Key result
Experimental models suggest that increases in extracellular K+, toxic metabolites, catecholamines, and autonomic nervous system activity play major roles in arrhythmogenesis during acute ischemia.
Understanding the cellular and pathophysiological mechanisms of ventricular arrhythmias in acute ischemia can help enhance prevention and target therapy.
May guide mechanistic targets for ischemia-related arrhythmias; leaves open clinical translation from experimental models.
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.
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Ehlert et al. (1997) conducted a review in Ventricular arrhythmias in acute myocardial ischemia and infarction. Experimental models suggest that increases in extracellular K+, toxic metabolites, catecholamines, and autonomic nervous system activity play major roles in arrhythmogenesis during acute ischemia.
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