Vulnerability in Simulated Ischemic Ventricular Transmural Tissues

Abstract

Vulnerability is an effective index to evaluate increased risk for unidirectional conduction block and reentry in hearts. Recent reports in animal experiments have indicated an opposite characteristics of the vulnerability in normal and ischemic transmural tissues. In order to clarify the differences and to investigate the mechanisms, a computer simulation method was used in this study to investigate the vulnerability relative to the premature pacing sites in normal and ischemic transmural tissues. Endo-, mid- and epi-cardial myocytes incorporating different severities of ischemia were developed across a tissue strand. The sodium channel inactivation gating variable h was calculated to provide the degree of sodium current recovery preceding the premature pacing. In the normal tissue, the measured vulnerable window was demonstrated to be wider by delivering an endocardial premature beat than that by applying an epicardial premature pacing. On the contrary, during ischemia the epicardium showed a wider vulnerable window than the endocardium. The results illustrated that during ischemia h decreased with accumulation of [K⁺]o, and action potential duration dispersion was obviously altered due to anoxia. In contrast, the elevated [K⁺]o was suggested to play an important role in the difference of the location-dependent vulnerability in normal and ischemic tissues.