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Am J Physiol Heart Circ Physiol 282: H212-H218, 2002;
0363-6135/02 $5.00
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Vol. 282, Issue 1, H212-H218, January 2002

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

Tetsu Watanabe1, Michiyasu Yamaki2, Sou Yamauchi1, Osamu Minamihaba1, Takehiko Miyashita1, Isao Kubota1, and Hitonobu Tomoike1

1 First Department of Internal Medicine and 2 Division of Medical Informatics, Yamagata University School of Medicine, Yamagata 990-9585, Japan

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.

restitution hypothesis; simulation


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