Cellular and pathophysiological mechanisms of ventricular arrhythmias in acute ischemia and infarction.

Ventricular arrhythmias in the setting of acute myocardial ischemia and infarction remain a serious health problem because of their sudden and unpredictable nature and their potentially grave results. Electrophysiological changes that may be responsible for these arrhythmias have been described in cardiac cells and in ischemic tissue. Experimental models have played a major role in elucidating the diversity of potential mechanisms for these arrhythmias. Increases in extracellular K+, the presence of toxic metabolites, and the accumulation of catecholamines in ischemic tissue all appear to have a role in arrhythmogenesis. The autonomic nervous system also appears to play a major role in these arrhythmias. With increased understanding of the pathophysiology underlying these arrhythmias, prevention can be enhanced and therapy can be better targeted.