Reversal of left ventricular hypertrophy after one-year treatment with clonidine: relationship between echocardiographic findings, blood pressure, and urinary catecholamines.

Previous studies have shown that some antihypertensive drugs, beside controlling arterial pressure (AP), reverse left ventricular hypertrophy (LVH) by reducing adrenosympathetic activity. The aim of our study was to evaluate the relationship between AP levels, echocardiographic LVH and 24-h urinary excretion of epinephrine (UE) and norepinephrine (UNE) in 23 previously untreated stable hypertensive individuals with LVH and in 18 healthy normotensive control subjects before and after 1-year treatment with oral clonidine. Intraventricular septal (IVS) and posterior wall (PW) thickness and left ventricular mass index (LVMI) were related to systolic (SAP), diastolic (DAP), and mean arterial pressure (MAP), as well as to UE and UNE by multivariate regression analysis. Before clonidine treatment increased values for IVS and PW thickness correlated with DAP (r = 0.54; p less than 0.05), and MAP (r = 0.50; p less than 0.05), a positive relation between IVS thickness and LVMI and UNE was found. After clonidine treatment, in addition to a statistically significant reduction in SAP, DAP, MAP, and in NE and UNE (all p less than 0.01), a decrease in IVS (12.5 to 9.5 mm; p less than 0.01) and in PW (11.2 to 9.3 mm; p less than 0.01) thickness as well as in LVMI (152.3 to 108.6 g/m2; p less than 0.01) was observed in hypertensive patients. LVMI weakly correlated with UNE change (r = 0.50; p less than 0.05). These data support a possible influence of catecholamines in modulating the development of LVH. They also confirm the parallel action of clonidine in controlling AP, in reducing UE and UNE, and in reversing LVH in hypertensive patients.