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与急性心肌梗死相关的电生理紊乱。

Electrophysiological disturbances associated with acute myocardial infarction.

作者信息

Sheridan D J, Culling W, Penny W J

出版信息

Eur Heart J. 1986 Jul;7 Suppl B:11-8. doi: 10.1093/eurheartj/7.suppl_b.11.

Abstract

By the time most patients reach hospital with acute myocardial infarction the risk of developing ventricular fibrillation (VF) is receding and Q wave evolution is complete. While these changes are the culmination of a single irreversible ischaemic insult, this may follow several reversible episodes of ischaemia associated with marked ECG changes during the preceding hours or days and further ischaemic episodes may follow the development of Q waves. Cellular electrophysiological changes associated with experimental myocardial ischaemia in an isolated guinea pig preparation were a reduction in refractory period and action potential amplitude, Vmax and duration while conduction time and QRS width were prolonged. Spontaneous recovery in action potential amplitude and Vmax was observed after 12 min of ischaemia and depended on the presence of residual coronary flow. Electrophysiological recovery commenced rapidly on reperfusion but with further shortening of action potential duration. Reperfusion VF was most likely to occur when the associated ischaemic insult was 20-30 min in duration. Myocardial catecholamine depletion significantly reduced these arrhythmias and this antiarrhythmic action was associated with marked attenuation of the electrophysiological effects of ischaemia and reperfusion.

摘要

大多数急性心肌梗死患者入院时,发生心室颤动(VF)的风险正在降低,Q波演变已完成。虽然这些变化是单一不可逆缺血性损伤的最终结果,但在此之前的数小时或数天内,这可能继发于几次与明显心电图变化相关的可逆性缺血发作,并且在Q波形成后可能会出现更多的缺血发作。在豚鼠离体心脏制备中,与实验性心肌缺血相关的细胞电生理变化包括不应期缩短、动作电位幅度、Vmax和时程降低,而传导时间和QRS波宽度延长。缺血12分钟后观察到动作电位幅度和Vmax的自发恢复,且这取决于残余冠脉血流的存在。再灌注时电生理恢复迅速开始,但动作电位时程进一步缩短。当相关的缺血性损伤持续20 - 30分钟时,再灌注性VF最有可能发生。心肌儿茶酚胺耗竭显著减少了这些心律失常,这种抗心律失常作用与缺血和再灌注电生理效应的明显减弱有关。

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