Relationship between left ventricular mass and endothelium-dependent vasodilation in never-treated hypertensive patients

Background-Hypertensive patients are characterized by development of both l eft ventricular hypertrophy (LVH) and endothelial dysfunction Methods and Results-We enrolled 65 never-treated hypertensive patients (36 men and 29 women aged 45.6+/-6.0 years) to assess the possible relationship between echocardiographic left ventricular mass (LVM) and endothelium-depe ndent vasodilation. Left ventricular measurements were performed at end dia stole and end systole according to the recommendations of the American Soci ety of Echocardiography and the Penn Convention. LVM was calculated with th e Devereux formula and indexed by body surface area and height raised to th e 2.7th power. The endothelial function was tested as responses of forearm vasculature to acetylcholine (ACh), an endothelium-dependent vasodilator (7 .5, 15, and 30 mu g mL(-1) min(-1), each for 5 minutes), and sodium nitropr usside (SNP), an endothelium-independent vasodilator (0.8, 1.6, and 3.2 mu g mC(-1) min(-1), each for 5 minutes). Drugs were infused into the brachial artery, and forearm blood flow (FBF) was measured by strain-gauge plethysm ography. A negative significant relationship between indexed LVM and peak o f increase in FBF was found during ACh infusions (r = -0.554; P<0.0001). in addition, hypertrophic patients had a significantly lower responsive to AC h than patients without LVH (the peak increase in FBF was 9.9+/-3.7 versus 16.1+/-8.1 mt per 100 mt of tissue per minute; P<0.0001). No significant co rrelation was observed between LVM and FBF during SNP infusion. Conclusions-Our data provide the first evidence that echocardiographic LVM in hypertensive patients is inversely related to FBF responses to the endot helium-dependent vasodilating agent ACh, but it is likely that both endothe lium and LVM are damaged by hypertension.