[Content of circulating endothelial progenitor cells in patients with chronic ischemic heart failure with preserved
Insights
Endothelial progenitor cells (EPC) with specific phenotypes are reduced in patients with chronic heart failure (CHF). Cardiovascular risk factors, including diabetes and hyperlipidemia, independently predict lower levels of these crucial EPC subpopulations.
Area of Science:
- Cardiovascular Research
- Cell Biology
- Immunology
Purpose:
To assess content of various subpopulations of endothelial progenitor cells (EPC) with CD45-CD34+, CD14+CD309+ and CD14+CD309+Tie2+ phenotypes in patients with chronic heart failure (CHF) of ischemic origin with preserved left ventricular ejection fraction.
Material And Methods:
We included into the study 126 patients (54 men) aged 48-62 years with angiographically confirmed ischemic heart disease (IHD) and 25 healthy volunteers. Eighty two (65%) patients had NYHA class I-II CHF. Phenotyping of populations of mononuclear cells was performed by flow cytometry with the use of fluorochrome-labeled monoclonal antibodies. Circulating EPC were determined as CD45-CD34+. For identification of subpopulations of EPC coexpressing CD14 antigen we determined CD309(VEGFR2) and Tie2 antigens.
Results:
In the group of patients with IHD level of circulating proatherogenic mononuclear cells of CD14+CD309+ and CD14+CD309+Tie2+ phenotype depended more on the presence of CHF and number of risk factors of cardiovascular complications (CVC) but not on severity and extent of coronary atherosclerosis. Most important independent predictors of lowering of circulating EPC with CD14+CD309+Tie2+ phenotype were CHF (odds ratio [OR] 1.45, 95% confidence interval [CI] 1.12 to 1.88, p = 0.004), type 2 diabetes (OR 1.21, 95% Cl 1.10 to 1.40; p = 0.008), NT-proBNP > 154 rg/ml (OR 1.13, 95% Cl 1.04 to 1.18, p = 0.003), hyperlipidemia (OR 1.12, 95% CI 1.05 to 1.23, p = 0.005), and presence of ± 3 traditional cardiovascular risk factors (OR 1.31, 95% CL 1.12 to 1.49, p = 0.008).
Conclusion:
Negative impact of factors of risk of CVC relative to manifestation of ischemic CHF might by mediated by deficit of nonhemopoetic circulating EPC, mobilization of which from peripheral tissues if reduced at early stages of formation of myocardial dysfunction.
