Delayed afterdepolarizations generate both triggers and a vulnerable substrate promoting reentry in cardiac tissue.

ABSTRACT:

Background

Delayed afterdepolarizations (DADs) have been well characterized as arrhythmia triggers, but their role in generating a tissue substrate vulnerable to reentry is not well understood.

Objective

The purpose of this study was to test the hypothesis that random DADs can self-organize to generate both an arrhythmia trigger and a vulnerable substrate simultaneously in cardiac tissue as a result of gap junction coupling.

Methods

Computer simulations in 1-dimensional cable and 2-dimensional tissue models were performed. The cellular DAD amplitude was varied by changing the strength of sarcoplasmic reticulum calcium release. Random DAD latency and amplitude in different cells were simulated using gaussian distributions.

Results

Depending on the strength of sp

SUBMITTER: Liu MB 

PROVIDER: S-EPMC4583816 | biostudies-literature | 2015 Oct

REPOSITORIES: biostudies-literature