The role of the size of infarcted area on two kinds of vulnerable window in two dimension ventricular tissue.

AIMS: Sudden cardiac death (SCD) is mainly induced by ventricular arrhythmia, especially among patients with myocardial infarction (MI). Previous studies have shown that ventricular tachycardia and fibrillation are thought to be caused by re-entrant waves of excitation. Although in heterogeneous tissue, the traditional vulnerable window of unidirectional block and the vulnerable window when bidirectional propagation was initiated could coexist, little studies are based on effects of infarcted areas on both vulnerable windows.

METHODS AND

RESULTS

The electrophysiology remodeling was based on TP06 model in the present study. In simulation of two-dimension (2D) ideal models, excitation wave conduction in ventricular tissue was simulated under three different types of stimulus. 2D ideal models of ventricular tissue were constructed as loop areas in the center of a square tissue with the resolution of 600×600 grid points and cell size of 0.35mm. Simulation results showed that the traditional vulnerable window when unidirectional propagation was initiated was consistent no matter where the position of stimulus is and how long and how wide the size of the infarcted area is. However, the vulnerable window when bidirectional propagation was initiated varies in different conditions.

CONCLUSION

The traditional vulnerable window could not reflect the role of the infarcted area on arrhythmogenesis. The vulnerable window when bidirectional propagation was initiated increases with the increasement of the width and the length of the infarcted area with the appropriate position of the stimulus, which could help us to conclude the arrhythmogenesis according to the size of infarcted areas.