Ventricular tachyarrhythmias during acute myocardial infarction: the role of endothelin-1.

Ventricular arrhythmogenesis during acute coronary syndromes is a common cause of sudden cardiac death, but the underlying mechanisms remain incompletely understood. Recent evidence indicates an emerging pathophysiologic role of endothelin-1 during myocardial ischaemia and evolving infarction. At the early stages post-coronary occlusion, endothelin-1 enhances sympathetic activation, an effect mediated via the ETA receptor, whereas the ETB receptor exerts protective actions. The importance of this interaction is clearly decreased during subsequent stages, during which endothelin-1 may participate in the genesis of ventricular tachycardia or fibrillation via other mechanisms; of these, the effects of endothelin-1 on repolarizing potassium currents and electrical conduction via gap junctions merit further research. The relative roles of ETA and ETB receptors during this phase are unclear. Evaluation of the arrhythmogenic effects of endothelin-1 during acute coronary syndromes may provide the tools towards lowering sudden cardiac death rates.