High Prevalence of Obesity in Young Patients with ST Elevation Myocardial Infarction

Login or register to view PDF.

Background: There is growing concern about increasing rates of obesity in young people, and increasing ST elevation myocardial infarction (STEMI) at a younger age. There are only a few studies performed to study the risk factors in STEMI among young populations. Methods: Retrospective chart reviews on all first event STEMI patients between December 2005 and July 2007 were performed. A young population was defined as: men <45 years of age and women <55 years of age. Results: Among 206 patients with STEMI, 36 were young. In young patients with STEMI, 78 % were obese compared with 35 % obese, non-young (p<0.001). Also, among young patients with STEMI, family history of coronary heart disease (CHD) was positive in 39 %, compared with 19 % in non-young patients (p=0.009). This significance for obesity and family history persisted after adjusting for other risk factors using logistic regression (OR 2.96 to 17.75, 95 % CI, p<0.0001 and OR 1.36 to 7.47, 95 % CI, p=0.008, respectively). Conclusion: Obesity and family history of CHD were major risk factors with a higher prevalence in young patients with STEMI than non-young patients.

American Heart Hospital Journal 2011;9(1):37-40

There is an increasing prevalence of obesity in the young population as well as in older people.1,2 One report showed an increasing incidence of coronary heart disease (CHD) in the young population.3 Obesity is now considered a major and independent risk factor for CHD.4 The role of obesity as a cause of CHD in young patients is a growing concern. Only a few studies have reported an increased prevalence of obesity in young patients with CHD3 or STEMI.5,6,7 Our study examines various risk factors for STEMI in young patients, and demonstrates an association between obesity in young patients and STEMI.


We hypothesized that in STEMI, young patients might have a higher prevalence of obesity compared to non-young patients.


A retrospective chart review on all patients with a first episode of STEMI between December 2005 and July 2007 was performed at our community/teaching hospital. Investigations were in accordance with the Declaration of Helsinki. Institutional Review Board approval was obtained.

International Classification of Diseases 9 Clinical Modification (ICD 9 CM) codes 410.0–410.6, 410.8, and 410 were used to identify patients with STEMI. We included only patients with a first episode of STEMI. Demographic information, secondary diagnoses, length of hospital stay, and disposition were retrieved from electronic billing records. Electronic medical records were used for findings at cardiac catheterization, risk factors (including family history for CHD), body mass index (BMI), and outcome.

Young patients in our study were defined as men <45 years and women <55 years of age. This definition was based on the age of risk for CHD in men and women. At any given age, men are at greater risk for coronary disease than women.8,9 The average age of men with a first coronary event is 64.5 years and women 70.3 years.10 Risk for CHD in women lags about five to 15 years behind that of men.9 Our definition for young corresponded with the age recommended for treatment of dyslipidemia in men and women in the Adult Treatment Panel III report.9

History of tobacco use and/or tobacco use disorder was based on ICD-9-CM discharge codes. Both men and women were defined as obese if their BMI was ≥30 kg/m2.

Statistical Methods

Continuous variables are presented as mean ± standard deviation and categorical variables as frequencies and percentages. The 95 % confidence intervals are shown where appropriate. Independent Student’s t-test was used to compare continuous variables, and Pearson Chi-square test used to compare categorical variables. Fisher exact test was used instead of chi-square if any one value in calculation was five or less. Multivariate analysis was performed using regression analysis and a binary logistic regression model to look for independent association. A p-value of ≤0.05 was considered statistically significant. Statistical tests used were derived from MiniTab 15.3, version #8 (MiniTab Inc. State College, PA, US).

Patient Characteristics and Risk Factors

Between December 2005 and July 2007, 206 patients were hospitalized with STEMI. Men were 65 % (134 of 206) of the patient sample. The mean age was 61.3 ± 14.6 years (mean ± standard deviation). Women were older than men, at 67.1 ± 15.6 versus 58.2 ± 13.1 years (p<0.0001).

Among patients with STEMI, 17.5 % (36 of 206) were young. Of the young patients with STEMI, 78 % (28 of 36) were obese compared with 35 % (60 of 170) of obese, non-young (p<0.001) (see Table 1). Also, among young patients with STEMI, family history of CHD was positive in 39 % (14 of 36) compared with 19% (32 of 170) in non-young (p=0.009). The proportion of young and non-young patients with obesity and family history for CHD is shown in Figure 1. After adjusting for other risk factors using logistic regression, both obesity and family history of CHD continued to be significantly associated with STEMI in young compared with non-young patients (see Table 2). Only obesity and family history of CHD were more prevalent among young compared with non-young STEMI patients (see Table 1).

Obesity was diagnosed in 43 % (88 of 206) of the total sample. Risk factors among obese and non-obese patients are shown in Table 3. Risk factors and outcome based on various levels of BMI are shown in Table 4. With increasing BMI, age decreased (p<0.0001) and the prevalence of diabetes mellitus increased (p=0.01) (see Table 4).


