Pattern of circulating microparticles in chronic heart failure patients with metabolic syndrome: Relevance to neurohumoral and inflammatory activation

BBA Clin. 2015 Aug 3:4:69-75. doi: 10.1016/j.bbacli.2015.07.002. eCollection 2015 Dec.

Abstract

Background: The 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.

Methods: The 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.

Results: The 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.

•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.

Keywords: Cardiovascular risk factors; Chronic heart failure; Circulating microparticles; Inflammation; Metabolic syndrome; Neurohumoral activation.