Long-term hemodynamic effects of nifedipine on congenital heart disease with Eisenmenger's mechanism in children.

The hemodynamic effect of long-term nifedipine medication was studied in 10 children, 3-12 years of age, five with ventricular septal defect and five with complete atrioventricular septal defect; all had Eisenmenger's reaction, seven also had Down's syndrome. They underwent heart catheterization prior to and during 1-4 years of nifedipine therapy. Fick's principle was used to calculate the ratio of pulmonary arterial pressure to aortic pressure (PAP/PAO), the ratio of pulmonary flow to aortic flow (QP/QS), as well as the ratio of pulmonary vascular resistance to aortic vascular resistance (RP/RS). In the seven children under 8.8 years, nifedipine caused a significant drop in PAP/PAO (p less than 0.004), a slight increase in arterial O2 saturation, a significant increase in QP/QS (p less than 0.02), and a decrease in RP/RS (p less than 0.02). The nifedipine effect was age related. On nifedipine, breathing oxygen resulted in, independent of age, a significant increase in QP/QS (p less than 0.003) and a significant decrease in PAP/PAO (p less than 0.04) and in RP/RS (p less than 0.003). Direct O2 consumption measurements before and during oxygen breathing in six patients demonstrated no significant change in RP, RS, QP, or QS indices. Nifedipine had a relaxing effect on the pulmonary vascular bed, especially in the younger child with Eisenmenger's mechanism. On nifedipine therapy, O2 produced a more complex hemodynamic reaction that was not restricted to the pulmonary circulation alone.