2019
Renewal Theory as a Universal Quantitative Framework to Characterize Phase Singularity Regeneration in Mammalian Cardiac Fibrillation
Dharmaprani D, Schopp M, Kuklik P, Chapman D, Lahiri A, Dykes L, Xiong F, Aguilar M, Strauss B, Mitchell L, Pope K, Meyer C, Willems S, Akar FG, Nattel S, McGavigan AD, Ganesan AN. Renewal Theory as a Universal Quantitative Framework to Characterize Phase Singularity Regeneration in Mammalian Cardiac Fibrillation. Circulation Arrhythmia And Electrophysiology 2019, 12: e007569. PMID: 31813270, DOI: 10.1161/circep.119.007569.Peer-Reviewed Original ResearchMeSH KeywordsAction PotentialsAnimalsAtrial FibrillationBiological EvolutionComputer SimulationDisease Models, AnimalHeart Conduction SystemHeart RateHumansModels, CardiovascularMulticenter Studies as TopicObservational Studies as TopicRatsReproducibility of ResultsSheep, DomesticStochastic ProcessesTime FactorsVentricular FibrillationConceptsPoisson renewal processRenewal theoryRenewal processPhase singularityMaximum entropy theoryExponential probability distribution functionProbability distribution functionFormation/destructionConstant rate parametersEntropy theoryInterevent timesDistribution functionExponential distributionRotational eventsRecurrence quantification analysis of complex‐fractionated electrograms differentiates active and passive sites during atrial fibrillation
Baher A, Buck B, Fanarjian M, Mounsey J, Gehi A, Chung E, Akar FG, Webber CL, Akar JG, Hummel JP. Recurrence quantification analysis of complex‐fractionated electrograms differentiates active and passive sites during atrial fibrillation. Journal Of Cardiovascular Electrophysiology 2019, 30: 2229-2238. PMID: 31507008, DOI: 10.1111/jce.14161.Peer-Reviewed Original Research
2011
Disruption of Hexokinase II–Mitochondrial Binding Blocks Ischemic Preconditioning and Causes Rapid Cardiac Necrosis
Smeele KM, Southworth R, Wu R, Xie C, Nederlof R, Warley A, Nelson JK, van Horssen P, van den Wijngaard JP, Heikkinen S, Laakso M, Koeman A, Siebes M, Eerbeek O, Akar FG, Ardehali H, Hollmann MW, Zuurbier CJ. Disruption of Hexokinase II–Mitochondrial Binding Blocks Ischemic Preconditioning and Causes Rapid Cardiac Necrosis. Circulation Research 2011, 108: 1165-1169. PMID: 21527739, DOI: 10.1161/circresaha.111.244962.Peer-Reviewed Original ResearchConceptsIschemic preconditioningWild-type heartsCardiac functionProtective effectHKII levelsBaseline cardiac functionIschemia-reperfusion injuryNormal cardiac functionMitochondrial permeability transition openingContractile impairmentReperfusion injuryAcute reductionCardiac necrosisMyocardial functionGlycolytic enzymes hexokinaseCardiac contractionMild mitochondrial uncouplingMembrane depolarizationMitochondrial membrane depolarizationHKIIMitochondrial hexokinaseControl peptideHeartPreconditioningTissue disruption
2010
Use‐Dependent Modulation of Myocardial Conduction by a New Class of HERG Agonists: Deal Breaker or Cherry on Top?
AKAR FG. Use‐Dependent Modulation of Myocardial Conduction by a New Class of HERG Agonists: Deal Breaker or Cherry on Top? Journal Of Cardiovascular Electrophysiology 2010, 21: 930-932. PMID: 20367661, DOI: 10.1111/j.1540-8167.2010.01747.x.Commentaries, Editorials and Letters
2007
Dynamic changes in conduction velocity and gap junction properties during development of pacing-induced heart failure
Akar FG, Nass RD, Hahn S, Cingolani E, Shah M, Hesketh GG, DiSilvestre D, Tunin RS, Kass DA, Tomaselli GF. Dynamic changes in conduction velocity and gap junction properties during development of pacing-induced heart failure. AJP Heart And Circulatory Physiology 2007, 293: h1223-h1230. PMID: 17434978, DOI: 10.1152/ajpheart.00079.2007.Peer-Reviewed Original ResearchMeSH KeywordsAction PotentialsAnimalsCardiac Pacing, ArtificialConnexin 43Disease Models, AnimalDogsDown-RegulationGap JunctionsHeart Conduction SystemHeart FailureMalePhosphorylationProtein IsoformsTachycardia, VentricularTime FactorsVentricular Function, LeftVentricular PressureVentricular RemodelingConceptsEnd-stage heart failureHeart failureConduction velocityMechanical dysfunctionCV slowingPacing-induced heart failureDevelopment of HFOnset of HFMechanical functionCx43 isoformConduction abnormalitiesCx43 lateralizationAdvanced stageBaseline levelsMyocardial preparationsPhosphorylation of Cx43High-resolution optical mappingSustained downregulationMarked increaseDephosphorylated Cx43LVEDPGap junction propertiesConduction changesDysfunctionTime course
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