2021
B-PO04-006 CARDIAC SPECIFIC TSPO GENE SILENCING IMPROVES ELECTRICAL REMODELING AND POST-ISCHEMIC ARRHYTHMIAS IN HYPERTROPHIED HEARTS
Cacheux M, Tieu A, Ilkan Z, Jirak P, Motloch L, O'Rourke B, Akar F. B-PO04-006 CARDIAC SPECIFIC TSPO GENE SILENCING IMPROVES ELECTRICAL REMODELING AND POST-ISCHEMIC ARRHYTHMIAS IN HYPERTROPHIED HEARTS. Heart Rhythm 2021, 18: s282. DOI: 10.1016/j.hrthm.2021.06.703.Peer-Reviewed Original ResearchB-PO02-027 RIGHT PREDOMINANT ELECTRICAL REMODELING IN A PURE MODEL OF PULMONARY HYPERTENSION PROMOTES REENTRANT ARRHYTHMIAS
Strauss B, Obus E, Katz M, Fargnoli A, Cacheux M, Akar J, Hummel J, Sassi Y, Akar F. B-PO02-027 RIGHT PREDOMINANT ELECTRICAL REMODELING IN A PURE MODEL OF PULMONARY HYPERTENSION PROMOTES REENTRANT ARRHYTHMIAS. Heart Rhythm 2021, 18: s106. DOI: 10.1016/j.hrthm.2021.06.284.Peer-Reviewed Original Research
2018
Optical Action Potential Mapping in Acute Models of Ischemia–Reperfusion Injury: Probing the Arrhythmogenic Role of the Mitochondrial Translocator Protein
Ilkan Z, Strauss B, Campana C, Akar FG. Optical Action Potential Mapping in Acute Models of Ischemia–Reperfusion Injury: Probing the Arrhythmogenic Role of the Mitochondrial Translocator Protein. Methods In Molecular Biology 2018, 1816: 133-143. PMID: 29987816, DOI: 10.1007/978-1-4939-8597-5_10.Peer-Reviewed Original ResearchConceptsOptical action potential mappingIschemia-reperfusion injuryTranslocator proteinPost-ischemic arrhythmiasIonotropic propertiesPostischemic arrhythmiasR injuryHypertensive ratsAcute modelArrhythmogenic roleElectrophysiological substrateElectrophysiological propertiesArrhythmia mechanismsPharmacological inhibitionIntact heartInjuryTSPO ligandsMitochondrial translocator proteinArrhythmiasTSPO geneHeartPatientsRatsQuantitative assessmentIncidence
2017
Oxidative stress and inflammation as central mediators of atrial fibrillation in obesity and diabetes
Karam BS, Chavez-Moreno A, Koh W, Akar JG, Akar FG. Oxidative stress and inflammation as central mediators of atrial fibrillation in obesity and diabetes. Cardiovascular Diabetology 2017, 16: 120. PMID: 28962617, PMCID: PMC5622555, DOI: 10.1186/s12933-017-0604-9.Peer-Reviewed Original ResearchConceptsAtrial fibrillationOxidative stressCommon sustained cardiac arrhythmiaMaintenance of AFSustained cardiac arrhythmiaDiabetic heartElectrical remodelingRisk factorsAtrial excitabilityTherapeutic strategiesCardiac arrhythmiasInflammationCentral mediatorObesityDiabetesFibrillationMechanistic linkMellitusArrhythmiasExcitabilityIncreased Afterload Following Myocardial Infarction Promotes Conduction-Dependent Arrhythmias That Are Unmasked by Hypokalemia
Motloch LJ, Ishikawa K, Xie C, Hu J, Aguero J, Fish KM, Hajjar RJ, Akar FG. Increased Afterload Following Myocardial Infarction Promotes Conduction-Dependent Arrhythmias That Are Unmasked by Hypokalemia. JACC Basic To Translational Science 2017, 2: 258-269. PMID: 28798965, PMCID: PMC5547890, DOI: 10.1016/j.jacbts.2017.02.002.Peer-Reviewed Original ResearchAdvanced ischemic heart diseasePost-myocardial infarction patientsIschemic heart diseaseSudden cardiac deathNew large animal modelLarge animal modelMechanisms of arrhythmiasIncreased afterloadResistant hypertensionCardiac deathWorsen outcomesAnterior MIInfarction patientsHeart diseasePathophysiological significanceAnimal modelsElectrophysiological substrateAfterloadHypokalemiaDisease phenotypePatientsArrhythmiasRelevant modelHypertensionMI
