Literature DB >> 22958452

Atrial arrhythmia, triggering events and conduction abnormalities in isolated murine RyR2-P2328S hearts.

J H King1, Y Zhang, M Lei, A A Grace, C L-H Huang, J A Fraser.   

Abstract

AIM: RyR2 mutations are associated with catecholaminergic polymorphic tachycardia, a condition characterized by ventricular and atrial arrhythmias. The present experiments investigate the atrial electrophysiology of homozygotic murine RyR2-P2328S (RyR2(S/S)) hearts for ectopic triggering events and for conduction abnormalities that might provide a re-entrant substrate.
METHODS: Electrocardiograph recordings were made from regularly stimulated RyR2(S/S) and wild type (WT) hearts, perfused using a novel modified Langendorff preparation. This permitted the simultaneous use of either floating intracellular microelectrodes to measure action potential (AP) parameters, or a multielectrode array to measure epicardial conduction velocity (CV).
RESULTS: RyR2(S/S) showed frequent sustained tachyarrhythmias, delayed afterdepolarizations and ectopic APs, increased interatrial conduction delays, reduced epicardial CVs and reduced maximum rates of AP depolarization ((dV/dt)(max)), despite similar effective refractory periods, AP durations and AP amplitudes. Effective interatrial CVs and (dV/dt)(max) values of APs following ectopic (S2) stimulation were lower than those of APs following regular stimulation and decreased with shortening S1S2 intervals. However, although RyR2(S/S) atria showed arrhythmias over a wider range of S1S2 intervals, the interatrial CV and (dV/dt)(max) of S2 APs provoking such arrhythmias were similar in RyR2(S/S) and WT.
CONCLUSIONS: These results suggest that abnormal intracellular Ca(2+) homoeostasis produces both arrhythmic triggers and a slow-conducting arrhythmic substrate in RyR2(S/S) atria. A similar mechanism might also contribute to arrhythmogenesis in other conditions, associated with diastolic Ca(2+) release, such as atrial fibrillation.
© 2012 The Authors Acta Physiologica © 2012 Scandinavian Physiological Society.

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Year:  2012        PMID: 22958452     DOI: 10.1111/apha.12006

Source DB:  PubMed          Journal:  Acta Physiol (Oxf)        ISSN: 1748-1708            Impact factor:   6.311


  32 in total

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5.  Treatment of catecholaminergic polymorphic ventricular tachycardia in mice using novel RyR2-modifying drugs.

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7.  Atrial arrhythmogenesis in catecholaminergic polymorphic ventricular tachycardia--is there a mechanistic link between sarcoplasmic reticulum Ca(2+) leak and re-entry?

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Review 9.  Atrial remodelling in atrial fibrillation: CaMKII as a nodal proarrhythmic signal.

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