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Cardiac Events Theoretically Cannot Be Produced By Non-Ischemic And/Or Iso-Ischemic Myocardium: Challenging Postulations And Vitality Of The Concept Of Ischemia-Dependent Conflictogenic Arrhythmias

机译:理论上非缺血性和/或缺血性心肌不能产生心脏事件:缺血相关的冲突性心律失常概念的挑战性和生命力

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摘要

Ischemia plays a key role in cardiac arrhythmogenesis, particularly in elderly patients. Healthy, non-ischemic and structurally normal myocardium is universally free from dysrhythmias. Thereby intact coronary blood flow prevents potential cardiac events. Hypothetically, ischemia-related electrophysiological differences are responsible for the supraventricular and/or ventricular rhythm irregularities. The goal of this review is to determine the role of systemic and coronary circulatory peculiarities and their association with heart rhythm abnormalities. The current analytical review extends and enriches previous knowledge about the influence of these peculiarities on the genesis of ischemia-dependent conflictogenic arrhythmias. Different intensity of coronary blood flow resulting from stenotic obstacles or vasospasm potentially leads to the non-uniform perfusion of myocites thus creating albeit subtle but vulnerable and powerful electrophysiologic substrate impending cardiac rhythm disturbances. Apparently, the behavior of both non-ischemic and iso-ischemic myocardium in respect to electric cardiac activity is very similar, at least theoretically. Some different clinical entities, e.g. arterial hypotension and/or anemia containing ischemic component, in most cases are free from arrhythmias. This postulation may be helpful in furthering arrhythmogenicity insights which have been generated previously. On the contrary, increased blood pressure often concurs with the supraventricular and/or ventricular arrhythmias; this pattern also favorably reflects our previous hypothetical assumptions associated with the mechanisms of arrhythmogenesis. Conclusively, both non-ischemic and iso-ischemic myocardium may be attributed to nonarrhythmogenic milieu. Nevertheless, the inventive analysis and more explorative data are required to support the suggested postulations.
机译:缺血在心律不齐的发生中起着关键作用,尤其是在老年患者中。健康,非缺血且结构正常的心肌普遍无心律失常。因此,完整的冠状动脉血流可防止潜在的心脏事件。假设与缺血有关的电生理差异是导致室上和/或心室节律不规则的原因。这篇综述的目的是确定全身性和冠状动脉循环异常的作用以及它们与心律异常的关系。当前的分析综述扩展并丰富了有关这些特殊性对缺血依赖性冲突性心律失常的发生的影响的先前知识。由狭窄障碍或血管痉挛引起的不同强度的冠状动脉血流可能导致肌钙蛋白的灌注不均匀,从而尽管产生微妙但脆弱且强大的电生理底物,从而导致心律失常。显然,至少在理论上,非缺血性和等缺血性心肌在心电活动方面的行为非常相似。一些不同的临床实体,例如动脉低血压和/或贫血中含有缺血性成分,多数情况下无心律不齐。这种假设可能有助于进一步了解以前产生的心律失常性见解。相反,血压升高通常与室上和/或室性心律失常有关。这种模式也有利地反映了我们以前与心律失常发生机制相关的假设。结论是,非缺血性和等缺血性心肌均可归因于非心律失常性环境。然而,需要有创造性的分析和更多的探索性数据来支持建议的假设。

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