Internal Medicine Section DOI : 10.7860/JCDR/2016/20206.8517
Year : 2016 | Month : Sep | Volume : 10 | Issue : 09 Page : OE08 - OE12

Vascular Disease in Young Indians (20-40 years): Role of Ischemic Heart Disease

Jamshed Dalal1, Murugesh Shantaveeraya Hiremath2, Mrinal Kanti Das3, Devangkumar M Desai4, Vijay Kumar Chopra5, Arup Das Biswas6

1 Director, Centre for Cardiac Sciences, Kokilaben Dhirubhai Ambani Hospital, Mumbai, Maharashtra, India.
2 Director, Cardiac Cath Lab, Ruby Hall Clinic, Pune, Maharashtra, India.
3 Consultant Cardiologist, Birla Heart Research Centre, Kolkata, West Bengal, India.
4 Technical Director, Department of Cardiology, B. D. Mehta Mahavir Heart Institute, Surat, Gujarat, India.
5 Director, Heart Failure Program, Medanta - The Medicity, Gurgaon, Haryana, India.
6 Ex-Professor and Head, Department of Cardiology, NRS Medical College, Kolkata, West Bengal, India.

NAME, ADDRESS, E-MAIL ID OF THE CORRESPONDING AUTHOR: Dr. Jamshed Dalal, Centre for Cardiac Sciences, Kokilaben Dhirubhai Ambani Hospital, Rao Saheb Achutrao Patwardhan Marg, Four Bunglows, Andheri West, Mumbai- 400053, Maharashtra, India.

Coronary Artery Disease (CAD) occurs at a younger age in Indians with over 50% of Cardiovascular Disease (CVD) mortality occurring in individuals aged less than 50 years. Although several risk factors have been suggested; smoking, dyslipidemia and hypertension are major risk factors in the young. In this review, we have pooled the current evidence on Ischemic Heart Disease (IHD) in young (20-40 years) and provided an opinion for the effective management of IHD in young Indians.


Coronary Artery Disease (CAD) occurs at a younger age in Indians [14], with over 50% of CAD mortality occurring in individuals aged less than 50 years, and one-fourth of all acute Myocardial Infarctions (MIs) are reported in patients below 40 years [3]. Projection suggests that by 2015, 62 million Indians will have CAD of which 23 million are expected to be below 40 years [5].

Differing pattern of dyslipidemia combined in inherent insulin resistance and contribution from varying lifestyle makes Indians more vulnerable to CAD at a younger age [4]. Although several risk factors have been suggested; smoking and other forms of tobacco, dyslipidemia and hypertension are major risk factors in the young [6,7]. Clinical presentation of CAD in young Indians may vary from multiple vessel disease without any clues offered from risk factors to extensive ischemia in an asymptomatic individual [8]. Occurrence of CAD in absence of any conventional risk factors at a young age makes it difficult to understand the aetiopathogenesis [911]. A dilemma may exist among clinicians as to adopting specific management strategies in young CAD patient. Appropriate selection of medical and/or interventional strategies to improve morbidity and mortality outcome may be difficult; however, effective risk stratification is necessary to improve outcomes [1214].

In pursuit of such enormous premature CVD burden, we pool current evidence on IHD in young (20-40 years) and provide an opinion for the effective management of IHD in young Indians.

Epidemiology in India

Increasing rates of CAD in India in last three decades sends an alarm to look for the factors responsible for its increasing prevalence. In Asian Indians, risk of CAD is 3-4 times higher than Americans, 6 times higher than Chinese and 20 times higher than Japanese [1517]. In the Framingham Heart Study, the incidence of an MI over a 10-year follow-up was 12.9/1000 in men 30 to 34-year-old and 5.2/1000 in women 35 to 44-year-old [18]. In a multinational study, Awad et al.,, observed prevalence of 23% in young adults (<55 years) how were hospitalized for Acute Coronary Syndrome (CAD) [19]. Prevalence data among young Indians is limited. In young patients increasing rates of CAD prevalence in adults have been reported previously [20]. Investigations in 1990s reported CAD prevalence of around 12-16% in the Youth/Young-population [21]. Prevalence of acute MI as high as 25 to 40% has also been reported in the young [22]. Analysis of INTERHEART data in South Asians revealed acute MI prevalence of 11.7% (n=55/470) in India in patients aged below 40 years [23]. In 25 748 ACS patients from Kerala state; Mohanan et al., observed ACS prevalence of 22.2%, 57.2% and 20.6% in age group of < 50 years, 51 to 70 years and > 70 years respectively. Further they found similar prevalence of three ACS types (22.4% for ST-elevation myocardial infarction {STEMI}, 22.2% for Non-St Elevation MI {NSTEMI} and 22.0% for Unstable Angina {UA}) in patients below 50 years [24]. We need a detailed, large pan India prospective study to estimate the prevalence of CAD in young Indians, both male and female.

Gender Differences

In general population, prevalence of CAD especially MI is more common in males than in females. In a small observational study in young Indians, Aggarwal et al., found CAD prevalence of 94.94% (n=75/79) and 86.75% (n=72/83) in periods 2001-2002 and 2009-2010 respectively [25]. Other reports also suggest a higher CAD prevalence in young Indian males than females [26]. Bhardwaj et al., also reported acute MI almost exclusively in young males (n=123/124) [6].


