Abstract
Acute myocardial ischemia induces an increase in interstitial extracellular potassium ([K+]e ). In the present overview, we review the electrophysiologic and metabolic consequences of [K+]e during acute myocardial ischemia, based upon findings from myself and my colleagues. 1) Heterogeneous increases in [K+]e between the endocardial and epicardial ischemic zones, and between the ischemic and border zones were demonstrated. 2) Intramyocardial conduction delay of the ischemic myocardium could not be explained by the increased [K+]e alone. However, hypoxia, acidosis, and isoproterenol also contribute to the conduction delay. Action potential duration was decreased by hypoxia, and the increased [K+]e led to a decrease in the action potential duration. However, isoproterenol increased the duration of the action potential in the setting of hypoxia and the increased [K+]e . 3) Treatments with CoQ10, GIK-P, and OKY-046 were shown to attenuate the increased [K+]e during acute myocardial ischemia. 4) The calcium antagonists, verapamil and nicardipine, also attenuate the increased [K+]e during acute myocardial ischemia. However, the effects were more pronounced with verapamil. 5) While the positive inotropic agents, isoproterenol, amrinone, and dopamine exacerbated the increased [K+]e , ouabain did not affect the rise in [K+]e during acute myocardial ischemia. 5) The class 3 antiarrhythmic drugs, bretylium, sotalol and amiodarone did not affect the increased [K+]e during acute myocardial ischemia. Bretylium and sotalol suppressed the shortening of the effective refractory period of the ischemic myocardium without affecting the conduction delay. However, amiodarone increased the effective refractory period of the ischemic myocardium without affecting the conduction delay.
