhomocystneimia (in patients <45 years of age).[27] Smoking and homocysteine were independent predictors of severe CAD in young patients according to logistic regression analysis with an odds ratio of 3.7 and 1.2, respectively. For predicting significant CAD, the cutoff value of homocysteine was 11.6 μmol/l with sensitivity and specificity of 53% and 77%, respectively.[28] The difference between Lp (a) in significant CAD and nonsignificant CAD was found to be nonsignificant; this was in closed agreement with Gambhir et al.[29] On multivariate analysis, Lp (a) along with low molecular weight isoform size and positive family history of PCAD classified the risk of CAD by 74%. In our study, the difference in fibrinogen level between significant CAD and nonsignificant CAD was found to be nonsignificant. Contrary to these results, Pineda et al.[30] found that young CAD patients had significantly higher Lp (a), TGs, fibrinogen, fibrin D-dimer, and von Willebrand factor (vWf) but lower HDL-C.

The present study showed SVD in 57.1% of the cases followed by DVD (11.5%) and TVD (7.1%). This finding was similar to previous studies.[16],[25] No patient had LMCA involvement in our study, while other studies[31],[32] showed a low prevalence of LMCA involvement. In patients with SVD, LAD was predominantly involved (82.5%) followed by RCA (12.5%) and LCX (5%). Our findings corroborate the results of different studies.[16],[25] There was a significant difference between significant CAD (≥70% stenosis) and nonsignificant CAD (<70% stenosis) groups when risk factors such as positive family history of PCAD, serum TGs, TC/HDL-C, and LDL-C/HDL-C were considered. No significant difference was found between significant CAD and nonsignificant CAD when other various conventional risk factors were compared.

In our study, newer risk factors such as Lp (a), homocysteine, and fibrinogen were not found to be associated with significant CAD. When comparison between proximal and mid-LAD lesions versus non-LAD lesion was done in relation to other various conventional risk factors, only positive family history of PCAD, tobacco intake, and LDL-C/HDL-C ratio were found to be significantly (P < 0.05) associated with LAD lesion. No significant correlation was found between LAD and non-LAD vessel involvement in relation to newer risk markers such as Lp (a), homocysteine, and fibrinogen may be due to small sample size.


Based on the observations from the present study, authors suggest screening of risk factors for CAD should start at an earlier age in Indian males and cessation of smoking and tobacco chewing, promotion of physical activities, and avoidance of high-fat diets have to be strongly encouraged to this vulnerable group. Parameters such as serum TGs, history of PCAD, and TC/HDL-C should be considered significant risk factors as they were associated with significant CAD. Optimal control of conventional risk factors such as DM, systemic HT, and dyslipidemia must be done. Newer risk factors such as hyperhomocysteinemia should be controlled by increased intake of fresh fruits and less cooking of food. All young patients presenting with MI with or without LV dysfunction should be screened by CAG as early as possible, and necessary interventions should be done so that they will lead a good quality of life in their prime age.


The authors would like to thank the Department of Cardiology and administration of Government Medical College and Superspeciality Hospital, Nagpur, Maharashtra, for permission to study and providing facility to carry out the work.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


