2 series of patients with angiographically proven coronary artery disease were studied under the influence of an infusion of a beta-receptor stimulating drug (heptaminole) and of kalium-magnesium-aspartate (KMA) in high (series: I: 1000 mg of heptaminole in 25 min) and low doses (series II: 200 mg of heptaminole in 25 min) of beta-receptor stimulation. The results confirm the finding that high dose beta-receptor stimulation in patients with severe coronary artery disease results in failure of the contractile mechanism of the heart with the beta-receptor angina. However, administration of KMA simultaneously with the beta-receptor stimulator seems to be able to prevent the expected decrease of lactate extraction and results in no change in lactate AVD in series I and even in an 11% increase in lactate AVD in series II. Experimental data concerning the biochemical effects of KMA suggest that its ability to provide adequate amounts of oxaloacetone and hence to improve the function of the bricarbonic acid cycle seems to be of special importance. For this action to become relevant in coronary artery disease a situation would have to be postulated, in which an additional limiting factor of oxydative metabolism would be an inadequate supply of Krebs-cycle intermediates.