|Year : 2017 | Volume
| Issue : 2 | Page : 84-91
A study of risk factors for acute myocardial infarction in patients below 35 years in eastern India
Monika Bhandari1, Vikas Singh2, Deepesh Venkatraman3
1 Department of Cardiology, King George's Medical University, Lucknow, Uttar Pradesh, India
2 Department of Cardiovascular and Thoracic Surgery, King George's Medical University, Lucknow, Uttar Pradesh, India
3 Consultant Cardiologist, BGS Global Hospital, Bengaluru, Karnataka, India
|Date of Web Publication||26-Oct-2017|
Department of Cardiology, KGMU, Lucknow, Uttar Pradesh
Source of Support: None, Conflict of Interest: None
Background: Coronary artery disease (CAD) is most common cause of mortality. Its incidence in young Indians is about 12%–16%. Myocardial infarction (MI) in young can be divided into two groups, those with angiographically normal coronaries and those with CAD. 15%–20% of those with CAD have no identifiable risk factors and therefore miss the opportunity for primary prevention. Recent reports have suggested that increased lipoprotein a (Lp[a]) and hyperhomocysteinemia play an important role in MI. The true prevalence of CAD in young is grossly underestimated.
Aims: (1) Study of risk factors for MI in patients <35 years. (2) Clinical presentation. (3) Disease pattern in coronary angiography. (4) To assess the relationship of emerging risk factors such as homocysteine and Lp(a) with MI.
Materials and Methods: Fifty patients aged 35 years or younger diagnosed with acute MI were included.
Results: The majority of patients were males (80%). The mean age was 33.3 in males and 31.8 years in females. Chest pain was the most common presenting complaint (94%). Smoking was the most prevalent risk factor (72%). Hyperhomocysteinemia (42%) and raised Lp(a) (24%) were emerging risk factors. Anterior wall MI was most prevalent (64%) and most patients had single vessel disease with left descending coronary being the most commonly involved artery.
Conclusions: Homocysteine and Lp(a) should be measured in young MI patients. Smoking cessation and prevention of diabetes and hypertension should be encouraged. As young patients have more discrete lesion, timely revascularization will reduce myocardial damage.
Keywords: Coronary artery disease, hyperhomocysteinemia, lipoprotein a, myocardial infarction
|How to cite this article:|
Bhandari M, Singh V, Venkatraman D. A study of risk factors for acute myocardial infarction in patients below 35 years in eastern India. Nig J Cardiol 2017;14:84-91
|How to cite this URL:|
Bhandari M, Singh V, Venkatraman D. A study of risk factors for acute myocardial infarction in patients below 35 years in eastern India. Nig J Cardiol [serial online] 2017 [cited 2021 Nov 29];14:84-91. Available from: https://www.nigjcardiol.org/text.asp?2017/14/2/84/217267
| Introduction|| |
Coronary artery disease (CAD) is the most common cause of mortality in the entire world. CAD in the absence of atherosclerosis, uncommon in older patients accounts for approximately 20% of cases in patients under age 45.,,
The prevalence of CAD in young Indians (below 45 years) is about 12%–16%., About 50% of CAD-related deaths in the young below 50 years and about 25% of myocardial infarction (MI) in India occurs under the age of 40 years.,
MI in the young can be divided into two groups, those with angiographically normal coronary arteries and those with CAD. The prevalence of MI with normal coronary arteries varies between 1% and 12%. Young MI patients have a higher percentage of normal coronary arteries. MI in them can be caused by arteritis, thrombosis, embolization, or spasm. As is the case with venous thrombosis, coronary thrombosis can be seen in hypercoagulable states, such as protein C and protein S deficiency, antiphospholipid syndrome, or nephrotic syndrome., Coronary artery spasm can cause MI in patients with cocaine abuse and also in association with alcohol binges., Other unusual causes include hypertension, coronary aneurysms, mediastinal irradiations, valvular abnormalities, and infective endocarditis.
Although traditional risk factors such as hypertension, insulin resistance, diabetes mellitus, smoking, hyperlipidemia, physical inactivity and obesity explain most of CAD, 15%–20% of those with CAD have no identifiable risk factors and therefore miss the opportunity for primary prevention.
