Endothelial dysfunction predicts regression of hypertensive cardiac mass

Background: Subclinical organ damage is a condition with an increased risk for fatal and nonfatal cardiovascular events. Particularly, endothelial dysfunction and left ventricular mass (LVM) are recognized as independent predictors of cardiovascular events in hypertensive patients. Besides, LVM in hypertensives is inversely related to forearm blood flow (FBF) responses to the endothelium-dependent vasodilating agent. We evaluated the role of endothelium-dependent vasodilation in the progression/regression of LVM in a group of hypertensive subjects.

Methods: We enrolled 170 hypertensive outpatients (88 men, 92 women; age 47 ± 11 years). LVM was calculated with the Devereux formula and indexed by surface area (LVMI). Endothelium-dependent vasodilation was investigated by intra-arterial infusions of acetylcholine (ACh).

Results: During the follow-up blood pressure (BP) decreased from 150/91 ± 17/11 to 135/80 ± 14/9 mm Hg (P=0.0001), and LVMI from 120 ± 28 to 118 ± 28 g/m(2) (P=0.194). The mean annual rate of variation of LVMI was -0.38 ± 3.9 g/m(2), which was not statistically different in men and women. It was correlated with baseline ACh-stimulated FBF (r=-0.272, P=0.0001) and BMI (r=0.164, P=0.016). At multivariate analysis, FBF was the only baseline covariate that remained significantly associated with LVMI variation, also after correction for antihypertensive treatment and BP reduction. The interaction between baseline LVM and ACh-stimulated FBF was investigated in a multiple linear regression model showing that a fixed reduction in ACh-stimulated FBF (100%) induces different variation of annual rate of LVMI at different levels of baseline LVM.

Conclusions: Our data demonstrate, for the first time, the role of endothelial function in the progression/regression of LVMI, independently of traditional cardiovascular risk factors and antihypertensive therapy.