The effect of intracoronary nifedipine on regional and global left ventricular performance, coronary vasomotility, and myocardial oxygen consumption is reported. Left ventricular pressures and volume indices of contractility and relaxation were simultaneously recorded in five patients without coronary artery disease. In these patients, nifedipine in the left main coronary artery not only delayed (+115 ms) anterior wall contraction but also slowed (3.5 vs 1.9 cm/s) and depressed it (-26%), resulting in a depression of global left ventricular ejection. This asynchrony and depression of regional contraction is considered to be responsible for the slowed isovolumic contraction and relaxation of the whole ventricle. In 10 other patients with coronary artery disease, coronary sinus blood flow and myocardial oxygen consumption were measured before and after intracoronary nifedipine. The observed decrease in myocardial oxygen consumption (-28%) depended primarily on a decrease in contractility and left ventricular performance. In a third study group of 12 patients with coronary artery disease, the effects of intracoronary nifedipine on the coronary vasomotility of 40 coronary segments (normal, prestenotic, stenotic, poststenotic) were quantitatively determined. Left ventricular haemodynamics and coronary sinus saturation were monitored while the cineangiograms were recorded before and after nifedipine. Nifedipine provoked vasodilatation of the normal (+10.3%), prestenotic, stenotic (+4 to 30%), and poststenotic (+16.4%) coronary segments, which persisted after the disappearance of its direct effects on the myocardium. This transient regional "cardioplegic" effect of nifedipine, associated with an increase in coronary blood flow, a reduction in myocardial oxygen consumption, and a vasodilatation of the epicardial vessels is likely to be beneficial during temporary coronary occlusion such as occurs in spasm or transluminal angioplasty.
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