Regression of Left Ventricular Hypertrophy in Treated Hypertensive Patients with Dilevalol and Metoprolol—A Double Blind Randomized Study

This study was designed to evaluate the effects of a new beta‐adrenergic blocking agent with beta 2 agonist activity (dilevalol, an R‐R' isomer of labetalol) on left ventricular hypertrophy regression as seen by M‐mode echocardiography. The study design was a 2:1 double blind randomization of dilevalol versus metoprolol. There was an equal blood pressure reduction in the two groups (supine diastolic blood pressure fell from 101 ± 4.5 mm Hg to 87 ± 13.7 mm Hg , P < .001 in the dilevalol group, and 101 ± 4.3 mm Hg to 87 ± 8.6 mm Hg , P < .01, in the metoprolol group). At the end of 2 months, there was an overall 7.5% decrease in left ventricular mass index in the 16 dilevalol treated patients (this was due to a 4.4% decrease in posterior wall thickness, end diastolic dimension increased by only 1%). Of the seven patients with an increased left ventricular mass index, all demonstrated hypertrophy regression (mean 17.14%). In contrast, no significant change in left ventricular mass was seen in the metoprolol treated group. Echocardiography left ventricular mass index and electrocardiographic evidence of left ventricular hypertrophy (using the Sokolow‐Lyons criteria and Romhilt‐Estes point score) had poor correlation (r = .30 and r = .38, respectively). Resting ejection fraction increased by 5% and velocity of circumferential fiber shortening by 14% in the dilevalol treatment group (not significant), in conclusion, 1) echocardiographic left ventricular hypertrophy regression occurred with dilevalol treatment 2) this left ventricular regression was a result of a decrease in intraventricular septal thickness and posterior wall thickness 3) the poor correlation between echocardiographic increased left ventricular mass and electrocardiographic left ventricular hypertrophy was supported 4) dilevalol and metoprolol had equal antihypertensive effects .