title: Rilmenidine in patients with left ventricular hypertrophy: beyond the reduction of left ventricular mass.
abstract: It is generally accepted that the development of left ventricular hypertrophy (LVH) represents a multifactorial phenomenon that also involves neurohormonal mechanisms. This finding may account for the ability of angiotensin-converting enzyme inhibitors to induce faster and more complete reversal of LVH than that observed with other antihypertensive treatments. The sympathetic system is also involved in the genesis of hypertension-induced LVH. We assessed the effects of satisfactory long-term treatment with rilmenidine, a new oxazoline with a potent antihypertensive action, on cardiovascular structural abnormalities and cardiac endocrine function in hypertensive patients with left ventricular hypertrophy. Eleven patients underwent M-mode and two-dimensional Doppler echocardiography, peripheral pulsed Doppler flowmetry, determination of plasma atrial natriuretic factor [(ANF) pg/ml] and renin activity, and 24-h urine electrolyte excretion under control conditions, after 4 weeks of blood pressure normalization, after 1 year of satisfactory antihypertensive treatment and, finally, 4 weeks after therapy withdrawal. I.VH (g/m2 body surface area) was reversed after 1-year treatment (from 152 +/- 5 to 131 +/- 4, p < 0.05). One-year treatment induced an improvement in brachial artery compliance (cm4/dyne.10(7)) (from 0.92 +/- 0.06 to 1.16 +/- 0.08, p < 0.05) that persisted after withdrawal of treatment (1.17 +/- 0.06, p < 0.05). Plasma renin activity and urinary electrolyte excretion did not change throughout the study, whereas ANF remained unchanged after blood pressure normalization (48.4 +/- 6.2 versus 44.7 +/- 2.9, NS), fell after reversal of LVH (28.6 +/- 3.4, p < 0.05), and remained significantly lower than under control conditions after therapy withdrawal (27.5 +/- 2.9, p < 0.05). These results demonstrate that a satisfactory long-term antihypertensive treatment with rilmenidine is able to reverse cardiovascular structural changes and to restore cardiac endocrine function.
authors.affiliation: Department of Internal Medicine, Federico II University, Naples, Italy.
authors.forename: B
authors.initials: B
authors.lastname: Trimarco
authors.forename: C
authors.initials: C
authors.lastname: Morisco
authors.forename: D
authors.initials: D
authors.lastname: Sarno
authors.forename: G
authors.initials: G
authors.lastname: Iovino
authors.forename: L
authors.initials: L
authors.lastname: Argenziano
authors.forename: R
authors.initials: R
authors.lastname: Russo
authors.forename: N
authors.initials: N
authors.lastname: De Luca
authors.forename: M
authors.initials: M
authors.lastname: Volpe
mesh_terms: D000959:Antihypertensive Agents / Q000627:therapeutic use*; D009320:Atrial Natriuretic Factor / Q000097:blood; D004334:Drug Administration Schedule; D004573:Electrolytes / Q000652:urine; D005260:Female; D006352:Heart Ventricles / Q000033:anatomy & histology / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000188:drug therapy; D017379:Hypertrophy, Left Ventricular / Q000188:drug therapy* / Q000209:etiology; D008297:Male; D008875:Middle Aged; D010080:Oxazoles / Q000627:therapeutic use*; D012083:Renin / Q000097:blood; D000077769:Rilmenidine
chemical_list: D000959:Antihypertensive Agents; D004573:Electrolytes; D010080:Oxazoles; D009320:Atrial Natriuretic Factor; D012083:Renin; D000077769:Rilmenidine