Minimally Symptomatic Hypertrophic Cardiomyopathy

We investigated the effects of nifedipine on left ventricular diastolic function in 17 asymptomatic or minimally symptomatic patients with hypertrophic cardiomyopathy by simultaneously measuring left ventricular pressure and volume with a catheter-tipped manometer and biplane cineangiography. Studies were performed before and 20 minutes after sublingual administration of nifedipine (20 mg). Heart rates were held constant (79±12 beats/min, mean±SD) by right atrial pacing. Left ventricular volumes and instantaneous rates of left ventricular volume were derived from frame-by-frame (20-msec) analyses of left ventricular biplane angiograms. Left ventricular peak systolic pressure (from 122±21 to 108±13 mm Hg, p<0.01 vs. control) and mean aortic pressure (from 96± 15 to 87± 11 mm Hg, p<0.01) decreased significantly with nifedipine. With afterload reduction, left ventricular ejection fraction (from 0.69±0.12 to 0.74±0.08, p<0.01) and cardiac output (from 6.4±2.0 to 7.2±2.2 1/min, p<0.05) increased significantly. However, there was a slight but significant increase in left ventricular enddiastolic pressure (from 15±8 to 18±8 mm Hg, p <0.05). Nifedipine did not improve left ventricular relaxation as assessed by the time constants of isovolumic pressure decay (t112, from 39.8±6.6 to 39.4±7.7 msec, NS; tlle, from 53.8±9.0 to 54.4±10.7 msec, NS). The peak filling rate of left ventricular volume during the rapid filling phase significantly increased with nifedipine (from 511± 127 to 627± 154 ml/sec, p<0.05), but when the peak filling rate was normalized for stroke volume, there was no statistically significant change (from 5.46+1.03 to 6.20±1.46 sec-', NS). The time from end systole to the peak filling rate also remained unchanged with nifedipine (from 204±36 to 196±34 msec, NS). The left ventricular diastolic pressure-volume relation was shifted downward (indicating improved left ventricular distensibility) in only one of 14 patients. We conclude that nifedipine does not improve left ventricular relaxation, diastolic filling, and distensibility in patients with hypertrophic cardiomiopathy who have minimal or no impairment of functional status. This finding suggests that abnormal left ventricular diastolic function is not necessarily associated with myocardial ischemia or intracellular calcium overload in hypertrophied myocardium in a mild form of hypertrophic cardiomyopathy. (Circulation 1990;81:593-601)