Introduction:
Ectopic fat depots may play a role in obesity-mediated cardiovascular disease (CVD). We tested the association of several distinct fat depots and incident CVD in an asymptomatic community-based sample.
Methods:
Participants from the Framingham Heart Study (n=3086, 49% women, mean age 50.2 years, free of CVD at baseline) underwent volumetric assessment of multiple fat depots using multidetector computed tomography from 2002–2005, and were followed longitudinally for CVD events. Fat depots included subcutaneous adipose tissue (SAT), visceral adipose tissue (VAT), pericardial adipose tissue, intra-thoracic adipose tissue and thoracic periaortic adipose tissue (TAT). Adipose volumes were standardized within sex to a mean of 0 and a standard deviation of 1. Cardiovascular events included coronary heart disease (myocardial infarction, coronary insufficiency or angina), cerebrovascular disease (stroke or transient ischemic attack), intermittent claudication, heart failure or CVD death. Using Cox proportional hazards regression models, we examined the association of each fat depot with the risk of CVD after adjustment for age, sex, systolic blood pressure, hypertension treatment, diabetes, total cholesterol, high-density lipoprotein cholesterol, smoking, and then additionally for BMI. We additionally examined the association of pericardial fat and incident coronary heart disease.
Results:
During a mean follow-up of 4.7 years, 90 CVD events occurred. After multivariable adjustment, VAT, VAT/SAT ratio, intra-thoracic fat and TAT were significantly associated with incident CVD events. The hazard ratios (95% confidence intervals) per each standard deviation higher were 1.37 (1.10–1.71, p=0.006 [VAT]), 1.30 (1.05–1.60, p=0.02 [VAT/SAT ratio]), 1.28 (1.03–1.59, p=0.03 [intra-thoracic fat]), and 1.30 (1.03–1.67, p=0.03 [TAT]), respectively. We observed no association between BMI (HR 1.15, 0.92–1.43, p=0.21), SAT (HR 1.13, 0.90–1.42, p=0.28) or pericardial fat (HR 1.14, 0.95–1.37, p=0.15) and incident CVD. After additional adjustment for BMI, VAT, VAT/SAT ratio and TAT remained significantly associated with incident CVD events [HR 1.44 (1.08–1.92, p=0.01 [VAT]), 1.34 (1.08–1.65, p=0.007 [VAT/SAT ratio]), and 1.31 (1.03–1.67, p=0.03 [TAT])], respectively. Pericardial fat was also not associated with incident coronary heart disease, even when limiting our events to myocardial infarction or coronary heart disease death (HR 0.97, p=0.81).
Conclusion:
Several distinct ectopic fat depots, including VAT, VAT/SAT ratio, intra-thoracic fat, and TAT, but not generalized obesity, are significantly associated with CVD events after adjustment for risk factors in our community-based sample. These findings support the growing recognition of several potentially pathogenic ectopic fat depots.
Ectopic fat deposition in populations of black African ancestry: A systematic review and meta-analysis