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Increase in circulating levels of endothelial progenitor cells after cardiac resynchronization therapy: what implications?
Session:
CO - Prémio Jovem Investigador (Investigação Básica)
Speaker:
James Milner
Congress:
CPC 2019
Topic:
O. Basic Science
Theme:
36. Basic Science
Subtheme:
36.3 Basic Science - Cardiac Diseases
Session Type:
Comunicações Orais
FP Number:
---
Authors:
James Milner; Gonçalo Cristóvão; Célia Domingues; Sofia S. Martinho; Catia Ferreira; Natália António; Miguel Ventura; João Cristóvão; Luis Elvas; Artur Paiva; Lino Gonçalves
Abstract
<p><strong>BACKGROUND: </strong>Endothelial Progenitor Cells (EPCs) are multipotent adult stem cells that circulate in the peripheral blood, playing an important role in postnatal neovascularization and repair of ischemic cardiac injury. Despite their established value as predictor of outcomes in coronary artery disease, little is known about the role of EPCs in patients with chronic heart failure, and whether their circulating levels evolve after response to cardiac resynchronization therapy (CRT).</p> <p><strong>AIM: </strong>To evaluate the influence of CRT on circulating EPC levels in patients with advanced heart failure (HF) submitted to CRT and to verify if EPCs levels have any value as a prognosticator in these patients.</p> <p><strong>METHODS: </strong>Prospective, single-center study of 50 patients with advanced HF submitted to cardiac resynchronization therapy (CRT), and followed up for 5.4±2.3 years. Two populations of circulating EPCs were quantified by flow cytometry: CD34<sup>+</sup>KDR<sup>+</sup>and CD133<sup>+</sup>KDR<sup>+</sup>cells. Levels of circulating EPCs were measured at baseline and 6 months post-CRT. Response to CRT was defined as a reduction in left ventricular end-systolic volume of ≥15% at 6-months follow up. </p> <p><strong>RESULTS: </strong>Mean age in this cohort was 62±11, and 64% of patients were males. Patients had HF of non-ischemic etiology in 78%, and 72% received a CRT with defibrillator. Most patients were in NYHA functional classes III-IV prior to CRT (89%), and most were receiving disease-modifying HF drugs (88% receiving beta-blockers, 86% on ACE-inhibitors or ARBs and 61% on mineralocorticoid-receptor antagonists). During long-term follow-up, the readmission rate due to acute decompensated HF was 44%, and all-cause mortality was 36%. Echocardiographic response to CRT occurred in 46% and functional response to CRT was 60%. After CRT, we verified a significant increase in circulating EPC levels for both studied populations, with an increase from 0.0024±0.0023 to 0.0047±0.0041 cells/100 leukocytes for the CD34<sup>+</sup>KDR<sup>+</sup>population and from 0.0007±0.0004 to 0.0016±0.0013 for the CD133<sup>+</sup>KDR<sup>+</sup>cells(p=0.01 and 0.007, respectively).Regarding, the potential value of circulating EPCs as predictor of outcomes, we did not verify neither an association between baseline EPCs levels and rate of rehospitalization for HF nor mortality rate. Time to the occurrence of first rehospitalization for HF was 43±39 months for patients in which CD34+KDR+ cells increased after CRT and 63±34 months for patients in which these EPCs did not increase with CRT, however this difference was not statistically significant (0.207).</p> <p><strong>CONCLUSIONS: </strong>Our results show that CRT directly or indirectly improves the endogenous pool of EPCs. However, baseline EPCs levels did not demonstrate any significant prognostic value in these patients. The importance of the increase in circulating EPCs associated with CRT and the mechanisms underlying this improvement needs further investigation.</p>
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