2012
Nicorandil Attenuates Monocrotaline-Induced Vascular Endothelial Damage and Pulmonary Arterial Hypertension
Sahara M, Sata M, Morita T, Hirata Y, Nagai R. Nicorandil Attenuates Monocrotaline-Induced Vascular Endothelial Damage and Pulmonary Arterial Hypertension. PLOS ONE 2012, 7: e33367. PMID: 22479390, PMCID: PMC3316574, DOI: 10.1371/journal.pone.0033367.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntihypertensive AgentsApoptosisBlotting, WesternCaspase 3Cells, CulturedDrug Therapy, CombinationEndothelium, VascularEnzyme InhibitorsFamilial Primary Pulmonary HypertensionGlyburideHuman Umbilical Vein Endothelial CellsHumansHypertension, PulmonaryInjections, IntraperitonealMaleMAP Kinase Signaling SystemMonocrotalineNG-Nitroarginine Methyl EsterNicorandilPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRandom AllocationRatsRats, Sprague-DawleySignal TransductionVentricular PressureConceptsRight ventricular systolic pressurePulmonary arterial hypertensionHuman umbilical vein endothelial cellsVascular endothelial damageMCT injectionArterial hypertensionEndothelial damageNitro-L-arginine methyl esterNitric oxide synthase inhibitorBeneficial effectsEndothelial NOS expressionVentricular systolic pressureVehicle-treated groupChannel blocker glibenclamideOxide synthase inhibitorChannel opener nicorandilSprague-Dawley ratsCaspase-3 expressionAnti-apoptotic effectsUmbilical vein endothelial cellsPromising therapeutic potentialBcl-2 expressionAnti-apoptotic factorsNicorandil administrationVein endothelial cells
2011
The ATP-Binding Cassette Transporter ABCG2 Protects Against Pressure Overload–Induced Cardiac Hypertrophy and Heart Failure by Promoting Angiogenesis and Antioxidant Response
Higashikuni Y, Sainz J, Nakamura K, Takaoka M, Enomoto S, Iwata H, Tanaka K, Sahara M, Hirata Y, Nagai R, Sata M. The ATP-Binding Cassette Transporter ABCG2 Protects Against Pressure Overload–Induced Cardiac Hypertrophy and Heart Failure by Promoting Angiogenesis and Antioxidant Response. Arteriosclerosis Thrombosis And Vascular Biology 2011, 32: 654-661. PMID: 22116099, DOI: 10.1161/atvbaha.111.240341.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornAntioxidantsATP Binding Cassette Transporter, Subfamily G, Member 2ATP-Binding Cassette TransportersCells, CulturedDisease Models, AnimalEndothelial CellsGenotypeGlutathioneHeart FailureHindlimbHumansHypertrophy, Left VentricularIschemiaMaleMiceMice, KnockoutMuscle, SkeletalMyocytes, CardiacNeoplasm ProteinsNeovascularization, PhysiologicOxidative StressPhenotypeRatsRats, WistarRNA InterferenceTime FactorsTransfectionVentricular FunctionVentricular RemodelingConceptsTransverse aortic constrictionWild-type micePressure overload-induced cardiac hypertrophyMicrovascular endothelial cellsOverload-induced cardiac hypertrophyCardiac hypertrophyHeart failureEndothelial cellsCassette transporter subfamily G member 2Exaggerated cardiac hypertrophyAntioxidant responseG member 2Tissue defense mechanismsSuperoxide dismutase mimeticCassette transporter ABCG2Cardiac dysfunctionImportant endogenous antioxidantPressure overloadVentricular remodelingAortic constrictionFunctional impairmentATP-Binding Cassette Transporter ABCG2Cardiomyocyte hypertrophyImpaired angiogenesisDismutase mimetic
2010
A Phosphodiesterase-5 Inhibitor Vardenafil Enhances Angiogenesis Through a Protein Kinase G-Dependent Hypoxia-Inducible Factor-1/Vascular Endothelial Growth Factor Pathway