Risk factors for CAD: Smoking, Apolipoprotein B/Apolipoprotein A1 (ApoB/ApoA1 ratio), hypertension, diabetes, abdominal obesity, psychological factors, poor daily consumption of fruits and vegetables, regular alcohol consumption, and absence of regular physical activity are risk factors for CAD validated by INTERHEART study and these account for 90% population attributable risk [27]. Presence of these factors in the young also predisposes them to CAD. Kerala ACS registry reported hypertension (48.4%), diabetes (37.6%), and smoking (34.4%) in patients who had ACS [24]. Many investigators reported similar risk factor profile even in the young as observed by INTERHEART study [9,26]. Ghosh et al., compared the risk factors amongst different groups. They observed increasing prevalence of risk factors with increasing age signifying prevention of risk factors in early age to prevent future complications [28].

Though difficult to quantify, stress, adverse childhood experiences and psychological behavior also play an important role in the development of CAD. Essentially, INTERHEART study found odd ratio of 2.67 for psychological factors in the causation of CAD in the general population, with population attributable risk as high as 32.5% [27].


Pathophysiologically, young CAD can be classified in to four major mechanisms namely atheromatous, non-atheromatous, hypercoagulable states and associated with substance misuse [12].

Atheromatous CAD is common in young and previous investigations provide agreement for this mechanism [2931]. Close look at risk factors in young also validate atheromatous CAD aetiology. A high degree cigarette smoking was found in young atheromatous CAD [3234]. Characteristic dyslipidemia with high prevalence low High-Density Lipoprotein Cholesterol (HDL-C) and high triglycerides can also promote atherosclerotic CAD [35].

Apart from conventional risk factors, other factors like increased levels of Lipoprotein-a (LP-a), hyperhomocysteinemia, have also been investigated [36,37]. A prospective study in north-Indian adult population identified significantly higher levels of LP-a in patients with ACS than controls [38]. In patients below 40 years, Gambhir et al., reported LP-a as independent risk factor for CAD. In their small sample evaluation of young CAD (n=50) compared to age matched controls (n=50), significantly higher levels of Lp-a (35.0±32.4mg/dL vs. 20.3±17.0mg/dL, p<0.002, respectively) were found [39]. Hyperhomocysteinemia is associated with vascular diseases including CAD [37]. Significant association of increased homocysteine levels with CAD in the young (<45 or <55 years) has been reported in many studies including investigations from India [4043].

Non-atheromatous CAD is may be majorly associated with congenital anomalies of coronary arteries that manifest in young age [44]. Myocardial bridging causing direct coronary compression or augmentation of existing coronary atherosclerotic lesion may also affect young and present with ischemia [45,46]. Spontaneous coronary dissection can also manifest as ACS in young. In young females (31-50 years) with ACS (n=77) who underwent coronary angiography, Saw et al., reported different aetiologies like Spontaneous Coronary Artery Dissection (SCAD), coronary fibro-muscular dysplasia, coronary vasculitis and coronary ectasia [47]. Paradoxical coronary embolism can also be a cause of ischemic disease in non-atheromatous coronaries [48]. Coronary artery aneurysm, MI resulting from septic vegetations from infected aortic valve also has been reported [12]. In our view, non-atheromatous CAD is not an uncommon entity and clinician should have high index suspicion in young individuals for this aetiology.

Evidence related to hypercoagulable states like antiphospholipid syndrome, nephrotic syndrome, factor V Leiden mutation, etc., suggests possibility of ACS or MI in young [12]. Acute MI can be the presentation of antiphospholipid syndrome associated with disease like systemic lupus erythematosus [49]. Long term use of contraceptive pills poses risk of MI [50,51]. Compared to noncurrent Oral Contraceptive (OC) pill users, Peragallo et al., in a meta-analysis observed significantly increased risk of venous thromboembolism (odds ration {OR} 2.97) and ischemic stroke (OR 1.90) but not that of MI (OR 1.34) or hemorrhagic stroke (OR 1.03) in patients with current use of OC pills [52]. This aetio-pathogenic mechanism should be explored in unexplained young CAD cases.

Being young at age, this population is often involved in illicit drug abuse. Cocaine use association with MI has previously been reported. Increased sympathetic activity, coronary arterial spasm and increased coagulability are proposed mechanism for MI [5355]. Enquiry into recreational drugs use should be done in all young ACS cases.

Issues in females

Epidemiological data suggests that CAD is relatively infrequent in women. High mortality in CAD is attributed to failure to recognize ACS in young women. Hormonal protection possibly prolongs development of atherosclerosis in women. Impaired coronary microcirculation, coronary spasm, coronary dissection and endothelial rupture culminating in to thrombosis are more frequent in women [56]. Apart from classical risk factors, psychosocial factors are especially important in Indian women. Literature suggests that young women have worse outcomes when compared to men and may have more iatrogenic complications [56,57].


All individuals should be investigated for risk factor profile including diabetic profile [fasting and postprandial blood glucose, glycosylated hemoglobin (HbA1c)], lipid profile (LDL-C, HDL-C, total cholesterol, triglyceride levels, non-HDL-C cholesterol, serum lipoprotein-a), and serum homocysteine. Some of the investigations are to be performed in selected cases based on clinical suspicion including protein C, protein S, antiphospholipid antibodies, and urine screen for cocaine.

