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心肌缺血与心室颤动:病理生理学及临床意义

Myocardial ischemia and ventricular fibrillation: pathophysiology and clinical implications.

作者信息

Luqman Nazar, Sung Ruey J, Wang Chun-Li, Kuo Chi-Tai

机构信息

The Department of Cardiology, RIPAS Hospital, Brunei Darussalam.

出版信息

Int J Cardiol. 2007 Jul 31;119(3):283-90. doi: 10.1016/j.ijcard.2006.09.016. Epub 2006 Dec 12.

DOI:10.1016/j.ijcard.2006.09.016
PMID:17166606
Abstract

Ventricular fibrillation (VF) and myocardial ischemia are inseparable. The first clinical manifestation of myocardial ischemia or infarction may be sudden cardiac death in 20-25% of patients. The occurrence of potentially lethal arrhythmia is the end result of a cascade of pathophysiological abnormalities that result from complex interactions between coronary vascular events, myocardial injury, and changes in autonomic tone, metabolic conditions and ionic state of the myocardium. It is also related to the time from the onset of ischemia. Within the first few minutes there is abundant ventricular arrhythmogenesis usually lasting for 30 min. Triggers for ischemic VF occur at the border zone or regionally ischemic heart. The border zone of ischemia is the predominant site of fragmentation. Acute ischemia opens K(ATP) channels and causes acidosis and hypoxia of myocardial cells leading to a large dispersion in repolarization across the border zone. Abnormalities of intracellular Ca2+ handling also occur in the first few minutes of acute myocardial ischemia and may be an important cause of arrhythmias in human coronary artery disease. Substrate on the other hand transforms triggers into VF and serves to maintain it through fragmentation of waves in the ischemic zone. Thrombin levels, stretch, catecholamine, genetic predisposition, etc. are some of these factors. Reentry models described are spiral wave reentry, 3 dimensional rotors, reentry around 'M' cells and figure-of-eight reentry. Continuing efforts to better understand these arrhythmias will help identify patients of myocardial ischemia prone to arrhythmias.

摘要

心室颤动(VF)与心肌缺血密切相关。在20%-25%的患者中,心肌缺血或梗死的首个临床表现可能是心源性猝死。潜在致命性心律失常的发生是一系列病理生理异常的最终结果,这些异常是由冠状动脉血管事件、心肌损伤以及自主神经张力、代谢状况和心肌离子状态的变化之间复杂相互作用导致的。它还与缺血发作后的时间有关。在最初几分钟内会出现大量室性心律失常,通常持续30分钟。缺血性室颤的触发因素出现在缺血边缘区或局部缺血的心脏区域。缺血边缘区是碎裂的主要部位。急性缺血会打开ATP敏感性钾通道,导致心肌细胞酸中毒和缺氧,进而导致整个边缘区复极化出现大的离散。在急性心肌缺血的最初几分钟内,细胞内钙处理也会出现异常,这可能是人类冠状动脉疾病中心律失常的一个重要原因。另一方面,基质将触发因素转化为室颤,并通过缺血区的波碎裂来维持室颤。凝血酶水平、牵张、儿茶酚胺、遗传易感性等都是这些因素。所描述的折返模型有螺旋波折返、三维转子、围绕“M”细胞的折返和8字形折返。持续努力更好地理解这些心律失常将有助于识别易发生心律失常的心肌缺血患者。

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