2014
Gene therapies for arrhythmias in heart failure
Akar FG, Hajjar RJ. Gene therapies for arrhythmias in heart failure. Pflügers Archiv - European Journal Of Physiology 2014, 466: 1211-1217. PMID: 24566976, PMCID: PMC4070506, DOI: 10.1007/s00424-014-1485-3.Peer-Reviewed Original Research
2013
Electrophysiological Remodeling in Heart Failure
Akar F, Tomaselli G. Electrophysiological Remodeling in Heart Failure. 2013, 369-386. DOI: 10.1007/978-1-4471-4881-4_22.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsHeart failureTreatment of arrhythmiasCellular electrophysiological propertiesIon channelsSafe therapyConduction abnormalitiesElectrophysiological remodelingSudden deathNovel pharmacologicalArrhythmogenic triggersElectrophysiological propertiesAction potentialsArrhythmiasFunctional consequencesIonic mechanismsMolecular mechanismsOrgan levelFailureTherapyAbnormalitiesPharmacologicalRepolarization
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
2010
Left ventricular repolarization heterogeneity as an arrhythmic substrate in heart failure.
Akar FG. Left ventricular repolarization heterogeneity as an arrhythmic substrate in heart failure. Minerva Cardioangiologica 2010, 58: 205-12. PMID: 20440250.ChaptersConceptsHeart failureElectrophysiological substrateSudden cardiac deathCalcium handling proteinsRepolarization gradientsVentricular repolarization heterogeneityHeterogeneous remodelingCardiac deathCardiac functionArrhythmic substrateLeft ventriculeHandling proteinsMuscle layerPathophysiological remodelingRepolarization heterogeneityTissue levelsOrgan system levelArrhythmiasGap junctionsIon channelsOverview of mechanismsSub-cellular changesRemodelingFailureVentricule
2008
Arrhythmia Mechanisms in the Failing Heart
JIN H, LYON AR, AKAR FG. Arrhythmia Mechanisms in the Failing Heart. Pacing And Clinical Electrophysiology 2008, 31: 1048-1056. PMID: 18684263, DOI: 10.1111/j.1540-8159.2008.01134.x.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsHeart failureArrhythmia mechanismsFundamental arrhythmia mechanismsSudden cardiac deathLethal ventricular tachyarrhythmiasCalcium handling proteinsEffective treatment strategiesCardiac deathMalignant arrhythmiasVentricular tachyarrhythmiasElectrical remodelingConduction abnormalitiesFailing HeartTreatment strategiesLethal arrhythmiasElectrophysiological substrateHandling proteinsAction potentialsPatientsArrhythmiasIon channelsDeathHeartTachyarrhythmiasAbnormalitiesA ligand to the mitochondrial benzodiazepine receptor prevents ventricular arrhythmias and LV dysfunction after ischemia or glutathione depletion
Brown D, Aon M, Akar F, O’Rourke B. A ligand to the mitochondrial benzodiazepine receptor prevents ventricular arrhythmias and LV dysfunction after ischemia or glutathione depletion. The FASEB Journal 2008, 22: 747.7-747.7. DOI: 10.1096/fasebj.22.1_supplement.747.7.Peer-Reviewed Original ResearchContractile dysfunctionBenzodiazepine receptorsGlobal ischemia/reperfusionOxidative stressMitochondrial benzodiazepine receptorIschemia/reperfusionGuinea pig heartsSignificant clinical implicationsAnti-oxidant defensesReduced arrhythmiasLV dysfunctionVentricular dysfunctionR injuryVentricular arrhythmiasInduced arrhythmiasNormoxic perfusionIsolated myocytesDysfunctionClinical implicationsArrhythmiasIntact heartMetabolic challengesPig heartsGlutathione depletionMitochondrial membrane potential
2007
