Rilmenidine in patients with left ventricular hypertrophy: Beyond the reduction of left ventricular mass

B. Trimarco, C. Morisco, D. Sarno, G. Iovino, L. Argenziano, R. Russo, N. De Luca, M. Volpe

Research output: Contribution to journalArticle

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. LVH (g/m2 body surface area) was reversed after 1-year treatment (from 152 ± 5 to 131 ± p <0.05). One-year treatment induced an improvement in brachial artery compliance (cm4/dyne · 107) (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.

Original languageEnglish
JournalJournal of Cardiovascular Pharmacology
Volume26
Issue numberSUPPL. 2
Publication statusPublished - 1995

Fingerprint

rilmenidine
Left Ventricular Hypertrophy
Antihypertensive Agents
Therapeutics
Atrial Natriuretic Factor
Renin
Electrolytes
Cardiovascular Abnormalities
Blood Pressure
Brachial Artery
Rheology
Doppler Echocardiography
Body Surface Area
Angiotensin-Converting Enzyme Inhibitors
Compliance

Keywords

  • Antihypertensive treatment
  • Atrial natriuretic factor
  • Hypertension

ASJC Scopus subject areas

  • Pharmacology
  • Cardiology and Cardiovascular Medicine

Cite this

Rilmenidine in patients with left ventricular hypertrophy : Beyond the reduction of left ventricular mass. / Trimarco, B.; Morisco, C.; Sarno, D.; Iovino, G.; Argenziano, L.; Russo, R.; De Luca, N.; Volpe, M.

In: Journal of Cardiovascular Pharmacology, Vol. 26, No. SUPPL. 2, 1995.

Research output: Contribution to journalArticle

Trimarco, B, Morisco, C, Sarno, D, Iovino, G, Argenziano, L, Russo, R, De Luca, N & Volpe, M 1995, 'Rilmenidine in patients with left ventricular hypertrophy: Beyond the reduction of left ventricular mass', Journal of Cardiovascular Pharmacology, vol. 26, no. SUPPL. 2.
Trimarco, B. ; Morisco, C. ; Sarno, D. ; Iovino, G. ; Argenziano, L. ; Russo, R. ; De Luca, N. ; Volpe, M. / Rilmenidine in patients with left ventricular hypertrophy : Beyond the reduction of left ventricular mass. In: Journal of Cardiovascular Pharmacology. 1995 ; Vol. 26, No. SUPPL. 2.
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AU - Argenziano, L.

AU - Russo, R.

AU - De Luca, N.

AU - Volpe, M.

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AB - 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. LVH (g/m2 body surface area) was reversed after 1-year treatment (from 152 ± 5 to 131 ± p <0.05). One-year treatment induced an improvement in brachial artery compliance (cm4/dyne · 107) (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.

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