ArticleJournal of molecular and cellular cardiology plus2025
Disruption of ventricular activation by subthreshold delayed afterdepolarizations in RyR2-R420Q catecholaminergic polymorphic ventricular tachycardia.
Article in Journal of molecular and cellular cardiology plus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Ca2+ signalling in cardiac muscle: the importance of balances.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2026Review
- Abnormal calcium release and delayed afterdepolarizations: A comparison of two mathematical models for human ventricular myocytes.PloS one · 2026Article
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Authors and funding
4 authors.
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Abstract
Background: Catecholaminergic polymorphic ventricular tachycardia (CPVT) carries increased risk of ventricular arrhythmias due to altered Ca Methods: Heterozygous R420Q and wildtype (WT) control hearts were perfused on a Langendorff apparatus. Electrical activity was monitored using volume conducted ECG electrodes and monophasic action potential (MAP) electrode recordings. Left ventricular activation and membrane potential changes were recorded using an 8 × 8 multielectrode array and optical mapping, respectively. Results: ECG recordings showed spontaneous ventricular arrhythmias in isolated R420Q hearts. More severe arrhythmias occurred in R420Q hearts following rapid electrical pacing combined with isoproterenol stimulation. Ventricular activation time was not different between genotypes, regardless of stimulation frequency or isoproterenol. Phase differences in local activation times were greater in R420Q hearts during 10 Hz pacing with isoproterenol, suggesting local conduction slowing. Optical mapping experiments revealed subthreshold DADs occurring in R420Q hearts during diastolic pauses. DADs prolonged the subsequent action potential and were associated with conduction slowing during the second beat after the DAD, but not the first beat. 2D tissue simulations revealed that direct inactivation of I Conclusions: Increased activation dispersion could arise from subthreshold DADs in R420Q mouse hearts and may contribute to conduction block. This could increase the propensity for re-entrant arrhythmias in CPVT without directly triggering ectopic beats.
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