The American Heart Hospital Journal
Table 4: Baseline Characteristics and Outcomes of the Cohort, by Body Mass Index PATIENT CHARACTERISTIC BMI (kg/m2
BMI <18.5 N=7
)
Age (in years) Male gender Hypertension Diabetes
Dyslipidemia Tobacco use
17.2 +/- 1.3 71.1 +/- 10.2 1 (14) 3 (43) 1 (14) 4 (57) 3 (43)
Family history of CHD 0 (0) LOS (days) Death
3.7 +/- 2.6 2 (29)
N=68
22.9 +/- 1.5 66.6 +/- 15.1 26 (60) 31 (72) 11 (26) 30 (70) 27 (63) 15 (35)
4.7 +/- 4.5 7 (16)
27 +/- 1.4
64.4 +/- 14.2 47 (69) 45 (66) 17 (25) 48 (71) 29 (43) 11 (16)
4.4 +/- 4.6 12 (18)
Original Contribution
BMI ≥18.5 AND < 25 BMI ≥25 AND <30 BMI ≥30 AND <40 BMI ≥40 N=43
N=78
33.6 +/- 2.7 55.6 +/- 12.7 56 (72) 59 (76) 25 (32) 54 (69) 36 (46) 17 (22)
3.9 +/- 3.8 5 (6)
N=10
TOTAL COHORT N=206
44.9 +/- 4.7 29.2 +/- 6.2 55.8 +/- 15 61.3 +/-14.6 4 (40) 8 (80) 6 (60) 7 (70) 6 (60) 3 (30)
134 (65) 146 (71) 60 (29) 143 (69) 101 (49) 46 (22)
5 +/- 2.7 0 (0)
4.3 +/- 4.2 26 (13)
Values are mean +/- standard deviation or number of patients (percentages). BMI = body mass index; CHD = coronary heart disease; LOS = length of hospital stay.
Mortality
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).
Discussion
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
The root causes of metabolic syndrome are overweight/obesity, physical inactivity, and genetic factors.9
It has been shown that individuals with metabolic syndrome, which includes obesity, are at increased risk for CHD.12
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
Summer 2011
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
with obesity23,24 paradox.25
Others, however, showed an increased mortality and suggest that there is no obesity
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
High Prevalence of Obesity in Young Patients with ST Elevation Myocardial Infarction 39
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