The hemodynamic effects of sublingual nifedipine were examined in 36 patients with hypertrophic cardiomyopathy. Twenty-one patients were initially given 20 mg and 15 patients were given 10 mg of the drug; 30 min after this first dose 26 patients received 10 mg and one patient 20 mg as a second dose. Hemodynamic findings in patients who received different doses of the drug were similar. Peak effects included an increase in heart rate from 79 ± 12 to 91 ± 14 (mean ± 1 SD) beats/min (p < .01) and a decrease in mean blood pressure from 89 ± 12 to 77 ± 10 mm Hg (p < .01). Cardiac index increased after nifedipine (2.8 ± 0.6 to 3.3 ± 0.8 liters/min/m2; p < .01); stroke volume index, however, did not change (36 ± 7 to 36 ± 8 ml/beat/m2; NS). Peripheral vascular resistance index fell significantly from 822 ± 261 to 610 ± 197 dynes·sec·cm-5 (p < .01). Overall, left ventricular outflow tract gradient (LVOTG) did not change in patients with significant (≥30 mm Hg) basal LVOTG (75 ± 22 to 83 ± 22 mm Hg; NS), but it increased significantly in those six patients in whom peripheral vascular resistance fell by 25% or more (73 ± 28 to 99 ± 22 mm Hg; p < .05). Pulmonary arterial wedge pressure increased significantly in patients with normal (≤15 mm Hg) basal values (9 ± 3 to 14 ± 7 mm Hg; p < .01) and in patients with significant basal LVOTG (15 ± 8 to 20 ± 10 mm Hg; p < .01). In 10 patients, systolic and diastolic function were studied simultaneously by a nonimaging scintillation probe. No changes in systolic or diastolic function were detected when determinations obtained at the time of the peak nifedipine effect were compared with control values recorded at similar heart rates obtained by atrial pacing. The pattern of change in the pressure-counts loops after administration of nifedipine was not consistent; in only three of 10 patients was an improvement in the diastolic pressure-volume relationship observed. These results indicate that in patients with hypertrophic cardiomyopathy sublingual nifedipine induces a marked reduction in afterload without demonstrating any beneficial effects on LVOT obstruction and diastolic function. Moreover, in patients with normal pulmonary arterial wedge pressure and/or significant LVOTGs, nifedipine seems to be detrimental because it increases filling pressures, with these changes being exaggerated in patients with more marked falls in peripheral vascular resistance.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Physiology (medical)