Abstract
Myocardial ischemia could induce arrhythmias such as ventricular tachycardia and ventricular fibrillation, leading to sudden death and other serious consequences. This manuscript adopted the cardiac modeling and simulation method to study the activity pattern of myocardial ischemia-related ventricular tachycardia and the effect of increased extracellular potassium concentration on arrhythmia vulnerability. A whole ventricular electrophysiological model of endocardial ischemia caused by distal occlusion of left anterior descending coronary artery was established. The simulation results suggested that the relationship between the vulnerability of ventricular arrhythmias and extracellular potassium concentration was bell shaped with a peak in susceptibility at 12 mM. This result was caused by the effect of extracellular potassium concentration on the dispersion of repolarization and the effective refractory period of cardiomyocytes. The extension of the effective refractory period was due to the electrical remodeling of the ventricle. Specifically, it was because of the delayed recovery of the INa current. In addition, the regularity of endocardial/epicardial reentrant pattern during non-transmural ischemia was also analyzed. The endocardium formed micro-reentrant, while the epicardium established macro-reentrant rotating around the ischemic regions provided a new idea for the determination of clinical ablation targets.
Highlights
Ischemic heart disease is a leading cause of sudden arrhythmic death, causing 7 million deaths worldwide every year [1]
The ischemic tissue showed a high resting potential, which was caused by the increase of extracellular potassium concentration
The simulation results suggested that the relationship between the vulnerability of ventricular arrhythmias and extracellular potassium concentration was bell shaped with a peak in susceptibility at 12 mM
Summary
Ischemic heart disease is a leading cause of sudden arrhythmic death, causing 7 million deaths worldwide every year [1]. Clinical studies have shown that the incidence of arrhythmias increases significantly when cardiomyocytes are ischemic [2]. It is of great clinical significance to study the relationship between myocardial ischemia and arrhythmia. Ischemia could lead to three main ischemic effects in cardiomyocytes: reduced oxygen supply (hypoxia), increased extracellular potassium concentration (hyperkalemia) and tissue acidification (acidosis). These metabolic changes make the amplitude and duration of action potential decrease, the conduction velocity slow down and the effective refractory period increase [4]. The elevation of resting membrane potential and the change of cellular excitability caused by the increase of extracellular potassium concentration may provide substrate conditions for the occurrence and maintenance of arrhythmia [5]. The relationship between extracellular potassium concentration and arrhythmia has been studied in animal experiments, the mechanism has not been analyzed and confirmed from micro to macro scale; further study is needed
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