Ventricular arrhythmias, sudden death, and silent myocardial ischemia.

摘要: T HE ASSOCIATION between acute ischemia and ventricular arrhythmia in experimental animals is well established. Kaplinsky et al’ found two periods of early within 30 minutes coronary occlusion dogs. Janse al* described mechanisms during ischemia. At the normal side ischemic border they a focal mechanism, induced possibly by injury currents Purkinje fibers, whereas myocardium macroand microreentry arrhythmia. Coronary cats3 caused increased conduction time through epicardial regions, asynchronous depolarization shortening refractory period, accompanied arrhythmias. Kabell al4 demonstrated that reduction collateral flow to an infarcted area animals, fractionation delay electrogram zone higher frequency pacing-induced tachycardia (VT). The effect repeated 5-minute followed reperfusion on was assessed Shiki Hearse5 rats; all exhibited VT 83% them fibrillation (VF). After conversion sinus rhythm following recovery, were again subjected reperfusion. Following short recovery period from initial bout only 8% 17% developed none had VF, longer associated with progressive return vulnerability. Thus, very “preconditioned” protected arrhythmias, but for time. Recent evidence suggests platelet activation may contribute arrhythmogenesis myocardial Flores al6 platelets reduced action potential duration. Further support role inducing life-threatening arrhythmias provided Davies al7 who aggregation as frequent finding patients unstable angina suffering sudden cardiac death. association catecholamines, ischemia, complex one. Within 10 noradrenaline concentration increased.8l” accumulation catecholamines extracellular space viable can cause malignant acceleration cell damage.‘O High doses epinephrine decrease resting membrane amplitude, slow conduction, produce undirectional block; these alterations predispose reentrant Epinephrine also induce triggered activity, underlying automatic i1,12 importance sympathetic system ischemia-induced further substantiated protective effects beta blockers both against necrosisi3s14 15.1h In human hearts no enhanced release angioplastyinduced could be detected sampling blood.17 An humans Garan al’s 17 multivessel disease survived out-ofhospital arrest. Before bypass surgery ischemia; after or VF not patients, suggesting major contributing factor patients. Morady al’” performed electrophysiological stimulation 15 survivors