Recent studies show that increased Lp(a), hyperhomocysteinemia plays an important role in MI. Some 10%–20% of cases of CAD have been linked to elevated level of serum homocysteine. Lp(a) is considered to be 10 times more atherogenic than low-density lipoprotein-cholesterol (LDL-C) and is associated with a family history of MI in asymptomatic individuals, as well as with clinical MI, CAD, and restenosis of coronary artery vein grafts.,,,
Factor V Leiden mutation also has been shown to increase the risk for MI. It may be possible that there is increased prevalence of hyperhomocysteinemia and elevated Lp(a) levels in Indian subcontinent leading to an early age of onset of first MI in Indians. Recently in studies, it has been found that measuring apolipoprotein (Apo)-B and Apo-A1 is better than measuring LDL-C and high-density lipoprotein-cholesterol (HDL-C) as the type of HDL-C and LDL-C (size and density) is more important rather than the absolute values. Small dense LDL-C particles are more atherogenic.
Approximately, 50% of patients have single vessel disease (SVD) while the remainder has multivessel disease. The prevalence of left main coronary artery stenosis is approximately 5%.
The true prevalence of CAD in the young is grossly underestimated. Therefore, this study was done to find out the association of recently identified risk factors along with traditional risk factors with the premature onset of CAD in young patients who are 35-year-old or younger.
| Materials and Methods|| |
The study was carried out on fifty patients aged ≤35 years admitted with MI in the Department of Cardiology at ICVS, RG Kar Medical College, Kolkata. A detailed clinical history, physical examination, electrocardiography (ECG), biochemical, and echocardiographic evaluation were done using a pretest proforma.
All patients aged 35 years or younger admitted with MI.
The final diagnosis of acute MI (AMI) was based on the following criteria:
- Ischemic chest pain lasting 20 min or more
- ECG evidence of myocardial injury
- Greater than or equal to 0.1 mv ST elevation in two contiguous leads other than V2–V3 where the cutoff point of ≥0.2 mv in men ≥40 years; ≥0.25 mv in men <40 years; or ≥0.15 mv in women
- New horizontal or down sloping ST depression ≥0.05 mv in two contiguous leads and/or T wave inversion ≥0.1 mv in two contiguous leads with prominent R wave or R/S ratio >1.
- Positive biomarkers- creatine kinase-MB fraction, cardiac troponins.
Patients below 18 years and above 35 years were not included. Patients who refused to give consent.
Study period: 2013–2014.
Sample size: A total of fifty patients were analyzed.
Sample design: Purposive sampling.
Study design: Observational study of CAD risk factors among eastern Indians. Subjects studied were men and women aged 18–35 years.
Statistical analysis used
Chi-square test was used for statistical analysis.
- History of hypertension
- History of diabetes mellitus
- History of smoking and duration
- History of alcohol consumption and duration
- History of substance abuse-cocaine
- Family history premature CAD (defined as CAD occurring below the age of 65 in women and 55 in men)
- Symptoms-chest pain or dyspnea.
- Systolic and diastolic blood pressure
- Waist-hip ratio
- Body mass index.
ElectrocardiographyST-segment elevation myocardial infarction (STEMI) or non-STEMI (NSTEMI).Coronary angiography
- Lipid profile
- Total cholesterol
- Triglycerides (TGs)
- Inflammatory markers
- C-reactive protein.
- Glucose metabolism
- Single vessel or multi-vessel disease
- Discrete lesion or diffuse disease.
Preformed proforma to record patient data, ECG, cardiac enzymes, lipid profile, inflammatory markers, and other relevant blood investigations, echocardiography (Two-dimensional-Echo and Doppler), catheterization lab to analyze disease pattern on coronary angiography.
- Proper informed and written consent was taken from all patients in the study
- A detailed history was taken as per preformed pro forma.
| Results|| |
In this study, the risk factors, clinical and angiographic profile of fifty young patients of age between 18 and 35 years with MI were studied from January 2013 to December 2014 presenting to our hospital.
