Effects of one-year treatment with rilmenidine on systemic hypertension-induced left ventricular hypertrophy in hypertensive patients

Abstract

In patients with essential hypertension, left ventricular hypertrophy (LVH) increases the risk for cardiovascular morbidity and mortality. Thus its reversal represents one of the principal endpoints of antihypertensive treatment. We assessed the cardiovascular effects of 1-year antihypertensive treatment with rilmenidine (1 or 2 mg/day orally), a new oxazoline with a potent antihypertensive action that acts selectively through imidazoline-preferring receptors. In 11 hypertensive patients (mean age, 49 ± 2 years) with LVH, we measured systemic hemodynamics, large artery compliance, cardiac anatomy, and endocrine function. Patients underwent M-mode and 2-dimensional echocardiography as well as Doppler and peripheral pulsed Doppler flowmetry, determination of plasma atrial natriuretic factor (ANF) levels and renin activity (PRA), and of 24-hour urinary electrolyte and creatinine excretion in control conditions (systolic/diastolic blood pressure, 148 ± 3 102 ± 1 mm Hg ), 4 weeks after blood pressure normalization ( 131 ± 2 84 ± 2 mm Hg ; p < 0.01), after 1 year of satisfactory antihypertensive treatment ( 142 ± 3 90 ± 1 mm Hg ; p <0.01) and, finally, 1 month after therapy withdrawal ( 155 ± 3 106 ± 2 mm Hg ; difference not significant [NS]). One-year of rilmenidine treatment induced an improvement in brachial artery compliance (from 0.92 ± 0.06 to 1.16 ± 0.08 cm 4/dyne; p <0.05), which persisted after withdrawal of treatment (1.17 ± 0.06 cm 4/ dyne; p <0.05). LVH was reversed after 1 year of rilmenidine treatment (from 152 ± 5 to 131 ± 4 g/m 2 body surface area; p <0.05). Finally, PRA and urinary electrolyte excretion did not change throughout the study, and ANF remained unchanged after blood pressure normalization (48.4 ± 6.2 vs 44.7 ± 2.9 pg/mL; difference not significant) but fell after reversal of LVH (28.6 ± 3.4 pg/mL; p <0.05) and remained significantly lower than in control conditions after therapy withdrawal (27.5 ± 2.9 pg/mL; p <0.05). Our results demonstrate that long-term antihypertensive treatment with rilmenidine is able to induce a reversal of LVH and of the vascular structural changes associated with essential hypertension. In addition, they indicate that rilmenidine-induced regression of LVH is associated with significant and persistent reduction of ANF levels, which may suggest a favorable influence of the drug with the biosynthetic properties of ventricular myocardium.