We studied nine patients with arteriosclerotic coronary heart disease (Group I) and 10 patients with normal coronary arteries (Group II) to elucidate mechanisms by which nifedipine affects catecholamine arterial levels and myocardial extraction at rest and during pacing. Nifedipine induced signs of general and coronary vasodilatation and improved myocardial lactate metabolism during pacing. Noradrenaline arterial concentration increased significantly after nifedipine in both groups (p less than 0.01). In Group I, the values were 40-50% higher compared with Group II. The net myocardial extraction of noradrenaline was not significantly affected by nifedipine, except during pacing in Group II, in which an increase in myocardial release was seen (p less than 0.05). In Group I, there was no correlation between arterial concentration of noradrenaline and myocardial release, while there was a significant negative correlation in Group II (p less than 0.0001). Adrenaline arterial concentration and myocardial extraction were not altered by nifedipine, but there was a positive significant correlation in Group I between arterial concentration and myocardial extraction of adrenaline (p less than 0.001). In conclusion, nifedipine increased noradrenaline levels in both groups of patients, probably reflecting a rise in sympathetic activity. Because myocardial lactate production turned into extraction in patients with coronary artery disease, the increased sympathetic tone evidently did not outweigh the beneficial antianginal effects of nifedipine.
Adult Aged