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Our understanding has grown tremendously since CPVT was first described as a clinical syndrome in 1995. It is now established that the deadly arrhythmias are caused by unregulated \u2018pathological\u2019 calcium release from the sarcoplasmic reticulum (SR), the major calcium storage organelle in striated muscle. Important questions remain regarding the molecular mechanisms that are responsible for the pathological calcium release, regarding the tissue origin of the arrhythmic beats that initiate ventricular tachycardia, and regarding optimal therapeutic approaches. At present, mutations in six genes involved in SR calcium release have been identified as the genetic cause of CPVT: <jats:italic>RYR2<\/jats:italic> (encoding ryanodine receptor calcium release channel), <jats:italic>CASQ2<\/jats:italic> (encoding cardiac calsequestrin), <jats:italic>TRDN<\/jats:italic> (encoding triadin), <jats:italic>CALM1<\/jats:italic>, <jats:italic>CALM2<\/jats:italic> and <jats:italic>CALM3<\/jats:italic> (encoding identical calmodulin protein). Here, we review each CPVT subtype and how CPVT mutations alter protein function, RyR2 calcium release channel regulation, and cellular calcium handling. We then discuss research and hypotheses surrounding the tissue mechanisms underlying CPVT, such as the pathophysiological role of sinus node dysfunction in CPVT, and whether the arrhythmogenic beats originate from the conduction system or the ventricular working myocardium. Finally, we review the treatments that are available for patients with CPVT, their efficacy, and how therapy could be improved in the future.\n<jats:boxed-text content-type=\"graphic\" position=\"anchor\"><jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/tjp14037-gra-0001-m.png\"><jats:alt-text>image<\/jats:alt-text><\/jats:graphic><\/jats:boxed-text><\/jats:p>","DOI":"10.1113\/jp276757","type":"journal-article","created":{"date-parts":[[2020,3,2]],"date-time":"2020-03-02T08:46:43Z","timestamp":1583138803000},"page":"2817-2834","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":120,"title":["Molecular and tissue mechanisms of catecholaminergic polymorphic ventricular 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Center for Arrhythmia Research and Therapeutics Division of Clinical Pharmacology Vanderbilt University Medical Center  Nashville Tennessee USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2020,4,27]]},"reference":[{"key":"e_1_2_6_2_1","first-page":"e210","article-title":"2017 AHA\/ACC\/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: Executive Summary","volume":"138","author":"Al\u2010Khatib 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