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dc.contributor.authorRohde, Luis E
dc.contributor.authorAikawa, Masanori
dc.contributor.authorCheng, George Z
dc.contributor.authorSukhova, Galina K.
dc.contributor.authorSolomon, Scott David
dc.contributor.authorLibby, Peter
dc.contributor.authorPfeffer, Janice
dc.contributor.authorPfeffer, Marc Alan
dc.contributor.authorLee, Richard Theodore
dc.date.accessioned2018-03-27T18:31:12Z
dc.date.issued1999
dc.identifier.citationRohde, Luis E, Masanori Aikawa, George C Cheng, Galina Sukhova, Scott D Solomon, Peter Libby, Janice Pfeffer, Marc A Pfeffer, and Richard T Lee. 1999. “Echocardiography-Derived Left Ventricular End-Systolic Regional Wall Stress and Matrix Remodeling after Experimental Myocardial Infarction.” Journal of the American College of Cardiology 33 (3) (March): 835–842. doi:10.1016/s0735-1097(98)00602-0.en_US
dc.identifier.issn0735-1097en_US
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:35140980
dc.description.abstractOBJECTIVES We tested the hypothesis that regional end-systolic left ventricular (ESLV) wall stress is associated with extracellular matrix remodeling activity after myocardial infarction (MI). BACKGROUND Increased left ventricular (LV) wall stress is a stimulus for LV enlargement, and echocardiography can be used to estimate regional wall stress. A powerful validation of a noninvasive method of estimating wall stress would be predicting cellular responses after a MI. METHODS Echocardiographic images were obtained in rats 1, 7, 14 or 21 days after coronary ligation (n = 11) or sham surgery (n = 5). End-systolic left ventricular wall stress was calculated by finite element analysis in three regions (infarcted, noninfarcted and border) from short-axis images. Matrix metalloproteinase-9 (MMP-9) and macrophage density were determined by immunohistochemistry, and positive cells were counted in high power fields (hpf). RESULTS Average ESLV wall stress was higher in rats with MI when compared to shams irrespective of time point (p < 0.01), and ESLV wall stress in the infarcted regions increased with time (25.1 ± 5.9 vs. 69.9 ± 4.4 kdyn/cm2, day 1 vs. 21; p < 0.01). Matrix metalloproteinase-9 expression was higher in infarcted and border regions when compared to noninfarcted regions (22.1 vs. 25.7 vs. 0.10 cells/hpf, respectively; p < 0.01). Over all regions, ESLV wall stress was associated with MMP-9 (r = 0.76; p < 0.001), macrophage density (r = 0.72; p < 0.001) and collagen content (r = 0.67; p < 0.001). End-systolic left ventricular wall stress was significantly higher when MMP-9 positive cell density was greater than 10 cells/hpf (45 ± 20 vs. 14 ± 10 kdyn/cm2; p < 0.001). CONCLUSIONS Regional increases in ESLV wall stress determined by echocardiography-based structural analysis are associated with extracellular matrix degradation activity.en_US
dc.language.isoen_USen_US
dc.publisherElsevier BVen_US
dc.relation.isversionofdoi:10.1016/S0735-1097(98)00602-0en_US
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pubmed/10080489en_US
dash.licenseMETA_ONLY
dc.titleEchocardiography-derived left ventricular end-systolic regional wall stress and matrix remodeling after experimental myocardial infarctionen_US
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden_US
dc.relation.journalJournal of the American College of Cardiologyen_US
dash.depositing.authorLibby, Peter
dash.embargo.until10000-01-01
dc.identifier.doi10.1016/S0735-1097(98)00602-0*
workflow.legacycommentsnoap.needmanen_US
dash.authorsorderedfalse
dash.contributor.affiliatedCheng, George Z
dash.contributor.affiliatedPfeffer, Marc
dash.contributor.affiliatedAikawa, Masanori
dash.contributor.affiliatedSukhova, Galina
dash.contributor.affiliatedSolomon, Scott
dash.contributor.affiliatedLee, Richard
dash.contributor.affiliatedLibby, Peter
dc.identifier.orcid0000-0002-1502-502X


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