Regression of cardiac hypertrophy: experimental and clinical results.

Since left ventricular hypertrophy is considered to be a precursor of later hypertensive heart failure, a treatment that can prevent or even reverse myocardial hypertrophy is a highly desirable goal. In order to evaluate which type of antihypertensive treatment is able to induce regression of hypertensive hypertrophy, experimental and clinical studies were performed. Experimental studies were performed in spontaneously hypertensive rats (SHRs). Left ventricular hypertrophy and pumping function were studied after antihypertensive treatment with a beta-receptor blocker (metoprolol), an arteriolar vasodilator (hydralazine), and a calcium channel blocker (nifedipine) had been instituted for a period of 20-40 weeks. Patients with hemodynamically compensated hypertensive heart disease were treated with a calcium channel blocker (nifedipine), an angiotensin-converting enzyme (ACE) inhibitor (enalapril), an antisympathetic agent (clonidine), and prazosin. Comparing the amount of blood pressure reduction with the extent of hypertrophy reversal, nifedipine, prazosin, and enalapril were equipotent, whereas clonidine was most efficient in this respect. Muscle mass was overproportionally reduced in relation to blood pressure reduction following treatment with clonidine. It is likely that this was caused by lowered catecholamine levels secondary to clonidine therapy. Left ventricular pumping function was enhanced as a result of a reduction in left ventricular afterload, whereas myocardial contractility was found to be unchanged.