Abstract
Ventricular fibrillation (VF) is the major cause of sudden cardiac death by lethal arrhythmia. Regional abnormalities such as myocardial infarction are regarded as the cause of VF; however, VF is clinically caused without the organic heart disease. Then we hypothesized that a human heart equips a protective mechanism against VF and thus the breakdown of the protective mechanism induces VF. We considered that the essence of the mechanism is the ventricular transmural gradient (electrophysiological heterogeneity) . To confirm this hypothesis, we have developed a 3-D ventricular wall model and analyzed the dynamics of spiral wave reentry and filament (reentrant organizing center) . It was found that the ventricular gradient forces an intramural filament to drift out a boundary and reduces the sustainment of VF. On the other hand, the pharmacological modifications of ventricular gradient to increase transmural dispersion of repolarization (TDR) break the protective mechanism and sustain VF.
