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Dadun > Depósito Académico > CIMA (Centro de Investigación Médica Aplicada) > Área de Ciencias Cardiovasculares > Cardiopatía hipertensiva > DA - CIMA - Cardiovasculares - Cardiopatía hipertensiva - Artículos de Revista >

Cardiac resynchronization therapy-induced left ventricular reverse remodelling is associated with reduced plasma annexin A5
Authors: Ravassa, S. (Susana)
Garcia-Bolao, I. (Ignacio)
Zudaire, A. (Amaia)
Macias, A. (Alfonso)
Gavira, J.J. (Juan José)
Beaumont, J. (Javier)
Arias, T. (Teresa)
Huerta, A. (Ana)
Diez, J. (Javier)
Keywords: Annexin A5
Mitochondrial dysfunction
Heart failure
Resynchronization
Ventricular dyssynchrony
Issue Date: 2010
Publisher: Oxford University Press
Publisher version: http://cardiovascres.oxfordjournals.org/content/88/2/304
ISSN: 1755-3245
Citation: Ravassa 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.
Abstract
AIMS: 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.
Permanent link: http://hdl.handle.net/10171/21831
Appears in Collections:DA - CIMA - Cardiovasculares - Cardiopatía hipertensiva - Artículos de Revista

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