Shortened Ca2+ signaling refractoriness underlies cellular arrhythmogenesis in a postinfarction model of sudden cardiac death.

Abstract

The attainment of a certain threshold [Ca(2+)](SR) is not sufficient for the generation of DCWs. Postrelease Ca(2+) signaling refractoriness critically influences the occurrence of DCWs. Shortened Ca(2+) signaling refractoriness due to RyR2 phosphorylation and oxidation is responsible for the increased rate of DCWs observed in VF myocytes and could provide a substrate for synchronization of arrhythmogenic events at the tissue level in hearts prone to VF.

Full Text

DOI - Circulation research (DOI)
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Subjects

Authors

Publication date

2012-02-20

Journal

Circulation research
Circ Res (1524-4571)

Journal topics

Language

Eng.

Copyright

Circulation research

Davis Heart and Lung Research Institute, The Ohio State University Medical Center, 473 W 12th Ave., Columbus, OH 43210, USA.. Andriy.Belevych [at] osumc.edu

Release reference

Circ Res. 2012 Feb;110(4):569-77