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dc.contributor.authorTse, Gen
dc.contributor.authorYeo, JMen
dc.contributor.authorChan, Fionaen
dc.contributor.authorLai, ETHen
dc.contributor.authorYan, BPen
dc.date.accessioned2017-12-04T17:39:47Z
dc.date.available2017-12-04T17:39:47Z
dc.identifier.issn1664-042X
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/269915
dc.description.abstractSudden cardiac death (SCD) remains an unsolved problem in the twenty-first century. It is often due to rapid onset, ventricular arrhythmias caused by a number of different clinical conditions. A proportion of SCD patients have identifiable diseases such as cardiomyopathies, but for others, the causes are unknown. Viral myocarditis is becoming increasingly recognized as a contributor to unexplained mortality, and is thought to be a major cause of SCD in the first two decades of life. Myocardial inflammation, ion channel dysfunction, electrophysiological, and structural remodeling may play important roles in generating life-threatening arrhythmias. The aim of this review article is to examine the electrophysiology of action potential conduction and repolarization and the mechanisms by which their derangements lead to triggered and reentrant arrhythmogenesis. By synthesizing experimental evidence from pre-clinical and clinical studies, a framework of how host (inflammation), and viral (altered cellular signaling) factors can induce ion electrophysiological and structural remodeling is illustrated. Current pharmacological options are mainly supportive, which may be accompanied by mechanical circulatory support. Heart transplantation is the only curative option in the worst case scenario. Future strategies for the management of viral myocarditis are discussed.
dc.description.sponsorshipGT was awarded a BBSRC Doctoral Training Award and thanks for the Croucher Foundation for its generous support.
dc.publisherFrontiers Media
dc.rightsAttribution 4.0 International*
dc.rightsAttribution 4.0 Internationalen
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/en
dc.subjectviral myocarditisen
dc.subjectcardiac arrhythmiaen
dc.subjectmouse modelen
dc.subjectviral-induced cardiomyopathyen
dc.subjectconductionen
dc.subjectrepolarizationen
dc.titleWhat Is the Arrhythmic Substrate in Viral Myocarditis? Insights from Clinical and Animal Studiesen
dc.typeArticle
prism.number308en
prism.publicationNameFrontiers in Physiologyen
prism.volume7en
dc.identifier.doi10.17863/CAM.16790
dcterms.dateAccepted2016-07-06en
rioxxterms.versionofrecord10.3389/fphys.2016.00308en
rioxxterms.versionVoR*
rioxxterms.licenseref.urihttp://creativecommons.org/licenses/by/4.0/en
rioxxterms.licenseref.startdate2016-07-06en
dc.identifier.eissn1664-042X
rioxxterms.typeJournal Article/Reviewen
cam.issuedOnline2016-07-21en


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Attribution 4.0 International
Except where otherwise noted, this item's licence is described as Attribution 4.0 International