Sahara M, Sata M, Morita T, Nakajima T, Hirata Y, Nagai R. A Phosphodiesterase-5 Inhibitor Vardenafil Enhances Angiogenesis Through a Protein Kinase G-Dependent Hypoxia-Inducible Factor-1/Vascular Endothelial Growth Factor Pathway. Arteriosclerosis Thrombosis And Vascular Biology 2010, 30: 1315-1324. PMID: 20413734, DOI: 10.1161/atvbaha.109.201327.Peer-Reviewed Original ResearchMeSH KeywordsAngiogenesis Inducing AgentsAnimalsCapillariesCell HypoxiaCell MovementCells, CulturedCollateral CirculationCyclic GMPCyclic GMP-Dependent Protein KinasesCyclic Nucleotide Phosphodiesterases, Type 5Disease Models, AnimalEndothelial CellsGreen Fluorescent ProteinsHindlimbHumansHypoxia-Inducible Factor 1, alpha SubunitImidazolesIschemiaMaleMiceMice, Inbred C3HMice, Inbred C57BLMice, KnockoutMice, TransgenicMuscle, SkeletalNeovascularization, PhysiologicNitric Oxide Synthase Type IIIPhosphodiesterase 5 InhibitorsPhosphodiesterase InhibitorsPiperazinesRecovery of FunctionRegional Blood FlowRNA InterferenceSignal TransductionStem CellsSulfonesTime FactorsTransfectionTriazinesVardenafil DihydrochlorideVascular Endothelial Growth Factor AConceptsEndothelial progenitor cellsVascular endothelial growth factor (VEGF) pathwayEndothelial growth factor pathwayIschemia-induced angiogenesisGrowth factor pathwaysIschemic muscleMobilization of EPCsSca-1/flkFactor pathwaySoluble guanylate cyclase inhibitorEndothelial nitric oxide synthasePhosphodiesterase-5 inhibitor vardenafilRight femoral arteryBlood flow recoveryEffect of vardenafilPhosphodiesterase-5 inhibitionUnilateral hindlimb ischemiaGuanylate cyclase inhibitorVascular endothelial growth factorNitric oxide synthaseUpregulated protein expressionProtein kinase G inhibitorIschemic cardiovascular diseaseCapillary-like tube formationEndothelial growth factor
2009
Infective Endocarditis by Bartonellaquintana Masquerading as Antineutrophil Cytoplasmic Antibody-Associated Small Vessel Vasculitis
Sugiyama H, Sahara M, Imai Y, Ono M, Okamoto K, Kikuchi K, Nagai R. Infective Endocarditis by Bartonellaquintana Masquerading as Antineutrophil Cytoplasmic Antibody-Associated Small Vessel Vasculitis. Cardiology 2009, 114: 208-211. PMID: 19602882, DOI: 10.1159/000228645.Peer-Reviewed Case Reports and Technical NotesConceptsAntineutrophil cytoplasmic antibodySmall vessel vasculitisANCA-associated vasculitisANCA testVessel vasculitisInfective endocarditisBacterial endocarditisPresence of ANCAIdiopathic small vessel vasculitisPositive ANCA testCulture-negative infective endocarditisVariety of infectionsPolymerase chain reaction-restriction fragment length polymorphism analysisImportant causative agentCytoplasmic antibodiesSkin purpuraImmunosuppressive therapyClinical findingsClinical manifestationsEndocardial involvementDifferential diagnosisVasculitisAppropriate treatmentCorrect diagnosisEndocarditis
2007
Diverse Contribution of Bone Marrow–Derived Cells to Vascular Remodeling Associated With Pulmonary Arterial Hypertension and Arterial Neointimal Formation
Sahara M, Sata M, Morita T, Nakamura K, Hirata Y, Nagai R. Diverse Contribution of Bone Marrow–Derived Cells to Vascular Remodeling Associated With Pulmonary Arterial Hypertension and Arterial Neointimal Formation. Circulation 2007, 115: 509-517. PMID: 17242277, DOI: 10.1161/circulationaha.106.655837.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, Genetically ModifiedArteriolesBone Marrow CellsBone Marrow TransplantationCapillariesCell DifferentiationDisease Models, AnimalFemoral ArteryGreen Fluorescent ProteinsHypertension, PulmonaryMaleMonocrotalinePneumonectomyPulmonary ArteryPulmonary EmbolismRatsRats, Sprague-DawleyThrombosisTunica IntimaVentricular Dysfunction, RightConceptsPulmonary arterial hypertensionArterial neointimal formationBM-derived cellsPulmonary arterial remodelingArterial hypertensionPulmonary arteriolesProtein-positive cellsSmooth muscle cellsGreen fluorescent protein-positive cellsArterial remodelingFemoral arteryBM cellsNeointimal formationBone marrowMonocrotaline-induced pulmonary arterial hypertensionRight ventricular systolic pressureMuscle cellsVascular Remodeling AssociatedVentricular systolic pressureGreen fluorescent protein (GFP) transgenic ratsSmooth muscle-like cellsSprague-Dawley ratsWire-injured femoral arteriesMuscle-like cellsPulmonary hypertension
