Does verapamil improve left ventricular relaxation in patients with myocardial hypertrophy?

A beneficial effect of verapamil on left ventricular relaxation has been reported in patients with hypertrophic cardiomyopathy. The effect of 0.1 mg/kg intravenous verapamil on left ventricular relaxation and diastolic mechanics was studied in 10 patients with hypertrophic cardiomyopathy and 13 patients with aortic stenosis. M mode echocardiograms and left ventricular high-fidelity pressure measurements were obtained simultaneously in patients at rest and 10 to 15 min after verapamil. The time constant of left ventricular pressure decay (T; in msec) and the pressure intercept (PB; in mm Hg) were calculated from left ventricular pressure and negative dP/dt during isovolumetric relaxation with the use of a linear regression analysis. Left ventricular early and mean diastolic filling rates as well as diastolic pressure-diameter relationships before and after verapamil were determined from simultaneous echocardiographic and pressure measurements. After verapamil heart rate, left ventricular peak systolic pressure, and maximum and minimum dP/dt remained unchanged in both groups. Left ventricular end-diastolic pressure increased significantly from 15 to 17 mm Hg (p less than .02) in patients with aortic stenosis but did not change in those with hypertrophic cardiomyopathy. However, the time constant T decreased significantly from 79 to 60 msec (p less than .001) in patients with hypertrophic cardiomyopathy but increased significantly from 53 to 68 msec (p less than .025) in those with aortic stenosis. Parallel to the decrease in time constant, early (5.3 vs 7.3 cm/sec, p less than .05) and mean (3.0 vs 4.3 cm/sec, p less than .06) diastolic lengthening rate increased in patients with hypertrophic cardiomyopathy after verapamil. In contrast, early (7.7 vs 7.6 cm/sec, p = NS) and mean (4.3 vs 4.2 cm/sec, p = NS) diastolic lengthening rate remained unchanged in patients with aortic stenosis. The diastolic pressure-diameter relationship did not change in either group after verapamil. Cycle efficiency of the left ventricular pressure-diameter loop was significantly decreased in patients with hypertrophic cardiomyopathy when compared with that in those with aortic stenosis (71% vs 80%; p less than .01), but improved significantly from 71% to 77% (p less than .02) in patients with hypertrophic cardiomyopathy and remained unchanged in those with aortic stenosis (80% vs 80%) after verapamil. We conclude that verapamil improves left ventricular relaxation in patients with hypertrophic cardiomyopathy but delays relaxation in those with aortic stenosis.(ABSTRACT TRUNCATED AT 400 WORDS)