In-hospital all-cause mortality among all STEMI patients was 12.6 % (26 of 206). The mortality in women was 16.6 % (12 of 72) and 10.4 % (14 of 134) for men, but this did not differ significantly. All-cause mortality was lower for obese patients than non-obese patients 5.6 % (5 of 89) versus 17.9 % (21 of 117) (p=0.01). This significance, however, was lost with binary logistic regression using age, gender, tobacco use, hypertension, dyslipidemia, diabetes mellitus, family history, and obesity as co-variates. Only age was a significant predictor of all-cause mortality, based on binary logistic regression (p<0.0001).


In young patients with STEMI there was a higher prevalence of obesity and family history of CHD. Obesity is becoming a global epidemic.4 In the past 10 years in the US, there has been a dramatic increase in the prevalence of obesity in both children and adults.4 Over the last three decades, the age-adjusted prevalence of overweight and obesity has increased both in children and adults.11

It has been shown that individuals with metabolic syndrome, which includes obesity, are at increased risk for CHD.12 The root causes of metabolic syndrome are overweight/obesity, physical inactivity, and genetic factors.9 Furthermore obesity is associated with multiple comorbidities such as cardiovascular disease, type 2 diabetes, hypertension, certain cancers, and sleep apnea.4

The relationship of obesity with atherosclerosis and CHD in the past was uncertain, but it is now confirmed to be a major risk factor for CHD.4 Previous studies suggested that obesity was not an important contributor to coronary atherosclerosis. The Framingham Heart Study13 showed that the relation between body weight and risk of CHD was mediated largely through other risk factors, such as blood pressure, total cholesterol, high-density lipoprotein cholesterol, and diabetes. The Seven countries study14 found little association between body weight and the incidence of CHD. More recent studies suggested that obesity is an independent risk factor for CHD.15,16 The INTERHEART study of 27,000 participants showed abdominal obesity as an independent risk factor, but it failed to demonstrate BMI as a independent risk factor for CHD.17

The European prospective investigation into cancer and nutrition (EPIC) in Norfolk cohort study of more than 24,000 participants, showed both higher BMI and abdominal obesity to be independent risk factors for CHD. Although not when adjusted for factors such as age etc.18 The Emerging Risk Factors Collaboration analysis of 58 prospective studies showed similar findings.19

Several studies have observed a good prognosis with cardiovascular diseases associated with obesity.20–22 This counterintuitive observation was termed the ‘obesity paradox’.21 Others, however, showed an increased mortality with obesity23,24 and suggest that there is no obesity paradox.25 We found no evidence of the obesity paradox in our investigation after adjusting for confounding variables.

Obese individuals have a proinflammatory state that may predispose them to acute coronary syndrome.26 Surplus adipose tissue secretes increased amounts of several cytokines that underlie the proinflammatory state. Plasminogen activator inhibitor-1 (PAI-1), mainly produced by the endothelium, is also released in increased amounts by the adipose tissue, which in turn favors a prothrombotic state.27

CHD and Family History

Family history of CHD is a non-modifiable risk factor for the development of atherosclerotic disease. In our cohort study, family history of CHD was significantly more common in young patients compared to non-young patients with STEMI. This finding is supported by the current guidelines28 which has a class I recommendation to obtain the family history of CHD in all asymptomatic adults.


This was a retrospective review of patients with STEMI. This study was not designed as a case control study so multivariate analysis for STEMI versus control could not be performed for determining independent causal relationships.


Obesity and family history of CHD were major risk factors with a higher prevalence in young patients with STEMI than non-young patients.


The authors thank Ms Valerie Lauer for her assistance in electronic data retrieval and Mr Patrick Lowe for his statistical assistance.

