சுருக்கம்
Pattern of apoptotic endothelial cell-derived micro vesicles in patients with different phenotypes of chronic heart failure
Alexander E Berezin*, Alexander A Kremzer, Tatyana A Samura and Tatyana A BerezinaBackground: The aim of the study was to evaluate the associations between the signature of apoptotic endothelial cellderived microvesicles (MVs) and biomarkers of fibrosis, inflammation and cardiac remodeling in patients with different phenotypes of chronic Heart Failure (HF). Methods: The study cohort consisted of 388 prospectively involved subjects with established chronic HF. The phenotype of HF was determined according to left ventricular ejection fraction (LVEF) value per contemporary clinical guideline. HFrEF (LVEF ≤ 40%), HFmrEF (41-49%) and HFpEF (LVEF ≥ 50%) were determined. All biomarkers were measured at baseline. Results: The number of circulating CD31+/annexin V+MVs in HFpEF patients was significantly different from both HFrEF and HFmrEF individuals, but it was similar in HFrEF and HFmrEF patients. The number of circulating CD144+/ annexin V+MVs in HFrEF patients was significantly higher to HFmrEF and HFpEF. We determined that a combination of a number of circulating CD31+/annexin V+MVs and galectin-3 (AUC=0.68; 95% CI=0.61-0.77; P=0.001) was the best predictor of HFpEF. The predictive values of sST2 (AUC=0.65; 95% CI=0.60-0.69), number of circulating CD31+/annexin V+MVs (AUC=0.63; 95% CI=0.58-0.69) alone and their combination (AUC=0.65; 95% CI=0.59-0.70) for HFmrEF did not distinguished significantly (P=0.48). The double combinations of number of circulating CD144+/annexin V+MVs and sST2 (AUC=0.70; 95% CI=0.66-0.75) or number of circulating CD144+/annexin V+MVs and galectin-3 (AUC=0.71; 95% CI=0.650.76) were the best prognosticators for HFrEF. Conclusion: we found that the number of circulating CD31+/annexin V+MVs may improve a prediction of galectin-3 for HFpEF, and that number of circulating CD144+/annexin V+MVs is able to increase predictive capabilities of sST2 and galectin-3 for HFrEF.