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 impairment
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 dysfunctionAMPK deficiency in cardiac muscle results in dilated cardiomyopathy in the absence of changes in energy metabolism
Sung MM, Zordoky BN, Bujak AL, Lally JS, Fung D, Young ME, Horman S, Miller EJ, Light PE, Kemp BE, Steinberg GR, Dyck JR. AMPK deficiency in cardiac muscle results in dilated cardiomyopathy in the absence of changes in energy metabolism. Cardiovascular Research 2015, 107: 235-245. PMID: 26023060, PMCID: PMC4565988, DOI: 10.1093/cvr/cvv166.Peer-Reviewed Original ResearchConceptsHeart failureCardiac functionCardiac hypertrophyRole of AMPKAMPK deficiencyCompensatory cardiac hypertrophyWild-type littermatesFatty acid oxidation ratesMyocardial energy metabolismAlters cardiac functionMuscle-specific deletionFirst mouse modelDiastolic functionAbsence of changesCardiac dysfunctionWT miceBasal glucoseMyocardial functionMyocardial metabolismCell shorteningMouse modelCardiac muscle resultsHypertrophyImpaired activationTroponin I
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