For definitive diagnosis of CAD, investigations like Electro-cardiogram (ECG), cardiac troponin and coronary angiography are must. Specialized investigations are necessary in selected individual cases.

Electrocardiogram (ECG)

Immediate assessment of patient with suspected ACS should be done with a 12-lead ECG. Based on changes in ST-segment and T wave, clinical diagnosis of ACS can be differentiated. In case of no changes on ECG and physician has strong suspicion of ACS, repeat ECG can be taken after an interval. It is to be remembered that a normal ECG doesn’t rule out ACS or changes in ST-T segment do not always suggest MI [5860].

Cardiac troponin

Undoubtedly cardiac specific troponin and High-Sensitivity Troponin are diagnostic biomarkers for acute MI [59].

Exercise stress test

A suspected CAD can be ascertained with exercise stress test. After multivariate analysis, Uthamalingam et al., observed that stress induced ST-segment elevation in lead aVR was strongest predictor of left main coronary artery or ostial left anterior descending artery stenosis [61].

Echocardiography (ECHO)

Wall motion abnormalities diagnosed on transthoracic ECHO may suggest possible IHD. Some investigations using stress ECHO with exercise or pharmacotherapy suggest a greater sensitivity and specificity. It can be used as a screening test to select individuals [62].

Coronary angiography

Angiographic visualization of coronaries provides essentials of coronaries in order to optimize the treatment strategy. It is also a tool to distinguish between the atheromatous and non-atheromatous coronary involvement in young [63]. Uddin et al., compared angiographic profile of young (< 40 years, n=50) to the older population. The important observations for young were more family history of premature CAD, normal coronaries or single vessel disease, less extensive coronary atherosclerosis and lesser number of inoperable vessels [64]. In another study of young adults (<40 years, n=239), investigators observed angiographically normal coronaries in 16.9% and 37.2% of STEMI and CAD patients respectively [65]. In case of suspected acute MI without ST elevation, coronary angiography is advised for persistent or recurrent ischemia with or without ECG changes and also in presence of shock, severe pulmonary congestion or continuing hypotension [66]. Coronary angiography provides key details of coronary vasculature and helps differentiate atheromatous and non-atheromatous and can provides prognosis of CAD based on disease involvement.

Coronary Computed Tomography (CT) Angiography (CTA)

In selected individuals CTA can be helpful in determining the aetiology of CAD and delineating the coronary atherosclerosis. Kim et al., interestingly observed that individuals classified as low-risk (n=2133) by NCEP guidelines actually had atherosclerotic plaques (11.4%), significant stenosis (1.3%) significant stenosis due to non-calcified plaques (0.8%), on assessment by cardiac CTA. Excepting one patient, all patients who had non-calcific stenosis were young. This suggests prognostic role of CTA in otherwise low risk patients [67]. In a prospective study of young (<45 years, n=1635), Otaki et al., observed a stronger correlation between number of risk factors, and extent and severity of CAD. After adjustments for sex and risk factors, they reported family history of CAD being the strongest predictor of obstructive CAD (≥50% stenosis) (OR = 2.71) [68]. In selected individuals CTA is must where suspicion of either congenital anomalies of coronaries or spontaneous coronary dissection is high and patient has CAD. Retrospective evaluation by Ma et al revealed 13.6% patients having one or more myocardial bridge and mural coronary artery by 256-slice CTA. LAD was commonly involved (60.41%) and over one-third of mural coronaries had more than 50% stenosis in systole phase [69].



Optimal medical management of young CAD is essential to reduce recurrent CAD and mortality.

A large observational study in young individuals with ACS found significant reduction in atrial fibrillation, stroke, and major bleeding episode over the study period (1999-2007). Also, in-hospital mortality and 30-day adjusted mortality reduced by more than 30% in this population. Investigators attribute it to the aggressive management [19]. This medical management of CAD starts with risk factor reduction, lifestyle therapy incorporating dietary and exercise measures remains central to management of young IHD [70,71]. Control of blood pressure, lipids and sugars with recommended treatments should be aggressively followed. High-intensity statin treatment should be instituted. Treating non-conventional risk factors should be taken in to consideration based on overall CV risk. LP-a was found to be associated with increased residual risk in the AIM-HIGH Trial (Atherothrombosis Intervention in Metabolic Syndrome with Low HDL/High Triglyceride and Impact on Global Health Outcomes Trial). But simvastatin in combination with extended-release niacin could not improve CV outcomes regardless of significant reduction in LP-a at 1 year [72]. Decision in such cases should be on clinical judgment and patient preferences. Drug therapy prescribed to young remains the same as is recommended in guidelines [58,59].


Cole et al., in a fifteen years follow-up of young individuals with angiographically documented CAD identified single, double and triple vessel disease in 60.6%, 24.5%, 12.8% of women (n=94) and 55.8%, 27.2%, 14.8% of men respectively [73]. Depending on pathogenesis of CAD, interventional modality is directed in an individual.

