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Original Research

Inflammatory phenotype of circulating endothelial-derived microparticles in chronic heart failure patients with metabolic syndrome

Alexander E Berezin, Alexander A Kremzer, Tatyana A Samura, Tatyana A Berezina.


Metabolic syndrome (MetS) may have an adverse impact on cardiovascular events in unselected populations. However, the role of MetS in chronic heart failure (CHF) subjects remains controversial. Endothelial-derived microparticles (EMPs) may play a pivotal role in cell-to-cell cooperation, effects negatively on tissue reparation, and mediates vascular function. Pattern of circulating EMPs probably reflects imbalance between endothelial cell injury and endothelial repair. The aim of the study: to investigate an inflammatory pattern of circulating EMPs in MetS patients with CHF.
Methods: The study retrospectively evolved 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 EMPs were phenotyped by flow cytometry technique.
Results: We found CD62E+ EMPs and CD62E+ to CD31+/annexin V+ ratio were elevated in healthy persons when compared with MetS patients. CD62E+ to CD31+/annexin V+ ratio was found to be higher in the MetS patients without CHF compared with MetS patients with CHF. Using multiple linear regression analysis, independent impact of BMI, NT-proBNP, osteoprotegerin and hs-CRP on decreased CD62E+ to CD31+/annexin V+ ratio was found. We found that adding of combination of inflammatory biomarkers (hs-CRP, osteoprotegerin and NT-proBNP) to the based model (BMI) improved the relative integrated discrimination indices by 11.4% for decreased CD62E+ to CD31+/annexin V+ ratio.
In conclusion, 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.

Key words: Chronic heart failure; metabolic syndrome; circulating endothelial-derived microparticles; cardiovascular risk factors.

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