The total number of patients was fifty. Most of the patients (66%) were within the age of 31–35 years and 2% of the patients were in the age group of 21–25 years. The youngest patient was 22-year-old. 80% of the patients were males (P< 0.05) The mean age of female patients was 33.3 years while for males was 31.82 years [Table 1] and [Figure 1].
The most common symptom in young patients with MI was chest pain, which was present in 94% of the patients, followed by sweating (50%) and breathlessness (26%) [Table 2].
Smoking was the most common risk factor for MI (72%) in the young adults, hyperlipidemia being the second common risk factor (68%). 32% patients had body mass index (BMI) value of >25 kg/m 2. Twenty-four percent of the patients were diabetic, of which 10% were newly detected. Hypertension and a family history of premature CAD each formed 18% of the risk factors. 72% of the patients had multiple risk factors for AMI. 26% had a single risk factor, while 4% had none of the risk factors. Substance abuse (cocaine) was present in 4% patients [Table 3], [Table 4] and [Figure 2], [Figure 3].
|Table 4: Risk factors (lipid profile) of myocardial infarction in young adults|
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The serum TG levels were elevated in 76% of the patients [Figure 4]. HDL-C was below 40 mg/dl in 68% of patients overall, but when taking gender distinction into account, it was below normal in 66% of patients [Table 5]. LDL-C levels were high in 20% of the patients while 16% of the patients had very high levels of LDL-C [Figure 5]. Lp(a) levels were high (>30 mg/dl) in 24% of the patients [Table 6]. The homocysteine level was above normal (>15 μmol/L) in 42% of patients, of which 16% patients had homocysteine level between 15 and 30 μmol/L (moderate risk), 24% had levels between 30 and 100 μmol/L (intermediate risk), and 2% patients had levels above 100 μmol/L (high risk) [Figure 6]. The family history of premature CAD was positive in 18% of the patients [Table 7].
|Table 5: High-density lipoprotein-cholesterol level as a risk factor in myocardial infarction|
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The Apo-B/Apo-A1 ratio was elevated in 82% of the patients with 8% being under moderate risk category and 74% under high-risk category [Figure 7]. The mean ratio was 1.69.
|Figure 7: Apolipoprotein-B/apolipoprotein -A1 ratio and risk of myocardial infarction|
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Anterior wall MI was found in 64% of the patients, and 28% of the patients had inferior wall MI. Lateral wall MI was present in 4% of the patients[Figure 8], [Figure 11],[Figure 12],[Figure 13] and [Figure 15]. In our study, 64% of patients had SVD which was seen on coronary angiography, followed by double vessel disease (DVD) (24%), and 4% had multi vessel disease. Normal coronary angiography was found in 8% of cases. 68% of the patients had involvement of the left anterior descending (LAD) artery, 34% had involvement of the right coronary artery (RCA), and 16% had involvement of the left circumflex coronary artery (LCX) [Figure 9], [Figure 10] and [Figure 14].
|Figure 11: Electrocardiography of patient showing anterior wall myocardial infarction|
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|Figure 12: Electrocardiography of patient showing inferior wall myocardial infarction|
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|Figure 13: Electrocardiography of patient showing non-ST-segment elevation myocardial infarction|
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|Figure 14: Coronary angiogram showing critical stenosis in left anterior descending|
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|Figure 15: Two-dimensional-echo of patient showing thinning of anterior wall myocardial infarction|
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| Discussion|| |
AMI is rare before 35 years of age, but there is a rising trend in young population nowadays. Most of the patients belonged to higher range of age group that is 31–35 years which contributed 66% of the patients and only 2% of the patients were below 25 years of age. The mean age was 33.3 years for females and 31.82 years for males. The distribution of age group showed a striking increase in the disease with increasing age. This in accordance to previous studies which also showed increasing trend with increasing age even in young patients. In a study done by Sricharan et al. also the maximum number of the patients (70%) were within in the age of 35–40 years and 3.33% patients being in the age group of 25–30 years. In addition, in a study by Prajapati et al. the mean age was 34.5 ± 4.7 years. Male sex is an important risk factor for IHD. In our study 80% of the patients were male. A study by Prajapati et al., also 89.9% patients were male. Thus, the demographic profile of our patients was similar to previous studies.