Atherosclerotic obstructive CAD

Major therapeutic options for obstructive CAD in young include cardiac catheterization, Percutaneous Coronary Intervention (PCI) or Coronary Artery Bypass Grafting (CABG). Awad et al., reported data of young adults with CAD and use of hospital therapies for management at three different time-periods of hospitalization. They observed declining trend in use of thrombolysis and CABG whereas increasing use of PCI (P for trend < 0.05) [19]. This is possibly also true for Indian setting. A limited accessibility to PCI facility in India is a major challenge for timely intervention with PCI. Thrombolysis following STEMI, remains a major modality of intervention in India. Vaidya et al., studied young adults with STEMI and identified that 78.7% were thrombolysed in a government hospital set up whereas 38.7% were referred to higher centre for further intervention [74]. In a small study comparing tenecteplase (n=14) and streptokinase (n=10), Dhoot et al., observed higher rate of recanalization with tenecteplase (86%) compared to streptokinase (50%) [75], and though more expensive, should be the agent of choice.

PCI should be the choice for young patients where feasible. Ergelen et al., observed favorable short term and intermediate outcome in young (<45 years, n=465) than old (n=1959). Also, PCI was safe, more feasible and an effective modality for young than old [76]. Similarly Chua et al., observed better outcomes in younger patients without significant differences in repeated PCI or reinfarction compared to older adults [77]. With use of drug eluting stents with PCI, and use of better antiplatelet agents, we expect higher success rates with better long-term outcomes. However, long-term prospective studies are warranted to establish this hypothesis.

CABG is an option for more severe involvement of coronaries especially for complex triple vessel disease or with impaired left ventricular dysfunction specially when associated with diabetes. Christus et al., observed that CABG was needed in 13.5% of young adults below 35 years of Asian ethnicity. Most patients were managed medically (54.5%) and PCI with stenting was performed in 32% of patients [78]. CABG also has better success rate with preference of arterial than venous grafts [79].

Lone Aspiration Thrombectomy (LAT) is also another intervention in young adults with STEMI. Jamil et al., reported outcome of 10 patients who underwent LAT without stenting for STEMI. Nine patients at one month had no major CV events. Also, five patients at 2 months and three patients at 2 years had no major adverse consequences [13]. It can be alternative option in select individuals. The reason for this is that often in the young the underlying lesion is non-significant, with plaque rupture and thrombotic occlusion being the main reason for the STEMI. However, long-term, large scale, comparator studies are warranted.

The Coronary aRterydiseAse in young adults (CRAGS) study in adults below 50 years who underwent PCI suggests that disease progressed in 13.5% of the patients who required repeat revascularization. Hypertension, diabetes and multivessel disease were independent predictors of disease progression. Investigators identified need for effective use of currently available therapies for secondary prevention in young adults [80].

Non-obstructive CAD

It is more common in young adults than the elderly, and has lower 30-day and six months mortality as well as lower MI rates as compared to obstructive CAD [81]. Revascularization in such case should be decided on individual basis. Patients who have high-ischemic risk as identified by risk factor investigations, revascularization may be offered. Antiplatelet agents may be advised to reduce future coronary events. Patients who are not amenable to revascularization tend to have higher mortality and outcome may vary depending on various factors including age [82]. Optimal medical management of such individuals should be done. Regular follow-up for disease progression are mandated.

CAD associated with other causes

Aetio-pathophysiological causes like hypercoagulable states, illicit drug use, etc. need to be looked into while evaluating CAD in young. Undiagnosed familial hypercholesterolemia may sometimes present as acute MI. Clues from detail patient’s family history and clinical examination should be evaluated to make an early diagnosis and to reduce morbidity and mortality in young CAD.


Indians have higher risk of CAD at young age compared to other populations.

Risk factor profile remains similar to those of old adults such as dyslipidemia, tobacco, diabetes, and hypertension but conditions like hyperhomocysteinemia, hypercoagulable states, and cocaine use, etc. are specific to younger population and should be evaluated in CAD cases.

CAD in the young is increasing in prevalence in India due to changing lifestyle.

Family history of premature CAD is one of the strongest risk factor in young individuals.

Obstructive as well as non-obstructive pathologies prevail in young individuals.

Search for causes like coronary dissection, myocardial bridging, coronary anomalies, aorto-arteritis etc., is necessary in cases where causes remain unidentified.

Investigations like exercise stress testing, stress echocardiography, coronary angiography can help identify young individuals at higher risk of CAD.

Risk factor prevention is essential to prevent CAD in young.

Optimal medical management can be helpful in non-obstructive CAD.

For obstructive CAD, PCI with stenting should be preferred if available and affordable.

Thrombolysis still remains one of the major therapeutic approaches even for the young CAD due to ease of availability. Preference to newer fibrinolytics like reteplase, or tenecteplase should be given if available and affordable.

For complex coronary lesions, multivessel disease or with LV dysfunction, especially when associated with diabetes CABG can be a method of choice. Preference to total arterial grafting should be given.

Lone aspiration thrombectomy is another approach, when underlying lesion is insignificant and occlusion is predominantly due to a large thrombus. In absence of strong clinical evidence, it should be reserved for selected patients where it would be safe to leave them unstented.

Optimal secondary prevention medications and strict adherence to life style changes should be ensured to reduce future coronary events.