2006
New Insights in the Treatment Strategy for Pulmonary Arterial Hypertension
Sahara M, Takahashi T, Imai Y, Nakajima T, Yao A, Morita T, Hirata Y, Nagai R. New Insights in the Treatment Strategy for Pulmonary Arterial Hypertension. Cardiovascular Drugs And Therapy 2006, 20: 377-386. PMID: 17124557, DOI: 10.1007/s10557-006-0498-3.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsMeSH KeywordsAnticoagulantsAntihypertensive AgentsCalcium Channel BlockersDiureticsDrug Therapy, CombinationHumansHypertension, PulmonaryMaleMiddle AgedNicorandilNitric Oxide DonorsOxygen Inhalation TherapyPhosphodiesterase InhibitorsPiperazinesPurinesPyridazinesSildenafil CitrateSulfonesVasodilator AgentsConceptsPulmonary arterial hypertensionFunctional class IVArterial hypertensionNew York Heart Association functional class IVNYHA functional class IVPhosphodiesterase type 5 inhibitorsClass IVIntravenous prostacyclin therapyOral combination therapyRational pharmacological therapyFirst-line therapyPhosphodiesterase type 3 inhibitorPrimary pulmonary hypertensionEndothelin receptor antagonistsCurrent treatment optionsCalcium channel blockersLong-term efficacyType 5 inhibitorsNovel therapeutic approachesLong-term survivalProstacyclin therapyExercise tolerancePulmonary hypertensionMale patientsPharmacological therapy
2004
Soft plaque detected on intravascular ultrasound is the strongest predictor of in-stent restenosis: an intravascular ultrasound study
Sahara M, Kirigaya H, Oikawa Y, Yajima J, Nagashima K, Hara H, Ogasawara K, Aizawa T. Soft plaque detected on intravascular ultrasound is the strongest predictor of in-stent restenosis: an intravascular ultrasound study. European Heart Journal 2004, 25: 2026-2033. PMID: 15541839, DOI: 10.1016/j.ehj.2004.07.039.Peer-Reviewed Original ResearchConceptsIntravascular ultrasoundSoft plaqueStent restenosisStrongest predictorLarger neointimal areaPercent plaque volumeSerial IVUS studiesNative coronary lesionsOnly independent predictorIntravascular ultrasound studyPercent plaque areaQuantitative coronary angiographyCoronary angiographyCoronary lesionsIndependent predictorsISR groupWorse prognosisStent implantationPlaque volumeNeointimal areaPlaque areaIVUS studiesUltrasound studyMultivariate analysisPlaque morphologyA serum amyloid A and LDL complex as a new prognostic marker in stable coronary artery disease
Ogasawara K, Mashiba S, Wada Y, Sahara M, Uchida K, Aizawa T, Kodama T. A serum amyloid A and LDL complex as a new prognostic marker in stable coronary artery disease. Atherosclerosis 2004, 174: 349-356. PMID: 15136066, DOI: 10.1016/j.atherosclerosis.2004.01.030.Peer-Reviewed Original ResearchConceptsStable coronary artery diseaseCoronary artery diseaseSerum amyloid AC-reactive proteinArtery diseaseEnzyme-linked immunosorbent assayCoronary angiographyLDL complexSerum levelsAmyloid ADiagnostic coronary angiographyAcute coronary syndromeProspective cohort studyEnd-point eventsNew prognostic markerPrediction of prognosisAcute phase proteinsNew markersSandwich enzyme-linked immunosorbent assayCoronary revascularizationCoronary syndromeInflammatory markersCerebral infarctionCohort studyIntravascular inflammation[Sex differences in coronary atherosclerosis: coronary angiography and intravascular ultrasonography].
