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|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|
|Issue Date: ||2010|
|Publisher: ||Oxford University Press|
|Publisher version: ||http://cardiovascres.oxfordjournals.org/content/88/2/304|
|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.|
|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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