Regulation of ion channels and arrhythmias in the ischemic heart
Akar JG, Akar FG. Regulation of ion channels and arrhythmias in the ischemic heart. Journal Of Electrocardiology 2007, 40: s37-s41. PMID: 17993326, DOI: 10.1016/j.jelectrocard.2007.05.020.Peer-Reviewed Original ResearchConceptsIschemic injuryElectrophysiological changesIschemic heart diseaseBest treatment strategyCoronary eventsReperfusion phaseVentricular arrhythmiasIschemic episodesHeart diseaseLeading causeElectrical dysfunctionTreatment strategiesIschemic heartMetabolic substratesPatientsArrhythmiasKey cellularTime courseInjuryIon channelsHeartDysfunctionMortalityDisease
2006
Mapping arrhythmias in the failing heart: from Langendorff to patient
Akar JG, Akar FG. Mapping arrhythmias in the failing heart: from Langendorff to patient. Journal Of Electrocardiology 2006, 39: s19-s23. PMID: 16920143, DOI: 10.1016/j.jelectrocard.2006.03.011.Peer-Reviewed Educational MaterialsConceptsHeart failureVentricular arrhythmiasOptical action potential mappingSudden cardiac deathCardiac deathIntact tissue preparationsCardiac remodelingMost arrhythmiasArrhythmic substrateArrhythmiasElectrophysiological propertiesMapping arrhythmiasTissue levelsIndividual myocytesMajor causeReentrant excitationOrgan system levelPatientsMultiple mechanismsTissue preparationsHeartRecent findingsHost of changesCellular studiesLangendorff
2005
The mitochondrial origin of postischemic arrhythmias
Akar FG, Aon MA, Tomaselli GF, O'Rourke B. The mitochondrial origin of postischemic arrhythmias. Journal Of Clinical Investigation 2005, 115: 3527-3535. PMID: 16284648, PMCID: PMC1280968, DOI: 10.1172/jci25371.Peer-Reviewed Original ResearchMeSH KeywordsAction PotentialsAnimalsAnionsArrhythmias, CardiacDose-Response Relationship, DrugElectrophysiologyGuinea PigsHeartIntracellular MembranesIon ChannelsIschemiaMembrane PotentialsMicroscopy, ConfocalMitochondria, HeartMyocardial IschemiaMyocardial ReperfusionMyocardial Reperfusion InjuryMyocardiumMyocytes, CardiacOscillometryReactive Oxygen SpeciesReceptors, GABA-AReperfusion InjuryTemperatureTime FactorsConceptsAction potentialsVentricular fibrillationPostischemic functional recoveryIschemic heart diseaseGuinea pig heartsNew therapeutic targetsAbnormal electrical activationPostischemic arrhythmiasReperfusion arrhythmiasFunctional recoveryGlobal ischemiaHeart diseaseBolus infusionArrhythmia preventionElectrophysiological changesAP shorteningControl heartsPostischemic heartsBenzodiazepine receptorsElectrophysiological substrateTherapeutic targetArrhythmiasReperfusionPig heartsMitochondrial benzodiazepine receptor
2002
The Electrophysiological Substrate for Reentry: Unique Insights from High-Resolution Optical Mapping with Voltage-Sensitive Dyes
Rosenbaum D, Akar F. The Electrophysiological Substrate for Reentry: Unique Insights from High-Resolution Optical Mapping with Voltage-Sensitive Dyes. 2002, 568-595. DOI: 10.1201/b14064-18.Peer-Reviewed Original ResearchMajor public health problemReentrant arrhythmiasSudden cardiac deathPublic health problemNormal cardiac rhythmHemodynamic deteriorationCardiac deathVentricular arrhythmiasConduction disturbancesLethal arrhythmiasVoltage-sensitive dyeCardiac rhythmElectrophysiological substrateReentrant circuitMaintenance of reentryArrhythmiasElectrical defibrillationHealth problemsArrhythmia mechanismsMyocardial excitabilityFocal arrhythmiasIntact heartCardiac impulseResolution optical mappingReentrant excitation