Potential electrophysiologic mechanisms responsible for dysrhythmias associated with reperfusion of ischemic myocardium.
Dysrhythmia associated with reperfusion may not only play a critical role in sudden cardiac death, but also, the presence of dysrhythmia during intracoronary administration of thrombolytic agents may reflect heterogeneity of recovery of excitability and, hence, salvage of ischemic myocardium. The electrophysiologic basis for these dysrhythmias appears to be heterogeneity of electrical recovery resulting in reentry or enhanced ventricular automaticity. Although the precise mechanisms are unknown, rapid changes in K+, PCO2 and intracellular Ca++ appear to play major roles. In addition, alterations in the regional concentration or tissue compartment localization of amphiphilic lipid metabolites such as lysophosphoglycerides and long-chain acyl carnitines may affect not only the development of dysrhythmia during reperfusion, but also the salvage of ischemic myocardium. Recent experimental evidence in several species also suggests a prominent role of alpha 1-adrenergic stimulation in the evolution of dysrhythmia associated with reperfusion.
D001145:Arrhythmias, Cardiac / Q000209:etiology* / Q000503:physiopathology; D002118:Calcium / Q000502:physiology; D003326:Coronary Circulation; D003327:Coronary Disease / Q000188:drug therapy* / Q000503:physiopathology; D005343:Fibrinolytic Agents / Q000009:adverse effects*; D006329:Heart Conduction System / Q000187:drug effects* / Q000503:physiopathology; D006801:Humans; D011188:Potassium / Q000502:physiology; D011942:Receptors, Adrenergic, alpha / Q000502:physiology
D005343:Fibrinolytic Agents; D011942:Receptors, Adrenergic, alpha; D011188:Potassium; D002118:Calcium