What does this research mean for the field?

Abnormalities in intracellular calcium regulation, driven by mutations in the ryanodine receptor and cardiac calsequestrin, form the molecular basis of catecholaminergic polymorphic ventricular tachycardia (CPVT) and profoundly disrupt cardiac electrophysiology. Novelty: ClaimNovelty.SYNTHESIS. Consensus alignment: ConsensusAlignment.NEUTRAL.

March 31, 2011Circulation ResearchOpen Access

Inherited Dysfunction of Sarcoplasmic Reticulum Ca 2+ Handling and Arrhythmogenesis

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Population

Patients with Catecholaminergic polymorphic ventricular tachycardia (CPVT)

Design

Review

Authors

Silvia G. PrioriUniversity of Siena SCS.R. Wayne ChenElectrophysiology

Discussion

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Implication

Informs mechanistic CPVT approaches; leaves open whether Ca2+ targeting improves outcomes.

Structured PICO

Population

Patients with Catecholaminergic polymorphic ventricular tachycardia (CPVT)

This review highlights the translational importance of understanding intracellular Ca2+ regulation abnormalities in the diagnosis and management of CPVT.

Cite This Study

Priori et al. (2011) studied this question.

synapsesocial.com/papers/6a1a29e80fc4dc4e42436b5a https://doi.org/10.1161/circresaha.110.226845

Topics

Ventricular arrhythmias

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Inherited Dysfunction of Sarcoplasmic Reticulum Ca 2+ Handling and Arrhythmogenesis

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Topics

Inherited Dysfunction of Sarcoplasmic Reticulum Ca 2+ Handling and Arrhythmogenesis

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Topics

Also Consider