An Association of Insulin Resistance with Numerous of Circulating Microparticles Originated from Endothelial Cells in Cardiac Failure Individuals without History of Diabetes Mellitus

Background: The causality role of insulin resistance (IR) in chronic heart failure (CHF) subjects has not determined. The study was conducted to examine a relationship between IR and numerous of circulating endothelial cell-derived microparticles (EMPs) in patients with CHF. Methods: Three hundreds ischemic-induced CHF patients aged 48 to 62 years who underwent multispiral computed tomography angiography or coronary angiography was involved in the study. Ischemic-induced CHF has documented when atherosclerotic stenos is > 50% of at least one coronary artery was presented or previously defined myocardial infarction was reported. Biomarkers were measured at baseline of the study. Circulating EMPs were isolated from peripheral blood and measured using flow cytometry technique. Results: These were not significant differences between patients with and without IR in EMPs labeled as CD144+/CD31+, CD144+/annexin V+, and CD62E+ microparticles. Higher concentrations of CD144+/CD31+/annexin V+ EMPs and CD31+/annexin V+ EMPs were found in IR subjects when compared with none IR patients. Multivariate linear regression analyses has shown HOMAIR (OR = 1.14, 95% CI=1.08-1.21, P = 0.001), NT-proBNP (OR = 1.07, 95% CI=1.04-1.10, P = 0.001), hs-CRP (OR = 1.04, 95% CI=1.02-1.07, P = 0.001), and NYHA class (OR = 1.03, 95% CI=1.01-1.05, P = 0.001) were predictors for increased CD31+/annexin V+ EMPs. Additionally, HOMA-IR (OR = 1.10, 95% CI=1.05-1.17, P = 0.001), NT-proBNP (OR = 1.08, 95% CI=1.04-1.12, P = 0.001), and NYHA class (OR = 1.05, 95% CI=1.02-1.09, P = 0.001) significantly predicted elevation of CD144+/CD31+/annexin V+ EMPs. C-statistics for Models with HOMA-IR, NYHA class, and CHF biomarkers (hs-CRP, NT-proBNP) as continuous variables reported that adding of combination of these biomarkers to the based model constructed with HOMA-IR did not improve the relative IDI for increased CD144+/CD31+/annexin V+ and CD31+/annexin V+ microparticles. Conclusion: we found that IR was statistically significant predictor for increased apoptotic EMPs labelled as CD144+/CD31+/annexin V+ and CD31+/ annexin V+ microparticles in CHF patients without history of T2DM. We suggest that these findings might reflect an impaired phenotype of circulating EMPs in this patient population.