Hara H, Yajima J, Kirigaya H, Nagashima K, Oikawa Y, Sahara M, Nakatsu Y, Aizawa T. [Sex differences in coronary atherosclerosis: coronary angiography and intravascular ultrasonography]. Journal Of Cardiology 2004, 43: 215-21. PMID: 15188608.Peer-Reviewed Original ResearchConceptsQuantitative coronary angiographyIntravascular ultrasonographyCoronary angiographyVessel areaHigh mortalityFrequency of complicationsMinimal lumen diameterPercentage diameter stenosisPresence of calcificationPercentage area stenosisCoronary atherosclerosisCoronary interventionDiameter stenosisArea stenosisReference diameterLumen diameterLumen areaUltrasonographyLesion lengthWomenCalcificationStenosisSignificant differencesAngiographyMen
2003
Arterial remodeling patterns before intervention predict diffuse in-stent restenosis An intravascular ultrasound study
Sahara M, Kirigaya H, Oikawa Y, Yajima J, Ogasawara K, Satoh H, Nagashima K, Hara H, Nakatsu Y, Aizawa T. Arterial remodeling patterns before intervention predict diffuse in-stent restenosis An intravascular ultrasound study. Journal Of The American College Of Cardiology 2003, 42: 1731-1738. PMID: 14642680, DOI: 10.1016/j.jacc.2003.05.009.Peer-Reviewed Original ResearchConceptsArterial remodeling patternsDiffuse ISRIntravascular ultrasound studyISR groupBaseline RIISR lesionsUltrasound studyStent restenosisRemodeling patternOnly independent predictorSuccessful stent implantationQuantitative coronary angiographyLogistic regression analysisCoronary angiographyIndependent predictorsRetrospective studyDiameter stenosisPositive remodelingNegative remodelingStent implantationTarget lesionsProcedural characteristicsHigh riskPlaque growthReference segmentsNifekalant Hydrochloride, a Novel Class III Antiarrhythmic Agent, Suppressed Postoperative Recurrent Ventricular Tachycardia in a Patient Undergoing Coronary Artery Bypass Grafting and the Dor Approach
Sahara M, Sagara K, Yamashita T, Iinuma H, Fu L, Watanabe H. Nifekalant Hydrochloride, a Novel Class III Antiarrhythmic Agent, Suppressed Postoperative Recurrent Ventricular Tachycardia in a Patient Undergoing Coronary Artery Bypass Grafting and the Dor Approach. Circulation Journal 2003, 67: 712. PMID: 12890916, DOI: 10.1253/circj.67.712.Peer-Reviewed Case Reports and Technical NotesConceptsVentricular premature contractionsVentricular tachycardiaNifekalant hydrochlorideAntiarrhythmic agentsPremature contractionsCoronary Artery Bypass GraftingNovel class III antiarrhythmic agentClass III antiarrhythmic agentRecurrent ventricular tachyarrhythmiasArtery Bypass GraftingCoronary artery bypassRecurrent ventricular tachycardiaCoronary artery diseaseClass III drugsArtery bypassBypass GraftingArtery diseaseElectrical cardioversionVentricular aneurysmVentricular tachyarrhythmiasIb drugsChannel blockersElectrical stormTachycardiaDrugs
2002
Mechanisms of acute gain and late lumen loss after atherectomy in different preintervention arterial remodeling patterns
Oikawa Y, Kirigaya H, Aizawa T, Nagashima K, Yajima J, Ishimura K, Hara H, Sahara M, Iinuma H, Fu L. Mechanisms of acute gain and late lumen loss after atherectomy in different preintervention arterial remodeling patterns. The American Journal Of Cardiology 2002, 89: 505-510. PMID: 11867032, DOI: 10.1016/s0002-9149(01)02288-3.Peer-Reviewed Original ResearchConceptsDirectional coronary atherectomyNegative remodeling groupLumen area lossLate lumen lossRemodeling groupIntravascular ultrasoundLate lumen area lossLumen lossPlaque areaVessel areaArterial remodeling patternsPlaque area increaseCoronary artery restenosisDifferent coronary arteriesLumen area increaseMechanism of restenosisNovo lesionsCoronary atherectomyArtery restenosisAcute gainCoronary arteryNegative remodelingIVUS findingsVessel shrinkageRemodeling patternJ Wave and ST Segment Elevation in the Inferior Leads
Sahara M, Sagara K, Yamashita T, Abe T, Kirigaya H, Nakada M, Iinuma H, Fu L, Watanabe H. J Wave and ST Segment Elevation in the Inferior Leads. International Heart Journal 2002, 43: 55. PMID: 12041890, DOI: 10.1536/jhj.43.55.Peer-Reviewed Case Reports and Technical NotesConceptsST-segment elevationSegment elevationInferior leadsNon-sustained monomorphic ventricular tachycardiaJ wavesStructural heart diseaseMonomorphic ventricular tachycardiaSodium channel blockersElectrophysiologic studyECG findingsHeart diseaseVentricular tachycardiaBrugada syndromeVentricular fibrillationChannel blockersHolter recordingsCircadian variationDiagnostic signsElevationPilsicainideTachycardiaPatientsFibrillationBlockersSyndrome