Tobacco smoking is an established conventional coronary risk factor for CAD. Casual association between tobacco chewing (smokeless tobacco) and CAD is found in some case control studies. Tobacco increases the risk of cardiovascular (CV) disease by raising blood pressure, damaging vascular endothelium, increasing LDL-cholesterol oxidation, and lowers the HDL-cholesterol. Smoking was found to be a most prevalent risk factor (72%) in our study also. This was in line with a previously reported prevalence of 77% in Swiss patients aged ≤35 years by Schoenenberger et al. Studies done in India also showed smoking the most prevalent risk factor.,,
Thus, an effort should be made to educate people about the hazards of cigarette smoking, and people should be educated at an early age to avoid smoking, and smoking cessation programs need to be established.
About 24% of the patients were diabetic, of which 10% were newly detected and hypertension was present in 18% of the patients. BMI more than 25 kg/m 2 was seen in 32% of the patients. A study by Sricharan et al. and Jamil et al. also showed a similar trend.
The excess burden of CAD among South Asians appears to be primarily due to dyslipidemia that is characterized by: high levels of ApoB, TGs, Lp(a), borderline high levels of LDL-C, low levels of HDL-C and Apo-A1. Total cholesterol levels and LDL-C levels are correlated with extent and severity of CAD in Asian Indians as in whites. However, at any given total cholesterol or LDL-C level, Asian Indians have a greater CAD risk than whites. In our study, hyperlipidemia was present in 68% of the patients, with 54% of the patients having increased LDL-C levels.
In previous studies also hyperlipidemia was found to be a common risk factor. In a study by Sricharan et al. hyperlipidemia was the second most common risk factor (36.67%). Hyperlipidemia was documented in 46% of the study population in the study by Hassan et al. Similar results were obtained in the study by Prajapati et al.
Therefore, Asian Indians with dyslipidemia should be treated as aggressively as if they had a CAD risk equivalent similar to the treatment of patients with diabetes or heart disease.
Lp(a) appears to be a major risk factor in Asian Indians as compared to whites. A high level of Lp(a) is shown to the most prevalent dyslipidemia in our young patients with premature CAD. Lp(a) levels are governed almost exclusively by race, ethnicity, and genetics, unlike other lipids, where the levels are influenced by age, gender, diet, and other environmental factors. The effect of Lp(a) on the atherogenicity is not additive but multiplicative. It constitutes an important inherited risk factor for atherosclerosis and is also regarded as a biological marker for familial CAD.
In our study, Lp(a) levels were above 30 mg/dl in 24% of the patients representing an important risk factor in young patients with MI. In the study by Prajapati et al. 26 (21.5%), patients had a high level of Lp(a) similar to our study. Similarly, in the studies by Schaefer et al. (elevated in 21.5% of patients) the Lp(a) level was significantly higher in young patients with MI as compared with controls.
Homocysteine levels are higher among Asian Indians than others. In India, most people adhere to a vegetarian diet and vegetarians have 3.0 times higher risk of hyperhomocysteinemia compared to those who eat nonvegetarian. In our study, homocysteine levels were above normal in 42% of the patients. Furthermore, in the study done by Arumalla and Reddy  hyperhomocysteinemia was found in 66% of the patients with AMI. The slightly lower prevalence of hyperhomocysteinemia in our patients might be due to increased fish consumption and fruits. Hence, we should encourage higher intake of fruits and avoid overcooking of vegetables to prevent hyperhomocysteinemia.
Our study showed that 72% patients had multiple risk factors, 26% had a single risk factor, and 4% of the patients had no risk factors. According to Sricharan et al. 46.67% of the patients had multiple risk factors for AMI, 46.67% had a single risk factor, while 6.67% had none of the risk factors.
