Abstract MP76: The Association of “Metabolically Benign Obesity” with Subclinical Myocardial Damage
Background: The term “metabolically benign obesity” refers to obese individuals who have a favorable metabolic profile (i.e., normal glucose, lipid, and blood pressure levels). However, the cardiovascular risk among these persons is largely uncharacterized. High sensitivity cardiac troponin (hs-cTnT) reflects occult cardiac injury. We hypothesized that hs-cTnT would be associated with obesity across the spectrum of metabolic abnormalities, and that persons with metabolically benign obesity would have a high prevalence of subclinical cardiac injury.
Methods: We conducted a cross-sectional analysis of 9477 participants from the ARIC Study with no history of coronary heart disease (CHD) or heart failure (HF). Participants were classified as normal, overweight, or obese, and by benign or adverse metabolic profile. An adverse profile was defined as >2 of the following factors: elevated blood pressure (systolic ≥130 mmHg, diastolic ≥85 mmHg or medication use), elevated glucose (fasting glucose≥100 mg/dl or diabetes), elevated triglycerides (≥150 mg/dl), decreased HDL-cholesterol (<50 mg/dl for women; 40 mg/dl for men).
Results: In this community-based population (mean age 63 years, 59% women, 78% white) without CHD or HF, 13% had metabolically adverse obesity and 22% had metabolically benign obesity. Overall 7% had elevated hs-cTnT (above the 99th percentile for a healthy reference population [0.014 μg/L]) and 66% had detectable hs-cTnT. The adjusted mean of hs-cTnT was highest among persons with metabolically adverse obesity (Figure). Among obese individuals, a higher proportion in the metabolically adverse group had elevated hs-cTnT (12% versus 7%, p<0.01) and detectable hs-cTnT (75% versus 67%, p <0.01). However, within individuals with metabolically benign profile, those with obesity were significantly more likely to have elevated hs-cTnT (OR 1.47, 95%CI 1.11, 1.96)
Conclusions: Adults with “metabolically benign obesity” had evidence of subclinical myocardial damage in this community-based population.
- © 2013 by American Heart Association, Inc.