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dc.creatorRavassa, S. (Susana)-
dc.creatorGarcia-Bolao, I. (Ignacio)-
dc.creatorZudaire, A. (Amaia)-
dc.creatorMacias, A. (Alfonso)-
dc.creatorGavira, J.J. (Juan José)-
dc.creatorBeaumont, J. (Javier)-
dc.creatorArias, T. (Teresa)-
dc.creatorHuerta, A. (Ana)-
dc.creatorDiez-Martinez, J. (Javier)-
dc.date.accessioned2012-04-30T10:19:02Z-
dc.date.available2012-04-30T10:19:02Z-
dc.date.issued2010-
dc.identifier.citationRavassa S, Garcia-Bolao I, Zudaire A, Macias A, Gavira JJ, Beaumont J, et al. Cardiac resynchronization therapy-induced left ventricular reverse remodelling is associated with reduced plasma annexin A5. Cardiovasc Res 2010 Nov 1;88(2):304-313.es_ES
dc.identifier.issn1755-3245-
dc.identifier.urihttps://hdl.handle.net/10171/21831-
dc.description.abstractAIMS: Cardiac resynchronization therapy (CRT) diminishes cardiac apoptosis and improves systolic function in heart failure (HF) patients with ventricular dyssynchrony. Plasma annexin A5 (AnxA5), a protein related to cellular damage, is associated with systolic dysfunction. We investigated whether the response to CRT is associated with plasma AnxA5. We also studied AnxA5 overexpression effects in HL-1 cardiomyocytes. METHODS AND RESULTS: AnxA5 ELISA was performed in plasma from 57 patients with HF and ventricular dyssynchrony at baseline and after 1 year of CRT. Patients were categorized as responders if they presented both a reduction in left ventricular (LV) end-systolic volume index (LVESVi) >10% and an increase in LV ejection fraction (LVEF) >10%. HL-1 cells were transfected with human AnxA5 cDNA, and AnxA5, PKC, Akt, p38MAPK, Bcl-2, mitochondrial integrity, caspase-3, and ATP were assessed. At baseline, an increased plasma AnxA5 level was associated with decreased LVEF and increased LVEDVi values (P < 0.05). No differences in baseline AnxA5 were observed between responders and non-responders. After CRT, AnxA5 decreased (P = 0.001) in responders but remained unchanged in non-responders. Final values of AnxA5 were independently associated with LVEF (r = -0.387, P = 0.003) and LVESVi (r = 0.403, P = 0.004) in all patients. Compared with control cells, AnxA5-transfected cells exhibited AnxA5 overexpression, decreased PKC and Akt and increased p38MAPK and Bcl-2 phosphorylation, loss of mitochondrial integrity, caspase-3 activation, and decreased ATP. CONCLUSION: CRT-induced LV reverse remodelling is associated with reduction in plasma AnxA5. The excess of AnxA5 is detrimental for HL-1 cardiomyocytes. Collectively, these data suggest that the beneficial effects of CRT might be related to an AnxA5 decrease.es_ES
dc.language.isoenges_ES
dc.publisherOxford University Presses_ES
dc.rightsinfo:eu-repo/semantics/closedAccess-
dc.subjectAnnexin A5es_ES
dc.subjectMitochondrial dysfunctiones_ES
dc.subjectHeart failurees_ES
dc.subjectResynchronizationes_ES
dc.subjectVentricular dyssynchronyes_ES
dc.titleCardiac resynchronization therapy-induced left ventricular reverse remodelling is associated with reduced plasma annexin A5es_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.relation.publisherversionhttp://cardiovascres.oxfordjournals.org/content/88/2/304es_ES
dc.type.driverinfo:eu-repo/semantics/articlees_ES

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