  1. Cooper R, Cutler J, Desvigne-Nickens P, et al., Trends and disparities in coronary heart disease, stroke, and other cardiovascular diseases in the United States: findings of the national conference on cardiovascular disease prevention, Circulation, 2000;102:3137–47.
  2. Berenson GS, Srinivasan SR, Emergence of obesity and cardiovascular risk for coronary artery disease: the Bogalusa Heart Study, Prev Cardiol, 2001;4:116–21.
  3. Imamura H, Izawa A, Kai R, et al., Trends over the last 20 years in the clinical background of young Japanese patients with coronary artery disease, Circ J, 2004;68:186–91.
  4. Poirier P, Giles TD, Bray GA, et al., Obesity Committee of the Council on Nutrition, Physical Activity, and Metabolism. Obesity and cardiovascular disease: pathophysiology, evaluation, and effect of weight loss: an update of the 1997 American Heart Association Scientific Statement on Obesity and Heart Disease from the Obesity Committee of the Council on Nutrition, Physical Activity, and Metabolism, Circulation, 2006;113:898–918.
  5. Chua SK, Hung HF, Shyu KG, et al., Acute ST-elevation myocardial infarction in young patients: 15 years of experience in a single center, Clin Cardiol, 2010;33:140–8.
  6. Wienbergen H, Gitt AK, Juenger C, et al., Impact of the body mass index on occurrence and outcome of acute ST-elevation myocardial infarction, Clin Res Cardiol, 2008;97:83–8.
  7. Wells B, Gentry M, Ruiz-Arango A, et al., Relation between body mass index and clinical outcome in acute myocardial infarction, Am J Cardiol, 2006;98:474–7.
  8. Wilson PWF, D’Agostino RB, Levy D, et al., Prediction of coronary heart disease using risk factor categories, Circulation, 1998;97:1837–47.
  9. Third report of the National Cholesterol Education Program (NCEP) expert panel on detection, evaluation, and treatment of high blood cholesterol in adults (Adult Treatment Panel III). Final report, Circulation, 2002;106:3143–421.
  10. Hurst’s The Heart, Arteries and Veins, 10th ed, New York, NY: McGraw-Hill, 2001:3–7; Am J Cardiol, 2002;90:927–31.
  11. Roger VL, Go AS, Lloyd-Jones DM, et al., Heart disease and stroke statistics—2011 update: a report from the American Heart Association, Circulation, 2011;123:e18–e209.
  12. Lakka HM, Laaksonen DE, Lakka TA, et al., The metabolic syndrome and total and cardiovascular disease mortality in middle-aged men, JAMA, 2002;288:2709–16.
  13. Hubert HB, Feinleib M, McNamara PM, et al., Obesity as an independent risk factor for cardiovascular disease: A 26-year follow up of participants in the Framingham Heart Study, Circulation, 1983;67:968–77.
  14. Keys A, Menotti A, Aravanis C, et al., The seven countries study: 2,289 deaths in 15 years, Prev Med, 1984;13:141–54.
  15. Rimm EB, Stampfer MJ, Giovannucci E, et al., Body size and fat distribution as predictors of coronary heart disease among middle-aged and older US men, Am J Epidemiol, 1995;141:1117–27.
  16. Calle EE, Thun MJ, Petrelli JM, et al., Body-mass index and mortality in a prospective cohort of U.S. adults, N Engl J Med, 1999;341:1097–105.
  17. Yusuf S, Hawken S, Ounpuu S, et al., Obesity and the risk of myocardial infarction in 27,000 participants from 52 countries: a case-control study, Lancet, 2005;366:1640–9.
  18. Canoy D, Boekholdt SM, Wareham N, et al., Body fat distribution and risk of coronary heart disease in men and women in the European Prospective Investigation Into Cancer and Nutrition in Norfolk cohort: a population-based prospective study, Circulation, 2007;116:2933–43.
  19. The Emerging Risk Factors Collaboration, Separate and combined associations of body-mass index and abdominal adiposity with cardiovascular disease: collaborative analysis of 58 prospective studies, Lancet, 11 March 2011(Article in Press DOI: 10.1016/S0140-6736(11)60105-0).
  20. Buettner HJ, Mueller C, Gick M, et al., The impact of obesity on mortality in UA/non-ST-segment elevation myocardial infarction, Eur Heart J, 2007;28:1694–701.
  21. Uretsky S, Messerli FH, Bangalore S, et al., Obesity paradox in patients with hypertension and coronary artery disease, Am J Med, 2007;120:863–70.
  22. Romero-Corral A, Montori VM, Somers VK, et al., Association of body-weight with total mortality and with cardiovascular events in coronary artery disease: a systematic review of cohort studies, Lancet, 2006;368:666–78.
  23. Pencina M, D’Agostino RB, Fox CS, et al., Obesity is independently associated with long-term risk of cardiovascular mortality and underweight with risk of non-cardiovascular mortality in Framingham Offspring Cohort [abstract 1466], Circulation, 2009;120:S508.
  24. Peeters A, Barendregt JJ, Willekens F, et al., Obesity in adulthood and its consequences for life expectancy: a life-table analysis, Ann Intern Med, 2003;138:24–32.
  25. Ades PA, Savage PD, The Obesity Paradox: Perception vs Knowledge, Mayo Clin Proc, 2010;85:112–4.
  26. Chambers JC, Eda S, Bassett P, et al., C-reactive protein, insulin resistance, central obesity, and coronary heart disease risk in Indian Asians from the United Kingdom compared with European whites, Circulation, 2001;104:145–50.
  27. Mertens I, Van der Planken M, Corthouts B, et al., Visceral fat is a determinant of PAI-1 activity in diabetic and non-diabetic overweight and obese women, Horm Metab Res, 2001;33:602–7.
  28. Greenland P, Alpert JS, Beller GA, et al., American Heart Association. 2010 ACCF/AHA guideline for assessment of cardiovascular risk in asymptomatic adults: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, J Am Coll Cardiol, 2010;56:2182–99.