Published online Nov 26, 2020. doi: 10.4330/wjc.v12.i11.526
Peer-review started: June 24, 2020
First decision: July 25, 2020
Revised: July 28, 2020
Accepted: October 5, 2020
Article in press: October 5, 2020
Published online: November 26, 2020
Processing time: 154 Days and 16.2 Hours
Vascular endothelial dysfunction is an underlying pathophysiological feature of chronic heart failure (CHF). Patients with CHF are characterized by impaired vasodilation and inflammation of the vascular endothelium. They also have low levels of endothelial progenitor cells (EPCs). EPCs have been used as an index of the endothelium restoration potential, therefore reflecting the vascular endothelial function. Exercise has a beneficial impact in the function of the vascular endothelium and EPCs.
Despite the proven beneficial effect of exercise training in patients with cardiovascular comorbidities, the effect of maximal exercise on EPCs in patients with CHF, and especially in patients of different severity, remains under investigation.
This study was conducted to assess, quantify and compare the acute mobilization of EPCs after maximal exercise in patients with CHF of both lower and higher severity.
Forty-nine consecutive patients with stable CHF underwent a cardiopulmonary exercise testing (CPET) on a cycle ergometer. Venous blood was sampled before and after CPET. Five circulating endothelial populations were quantified by flow cytometry. Patients were divided in two groups of severity according to the median value of peak oxygen uptake (VO2), predicted peak VO2, ventilation (VE)/carbon dioxide output (VCO2) slope and ejection fraction (EF).
Patients with lower peak VO2 increased the mobilization of CD34+/CD45-/CD133+, CD34+/CD45-/CD133+/VEGFR2, CD34+/CD45-/CD133- and CD34+/CD45-/CD133-/VEGFR2, while patients with higher VO2 increased the mobilization of CD34+/CD45-/CD133+, CD34+/CD45-/CD133+/VEGFR2, CD34+/CD133+/VEGFR2, CD34+/CD45-/CD133- and CD34+/CD45-/CD133-/VEGFR2. A similar increase in the mobilization of at least four out of five cellular populations was observed after maximal exercise within each severity group regarding predicted peak, VE/VCO2 slope and EF, as well (P < 0.05). However, there were no statistically significant differences in the mobilization of endothelial cellular populations between severity groups in each comparison (P > 0.05).
Our study has shown an increased EPC and CEC mobilization after maximal exercise in CHF patients, but this increase was not associated with syndrome severity.
EPCs could be the cornerstone to the treatment of CHF. Understanding their possible mechanisms of action on vascular endothelial function through exercise would create innovative ideas regarding their distribution and proliferation in these patients in order to take advantage of their beneficial effects on the endothelium and reverse cardiac remodeling.