Abstract 1471: Peri-vascular Fat Deposition is Associated With Peripheral Arterial Disease: The Framingham Heart Study
Background Fat deposits immediately surrounding the coronary arteries are independently correlated with coronary artery calcification, suggesting a local toxic effect of fat on the vasculature. Similarly, peri-aortic fat may be associated with localized diseases of the aorta and lower extremity arteries. We hypothesized that individuals with greater amounts of peri-aortic fat have more clinical peripheral arterial disease (PAD) and a low ankle-brachial index (ABI).
Methods We quantified peri-aortic fat surrounding the thoracic aorta using a novel volumetric quantitative approach in 1205 individuals from the Framingham Heart Study Offspring cohort (mean age 65.9 years, 54% women); visceral abdominal fat (VAT) was also measured using standard imaging techniques. Clinical PAD was defined as a history of intermittent claudication and ABI was dichotomized as low ABI≤0.9 or lower extremity revascularization vs ABI >0.9 to <1.4. Regression models were created to examine the association between peri-aortic fat and intermitten claudication or ABI after adjustment for age, sex, smoking, diabetes, hypertension, total/HDL cholesterol, lipid treatment, and triglycerides.
Results Overall, 45 participants had a low ABI, and 35 had intermittent claudication. In multivariable logistic regression, per 1 standard deviation increase in fat, the odds ratio (OR) for low ABI was 1.8 for peri-aortic fat (p-value<0.001); these results were strengthened with additional adjustment for BMI (OR 2.1, p<0.001), whereas no association was observed for VAT (p=0.06). Similarly, per standard deviation increase in peri-aortic fat, the OR for intermittent claudication was 1.54 (p=0.02); results persisted after additional adjustment for BMI (OR=1.62, p-value=0.02), whereas no association was observed with VAT and intermittent claudication (p-value=0.27).
Conclusions Peri-aortic fat, but not visceral fat, is associated with low ABI and intermittent claudication. These findings support the concept that peri-vascular fat deposition may be involved in the pathogenesis of PAD.