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- W2129258486 abstract "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). In normal heart, S2 beats failed to initiate reentry with either steep or flat APDR. However, when diseased heart was simulated by adding an ischemic region (modeled by lowered excitability due to increased extracellular potassium), reentry was more easily induced by an S2 when APDR slope was steep (left figure). Flattening APDR reduced the “vulnerability window,” defined as the set of S2 intervals for which reentry was induced (right figure, black bars), from 60msec to 30msec. (White bars indicate that a propagated beat was initiated by S2 without reentry, gray bars indicate that the S2 beat failed to propagate). Flattening APDR may therefore be a promising therapy for preventing both initiation of reentry and the subsequent transition from VT to VF." @default.
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- W2129258486 date "2005-05-01" @default.
- W2129258486 modified "2023-09-27" @default.
- W2129258486 title "The role of action potential duration restitution in vulnerability to reentry in a mathematical model of canine ventricle" @default.
- W2129258486 doi "https://doi.org/10.1016/j.hrthm.2005.02.951" @default.
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