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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”

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 (1). 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.

Credits: Dr. Petras Stirbys

Biosense Webster
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Introduction to AFib
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