2020
‘Social distancing’ of the neuronal nitric oxide synthase from its adaptor protein causes arrhythmogenic trigger-substrate interactions in long QT syndrome
Tieu A, Akar FG. ‘Social distancing’ of the neuronal nitric oxide synthase from its adaptor protein causes arrhythmogenic trigger-substrate interactions in long QT syndrome. Cardiovascular Research 2020, 117: 338-340. PMID: 32589704, PMCID: PMC7820852, DOI: 10.1093/cvr/cvaa179.Commentaries, Editorials and Letters
2011
Deciphering Arrhythmia Mechanisms: Tools of the Trade
Salama G, Akar FG. Deciphering Arrhythmia Mechanisms: Tools of the Trade. Cardiac Electrophysiology Clinics 2011, 3: 11-21. PMID: 21572551, PMCID: PMC3093299, DOI: 10.1016/j.ccep.2010.10.013.Peer-Reviewed Original ResearchArrhythmia mechanismsIschemia-reperfusion injuryCalcium handling propertiesLong QT syndromeMultiple cardiovascular disordersHeart failureCardiac functionCardiovascular disordersQT syndromeComplex arrhythmiasAction potentialsOptical action potentialsPathophysiological remodelingTissue levelsOrgan system levelRepolarization gradientsArrhythmiasSub-cellular changesSyndromeInjuryLevels
2008
Targeted deletion of kcne2 impairs ventricular repolarization via disruption of IK,slow1 and Ito,f
Roepke TK, Kontogeorgis A, Ovanez C, Xu X, Young JB, Purtell K, Goldstein PA, Christini DJ, Peters NS, Akar FG, Gutstein DE, Lerner DJ, Abbott GW. Targeted deletion of kcne2 impairs ventricular repolarization via disruption of IK,slow1 and Ito,f. The FASEB Journal 2008, 22: 3648-3660. PMID: 18603586, PMCID: PMC2537427, DOI: 10.1096/fj.08-110171.Peer-Reviewed Original ResearchConceptsAlpha subunitKv4 alpha subunitsAction potential durationVentricular action potential durationFunctional promiscuityVentricular membrane fractionsLong QT syndromeVentricular repolarizationAncillary subunitsWild typeNovel roleMembrane fractionKcne2 deletionKv1.5 proteinTargeted deletionSubunitsKcne2 disruptionMiRP1Cardiac roleProteinKCNE2DeletionKv1.5Sevoflurane anesthesiaDisruption
2005
Molecular Basis of Arrhythmias
Shah M, Akar FG, Tomaselli GF. Molecular Basis of Arrhythmias. Circulation 2005, 112: 2517-2529. PMID: 16230503, DOI: 10.1161/circulationaha.104.494476.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsIon channel subunit genesChannel subunit genesSubunit geneMolecular basisBasic biologySingle gene disordersNew molecular targetsCardiac arrhythmiasCellular basisGene disordersMolecular targetsMolecular pathogenesisPathophysiological conditionsCritical roleCatecholaminergic polymorphic ventricular tachycardiaPrimary electrical diseasePathological remodelingFundamental mechanismsPolymorphic ventricular tachycardiaImportant insightsLong QT syndromeElectrical diseaseVentricular tachycardiaBrugada syndromeGenes
2002
Unique Topographical Distribution of M Cells Underlies Reentrant Mechanism of Torsade de Pointes in the Long-QT Syndrome
Akar FG, Yan GX, Antzelevitch C, Rosenbaum DS. Unique Topographical Distribution of M Cells Underlies Reentrant Mechanism of Torsade de Pointes in the Long-QT Syndrome. Circulation 2002, 105: 1247-1253. PMID: 11889021, DOI: 10.1161/hc1002.105231.Peer-Reviewed Original ResearchConceptsLong QT syndromeSpecific ion channel mutationsCongenital long QT syndromeM cellsQT interval prolongationIon channel mutationsInterval prolongationReentrant mechanismTdP arrhythmiasConduction blockCanine wedge preparationReentrant circuitTransmural dispersionLeft ventricleAction potentialsTransmural wallIntact myocardiumTopographical distributionChannel mutationsWedge preparationsMidmyocardial cellsRepolarizationLQT2Cellular basisElectrical instability