The most common presenting complaint in our study was chest pain (94%) followed by sweating (50%) and breathlessness (26%). The study by Sricharan et al. showed that the most common symptom was chest pain, which was present in 90% of the patients, followed by sweating (50%), breathlessness (20%), restlessness (6.7%), and palpitations (3.3%). However, in the study by Hassan et al. 69% of the patients denied any chest pain. The chest pain was absent in our study mainly in females and diabetics.
There is now compelling evidence that the Apo-B/Apo-A1 ratio is a better index of the likelihood of vascular events than any of the corresponding cholesterol indices: The total cholesterol/HDL-C ratio, non-HDL-C/HDL-C ratio, or LDL-C/HDL-C ratio. Apo-B/Apo-A1 ratio >1 is associated with increased CV risk. The relation between risk and ApoB is continuous, whereas at the extremes of HDL concentration in plasma the relation to risk is not certain. In the present study, the Apo-B/Apo-A1 ratio was elevated in 82% of the patients. The mean ratio was 1.69. In a study by Prajapati et al., the mean ratio was 0.76.
In our study, most common presentation was with anterior wall MI which was found in 64% of the patients. It was followed by inferior wall MI in 28% and lateral wall MI in 4% of the patients. These results are in line with the prior studies done by Sricharan et al. and Prajapati et al., where also anterior wall MI was most common presentation followed by inferior wall MI.,
Regarding coronary angiographic findings, LAD was the most common coronary artery involved (68%) followed by RCA in 34% of the patients. The LCX was the least (16%) involved artery. Prior studies also ,, showed LAD as the most common coronary artery involved followed by RCA and LCX.
Normal coronary angiography was seen in 8% of the patients. 64% of the patients had SVD whereas DVD and multivessel disease was present in 24% and 4% of the patients respectively.
Studies done by Hassan et al. and Jamil et al. also showed that SVD was most common in young AMI patients followed by DVD and multivessel disease., Whereas in the study by Sricharan et al., the majority of the patients (57.14%) had SVD, followed by normal coronaries (22.45%). 16.3% patients had DVD and 4% patients had multivessel disease.
Thus, it is evident from angiographic findings that young patients usually have SVD and less diffuse disease which is highly amenable to treatment with better preservation of myocardial function if they are offered timely intervention.
| Conclusions|| |
The most important thing is to do risk factor modification which is a quite challenging task. Since cigarette smoking is highly prevalent in young, preventive educational programs along with smoking cessation clinics need to be established. Diabetes and cholesterol education should be provided to the population especially the youth by medical personnel on a priority basis. Young patients usually have discrete lesion which can be treated by angioplasty and if done early, much of the myocardium at risk can be rescued. Thus, all the patients should be subjected to an early revascularization and risk stratification for better outcomes and prognosis.
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Conflicts of interest
There are no conflicts of interest.
| References|| |
WHO. The Global Burden of Disease, Update. WHO Press: Geneva; 2004. p. 11-2.
Negus BH, Willard JE, Glamann DB, Landau C, Snyder RW 2nd
, Hillis LD, et al.
Coronary anatomy and prognosis of young, asymptomatic survivors of myocardial infarction. Am J Med 1994;96:354-8.
Mammi MV, Pavithran K, Abdu Rahiman P, Pisharody R, Sugathan K. Acute myocardial infarction in North Kerala – A 20 year hospital based study. Indian Heart J 1991;43:93-6.
Yater WM, Traum AH, Brown WG, Fitzgerald RP, Geisler MA, Wilcox BB. Coronary artery disease in men 18 to 39 years of age. Am Heart J 1948;36:334-48.
Kennelly BM. Aetiology and risk factors in young patients with recent acute myocardial infarction. S Afr Med J 1982;61:503-7.
Berenson GS, Srinivasan SR, Bao W, Newman WP 3rd
, Tracy RE, Wattigney WA, et al.
Association between multiple cardiovascular risk factors and atherosclerosis in children and young adults. The Bogalusa heart study. N
Engl J Med 1998;338:1650-6.
Bahuleyan CG. Hospital data on coronary artery disease from North Kerala. In Vijayaraghavan G (ed). Cardiovascular Disease Prevention. Trivandrum. 1996. p. 54-9.
