Beta-adrenoceptor antagonists and blood flow to the jeopardized myocardium.

The accepted rationale for the use of beta-adrenoceptor antagonists in the therapy of angina pectoris is that these drugs, by inhibiting the positive chronotropic and inotropic effects of sympathetic stimulation, reduce the myocardial oxygen consumption. In the present paper, another aspect of these agents, namely the effect on blood supply to the jeopardized myocardium, is discussed. In the presence of coronary artery stenosis, transmural blood flow to the ischaemic zone may be reduced and the endocardial perfusion, reactive hyperaemia and the contractile function of the myocardium are significantly affected. The administration of beta-adrenoceptor antagonists reduces the heart rate, myocardial contractility and myocardial oxygen demand, and improves the biochemical, electrical and mechanical function of the jeopardized myocardium, particularly during exercise or stress. The transmural blood flow may or may not increase but there is usually a redistribution of blood flow in favour of the endocardium where the imbalance between oxygen demand and supply is most marked. The main mechanisms responsible for this favourable redistribution appear to be: (i) an increase in the diastolic period, particularly in relation to the cardiac cycle, (ii) a restoration of autoregulation in the epicardium, and (iii) a vasoconstriction mediated by beta-adrenoceptors. The improvement of endocardial perfusion may play an additional role in the salvage of jeopardized myocardium.