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

Summary

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<0.004), a slight increase in arterial O₂ saturation, a significant increase in QP/QS (p<0.02), and a decrease in RP/RS (p<0.02). The nifedipine effect was age related. On nifedipine, breathing oxygen resulted in, independent of age, a significant increase in QP/QS (p<0.003) and a significant decrease in PAP/PAO (p<0.04) and in RP/RS (p<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.