Changes in truncal obesity and fat distribution predict arterial health

Background: Truncal obesity is associated with metabolic syndrome and cardiovascular risk. Although vascular health is influenced by weight, it is not known whether changes in fat distribution modulate arterial function.

Objective: We assessed how changes in truncal (android) fat at 1 year affect arterial stiffness and endothelial function.

Methods: We recruited 711 healthy volunteers (235 males, age 48 ± 11 years) into the Emory Predictive Health Study; 498 returned at 1 year. Measurements included anthropometric and chemistry panels, fat mass using dual-energy X-ray absorptiometry, arterial stiffness indices (pulse wave velocity [PWV], augmentation index [AIx], and subendocardial viability ratio [SEVR]; Sphygmocor), flow-mediated dilation (FMD), and reactive hyperemia index (Endo-PAT).

Results: At baseline, measures of body mass correlated with PWV, AIx, SEVR, and FMD. In a multivariable analysis including body mass index (BMI) and traditional risk factors, BMI remained an independent predictor of PWV, AIx, SEVR, and FMD. In a model including BMI and measures of fat distribution, android fat remained an independent predictor of PWV (β = 0.31, P = .004), AIx (β = 0.24, P = .008), and SEVR (β = -0.41, P < .001). The 1-year change in android fat correlated negatively with change in SEVR (β = -0.13, P = .005) and FMD (β = -0.13, P = .006) after adjustment for change in gynoid fat.

Conclusion: In addition to BMI, android fat is a determinant of arterial stiffness, independent of traditional risk factors. Changes in android fat over time are associated with simultaneous changes in vascular function, indicating fat distribution's effect on vascular health.