Stirbys Petras
Department of Cardiology, Lithuanian University of Health Sciences Hospital, Kaunas Clinic, Kaunas, Lithuania.
J Atr Fibrillation. 2013 Dec 31;6(4):976. doi: 10.4022/jafib.976. eCollection 2013 Dec.
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.
缺血在心律失常的发生中起关键作用，尤其是在老年患者中。健康、无缺血且结构正常的心肌通常不会出现心律失常。因此，完整的冠状动脉血流可预防潜在的心脏事件。据推测，缺血相关的电生理差异是室上性和/或室性节律异常的原因。本综述的目的是确定全身和冠状动脉循环特性的作用及其与心律异常的关联。当前的分析性综述扩展并丰富了先前关于这些特性对缺血依赖性冲突性心律失常发生影响的认识。由狭窄障碍或血管痉挛导致的不同强度的冠状动脉血流可能会导致心肌细胞灌注不均匀，从而产生尽管细微但脆弱且强大的电生理基础，易于引发心律失常。显然，至少在理论上，非缺血心肌和同等缺血心肌在心脏电活动方面的表现非常相似。一些不同的临床情况，如含有缺血成分的动脉低血压和/或贫血，在大多数情况下不会出现心律失常。这一假设可能有助于进一步深入了解先前产生的心律失常机制。相反，血压升高常与室上性和/或室性心律失常同时出现；这种模式也很好地反映了我们先前与心律失常发生机制相关的假设。总之，非缺血心肌和同等缺血心肌都可被认为处于无心律失常的环境中。然而，需要进行创新性分析和更多探索性数据来支持所提出的假设。
