The
calcium channel blocking agent,
nifedipine, has been shown to improve indexes of left ventricular relaxation, diastolic filling and compliance in patients with
hypertrophic cardiomyopathy. The mechanism of action of
nifedipine on diastolic properties in patients with
hypertrophic cardiomyopathy is unclear and could result from an improvement in myocardial inactivation or from systemic vasodilation and left ventricular unloading. To distinguish between these mechanisms, the effects of
nifedipine and the
vasodilator nitroprusside on left ventricular diastolic properties were compared in 10 patients with nonobstructive
hypertrophic cardiomyopathy using simultaneous micromanometer left ventricular pressure and echocardiographic measurements. Left ventricular peak systolic pressure was comparable during
nitroprusside infusion (132 +/- 38 mm Hg) and after
nifedipine (132 +/- 32 mm Hg). During
nitroprusside infusion, the decrease in left ventricular end-diastolic pressure (22 +/- 11 to 17 +/- 11 mm Hg, p less than 0.05) was associated with a decrease in left ventricular end-diastolic dimension. In contrast, the decrease in left ventricular end-diastolic pressure after
nifedipine (22 +/- 11 to 18 +/- 10 mm Hg, p less than 0.05) was associated with no reduction of left ventricular end-diastolic dimensions, suggesting an increase in left ventricular distensibility. Compared with
nitroprusside,
nifedipine was associated with less prolongation of the left ventricular isovolumic relaxation time and less depression of the peak left ventricular posterior wall thinning rate and peak left ventricular internal dimension filling rate. These data suggest that the effects of the
calcium channel blocker,
nifedipine, on diastolic mechanics in
hypertrophic cardiomyopathy result not only from systemic vasodilation but also from improved cardiac muscle inactivation.