African Americans with a family history of cardiovascular disease show lower endothelial-dependent vasodilation.

Normotensive African Americans (AAs) show attenuated vascular responses and reduced nitric oxide (NO) bioavailability compared to European Americans (EAs). Few studies have used diverse measures to examine differences in macrovascular function and structure in individuals with a family history of CV disease (CVD). We assessed 150 AAs (Mage, 23.57 ± 2.73 yr) and 104 EAs (Mage, 22.70 ± 2.86) with a confirmed family history of CVD. Age, sex, body mass index, and father's education were used as covariates, hemodynamic measures (heart-rate [HR], stroke volume [SV], cardiac output [CO], total peripheral resistance [TPR], mean arterial pressure [MAP], systolic and diastolic blood pressure [SBP/DBP], and pulse pressure [PP]), high-frequency heart-rate variability [HF-HRV], and endothelial-dependent arterial dilation [EDAD] were the dependent variables. AA's had lower EDAD (11.64 vs. 13.20%) and higher HF-HRV (7.31 vs. 7.11 ms2), TPR (17.60 vs. 15.93 mmHg/L/min), TPI (33.72 vs. 30.09 mmHg/L/min/m2), MAP (83.60 vs. 78.36 mmHg), SBP (115.44 vs. 110.23 mmHg), and DBP (65.35 vs. 60.57 mmHg). Lower EDAD alongside no ethnic differences in PP, HR, or SV suggests early onset endothelial dysfunction (lower NO availability) rather than inherited pathophysiological structural characteristics (arterial stiffness) in AAs. Future prospective studies are needed and should consider measures of sympathetic activity and potential moderators, including discrimination.