scholarly journals Improvement in circulating endothelial progenitor cells pool after cardiac resynchronization therapy: increasing the list of benefits

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Gonçalo Cristóvão ◽  
James Milner ◽  
Pedro Sousa ◽  
Miguel Ventura ◽  
João Cristóvão ◽  
...  
2020 ◽  
Author(s):  
Gonçalo Cristóvão ◽  
James Milner ◽  
Pedro Sousa ◽  
Miguel Ventura ◽  
João Cristóvão ◽  
...  

Abstract Background Recent studies suggest that circulating endothelial progenitor cells (EPCs) may influence the response to cardiac resynchronization therapy (CRT). The aim of this study was to evaluate the effect of CRT on EPCs levels and to assess the impact of EPCs on long-term clinical outcomes. Population and methods Prospective study of 50 patients submitted to CRT. Two populations of circulating EPCs were quantified previously to CRT implantation: CD34 + KDR + and CD133 + KDR + cells. EPCs levels were reassessed 6 months after CRT. Endpoints during the long-term follow-up were all-cause mortality, heart transplantation and hospitalization for heart failure (HF) management. Results The proportion of non-responders to CRT was 42% and tended to be higher in patients with an ischemic vs non-ischemic etiology (64% vs 35%, p=0.098). Patients with ischemic cardiomyopathy (ICM) showed significantly lower CD34+KDR+ EPCs levels when compared to non-ischemic dilated cardiomyopathy patients (DCM) (0.0010 ± 0.0007 vs 0.0030 ± 0.0024 cells/100 leukocytes, p=0.032). There were no significant differences in baseline EPCs levels between survivors and non-survivors nor between patients who were rehospitalized for HF management during follow-up or not. At 6-month follow-up, circulating EPCs levels were significantly higher than baseline levels (0.0024 ± 0.0023 vs 0.0047 ± 0.0041 CD34 + KDR + cells/100 leukocytes, p=0.010 and 0.0007 ± 0.0004 vs 0.0016 vs 0.0013 CD133 + /KDR + cells/100 leukocytes, p=0.007). Conclusions Patients with ICM showed significantly lower levels of circulating EPCs when compared to their counterparts. CRT seems to improve the pool of endogenously circulating EPCs and reduced baseline EPCs levels seem not influence long-term outcomes after CRT.


2020 ◽  
Author(s):  
Gonçalo Cristóvão ◽  
James Milner ◽  
Pedro Sousa ◽  
Miguel Ventura ◽  
João Cristóvão ◽  
...  

Abstract Background Recent studies suggest that circulating endothelial progenitor cells (EPCs) may influence the response to cardiac resynchronization therapy (CRT). The aim of this study was to evaluate the effect of CRT on EPCs levels and to assess the impact of EPCs on long-term clinical outcomes. Population and methods Prospective study of 50 patients submitted to CRT. Two populations of circulating EPCs were quantified previously to CRT implantation: CD34 + KDR + and CD133 + KDR + cells. EPCs levels were reassessed 6 months after CRT. Endpoints during the long-term follow-up were all-cause mortality, heart transplantation and hospitalization for heart failure (HF) management. Results The proportion of non-responders to CRT was 42% and tended to be higher in patients with an ischemic vs non-ischemic etiology (64% vs 35%, p=0.098). Patients with ischemic cardiomyopathy (ICM) showed significantly lower CD34+KDR+ EPCs levels when compared to non-ischemic dilated cardiomyopathy patients (DCM) (0.0010 ± 0.0007 vs 0.0030 ± 0.0024 cells/100 leukocytes, p=0.032). There were no significant differences in baseline EPCs levels between survivors and non-survivors nor between patients who were rehospitalized for HF management during follow-up or not. At 6-month follow-up, circulating EPCs levels were significantly higher than baseline levels (0.0024 ± 0.0023 vs 0.0047 ± 0.0041 CD34 + KDR + cells/100 leukocytes, p=0.010 and 0.0007 ± 0.0004 vs 0.0016 vs 0.0013 CD133 + /KDR + cells/100 leukocytes, p=0.007). Conclusions Patients with ICM showed significantly lower levels of circulating EPCs when compared to their counterparts. CRT seems to improve the pool of endogenously circulating EPCs and reduced baseline EPCs levels seem not influence long-term outcomes after CRT.


2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Richard Longeras ◽  
Krysten Farjo ◽  
Michael Ihnat ◽  
Jian-Xing Ma

Proliferative diabetic retinopathy is characterized by pathological retinal neovascularization, mediated by both angiogenesis (involving mature endothelial cells) and vasculogenesis (involving bone marrow-derived circulating endothelial progenitor cells (EPCs)). Pigment epithelium-derived factor (PEDF) contains an N-terminal 34-amino acid peptide (PEDF-34) that has antiangiogenic properties. Herein, we present a novel finding that PEDF-34 also possesses antivasculogenic activity. In the oxygen-induced retinopathy (OIR) model using transgenic mice that have Tie2 promoter-driven GFP expression, we quantified Tie2GFP+cells in bone marrow and peripheral blood by fluorescence-activated cell sorting (FACS). OIR significantly increased the number of circulating Tie2-GFP+at P16, correlating with the peak progression of neovascularization. Daily intraperitoneal injections of PEDF-34 into OIR mice decreased the number of Tie2-GFP+cells in the circulation at P16 by 65% but did not affect the number of Tie2-GFP+cells in the bone marrow. These studies suggest that PEDF-34 attenuates EPC mobilization from the bone marrow into the blood circulation during retinal neovascularization.


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