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• W2028487714 endingPage "1659" @default.
• W2028487714 startingPage "1652" @default.
• W2028487714 abstract "In the 8 years since the discovery of the genetic bases of catecholaminergic polymorphic ventricular tachycardia (CPVT), we have witnessed a remarkable improvement of knowledge on arrhythmogenic mechanisms involving disruption of cardiac Ca(2+) homeostasis. Studies on the consequences of RyR2 and CASQ2 mutations in cellular systems and mouse models have shed new light on pathways that are also implicated in arrhythmias occurring in highly prevalent diseases, such as heart failure. This research track has also led to the identification of therapeutic targets of potential clinical impact to abate the burden of sudden death in CPVT. Here, we review the current knowledge on the pathophysiology of CPVT also highlighting the existing controversies and possible future development." @default.
• W2028487714 created "2016-06-24" @default.
• W2028487714 creator A5008966758 @default.
• W2028487714 creator A5021196395 @default.
• W2028487714 creator A5033233937 @default.
• W2028487714 date "2009-11-01" @default.
• W2028487714 modified "2023-10-16" @default.
• W2028487714 title "Catecholaminergic polymorphic ventricular tachycardia: A paradigm to understand mechanisms of arrhythmias associated to impaired Ca2+ regulation" @default.
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• W2028487714 doi "https://doi.org/10.1016/j.hrthm.2009.06.033" @default.
• W2028487714 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19879546" @default.
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