Arrhythmia initiation in catecholaminergic polymorphic ventricular tachycardia type 1 depends on both heart rate and sympathetic stimulation

Catecholaminergic polymorphic ventricular tachycardia type 1 (CPVT1) predisposes to ventricular tachyarrhythmias (VTs) during high heart rates due to physical or psychological stress. The essential role of catecholaminergic effects on ventricular cardiomyocytes in this situation is well documented,...

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Bibliographic Details
Published in:PloS one 2018, Vol.13 (11), p.e0207100-e0207100
Main Authors: Danielsen, Tore K, Manotheepan, Ravinea, Sadredini, Mani, Leren, Ida S, Edwards, Andrew G, Vincent, Kevin P, Lehnart, Stephan E, Sejersted, Ole M, Sjaastad, Ivar, Haugaa, Kristina H, Stokke, Mathis K
Format: Article
Language:English
Subjects:
Adrenergic receptors
Arrhythmia
Bicycles
Biology and Life Sciences
Calcium (reticular)
Calcium ions
Calcium signalling
Cardiac arrhythmia
Cardiology
Cardiomyocytes
Computation
Computer applications
Electrocardiography
Electrophysiology
Fitness training programs
Heart rate
Kinases
Laboratories
Medical research
Medicine and Health Sciences
Mouse devices
Mutation
Patients
Phenotypes
Phosphorylation
Physical Sciences
Physical training
Physiology
Polyvinyl chloride
Psychological stress
Ryanodine receptors
Sarcoplasmic reticulum
Sensitivity
Stimulation
Tachycardia
Thresholds
Ventricle
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Summary:Catecholaminergic polymorphic ventricular tachycardia type 1 (CPVT1) predisposes to ventricular tachyarrhythmias (VTs) during high heart rates due to physical or psychological stress. The essential role of catecholaminergic effects on ventricular cardiomyocytes in this situation is well documented, but the importance of heart rate per se for arrhythmia initiation in CPVT1 is largely unexplored. Sixteen CPVT1 patients performed a bicycle stress-test. Occurrence of VT triggers, i.e. premature ventricular complexes (PVC), depended on high heart rate, with individual thresholds. Atrial pacing above the individual PVC threshold in three patients did not induce PVCs. The underlying mechanism for the clinical observation was explored using cardiomyocytes from mice with the RyR2-R2474S (RyR2-RS) mutation, which exhibit exercise-induced VTs. While rapid pacing increased the number of Ca2+ waves in both RyR2-RS and wild-type (p
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0207100