2023
Detection of Left Ventricular Systolic Dysfunction From Electrocardiographic Images
Sangha V, Nargesi A, Dhingra L, Khunte A, Mortazavi B, Ribeiro A, Banina E, Adeola O, Garg N, Brandt C, Miller E, Ribeiro A, Velazquez E, Giatti L, Barreto S, Foppa M, Yuan N, Ouyang D, Krumholz H, Khera R. Detection of Left Ventricular Systolic Dysfunction From Electrocardiographic Images. Circulation 2023, 148: 765-777. PMID: 37489538, PMCID: PMC10982757, DOI: 10.1161/circulationaha.122.062646.Peer-Reviewed Original ResearchMeSH KeywordsAdultElectrocardiographyHumansLongitudinal StudiesProspective StudiesVentricular Dysfunction, LeftVentricular Function, LeftConceptsLV systolic dysfunctionYale-New Haven HospitalVentricular systolic dysfunctionSystolic dysfunctionLV ejection fractionBrazilian Longitudinal StudyNew Haven HospitalEjection fractionCardiology clinicRegional hospitalLeft ventricular systolic dysfunctionCedars-Sinai Medical CenterAdult Health (ELSA-Brasil) cohort
2019
New approach for quantification of left ventricular function from low-dose gated bloodpool SPECT: Validation and comparison with conventional methods in patients
Liu YH, Fazzone-Chettiar R, Sandoval V, Tsatkin V, Miller EJ, Sinusas AJ. New approach for quantification of left ventricular function from low-dose gated bloodpool SPECT: Validation and comparison with conventional methods in patients. Journal Of Nuclear Cardiology 2019, 28: 939-950. PMID: 31338796, DOI: 10.1007/s12350-019-01823-8.Peer-Reviewed Original ResearchConceptsLV functionEquilibrium radionuclide angiocardiographyInter-observer reproducibilityRed blood cellsVentricular functionLeft ventricular functionExcellent inter-observer reproducibilityHigh-dose injectionLow-dose injectionsUnderwent standardRadionuclide angiocardiographyRadioactive doseShort-axis slicesRegional functionBlood cellsRadiation exposureGold standardImaging modalitiesAxis slicesPatientsDedicated cardiac SPECT cameraDoseSPECTInjectionDifferent quantification methods
2016
Longitudinal systolic strain, cardiac function improvement, and survival following treatment of light-chain (AL) cardiac amyloidosis
Salinaro F, Meier-Ewert HK, Miller EJ, Pandey S, Sanchorawala V, Berk JL, Seldin DC, Ruberg FL. Longitudinal systolic strain, cardiac function improvement, and survival following treatment of light-chain (AL) cardiac amyloidosis. European Heart Journal - Cardiovascular Imaging 2016, 18: 1057-1064. PMID: 27965280, DOI: 10.1093/ehjci/jew298.Peer-Reviewed Original ResearchMeSH KeywordsAgedAntineoplastic Combined Chemotherapy ProtocolsBiomarkersBortezomibBostonCardiomyopathiesCohort StudiesEchocardiography, Doppler, ColorFemaleFollow-Up StudiesHeart Function TestsHospitals, UniversityHumansImmunoglobulin Light-chain AmyloidosisKaplan-Meier EstimateMaleMelphalanMiddle AgedPrognosisRetrospective StudiesROC CurveSensitivity and SpecificitySurvival AnalysisTreatment OutcomeVentricular Dysfunction, LeftConceptsB-type natriuretic peptideFree light chainsLight-chain cardiac amyloidosisCardiac amyloidosisCardiac biomarkersCR groupGlobal LSHigh-dose melphalanLongitudinal systolic strainSerum free light chainsCardiac functional impairmentCardiac functional improvementStandard echocardiographic measuresCardiac function improvementShort-term improvementBNP reductionComplete responseDiastolic functionEchocardiographic measuresHematologic responseNatriuretic peptideSystolic strainFunctional improvementFunction improvementFunctional impairmentMitochondrial Reactive Oxygen Species Mediate Cardiac Structural, Functional, and Mitochondrial Consequences of Diet‐Induced Metabolic Heart Disease
