Article ID Journal Published Year Pages File Type
2773068 BBA Clinical 2015 7 Pages PDF
Abstract

•Circulating microparticles may interplay in vascular remodeling and tissue reparation.•Heart failure associates with elevated apoptotic and decreased activated endothelial cell-derived microparticles.•Imbalance between numbers of apoptotic and activated endothelial cell microparticles reflects impaired immune phenotype.•Impaired immune phenotype of microparticles might discuss a surrogate marker of heart failure development.•Brain natriuretic peptide, C-reactive protein, and osteoprotegerin predict impaired immune phenotype of microparticles.

BackgroundThe role of pattern of circulating endothelial cell-, platelet-, and monocyte-derived microparticles in metabolic syndrome (MetS) patients with chronic heart failure (CHF) is not still understood.The aim of the study was to investigate a pattern of circulating MPs in MetS patients with CHF in relation to neurohumoral and inflammatory activation.MethodsThe study retrospectively involved 101 patients with MetS (54 subjects with CHF and 47 patients without CHF) without documented coronary artery stenosis > 50% at least of one artery and 35 healthy volunteers. Biomarkers were measured at baseline of the study. Circulating MPs were phenotyped by flow cytometry technique.ResultsThe results of the study have shown that numerous of the circulating platelet-derived and monocyte-derived MPs in subjects with MetS (with or without CHF) were insufficiently distinguished from the level obtained in healthy volunteers. We found an elevated level of CD31 +/annexin V + MPs in association with a lower level of CD62E + MPs. All these led to decreased CD62E + to CD31 +/annexin V + ratio among patients with MetS in comparison with healthy volunteers, as well as in MetS patients with CHF compared with those who did not demonstrated CHF. Therefore, we found that biomarkers of biomechanical stress (NT-proBNP) and inflammation (hs-CRP, osteoprotegerin) remain statistically significant predictors for decreased CD62E + to CD31 +/annexin V + ratio in MetS patients with CHF.In conclusion, decreased CD62E + to CD31 +/annexin V + ratio reflected impaired immune phenotype of MPs may be discuss surrogate marker of CHF development in MetS population.

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