Effect of Electroporation on Cardiac Electrophysiology

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Abstract
Defibrillation shocks are commonly used to terminate life-threatening arrhythmias. According to the excitation theory of defibrillation, such shocks are aimed at depolarizing the membranes of most cardiac cells, resulting in resynchronization of electrical activity in the heart. If shock-induced transmembrane potentials are large enough, they can cause transient tissue damage due to electroporation. In this review, evidence is presented that electroporation of the heart tissue can occur during clinically relevant intensities of the external electrical field and that electroporation can affect the outcome of defibrillation therapy, being both pro- and antiarrhythmic. Here, we present experimental evidence for electroporation in cardiac tissue, which occurs above a threshold of 25 V/cm as evident from propidium iodide uptake, transient diastolic depolarization, and reductions of action potential amplitude and its derivative. These electrophysiological changes can induce tachyarrhythmia, due to conduction block and possibly triggered activity; however, our findings provide the foundation for future design of effective methods to deliver genes and drugs to cardiac tissues, while avoiding possible side effects such as arrhythmia and mechanical stunning.

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