[1]Enas EA, Yusuf S, Mehta JL, Prevalence of coronary artery disease in Asian Indians Am J Cardiol 1992 70(9):945-49.  [Google Scholar]

[2]Jha P, Enas E, Yusuf S, Coronary artery disease in Asian Indians: Prevalence and risk factors Asian Am Pac Isl J Health 1993 1(2):163-75.  [Google Scholar]

[3]Sharma R, Bhairappa S, Prasad SR, Manjunath CN, Clinical characteristics, angiographic profile and in hospital mortality in acute coronary syndrome patients in south Indian population Heart India 2014 2:65-69.  [Google Scholar]

[4]McKeigue PM, Miller GJ, Marmot MG, Coronary heart disease in south Asians overseas: a review J Clin Epidemiol 1989 42(7):597-609.  [Google Scholar]

[5]Indrayan A, Forecasting vascular disease cases and associated mortality in India Reports of the National Commission on Macroeconomics and Health, Ministry of Health and Family Welfare, India 2005   [Google Scholar]

[6]Bhardwaj R, Kandoria A, Sharma R, Myocardial infarction in young adults-risk factors and pattern of coronary artery involvement Niger Med J 2014 55(1)44-47doi: 10.4103/0300-1652.128161  [Google Scholar]

[7]Sharma M, Ganguly NK, Premature coronary artery disease in Indians and its associated risk factors Vascular Health and Risk Management 2005 1(3):217-25.  [Google Scholar]

[8]Dwivedi S, Dwivedi G, Chaturvedi A, Sharma S, Coronary artery disease in the young: heredofamilial or faulty life style or both Journal Indian Academy of Clinical Medicine 2000 1(3):222-29.  [Google Scholar]

[9]Gupta R, Gupta VP, Meta-analysis of coronary heart disease prevalence in India Indian Heart J 1996 48(3):241-45.  [Google Scholar]

[10]Krishnaswami S, Prasad NK, Jose VJ, A study of lipid levels in Indian patients with coronary arterial disease Int J Cardiol 1989 24(3):337-45.  [Google Scholar]

[11]Bhatnagar D, The metabolic basis of increased coronary risk attributed to people from the Indian sub-continent Curr Sci 1998 74:1087-94.  [Google Scholar]

[12]Egred M, Viswanathan G, Davis GK, Myocardial infarction in young adults Postgrad Med J 2005 81(962):741-45.  [Google Scholar]

[13]Jamil G, Jamil M, Abbas A, Sainudheen S, Mokahal S, Qureshi A, "Lone aspiration thrombectomy" without stenting in young patients with ST elevation myocardial infarction Am J Cardiovasc Dis 2013 3(2):71-8.Print 2013  [Google Scholar]

[14]Biancari F, Gudbjartsson T, Heikkinen J, Anttila V, Mäkikallio T, Jeppsson A, Comparison of 30-day and 5-year outcomes of percutaneous coronary intervention versus coronary artery bypass grafting in patients aged≤50 years (the coronary artery disease in young adults Study) Am J Cardiol 2014 114(2):198-205.  [Google Scholar]

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

[16]Enas EA, Yusuf S, Third meeting of the international working group on coronary artery disease in south asians. 29 March 1998, Atlanta, USA Indian Heart J 1999 51(1):99-103.  [Google Scholar]

[17]Ghaffar A, Reddy KS, Singhi M, Burden of non-communicable diseases in South Asia BMJ 2004 328:807-10.  [Google Scholar]

[18]Kannel WB, Abbott RD, Incidence and prognosis of unrecognized myocardial infarction. An update on the Framingham study N Engl J Med 1984 311(18):1144-47.  [Google Scholar]

[19]Awad HH, McManus DD, Anderson FA, Gore JM, Goldberg RJ, Young patients hospitalized with an acute coronary syndrome Coron Artery Dis 2013 24(1):54-60.  [Google Scholar]

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

[21]Hasan A, Agarwal A, Parvez A, Mohammed AS, Premature coronary artery disease and risk factors in India Indian Journal of Cardiology 2013 16(1-2):5-11.  [Google Scholar]

[22]Mammi MVI, Pavithran P, Rahman PA, Acute MI in North Kerala. A 20-year hospital based study Indian Heart J 1991 43:93-96.  [Google Scholar]

[23]Joshi P, Islam S, Pais P, Reddy S, Dorairaj P, Kazmi K, Risk factors for early myocardial infarction in South Asians compared with individuals in other countries JAMA 2007 297(3):286-94.  [Google Scholar]

[24]Mohanan PP, Mathew R, Harikrishnan S, Krishnan MN, Zachariah G, Joseph J, Kerala ACS Registry Investigators. Presentation, management, and outcomes of 25 748 acute coronary syndrome admissions in Kerala, India: results from the Kerala ACS Registry Eur Heart J 2013 34(2):121-29.  [Google Scholar]

[25]Aggarwal A, Aggarwal S, Sharma V, Cardiovascular risk factors in young patients of coronary artery disease: Differences over a decade J Cardiovasc Thorac Res 2014 6(3):169-73.  [Google Scholar]

