| pubmed-article:3354448 | pubmed:abstractText | The relation between nifedipine concentration and hemodynamic effects after sublingual administration of 10 or 20 mg was examined in 13 patients with nonobstructive hypertrophic cardiomyopathy (HC). Serum nifedipine concentrations were determined by gas chromatography and were not related to dose. Peripheral vascular resistance decreased as a function of nifedipine concentration (r = -0.63, p less than 0.001); this was associated with a concentration-related increase in heart rate (r = 0.56, p less than 0.001) and in cardiac index (r = 0.50, p less than 0.001). However, evidence for a pure vasodilator effect of nifedipine was inconsistent, in that the change in stroke volume index with nifedipine was not significant. Although stroke volume index increased at nifedipine concentrations between 60 and 120 ng/ml (38 +/- 6 to 42 +/- 4 ml/m2, p less than 0.01), it decreased at concentrations greater than 120 ng/ml (40 +/- 3 to 38 +/- 4 ml/m2, p less than 0.01). Moreover, pulmonary artery wedge pressure increased at nifedipine concentrations greater than 120 ng/ml (11 +/- 2 to 16 +/- 4 mm Hg, p less than 0.001), suggesting either depressed left ventricular (LV) systolic function or reduced LV filling. To investigate these possible mechanisms, LV systolic and diastolic function was studied during catheterization with a nonimaging scintillation probe in 6 of the 13 patients. In these subjects, heart rate was held constant by atrial pacing.(ABSTRACT TRUNCATED AT 250 WORDS) | lld:pubmed |
