Treatment and post-treatment effects of alpha- versus beta-receptor blockers on left ventricular structure and function in essential hypertension.

This study was undertaken to compare the effects of alpha-receptor blockade and beta-receptor blockade on left ventricular structure and function in essential hypertension. The increase in left ventricular mass in patients with essential hypertension is at least partly induced by the sympathetic nervous system. We conducted a double-blind, randomized, controlled clinical trial to compare the effects of alpha-blockers and beta-blockers on left ventricular structure and function. Forty-three patients with mild to moderate essential hypertension were randomly allocated to receive antihypertensive therapy with either the alpha-blocker bunazosin (n = 23) or the beta-blocker metoprolol (n = 20). Twenty-four-hour blood pressure measurements and echocardiographic measurements of left ventricular structure and function were performed before therapy, after 6 months of therapy, and 4 weeks after discontinuation of therapy. Bunazosin and metoprolol led to similar reductions in systolic/diastolic blood pressure (-11 +/- 11/-9 +/- 8 mm Hg vs -11 +/- 12/-8 +/- 9 mm Hg, respectively) and left ventricular mass (-25 +/- 42 gm vs -28 +/- 44 gm, respectively) (p = no significant difference, bunazosin vs metoprolol). Neither metoprolol nor bunazosin significantly affected left ventricular systolic function. Diastolic left ventricular filling, however, was increased with beta-blocker medication, as indicated by a decrease in atrial filling fraction (39% +/- 5% to 34% +/- 5%; p < 0.05), but not with the alpha-blocker. The effect of metoprolol resulted from its bradycardiac effect. Four weeks after discontinuation of therapy, blood pressure and left ventricular mass increased to pretreatment levels in both groups similarly. Furthermore, the increase in diastolic filling was lost shortly after withdrawal of metoprolol concomitant with the increase in heart rate. We conclude that alpha-blockers and beta-blockers are equally capable of reducing left ventricular mass in hypertensive patients. beta-Blockers lead to an increase in diastolic left ventricular filling. This effect may be of therapeutic value because diastolic dysfunction may precede systolic dysfunction in hypertensive heart disease.