[26]Aggarwal A, Aggarwal S, Goel A, Sharma V, Dwivedi S, A retrospective case-control study of modifiable risk factors and cutaneous markers in Indian patients with young coronary artery disease JRSM Cardiovasc Dis 2012 1(3)  [Google Scholar]

[27]Yusuf S, Hawken S, Ounpuu S, Dans T, Avezum A, Lanas F, INTERHEART Study Investigators. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study Lancet 2004 364(9438):937-52.  [Google Scholar]

[28]Ghosh A, Bhagat M, Das M, Bala SK, Goswami R, Pal S, Prevalence of cardiovascular disease risk factors in people of Asian Indian origin: Age and sex variation J Cardiovasc Dis Res 2010 1(2):81-5.  [Google Scholar]

[29]McGill HC Jr, McMahan CA, Zieske AW, Tracy RE, Malcom GT, Herderick EE, Association of coronary heart disease risk factors with microscopic qualities of coronary atherosclerosis in youth Circulation 2000 102:374  [Google Scholar]

[30]Milonig G, Malcolm GT, Wick G, Early inflammatory and immunological lesions in juvenile atherosclerosis from the pathological determinants of atherosclerosis in youth (PDAY) study Atherosclerosis 2002 160:444-48.  [Google Scholar]

[31]Berenson GS, Srinivasan SR, Bao W, Newman WP, Tracy RE, Wattigney WA, Association between multiple cardiovascular risk factors and atherosclerosis in children and young adults: the Bogalusa heart study N Engl J Med 1998 338:1650-56.  [Google Scholar]

[32]Zimmerman FH, Cameron A, Fisher LD, Myocardial infarction in young adults: Angiographic characteristics, risk factors and prognosis, coronary artery surgery study register (CASS) J Am Coll Cardiol 1995 26:654  [Google Scholar]

[33]Aggarwal A, Aggarwal S, Sharma V, Metabolic syndrome and coronary artery disease in indians younger than 40 years J Endocrinol Metab 2012 2(1):39-45.  [Google Scholar]

[34]Dwivedi S, Dwivedi G, Chaturvedi A, Sharma S, Coronary artery disease in the young: here do familial or faulty life style or both Journal Indian Academy of Clinical Medicine 2000 1(3):222-29.  [Google Scholar]

[35]Joshi SR, Anjana RM, Deepa M, Pradeepa R, Bhansali A, Dhandania for the ICMR– INDIAB Collaborative Study Group. Prevalence of Dyslipidemia in Urban and Rural India: The ICMR–INDIAB Study PLoS ONE 2014 9(5):e96808  [Google Scholar]

[36]Rajasekhar D, Saibaba KS, Srinivasa Rao PV, Latheef SA, Subramanyam G, Lipoprotein (A): Better assessor of coronary heart disease risk in south Indian population Indian J ClinBiochem 2004 19(2):53-9.  [Google Scholar]

[37]Clarke R, Daly L, Robinson K, Naughten E, Cahalane S, Fowler B, Hyperhomocysteinemia: an independent risk factor for vascular disease N Engl J Med 1991 324(17):1149-55.PubMed PMID: 2011158  [Google Scholar]

[38]Yusuf J, Yadav N, Mukhopadhyay S, Goyal A, Mehta V, Trehan V, Relook at lipoprotein (A): independent risk factor of coronary artery disease in north Indian population Indian Heart J 2014 66(3):272-79.  [Google Scholar]

[39]Gambhir JK, Kaur H, Gambhir DS, Prabhu KM, Lipoprotein(a) as an independent risk factor for coronary artery disease in patients below 40 years of age Indian Heart J 2000 52(4):411-15.  [Google Scholar]

[40]Sadeghian S, Fallahi F, Salarifar M, Davoodi G, Mahmoodian M, Fallah N, Tehran Heart Center. Homocysteine, vitamin B12 and folate levels in premature coronary artery disease BMC Cardiovasc Disord 2006 6:38  [Google Scholar]

[41]Wu Y, Huang Y, Hu Y, Zhong J, He Z, Li W, Hyperhomocysteinemia is an independent risk factor in young patients with coronary artery disease in southern China Herz 2013 38(7):779-84.  [Google Scholar]

[42]Gupta SK, Kotwal J, Kotwal A, Dhall A, Garg S, Role of homocysteine & MTHFR C677T gene polymorphism as risk factors for coronary artery disease in young Indians Indian J Med Res 2012 135(4):506-12.Erratum in: Indian J Med Res. 2013;138(4)574  [Google Scholar]

[43]Panwar RB, Gupta R, Gupta BK, Raja S, Vaishnav J, Khatri M, Atherothrombotic risk factors & premature coronary heart disease in India: a case-control study Indian J Med Res 2011 134:26-32.  [Google Scholar]

[44]Zeina AR, Peres D, Barmeir E, Single coronary artery as cause of non-atheromatous angina pectoris: multidetector computed tomography assessment Isr Med Assoc J 2007 9(8):624-25.  [Google Scholar]

[45]Ishikawa Y, Kawawa Y, Kohda E, Shimada K, Ishii T, Significance of the anatomical properties of a myocardial bridge in coronary heart disease Circ J 2011 75(7):1559-66.Epub 2011 Mar 31  [Google Scholar]