Girija G. Risk factors profile of patients with acute MI. In Vijayaraghavan G (ed). Cardiovascular Disease Prevention Trivandrum. 78-83. American Heart Association Heart and Stroke Statistical Update 1997;26-7.
Choudhury L, Marsh JD. Myocardial infarction in young patients. Am J Med 1999;107:254-61.
Padler FA, Comad AR. Myocardial infarction with normal coronary artery: A case report and review of literature. Am J Med Sci 1997;314:342-5.
Fujimura O, Gulamhusein S. Acute myocardial infarction: Thrombotic complications of Nephrotic syndrome. Can J Cardiol 1987;3:267-9.
Ross GS, Bell J. Myocardial infarction associated with inappropriate use of topical cocaine as treatment for epistaxis. Am J Emerg Med 1992;10:219-22.
Moreyra AE, Kostis JB, Passannante AJ, Kuo PT. Acute myocardial infarction in patients with normal coronary arteries after acute ethanol intoxication. Clin Cardiol 1982;5:425-30.
Smith SC Jr. Current and future directions of cardio-vascular risk prediction. Am J Cardiol 2006;97:28A-32A.
Tayal D, Goswami B, Koner BC, Mallika V. Role of homocysteine and lipoprotein (A) in atherosclerosis. An update. Biomedical Research 2011;22:391-405.
Lawn RM. Lipoprotein (a) in heart disease. Sci Am 1992;266:54-60.
Hoefler G, Harnoncourt F, Paschke E, Mirtl W, Pfeiffer KH, Kostner GM, et al.
Lipoprotein lp(a). A risk factor for myocardial infarction. Arteriosclerosis 1988;8:398-401.
Durrington PN, Ishola M, Hunt L, Arrol S, Bhatnagar D. Apolipoproteins (a), AI, and B and parental history in men with early onset ischaemic heart disease. Lancet 1988;1:1070-3.
Armstrong VW, Cremer P, Eberle E, Manke A, Schulze F, Wieland H, et al.
The association between serum lp(a) concentrations and angiographically assessed coronary atherosclerosis. Dependence on serum LDL levels. Atherosclerosis 1986;62:249-57.
Sweetnam PM, Bolton CH, Downs LG, Durrington PN, MacKness MI, Elwood PC, et al.
Apolipoproteins A-I, A-II and B, lipoprotein (a) and the risk of ischaemic heart disease: The Caerphilly study. Eur J Clin Invest 2000;30:947-56.
Hassan Z, Farooq S, Nazir N, Iqbal K. Coronary artery disease in young: A study of risk factors and angiographic characterization in the valley of Kashmir. Int J Sci Res Publ 2014;4:1.
Sricharan KN, Rajesh S, Rashmi K, Meghana HC, Badiger S, Mathew S. Study of acute myocardial infarction in young adults: Risk factors, presentation and angiographic findings. J Clin Diagn Res 2012;6:257-60.
Prajapati J, Jain S, Virpariya K, Rawal J, Joshi H, Sharma K, et al
. Novel atherosclerotic risk factors and angiographic profile of young Gujrati patients with acute coronary syndrome. JAPI 2014;62:584-8.
Schoenenberger AW, Radovanovic D, Stauffer JC, Windecker S, Urban P, Niedermaier G, et al
. Acute coronary syndromes in young patients: presentation, treatment and outcome. Int J Cardiol 2011;148:300-4.
Jamil G, Jamil M, Alkhazraji H, Haque A, Chedid F, Balasubramanian M, et al.
Risk factor assessment of young patients with acute myocardial infarction. Am J Cardiovasc Dis 2013;3:170-4.
Schaefer EJ, Lamon-Fava S, Jenner JL, McNamara JR, Ordovas JM, Davis CE, et al.
Lipoprotein(a) levels and risk of coronary heart disease in men. The lipid research clinics coronary primary prevention trial. JAMA 1994;271:999-1003.
Arumalla VK, Reddy KR. Plasma homocysteine and traditional risk factors in young acute myocardial infarction patients. IJABPT 2011;4;54-7.
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], [Figure 12], [Figure 13], [Figure 14], [Figure 15]
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7]