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Heart failure (HF) is one of the most common cardiac diseases that are associated with increased susceptibility of ventricular arrhythmia causing morbidity and mortality. Previous studies have found that HF causes a series of electrical and structural remodeling in the heart. The aim of this study was to determine the predominant factor of HF-induced remodeling responsible for ventricular arrhythmias. We developed a new family of cellular electrical models of canine ventricular and Purkinje fiber (PF) myocytes in control and HF condition based on experimental data. These models were validated by reproducing experimentally observed AP prolongation in HF condition. Single cell models were then incorporated into a 3D anatomical model with detailed electrical heterogeneity and structural anisotropy, as well as PF network. Re-entrant excitation waves were initiated using the phase distribution method. Role of each individual HF-induced electrical and structural remodeling on lifespan of re-entry was investigated. Among HF-induced remodeling, the reduction of intercellular conductivity plays an important role in sustaining ventricular arrhythmia. The ion channel remodeling though prolongs APD leading to increased vulnerability, it however reduces sustainability of re-entry.

Computational Investigation of Pro:arrhythmogenesis of Heart Failure Induced Electrical Remodelling in Ventricles