[46]Stables RH, Knight CJ, McNeill JG, Sigwart U, Coronary stenting in the management of myocardial ischaemia caused by muscle bridging Br Heart J 1995 74(1):90-2.  [Google Scholar]

[47]Saw J, Aymong E, Mancini GB, Sedlak T, Starovoytov A, Ricci D, Nonatherosclerotic coronary artery disease in young women Can J Cardiol 2014 30(7):814-19.  [Google Scholar]

[48]Ménager C, Bui HT, Rubin S, Nazeyrollas P, Metz D, Coronary embolism due to an adherent right atrium thrombus through a patent foramen ovale Ann Cardiol Angeiol (Paris) 2013 62(6):438-41.  [Google Scholar]

[49]Jouhikainen T, Pohjola-Sintonen S, Stephansson E, Lupus anticoagulant and cardiac manifestations in systemic lupus erythematosus Lupus 1994 3(3):167-72.  [Google Scholar]

[50]Dragoman M, Curtis KM, Gaffield ME, Combined hormonal contraceptive use among women with known dyslipidemias: a systematic review of critical safety outcomes Contraception 2016 94(3):280-87.  [Google Scholar]

[51]Lalude OO, Risk of cardiovascular events with hormonal contraception: insights from the Danish cohort study Curr Cardiol Rep 2013 15(7):374  [Google Scholar]

[52]Peragallo Urrutia R, Coeytaux RR, McBroom AJ, Gierisch JM, Havrilesky LJ, Moorman PG, Risk of acute thromboembolic events with oral contraceptive use: a systematic review and meta-analysis Obstet Gynecol 2013 122(2Pt1):380-89.  [Google Scholar]

[53]Hollander JE, Todd KH, Green G, Heilpern KL, Karras DJ, Singer AJ, Chest pain associated with cocaine: an assessment of prevalence in suburban and urban emergency departments Ann Emerg Med 1995 26:671-76.  [Google Scholar]

[54]Kolodgie FD, Virmani R, Cornhill JF, Herderick EE, Smialek J, Increase in atherosclerosis and adventitial cell mass in cocaine abusers—an alternative mechanism of cocaine associated coronary vosospasm and thrombosis J Am Coll Cardiol 1991 17:1553-60.  [Google Scholar]

[55]Lange RA, Hills CD, Cardiovascular complications of cocaine use N Engl J Med 2001 345:351-58.  [Google Scholar]

[56]Schiele F, Chopard R, Is coronary artery disease different in women? Presse Med 2014 43(7-8):796-802.  [Google Scholar]

[57]Majumder B, Haque A, Dastidar DG, Recent insights in coronary artery disease in women Medicine Update 2011 :9-11.  [Google Scholar]

[58]Amsterdam EA, Wenger NK, Brindis RG, Casey DE, Ganiats TG, Holmes DR, American college of cardiology; american heart association task force on practice guidelines; society for cardiovascular angiography and interventions; society of thoracic surgeons; american association for clinical chemistry. 2014 aha/acc guideline for the management of patients with Non-ST-Elevation Acute coronary syndromes: a report of the american college of cardiology/american heart association task force on practice guidelines J Am Coll Cardiol 2014 64(24):e139-228.  [Google Scholar]

[59]O’Gara PT, Kushner FG, Ascheim DD, Casey DE Jr, Chung MK, de Lemos JA, American College of Cardiology Foundation; american heart association task force on practice guidelines; american college of emergency physicians; society for cardiovascular angiography and interventions. 2013 ACCF/AHA guideline for the management of st-elevation myocardial infarction: executive summary: a report of the american college of cardiology foundation/american heart association task force on practice guidelines: developed in collaboration with the american college of emergency physicians and society for cardiovascular angiography and interventions Catheter CardiovascInterv 2013 82(1):E1-27.  [Google Scholar]

[60]Wang K, Asinger RW, Marriott HJ, ST-segment elevation in conditions other than acute myocardial infarction N Engl J Med 2003 349(22):2128-35.  [Google Scholar]

[61]Uthamalingam S, Zheng H, Leavitt M, Pomerantsev E, Ahmado I, Gurm GS, Exercise-induced ST-segment elevation in ECG lead aVR is a useful indicator of significant left main or ostial LAD coronary artery stenosis JACC Cardiovasc Imaging 2011 4(2):176-86.  [Google Scholar]

[62]Shah N, Soon K, Wong C, Kelly AM, Screening for asymptomatic coronary heart disease in the young ‘at risk’ population: Who and how? IJC Heart and Vasculature 2015 6:60-65.  [Google Scholar]

[63]Szamosi A, Hamsten A, Walldius G, de Faire U, Coronary angiography and pathogenesis of coronary artery disease in young male survivors of myocardial infarction Acta Radiol Diagn (Stockh) 1986 27(5):519-25.  [Google Scholar]

[64]Uddin SN, Siddiqui NI, Bagum F, Malik F, Rahman S, Ali MS, Coronary artery disease in young adults - angiographic profile Mymensingh Med J 2004 13(1):11-5.  [Google Scholar]

[65]Maroszy-ska-Dmoch EM, Wo-akowska-Kapłon B, [Coronary artery disease in young adults: clinical and angiographic characterization. A single centre study] Kardiol Pol 2016 74(4):314-21.  [Google Scholar]

