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dc.contributor.authorWatanabe, Shin
dc.contributor.authorFish, Kenneth
dc.contributor.authorKovacic, Jason C.
dc.contributor.authorBikou, Olympia
dc.contributor.authorLeonardson, Lauren
dc.contributor.authorNomoto, Koichi
dc.contributor.authorAguero, Jaume 
dc.contributor.authorKapur, Navin K.
dc.contributor.authorHajjar, Roger J.
dc.contributor.authorIshikawa, Kiyotake
dc.date.accessioned2018-11-22T08:10:52Z
dc.date.available2018-11-22T08:10:52Z
dc.date.issued2018
dc.identifierISI:000430009600007
dc.identifier.citationJ Am Heart Assoc. 2018; 7(6):e006462
dc.identifier.issn2047-9980
dc.identifier.urihttp://hdl.handle.net/20.500.12105/6682
dc.description.abstractBackground-Delivering therapeutic materials, like stem cells or gene vectors, to the myocardium is difficult in the setting of ischemic heart failure because of decreased coronary flow and impaired microvascular perfusion (MP). The aim of this study was to determine if mechanical left ventricular (LV) unloading with the Impella increases coronary flow and MP in a subacute myocardial infarction. Methods and Results-Anterior transmural myocardial infarction (infarct size, 26.0 +/- 3.4\%) was induced in Yorkshire pigs. At 2 weeks after myocardial infarction, 6 animals underwent mechanical LV unloading by Impella, whereas 4 animals underwent pharmacological LV unloading using sodium nitroprusside for 2 hours. LV unloading with Impella significantly reduced end-diastolic volume (-16 +/- 11mL, P=0.02) and end-diastolic pressure (EDP; -32 +/- 23 mm Hg, P=0.03), resulting in a significant decrease in LV end-diastolic wall stress (EDWS) (infarct: 71.6 +/- 14.7 to 43.3 +/- 10.8 kdynes/cm(2) [P=0.02]; remote: 66.6 +/- 20.9 to 40.6 +/- 13.3 kdynes/cm(2) [P=0.02]). Coronary flow increased immediately and remained elevated after 2 hours in Impella-treated pigs. Compared with the baseline, MP measured by fluorescent microspheres significantly increased within the infarct zone (109 +/- 81\%, P=0.003), but not in the remote zone. Although sodium nitroprusside effectively reduced LV-EDWS, 2 (50\%) of sodium nitroprusside-treated pigs developed profound systemic hypotension. A significant correlation was observed between the infarct MP and EDWS (r(2)=0.43, P=0.03), suggesting an important role of EDWS in regulating MP during LV unloading in the infarcted myocardium. Conclusions-LV unloading using an Impella decreased EDWS and increased infarct MP without hemodynamic decompensation. Mechanical LV unloading is a novel and efficient approach to increase infarct MP in patients with subacute myocardial infarction.
dc.description.sponsorshipThis study was partly supported by a research grant from ABIOMED Inc (Danvers, MA) (Ishikawa); National Institutes of Health (NIH) grants R01 HL139963 (Ishikawa) and HL117505, HL119046, HL129814, 128072, HL131404, R01HL135093, and P50 HL112324 (Hajjar); American Heart Association-Scientist Development Grant 17SDG33410873 (Ishikawa); and 2 Transatlantic Fondation Leducq grants. Bikou was supported by the Deutsche Herzstiftung. We would like to acknowledge the Gene Therapy Resource Program of the National Heart, Lung, and Blood Institute, NIH.
dc.language.isoeng
dc.publisherWiley
dc.relation.isversionofPublisher's version
dc.rights.urihttp://creativecommons.org/licenses/by-nc/4.0/*
dc.subjectcoronary flow
dc.subjectleft ventricular unloading
dc.subjectpercutaneous left ventricular assist device
dc.subjectperfusion
dc.subjectwall stress
dc.titleLeft Ventricular Unloading Using an Impella CP Improves Coronary Flow and Infarct Zone Perfusion in Ischemic Heart Failure
dc.typeArtículo
dc.rights.licenseAtribución-NoComercial 4.0 Internacional*
dc.identifier.pubmedID29514806
dc.format.volume7
dc.identifier.doi10.1161/JAHA.117.006462
dc.contributor.funderABIOMED Inc (Danvers, MA)
dc.contributor.funderNational Institutes of Health (Estados Unidos)
dc.contributor.funderAmerican Heart Association
dc.contributor.funderLeducq Foundation
dc.contributor.funderDeutsche Herzstiftung
dc.description.peerreviewed
dc.relation.publisherversionhttps://doi.org/10.1161/jaha.117.006462
dc.identifier.journalJournal of the American Heart Association
dc.repisalud.orgCNICCNIC::Grupos de investigación::Laboratorio Traslacional para la Imagen y Terapia Cardiovascular
dc.repisalud.institucionCNIC
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES


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