New Concepts of Antiarrhythmic Strategies

Abstract

Cardiac arrhythmias are an important cause of morbidity and mortality in hospital settings. They are more likely to occur in patients with heart disease, which provides the substrate for genesis of arrhythmias. However, arrhythmias often will not occur without some destabilizing factor (imbalance). For example, patients with chronic ischemic heart disease may have zones of fibrous scar tissue intermingled with surviving, normal fibers. The latter provide potential pathways (the substrate) for anatomical reentry. However, arrhythmias do not occur without some trigger, which could be premature beats from an automatic focus in response to digitalis excess, catecholamines, acute electrolyte or other imbalance. The latter might even be produced by an antiarrhythmic drug administered to suppress ventricular extrasystoles [1, 2]. If so, the premature beat encounters refractory tissue (due either to prematurity of the beat or increased refractoriness secondary to acute imbalance) and blocks in one direction. However, it conducts slowly in another part of the anatomical circuit and returns to re-excite no longer refractory tissues of the circuit. Thus, a reentry ventricular tachycardia could be initiated and sustained. With acute ischemic heart disease, we envision a different substrate, one not defined by anatomical boundaries. Rather, the substrate is defined by nonuniform electrophysiologic properties, produced by compromised coronary flow to some tissues. Consequently, depolarization and repolarization of myocardial fibers is inhomogeneous due to variable activation and inactivation of Na and K channels.