The signature of circulating microparticles in heart failure patients with metabolic syndrome

Authors

  • Alexander E Berezin Consultant of the Therapeutic Unit, Internal Medicine Department, State Medical University, Zaporozhye, Ukraine
  • Alexander Kremzer Consultant of the Therapeutic Unit, Internal Medicine Department, State Medical University, Zaporozhye, Ukraine
  • Tatyana Berezina Private center Vita-Center, Zaporozhye, Ukraine
  • Yu Martovitskaya Pathology Department, Dia-Service LTD, Zaporozhye, Ukraine

DOI:

https://doi.org/10.33393/jcb.2016.2064

Keywords:

Chronic heart failure, metabolic syndrome, circulating microparticles, cardiovascular risk factors inflammation, neurohumoral activation

Abstract

The role of pattern of circulating endothelial cell-derived microparticles, platelet-derived microparticles (PMPs), and monocyte-derived microparticles (MMPs) 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 microparticles (MPs) in MetS patients with CHF in relation to neurohumoral and inflammatory activation. The study retrospectively involved 101 patients with MetS and 35 healthy volunteers. Biomarkers were measured at baseline of the study. The results of the study have shown that numerous circulating PMPs- and MMPs in subjects with MetS (with or without CHF) insufficiently distinguished from level obtained in healthy volunteers. We found elevated level of CD31+/annexin V+ MPs in association with lower level of CD62E+ MPs. Therefore, we found that biomarkers of biomechanical stress serum N-terminal brain natriuretic peptide and inflammation (high-sensitive C-reactive protein ,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 that impaired immune phenotype of MPs may be discussed as a surrogate marker of CHF development in MetS population.