1Egred M, Viswanathan G, Davis GK. Myocardial infarction in young adults. Postgrad Med J 2005;81:741-5.
2Mohammad AM, Jehangeer HI, Shaikhow SK. Prevalence and risk factors of premature coronary artery disease in patients undergoing coronary angiography in Kurdistan, Iraq. BMC Cardiovasc Disord 2015;15:155.
3Enas EA, Singh V, Munjal YP, Bhandari S, Yadave RD, Manchanda SC, et al. Reducing the burden of coronary artery disease in India: Challenges and opportunities. Indian Heart J 2008;60:161-75.
4Enas EA. How to Beat the Heart Disease Epidemic among South Asians: A Prevention and Management Guide for Asian Indians and their Doctors. Downers Grove: Advanced Heart Lipid Clinic USA; 2007.
5Gupta R. Epidemiological evolution and rise of coronary heart disease in India. South Asian J Prev Cardiol 1997;1:14-20.
6Janus ED, Postiglione A, Singh RB, Lewis B. The modernization of Asia. Implications for coronary heart disease. Council on arteriosclerosis of the International Society and Federation of Cardiology. Circulation 1996;94:2671-3.
7Noeman A, Ahmad N, Azhar M. Coronary artery disease in young: Faulty life style or heredofamilial or both. Annals 2007;13:162-4.
8Killip T, Fisher L, Mock M; the CASS Investigations. National heart, lung and blood institute coronary artery surgery study (CASS): A multicenter comparison of the effects of randomized medical and surgical treatment of mildly symptomatic patients with coronary artery disease and a registry of consecutive patients undergoing coronary angiography. Circulation 1981;63:Il-81.
9Gensini GG. A more meaningful scoring system for determining the severity of coronary heart disease. Am J Cardiol 1983;51:606.
10Christus T, Shukkur AM, Rashdan I, Koshy T, Alanbaei M, Zubaid M, et al. Coronary artery disease in patients aged 35 or less – A different beast? Heart Views 2011;12:7-11.
11Imazio M, Bobbio M, Bergerone S, Barlera S, Maggioni AP. Clinical and epidemiological characteristics of juvenile myocardial infarction in Italy: The GISSI experience. G Ital Cardiol 1998;28:505-12.
12Wolfe MW, Vacek JL. Myocardial infarction in the young. Angiographic features and risk factor analysis of patients with myocardial infarction at or before the age of 35 years. Chest 1988;94:926-30.
13Doughty M, Mehta R, Bruckman D, Das S, Karavite D, Tsai T, et al. Acute myocardial infarction in the young – The University of Michigan experience. Am Heart J 2002;143:56-62.
14Chandrakasu A, Jayachandran A, Meyyappan C, Narayan G, Nayar PG, Abdul Bari AB, et al. Clinical and angiographic profile of coronary artery disease among young South Indian males. Kerala Heart J 2016;6:1/25-24/25.
15Yusuf S, Hawken S, Ounpuu S, Dans T, Avezum A, Lanas F, et al. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): Case-control study. Lancet 2004;364:937-52.
16Thomas Titus JA, Sivasankaran S, Padmakumar R, Krishnamoorthy KM, Dora S, Nair KK. Symptomatic coronary artery disease in patients less than 30 years of age: Clinical-and-angiographic profile. Indian Heart Journal 2001-5/Sept-Oct 03 (Abstract).
17Dalal J, Hiremath MS, Das MK, Desai DM, Chopra VK, Biswas AD, et al. Vascular disease in young Indians (20-40 years): Role of ischemic heart disease. J Clin Diagn Res 2016;10:OE08-12.
18Sanjeeva Kumar E, Sai Satish O, Srinivas M, Patnaik AN, Dubey BK, Srinivas B, et al. Clinical, biochemical and angiographic profile in young patients with acute-coronary syndrome: NIMS experience. Indian Heart Journal Sept-Oct 2006 (Abstract).
19Boden WE, O'rourke RA, Teo KK, Hartigan PM, Maron DJ, Kostuk W, et al. The evolving pattern of symptomatic coronary artery disease in the United States and Canada: Baseline characteristics of the Clinical Outcomes Utilizing Revascularization and Aggressive DruG Evaluation (COURAGE) trial. Am J Cardiol 2007;99:208-12.
20Hafeez S, Javed A, Kayani AM. Clinical profile of patients presenting with acute ST elevation myocardial infarction. J Pak Med Assoc 2010;60:190-3.
21Jackson R, Chambless L, Higgins M. Sex differences in ischemic heart disease mortality and risk factors in 46 communities: An etiologic analysis. Cardiovasc Risk Factors 1997;7:43-54.
22McKeigue PM, Marmot MG, Adelstein AM, Hunt SP, Shipley MJ, Butler SM, et al. Diet and risk factors for coronary heart disease in Asians in Northwest London. Lancet 1985;2:1086-90.
23Shah I, Faheem M, Shahzeb M, Hafizullah M. Clinical profile, angiographic characteristics and treatment recommendations in patients with coronary artery disease. J Pak Med Stud 2013;3:94-100.
24Choudhury L, Marsh JD. Myocardial infarction in young patients. Am J Med 1999;107:254-61.
25Bhardwaj R, Marwah R, Vaidya P, Sharma A. Risk factors and pattern of coronary artery disease in young myocardial infarction. Indian Heart J 2007;58:394-5.
26Kasliwal RR, Kulshreshtha A, Agrawal S, Bansal M, Trehan N. Prevalence of cardiovascular risk factors in Indian patients undergoing coronary artery bypass surgery. J Assoc Physicians India 2006;54:371-5.
27Morillas P, Bertomeu V, Pabón P, Ancillo P, Bermejo J, Fernández C, et al. Characteristics and outcome of acute myocardial infarction in young patients. The PRIAMHO II study. Cardiology 2007;107:217-25.
28Köz C, Celebi H, Yokuşoǧlu M, Baysan O, Haşimi A, Serdaroǧlu M, et al. The relation between coronary lesion distribution and risk factors in young adults. Anadolu Kardiyol Derg 2009;9:91-5.
29Gambhir JK, Kaur H, Prabhu KM, Gambhir DS. Association between apolipoprotein (a) polymorphism, plasma lipoprotein (a) levels and family history of premature coronary artery disease in young Asian Indians. Indian Heart J 2006;58:394-410.
30Pineda J, Marín F, Marco P, Roldán V, Valencia J, Ruiz-Nodar JM, et al. Premature coronary artery disease in young (age <45) subjects: Interactions of lipid profile, thrombophilic and haemostatic markers. Int J Cardiol 2009;136:222-5.
31Mishra BK, Sawhney JP, Manchanda SC, Khanna PK, et al. Coronary artery disease in young women less than 50 years of age. Indian Heart J 2008;60:401.
32Chris J, Jai Shankar K, Jaiswal PK, Nayar PG, Thomas JM, Meenakshi NA, et al. Evaluation of risk factor profile in acute coronary artery syndrome in the young. Indian Heart J 2006;58:394-410.