2023
Integrating Right Ventricular Pressure Waveform Analysis With Two-Point Volume Measurement for Quantification of Systolic and Diastolic Function: Experimental Validation and Clinical Application
Heerdt P, Martin-Flores M, Oakland H, Joseph P, Singh I. Integrating Right Ventricular Pressure Waveform Analysis With Two-Point Volume Measurement for Quantification of Systolic and Diastolic Function: Experimental Validation and Clinical Application. Journal Of Cardiothoracic And Vascular Anesthesia 2023, 37: 1929-1937. PMID: 37422337, PMCID: PMC10529383, DOI: 10.1053/j.jvca.2023.06.011.Peer-Reviewed Original ResearchConceptsRight heart catheterizationHeart catheterizationDiastolic functionRV volumesBeat measuresDiagnostic right heart catheterizationReference standardRight ventricular contractilityEnd-diastolic pressurePressure waveform analysisEnd-systolic elastancePotential clinical utilityClinical applicationRV volume measurementsVolume measurementsRV contractilityRV systolicVentricular contractilityRV pressureBland-Altman analysisClinical utilityAnesthetized swineNitric oxideExperimental modelContractilityCharacterizing the Spatiotemporal Transcriptomic Response of the Right Ventricle to Acute Pressure Overload
Kheyfets V, Kumar S, Heerdt P, Ichimura K, Brown R, Lucero M, Essafri I, Williams S, Stenmark K, Spiekerkoetter E. Characterizing the Spatiotemporal Transcriptomic Response of the Right Ventricle to Acute Pressure Overload. International Journal Of Molecular Sciences 2023, 24: 9746. PMID: 37298696, PMCID: PMC10253685, DOI: 10.3390/ijms24119746.Peer-Reviewed Original ResearchConceptsPressure overloadChronic RV pressure overloadExperimental pulmonary hypertension modelsRV pressure overloadTime pointsPulmonary hypertension modelRV outflow tractTranscriptomic signaturesAcute pressure overloadRight ventricular tissueDifferent time pointsPulmonary embolismHypertension modelSevere PEAcute increaseInitial insultOutflow tractRight ventricleRV apexVentricular tissueControl tissuesRatsSeverityWeeksTissue
2013
NHE Isoform Switching and KChIP2 Upregulation in Aging Porcine Atria
Kant R, Hu Z, Malhotra JK, Krogh-Madsen T, Christini DJ, Heerdt PM, Abbott GW. NHE Isoform Switching and KChIP2 Upregulation in Aging Porcine Atria. PLOS ONE 2013, 8: e82951. PMID: 24376615, PMCID: PMC3871617, DOI: 10.1371/journal.pone.0082951.Peer-Reviewed Original ResearchConceptsAtrial fibrillationMyocyte action potential durationHuman cardiac physiologyCessation of stimulationAction potential durationLarge animal modelSodium-hydrogen exchangerReperfusion arrhythmiasNHE1-specific inhibitorMyocardial responsivenessPharmacological responsivenessPharmacologic efficacyYoung adult pigsAtrial tissuePotential durationTherapeutic targetAnimal modelsCardiac pathologyKChIP2 expressionReal-time qPCRPotential molecular basisTherapeutic agentsCardiac physiologyFemale swineYoung adults
2002
Disease-specific remodeling of cardiac mitochondria after a left ventricular assist device
Heerdt PM, Schlame M, Jehle R, Barbone A, Burkhoff D, Blanck TJ. Disease-specific remodeling of cardiac mitochondria after a left ventricular assist device. The Annals Of Thoracic Surgery 2002, 73: 1216-1221. PMID: 11996266, DOI: 10.1016/s0003-4975(01)03621-9.Peer-Reviewed Original Research
2001
Comparison of Right and Left Ventricular Responses to Left Ventricular Assist Device Support in Patients With Severe Heart Failure
Barbone A, Holmes J, Heerdt P, The’ A, Naka Y, Joshi N, Daines M, Marks A, Oz M, Burkhoff D. Comparison of Right and Left Ventricular Responses to Left Ventricular Assist Device Support in Patients With Severe Heart Failure. Circulation 2001, 104: 670-675. PMID: 11489773, DOI: 10.1161/hc3101.093903.Peer-Reviewed Original ResearchMeSH KeywordsAdultAge FactorsAgedBlood PressureCalcium-Transporting ATPasesCardiac OutputFemaleFibrosisHeart FailureHeart TransplantationHeart VentriclesHeart-Assist DevicesHemodynamicsHumansIn Vitro TechniquesLungMaleMiddle AgedSarcoplasmic Reticulum Calcium-Transporting ATPasesTime FactorsVenous PressureConceptsSevere heart failureLVAD supportRight ventricleLeft ventricleReverse remodelingHeart failureHigh central venous pressurePulmonary artery diastolic pressureVentricular assist device supportLV myocyte diameterCentral venous pressureAssist device supportHigh cardiac outputHearts of patientsForce-frequency relationVentricular assist deviceComparison of rightPossible primary roleRV trabeculaeVenous pressureVentricular responseDiastolic pressureHemodynamic unloadingCardiac outputNeurohormonal factors
2000
Chronic Unloading by Left Ventricular Assist Device Reverses Contractile Dysfunction and Alters Gene Expression in End-Stage Heart Failure
Heerdt P, Holmes J, Cai B, Barbone A, Madigan J, Reiken S, Lee D, Oz M, Marks A, Burkhoff D. Chronic Unloading by Left Ventricular Assist Device Reverses Contractile Dysfunction and Alters Gene Expression in End-Stage Heart Failure. Circulation 2000, 102: 2713-2719. PMID: 11094037, DOI: 10.1161/01.cir.102.22.2713.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedBlotting, NorthernBlotting, WesternCalcium-Transporting ATPasesFemaleGene Expression RegulationHeart FailureHeart VentriclesHeart-Assist DevicesHumansMaleMiddle AgedMyocardial ContractionRNA, MessengerRyanodine Receptor Calcium Release ChannelSarcolemmaSodium-Hydrogen ExchangersConceptsEnd-stage heart failureLVAD supportHeart failureContractile strengthLVAD implantationSarcoplasmic reticular membranesNegative FFRIntact myocardiumVentricular assist deviceBlot analysisExpression of genesWestern blot analysisContractile dysfunctionSERCA2a proteinLV trabeculaeSubtype 2aChronic unloadingLV tissueAssist deviceContractile forcePatientsAlters gene expressionHigher mRNAReticular membranesRyanodine receptor