Changes in truncal obesity and fat distribution predict arterial health

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.

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

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).

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.

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.