Microvascular Function Contributes to the Relation Between Aortic Stiffness and Cardiovascular Events The Framingham Heart Study

Background Arterial dysfunction contributes to cardiovascular disease (CVD) progression and clinical events. Interrelations of aortic stiffness and vasodilator function with incident CVD remain incompletely studied. Methods and Results We used proportional hazards models to relate individual measures of vascular function to incident CVD in 4547 participants (mean age, 51 +/- 11 years; 54% women) in 2 generations of Framingham I Ieart Study participants. During follow-up (0,02-13,83 years), 232 participants (5%) experienced new-onset CVD events, In multivariable models adjusted for cardiovascular risk factors, both higher carotid-femoral pulse wave velocity (hazard ratio [HR], 1,32; 95% confidence interval ICU 1.07-1.63; P=0,01) and lower hyperemic mean flow velocity (HR, 0,84; 95% CI, 0.71-0,99; P=0,04) were associated significantly with incident CVD, whereas primary pressure wave amplitude (HR, 1,12; 95% CI, 0.99-1,27; P=0,06), baseline brachial diameter (HR, 1.09; 95% CI, 0,90-1,31; P=0,39), and flow-mediated vasodilation (11R, 0,85; 95% CI, 0,69-1,04; P=0.12) were not. In mediation analyses, 8% to 13% of the relation between aortic stiffness and CVD events was mediated by hyperemic mean flow velocity. Conclusions Our results suggest that associations between aortic stiffness and CVD events are mediated by pathways that include microvascular damage and remodeling,