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The role of action potential duration restitution in vulnerability to reentry in a mathematical model of canine ventricle

The mechanism of initiation of ventricular fibrillation (VF) in normal and diseased heart is poorly understood. It has been shown that VF starts with a simple reentry, or ventricular tachycardia (VT), which then degenerates into the multiple meandering wavelets that characterize VF. Although a steeply-sloped action potential duration restitution (APDR) curve promotes the transition of VT to VF, its role in the initiation of reentry is less clear. We performed a comprehensive study using a detailed anatomic model of the canine heart to investigate the role of APDR in initiating reentry by a single extrastimulus (S2).

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