Beta-Blocking Drugs and Myocardial Function

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Abstract
Beta-adrenoceptor antagonists do not directly depress myocardial contractile function. The primary pharmacological target of these drugs is to attenuate the increase in myocardial oxygen consumption resulting from sympathoadrenal stimulation of the heart. Pure beta blockade achieves this by modulating the increases in heart rate and myocardial contractility. This brings in its train the unwanted secondary and tertiary consequences of ventricular dilatation, impaired cardiac output response to exercise, and reflex increases in systemic vascular resistance and left ventricular afterload. Together these physiological effects offset much of the primary therapeutic benefit of these drugs. The ancillary pharmacological properties possessed by newer generations of beta-adrenoceptor antagonists have reduced some of the undesirable hemodynamic consequences of pure beta blockade. In this respect, positive inotropic activity and vasodilator effects, however achieved, are desirable properties in a drug with beta-blocking activity. Such additional pharmacodynamic activities afford direct support of cardiac contractile activity and reduce the undesirable increase in peripheral vasoconstriction that results from beta blockade alone. Celiprolol is a new dimension in beta-blocking therapy in that it achieves these additional hemodynamic benefits by widespread modulation of sympathoadrenal activity.

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