Vasodilatory capacity and vascular structure in long-standing hypertension: a LIFE substudy

Background Flow-mediated dilatation (FMD), which is considered a measure of endothelial function, has been found impaired in hypertension. However, it is unclear whether this impairment is explained solely by endothelial dysfunction, or whether it is associated with structural vascular changes and reduced vasodilatory capacity. Methods In 42 unmedicated patients with hypertension and electrocardiographic left ventricular hypertrophy, we measured the following: 24-h ambulatory blood pressure (BP), minimal forearm vascular resistance (MFVR) by plethysmography, intima-media cross-sectional area of the common carotid arteries (IMA), FMD, and nitroglycerin-induced dilatation (NID) in the brachial artery by ultrasound. Results: We found that FMD was correlated positively with NID (r = 0.38, P< .05). However, FMD as well as NID correlated negatively to 24-h systolic BP (r = −0.41, P = .01 and R = −0.52, P = .001), IMA/height (r = −0.41, P< .01 and R = −0.53, P< .001) and MFVRmen (r = −0.44, P< .05 and R = −0.42, P< .05). Conclusions Low FMD as well as low NID were related in parallel to high systolic BP and to the severity of vascular changes in different vascular beds, suggesting that elevated BP load in hypertension induces parallel abnormalities in conduit artery structure and overall vasodilatory capacity. Therefore, the decrease in FMD observed in severe hypertension may be caused by endothelial dysfunction as well as by structural vascular changes, suggesting difficulties in interpreting FMD solely as a measure of endothelial dysfunction in hypertensive patients with left ventricular hypertrophy.