Fibrosis in heart failure subtypes

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dc.contributor.authorToprak, G.
dc.contributor.authorYuksel, H.
dc.contributor.authorDemirpence, O.
dc.contributor.authorIslamoglu, Y.
dc.contributor.authorEvliyaoglu, O.
dc.contributor.authorMete, N.
dc.date.accessioned2024-04-24T17:34:01Z
dc.date.available2024-04-24T17:34:01Z
dc.date.issued2013
dc.departmentDicle Üniversitesien_US
dc.description.abstractBACKGROUND: The differences in concentrations of biomarkers between heart failure patients with dilated cardiomyopathy (HF-D) and with ischemic cardiomyopathy (HF-I) have yet to be defined. The objectives of this study were to compare the concentrations and correlation of biomarkers of inflammation, extracellular matrix (ECM) turnover and oxidative stress parameters between these populations. PATIENTS AND METHODS: Our study consisted of 36 subjects with HF-D (LVSD = 47.2 +/- 7.3 mm, LVDD = 65.1 +/- 6.3 mm), 44 subjects with HF-I (LVSD = 38.0 +/- 4.4 mm, LVDD = 58.5 +/- 6.0 mm) and 38 controls without heart failure. Concentrations of matrix metalloproteinase (MMP)-1, MMP-2, MMP-9, MMP-13, Galectin-3, prolidase, TNF-alpha, and oxidative stress index (OSI) were measured. RESULTS: Serum levels of MMP-2, MMP-9, and prolidase were significantly increased in HF-I group compared to healthy controls (p = 0.039, 0.019, 0.012 respectively), whereas the increases in MMP-1 and MMP-13 were not significant. This significance was stronger in the HF-D group than the HF-I group (p = 0.004, 0.001, 0.002 respectively). TNF-alpha, a marker of inflammation, was significantly increased in heart failure (p = 0.004) but there was no difference between HF-D and HF-I groups; however, Galectin-3 was significantly increased in the HF-D group compared to the HF-I group (p = 0.005). OSI showed the same response pattern as TNF-alpha (p = 0.019, 0.002 respectively). There was a positive correlation of MMP-9 levels with prolidase activity (r = 0.612, p: 0.003). CONCLUSIONS: MMPs and Galectin-3 are important in cardiac remodeling; prolidase may share an undefined role in fibrosis in heart failure and may have a role in the diffuse fibrosis of heart failure.en_US
dc.identifier.endpage2309en_US
dc.identifier.issn1128-3602
dc.identifier.issue17en_US
dc.identifier.pmid24065222
dc.identifier.scopus2-s2.0-84884244972
dc.identifier.scopusqualityQ2
dc.identifier.startpage2302en_US
dc.identifier.urihttps://hdl.handle.net/11468/20923
dc.identifier.volume17en_US
dc.identifier.wosWOS:000325204600006
dc.identifier.wosqualityQ4
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoenen_US
dc.publisherVerduci Publisheren_US
dc.relation.ispartofEuropean Review For Medical and Pharmacological Sciences
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectHeart Failureen_US
dc.subjectDilated Cardiomyopathyen_US
dc.subjectMmpen_US
dc.subjectProlidaseen_US
dc.titleFibrosis in heart failure subtypesen_US
dc.titleFibrosis in heart failure subtypes
dc.typeArticleen_US

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