Sverdlov AL, Elezaby A, Qin F, Behring JB, Luptak I, Calamaras TD, Siwik DA, Miller EJ, Liesa M, Shirihai OS, Pimentel DR, Cohen RA, Bachschmid MM, Colucci WS. Mitochondrial Reactive Oxygen Species Mediate Cardiac Structural, Functional, and Mitochondrial Consequences of Diet‐Induced Metabolic Heart Disease. Journal Of The American Heart Association 2016, 5: e002555. PMID: 26755553, PMCID: PMC4859372, DOI: 10.1161/jaha.115.002555.Peer-Reviewed Original ResearchMeSH KeywordsAdenosine TriphosphateAnimalsCatalaseDiet, High-FatDietary SucroseDisease Models, AnimalElectron Transport Complex IElectron Transport Complex IIEnergy MetabolismHypertrophy, Left VentricularMice, Inbred C57BLMice, TransgenicMitochondria, HeartMitochondrial DiseasesMutationOxidation-ReductionOxidative StressProtein Processing, Post-TranslationalReactive Oxygen SpeciesVentricular Dysfunction, LeftVentricular Function, LeftConceptsOxidative posttranslational modificationsMitochondrial reactive oxygen speciesPosttranslational modificationsReactive oxygen speciesMetabolic heart diseaseATP synthesisMitochondrial dysfunctionCardiac mitochondrial proteinsSite-directed mutationsMitochondrial proteinsTransgenic miceWild-type miceComplex IMitochondriaMitochondrial abnormalitiesHigh palmitateOxygen speciesCardiac mitochondriaCys100Mitochondrial consequencesCys103Key mediatorProteinH2O2 productionHigh-fat high-sucrose diet
2015
Partial Liver Kinase B1 (LKB1) Deficiency Promotes Diastolic Dysfunction, De Novo Systolic Dysfunction, Apoptosis, and Mitochondrial Dysfunction With Dietary Metabolic Challenge
Miller EJ, Calamaras T, Elezaby A, Sverdlov A, Qin F, Luptak I, Wang K, Sun X, Vijay A, Croteau D, Bachschmid M, Cohen RA, Walsh K, Colucci WS. Partial Liver Kinase B1 (LKB1) Deficiency Promotes Diastolic Dysfunction, De Novo Systolic Dysfunction, Apoptosis, and Mitochondrial Dysfunction With Dietary Metabolic Challenge. Journal Of The American Heart Association 2015, 5: e002277. PMID: 26722122, PMCID: PMC4859355, DOI: 10.1161/jaha.115.002277.Peer-Reviewed Original ResearchMeSH KeywordsAMP-Activated Protein KinasesAnimalsApoptosisApoptosis Regulatory ProteinsCaspase 3DiastoleDiet, High-FatDietary SucroseDisease Models, AnimalGenetic Predisposition to DiseaseHeterozygoteHypertrophy, Left VentricularMice, KnockoutMitochondria, HeartMyocardiumPhenotypeProtein Serine-Threonine KinasesSignal TransductionSystoleTime FactorsTumor Suppressor Protein p53Tumor Suppressor ProteinsVentricular Dysfunction, LeftVentricular Function, LeftVentricular RemodelingConceptsHigh-sucrose dietSystolic dysfunctionDiastolic dysfunctionLiver kinase B1Metabolic heart diseaseDietary excessHeart diseaseMyocardial hypertrophyDe novo appearanceControl dietRestrictive filling patternSevere diastolic dysfunctionLeft ventricular dilationMitochondrial dysfunctionMetabolic stressWild-type miceHigh-sucrose feedingNovo appearanceP53/PUMAMore hypertrophyDiastolic functionMyocardial dysfunctionVentricular hypertrophyVentricular dilationSevere mitochondrial dysfunction
2014
Preclinical Left Ventricular Diastolic Dysfunction in Metabolic Syndrome
Ayalon N, Gopal DM, Mooney DM, Simonetti JS, Grossman JR, Dwivedi A, Donohue C, Perez AJ, Downing J, Gokce N, Miller EJ, Liang CS, Apovian CM, Colucci WS, Ho JE. Preclinical Left Ventricular Diastolic Dysfunction in Metabolic Syndrome. The American Journal Of Cardiology 2014, 114: 838-842. PMID: 25084691, PMCID: PMC4162746, DOI: 10.1016/j.amjcard.2014.06.013.Peer-Reviewed Original ResearchConceptsHigher LA diameterLV diastolic dysfunctionVentricular diastolic dysfunctionDiastolic dysfunctionMetabolic syndromeLV massLA diameterLV hypertrophyYounger ageEarly risk factor modificationHigher left atrial diameterLeft ventricular diastolic dysfunctionAntihypertensive medication useLeft atrial diameterRisk factor modificationGender-adjusted analysesHigher LV massBody mass indexTissue Doppler imagingAtrial diameterDiastolic functionBlood pressureMedication useMass indexFactor modification