Relationship Between Left Ventricular Mass and Endothelium-Dependent Vasodilation in Never-Treated Hypertensive Patients

Abstract

Background —Hypertensive patients are characterized by development of both left 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-dependent vasodilation. Left ventricular measurements were performed at end diastole and end systole according to the recommendations of the American Society of Echocardiography and the Penn Convention. LVM was calculated with the Devereux formula and indexed by body surface area and height raised to the 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 μg · mL −1 · min −1 , each for 5 minutes), and sodium nitroprusside (SNP), an endothelium-independent vasodilator (0.8, 1.6, and 3.2 μg · mL −1 · min −1 , each for 5 minutes). Drugs were infused into the brachial artery, and forearm blood flow (FBF) was measured by strain-gauge plethysmography. A negative significant relationship between indexed LVM and peak of increase in FBF was found during ACh infusions ( r =−0.554; P <0.0001). In addition, hypertrophic patients had a significantly lower responsive to ACh than patients without LVH (the peak increase in FBF was 9.9±3.7 versus 16.1±8.1 mL per 100 mL of tissue per minute; P <0.0001). No significant correlation 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 endothelium-dependent vasodilating agent ACh, but it is likely that both endothelium and LVM are damaged by hypertension.