Left ventricular hypertrophy is associated with reduced vasodilatory capacity in the brachial artery in patients with longstanding hypertension. A LIFE substudy

Abstract

Background: Left ventricular (LV) hypertrophy has been found to be associated with endothelial dysfunction in untreated patients with mild, uncomplicated hypertension. Whether similar relations exist in patients with longstanding hypertension and target organ damage remain to be elucidated.

Methods: In 40 unmedicated, hypertensive patients with electrocardiographic LV hypertrophy we measured 24-h ambulatory blood pressure (n = 37), LV mass index by echocardiography (LVMI(echo)) and magnetic resonance imaging (LVMI(MRI), n = 31), flow-mediated (FMD) and nitroglycerin-induced dilatation (NID) in the brachial artery by ultrasound, acetylcholine- (AIR) and nitroprusside-induced relaxation (NIR) in isolated resistance arteries by wire-myography.

Results: LVMI(MRI) correlated negatively to NID (r = -0.60, p < 0.001, n = 30) and to FMD (r = -0.53, p < 0.01, n = 31), but were not significantly correlated to maximal AIR nor NIR. NID (r = -0.53, p < 0.001, n = 36), FMD (r = -0.43, p < 0.01, n = 37), LVMI(MRI) (r = 0.60, p < 0.001, n = 29) and LVMI(echo) (r = 0.39, p < 0.05, n = 37) were all significantly correlated to 24-h systolic blood pressure, whereas maximal AIR and NIR were not.

Conclusions: LV mass was related to NID and FMD, but not to AIR. The relationship to FMD was not independent of NID indicating that LV hypertrophy in patients with longstanding hypertension is more closely related to reduced overall vasodilatory capacity in the brachial artery than to endothelial dysfunction in conduit or subcutaneous resistance arteries. High LV mass and low NID were both related to high blood pressure, suggesting that vasodilatory capacity in conduit arteries is modified parallel to LV geometry by elevated blood pressure.