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Paradoxical Effect of Increased Diastolic Ca 2+ Release and Decreased Sinoatrial Node Activity in a Mouse Model of Catecholaminergic Polymorphic Ventricular Tachycardia: Depressed SAN Automaticity in CPVT
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Paradoxical Effect of Increased Diastolic Ca 2+ Release and Decreased Sinoatrial Node Activity in a Mouse Model of Catecholaminergic Polymorphic Ventricular Tachycardia: Depressed SAN Automaticity in CPVT

Patricia Neco, Angelo Torrente, Pietro Mesirca, Esther Zorio, Nian Liu, Silvia G. Priori, Carlo Napolitano, Sylvain Richard, Jean-Pierre Benitah, Matteo E. Mangoni, …
Circulation, Vol.126(4), pp.392-401
24/07/2012
DOI: https://doi.org/10.1161/CIRCULATIONAHA.111.075382
PMCID: PMC3434373
PMID: 22711277

Résumé

Action Potentials Adrenergic beta-Agonists Isoproterenol Male Mutation Mice Mice, Inbred C57BL Mice, Mutant Strains Middle Aged Patch-Clamp Techniques Adult Ryanodine Receptor Calcium Release Channel Animals Sarcoplasmic Reticulum Sinoatrial Node Tachycardia, Ventricular Aged Calcium Humans Calcium Signaling Disease Models, Animal Exercise Female In Vitro Techniques
Catecholaminergic polymorphic ventricular tachycardia is characterized by stress-triggered syncope and sudden death. Patients with catecholaminergic polymorphic ventricular tachycardia manifest sinoatrial node (SAN) dysfunction, the mechanisms of which remain unexplored.

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