[66]Scanlon PJ, Faxon DP, Audet AM, Carabello B, Dehmer GJ, Eagle KA, ACC/AHA guidelines for coronary angiography: executive summary and recommendations. A report of the american college of cardiology/american heart association task force on practice guidelines (committee on coronary angiography) developed in collaboration with the society for cardiac angiography and interventions Circulation 1999 99(17):2345-57.  [Google Scholar]

[67]Kim KJ, Choi SI, Lee MS, Kim JA, Chun EJ, Jeon CH, The prevalence and characteristics of coronary atherosclerosis in asymptomatic subjects classified as low risk based on traditional risk stratification algorithm: assessment with coronary CT angiography Heart 2013 99(15):1113-17.  [Google Scholar]

[68]Otaki Y, Gransar H, Cheng VY, Dey D, Labounty T, Lin FY, Gender differences in the prevalence, severity, and composition of coronary artery disease in the young: a study of 1635 individuals undergoing coronary CT angiography from the prospective, multinational confirm registry Eur Heart J Cardiovasc Imaging 2015 16(5):490-99.  [Google Scholar]

[69]Ma ES, Ma GL, Yu HW, Wu W, Li K, Assessment of myocardial bridge and mural coronary artery using ECG-gated 256-slice CT angiography: a retrospective study Scientific World Journal 2013 2013:947876  [Google Scholar]

[70]Arena R, Guazzi M, Lianov L, Whitsel L, Berra K, Lavie CJ, Healthy lifestyle interventions to combat noncommunicable disease-a novel nonhierarchical connectivity model for key stakeholders: a policy statement from the american heart association, european society of cardiology, european association for cardiovascular prevention and rehabilitation, and american college of preventive medicine Mayo Clin Proc 2015 90(8):1082-103.  [Google Scholar]

[71]Misra A, Nigam P, Hills AP, Chadha DS, Sharma V, Deepak KK, Physical Activity Consensus Group. Consensus physical activity guidelines for Asian Indians Diabetes Technol Ther 2012 14(1):83-98.  [Google Scholar]

[72]Albers JJ, Slee A, O’Brien KD, Robinson JG, Kashyap ML, Kwiterovich PO, Relationship of apolipoproteins A-1 and B, and lipoprotein(a) to cardiovascular outcomes: the AIM-HIGH trial (Atherothrombosis Intervention in Metabolic Syndrome with Low HDL/High Triglyceride and Impact on Global Health Outcomes) J Am Coll Cardiol 2013 62(17):1575-79.  [Google Scholar]

[73]Cole JH, Miller JI 3rd, Sperling LS, Weintraub WS, Long-term follow-up of coronary artery disease presenting in young adults J Am Coll Cardiol 2003 41(4):521-28.  [Google Scholar]

[74]Vaidya CV, Majmudar DK, A study of acute ST elevation myocardial infarction in young patients from government teaching hospital Sudan Med Monit 2015 10:45-49.  [Google Scholar]

[75]Dhoot KK, Gandhi R, Rawat A, Boben J, Benjamin B, Mahala BK, Angiographic comparison of thrombus load in young patients with stemi lysed with tenecteplase versus streptokinase (Abstract) Available from Accessed on 13-Oct-2015  [Google Scholar]

[76]Ergelen M, Uyarel H, Gorgulu S, Norgaz T, Ayhan E, Akkaya E, Comparison of outcomes in young versus nonyoung patients with ST elevation myocardial infarction treated by primary angioplasty Coron Artery Dis 2010 21(2):72-7.  [Google Scholar]

[77]Chua SK, Hung HF, Shyu KG, Cheng JJ, Chiu CZ, Chang CM, Acute ST-elevation myocardial infarction in young patients: 15 years of experience in a single center Clin Cardiol 2010 33(3):140-48.  [Google Scholar]

[78]Christus T, Shukkur AM, Rashdan I, Koshy T, Alanbaei M, Zubaid M, Coronary artery disease in patients aged 35 or less - a different beast? Heart Views 2011 12(1):7-11.  [Google Scholar]

[79]Ng WK, Vedder M, Whitlock RM, Milsom FP, Nisbet HD, Smith WM, Coronary revascularisation in young adults Eur J Cardiothorac Surg 1997 11(4):732-38.  [Google Scholar]

[80]Lautamäki A, Airaksinen KE, Kiviniemi T, Vinco G, Ribichini F, Gunn J, Prognosis and disease progression in patients under 50 years old undergoing PCI: the CRAGS (Coronary artery disease in young adults) study Atherosclerosis 2014 235(2):483-87.  [Google Scholar]

[81]De Ferrari GM, Fox KA, White JA, Giugliano RP, Tricoci P, Reynolds HR, Outcomes among non-ST-segment elevation acute coronary syndromes patients with no angiographically obstructive coronary artery disease: observations from 37,101 patients Eur Heart J Acute Cardiovasc Care 2014 3:37-45.  [Google Scholar]

[82]Authors/Task Force MembersRoffi M, Patrono C, Collet JP, 2015 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: Task force for the management of acute coronary syndromes in patients presenting without persistent ST-Segment Elevation of the European Society of Cardiology (ESC) Eur Heart J 2016 37(3):267-315.  [Google Scholar]