Regional prolongation of ARI and altered restitution properties cause ventricular arrhythmia in heart failure.

The mechanism of arrhythmogenicity in heart failure remains poorly understood. We examined the relationship between electrical abnormalities and ventricular arrhythmia by using experimental heart failure models. Sixty unipolar electrograms were recorded from the entire cardiac surface in control dogs (n = 13) and pacing-induced heart failure dogs (n = 16). In failing hearts, activation time (AT) was delayed at the apex, and AT dispersion increased in failing hearts. Activation-recovery intervals (ARI) were prolonged mainly at the apex and ARI dispersion was significantly augmented. The slope of the ARI restitution curve, interaction of diastolic interval, and ARI in failing hearts was significantly steeper than in control hearts. Ventricular fibrillation (VF) was easily induced by programmed stimulation in failing hearts, whereas no arrhythmia occurred in control hearts. Computer simulation studies could reproduce the experimental results. Altering the ARI restitution to the steep slope causes VF in a model heart. It is suggested that electrical remodeling, especially steepness of electrical restitution, may play a role in arrhythmogenicity in failing hearts.