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dc.contributor.authorChinyere, Ikeotunye Royal
dc.contributor.authorMoukabary, Talal
dc.contributor.authorHutchinson, Mathew D
dc.contributor.authorLancaster, Jordan J
dc.contributor.authorJuneman, Elizabeth
dc.contributor.authorGoldman, Steven
dc.date.accessioned2021-02-05T19:49:10Z
dc.date.available2021-02-05T19:49:10Z
dc.date.issued2021-01-01
dc.identifier.citationChinyere, I. R., Moukabary, T., Hutchinson, M. D., Lancaster, J. J., Juneman, E., & Goldman, S. (2021). Progression of infarct-mediated arrhythmogenesis in a rodent model of heart failure. American Journal of Physiology-Heart and Circulatory Physiology, 320(1), H108-H116.en_US
dc.identifier.issn0363-6135
dc.identifier.pmid33164577
dc.identifier.doi10.1152/ajpheart.00639.2020
dc.identifier.urihttp://hdl.handle.net/10150/651455
dc.description.abstractHeart failure (HF) post-myocardial infarction (MI) presents with increased vulnerability to monomorphic ventricular tachycardia (mmVT). To appropriately evaluate new therapies for infarct-mediated reentrant arrhythmia in the preclinical setting, chronologic characterization of the preclinical animal model pathophysiology is critical. This study aimed to evaluate the rigor and reproducibility of mmVT incidence in a rodent model of HF. We hypothesize a progressive increase in the incidence of mmVT as the duration of HF increases. Adult male Sprague-Dawley rats underwent permanent left coronary artery ligation or SHAM surgery and were maintained for either 6 or 10 wk. At end point, SHAM and HF rats underwent echocardiographic and invasive hemodynamic evaluation. Finally, rats underwent electrophysiologic (EP) assessment to assess susceptibility to mmVT and define ventricular effective refractory period (ERP). In 6-wk HF rats (n = 20), left ventricular (LV) ejection fraction (EF) decreased (P < 0.05) and LV end-diastolic pressure (EDP) increased (P < 0.05) compared with SHAM (n = 10). Ten-week HF (n = 12) revealed maintenance of LVEF and LVEDP (P > 0.05), (P > 0.05). Electrophysiology studies revealed an increase in incidence of mmVT between SHAM and 6-wk HF (P = 0.0016) and ERP prolongation (P = 0.0186). The incidence of mmVT and ventricular ERP did not differ between 6- and 10-wk HF (P = 1.0000), (P = 0.9831). Findings from this rodent model of HF suggest that once the ischemia-mediated infarct stabilizes, proarrhythmic deterioration ceases. Within the 6- and 10-wk period post-MI, no echocardiographic, invasive hemodynamic, or electrophysiologic changes were observed, suggesting stable HF. This is the necessary context for the evaluation of experimental therapies in rodent HF.NEW & NOTEWORTHY Rodent model of ischemic cardiomyopathy exhibits a plateau of inducible monomorphic ventricular tachycardia incidence between 6 and 10 wk postinfarction.en_US
dc.language.isoenen_US
dc.publisherAmerican Physiological Societyen_US
dc.rightsCopyright © 2021 the American Physiological Society.en_US
dc.rights.urihttp://rightsstatements.org/vocab/InC/1.0/
dc.subjectadverse remodelingen_US
dc.subjectIschemiaen_US
dc.subjectmonophasic action potentialen_US
dc.subjectrigor and reproducibilityen_US
dc.subjectVentricular Tachycardiaen_US
dc.titleProgression of infarct-mediated arrhythmogenesis in a rodent model of heart failureen_US
dc.typeArticleen_US
dc.contributor.departmentSarver Heart Center, University of Arizonaen_US
dc.contributor.departmentMD-PhD Program, College of Medicine, University of Arizonaen_US
dc.identifier.journalAmerican Journal of Physiology - Heart and Circulatory Physiologyen_US
dc.description.note12 month embargo; published 1 January 2021en_US
dc.description.collectioninformationThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.en_US
dc.eprint.versionFinal accepted manuscripten_US
dc.source.journaltitleAmerican journal of physiology. Heart and circulatory physiology
dc.source.volume320
dc.source.issue1
dc.source.beginpageH108
dc.source.endpageH116
dc.source.countryInternational
dc.source.countryUnited States


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