Abstract
Aim: To evaluate the prognostic value of circulating VE-catherinfor cumulative survivalin patients with ischemic chronic heart failure (CHF).Methods: A total of 154 patients withischemic symptomatic moderate-to-severe CHF were enrolled in the study on discharge from the hospital. Observation period was up to 3 years. Blood samples for biomarkers measurements were collected. ELISA method for measurements of circulating level of VE-catherin was used. Concentrations of VEcatherinfor cumulative survival cases due to advanced CHF were tested. Additionally, all-cause mortality, and CHFrelated death were examined.Results: During a median follow-up of 2.18 years, 21 participants died and 106 subjects were hospitalized repetitively. Medians of circulating levels of VE-catherin in survived and died patient cohort were 0.63 ng/ml (95% confidence interval [CI] = 0.55-0.64 ng/ml) and 1.03 ng/ml (95% CI = 0.97-1.07 ng/ml) (P<0.001). ROC analysis has been shown that cutoff point of VE-catherin concentration for cumulative survival function was 0.755ng/ml. It has beenfound a significantly divergence of Kaplan-Meier survival curves in patients with high (>0.755 ng/ml) and low (<0.755 ng/ml) concentrations of VE-catherin. Circulating VE-catherin independently predicted all-cause mortality (OR = 1.27; 95% CI = 1.081.59; P = 0.002), CHF-related death (OR = 1.16; 95% CI 1.021.50; P < 0.001), and also CHF-related rehospitalisation (OR = 1.12; 95% CI = 1.07 1.25; P<0.001) within 3 years of observation period.Conclusion: Increased circulating VE-catherinassociates with increased 3-year CHF-related death, all-cause mortality, and risk for recurrent hospitalization due to CHF.J MEDICINE July 2015; 16 (2) : 73-78
Highlights
Chronic heart failure (CHF) is considered as a leading cause of morbidity and mortality inworldwide.1Nature evolution of CHF is associated with endothelial dysfunction that results in shear stress disorders on endothelium, which is exerted several factors, such as angiotensin-aldosterone system activation, oxidative stress, proinflammatory response, exaggerated collagen synthesisand extracellular matrix remodelling in vasculature, degradation of vasodilators etc.[2]
Circulating VE-catherin level in survival and diedpatients Medians of circulating levels of VE-catherin in survived and died patient cohort were 0.63 ng/ml (95% confidence interval [CI] = 0.55-0.64 ng/ml) and 1.03 ng/ml (P
We found that VE-catherin(Model 1) and combination of VE-catherin with NT-pro-BNP (Model 2) remained statistically significant predictors for all-cause mortality (B-coefficient=1.18, p= 0.001, and Bcoefficient=1,13, p=0.001 respectively), CHF-related death (B-coefficient=2.36, p= 0.001, and B-coefficient=2,81, p=0.001 respectively), and CHF-related re-hospitalisations (B-coefficient=2.34, p= 0.001, and B-coefficient=2,26, p=0.001 respectively),whereas combination of VE-catherin with both NT-pro-BNP and Left ventricular ejection fraction (LVEF)(Model 3) did not (Bcoefficient= 0.011, p= 0.682, and B-coefficient=0,012, p=0.588, and B-coefficient=0,011, p=0.568 respectively)
Summary
Chronic heart failure (CHF) is considered as a leading cause of morbidity and mortality inworldwide.1Nature evolution of CHF is associated with endothelial dysfunction that results in shear stress disorders on endothelium, which is exerted several factors, such as angiotensin-aldosterone system activation, oxidative stress, proinflammatory response, exaggerated collagen synthesisand extracellular matrix remodelling in vasculature, degradation of vasodilators etc.[2] mechanical interaction of endothelial cells (ECs), which is mediated by blood flow,might lead to junction vascular remodelling.3Particularly this phenomenon is. 1. State Medical University, Internal Medicine Department, Zaporozhye, Ukraine. 2. State Medical University, Clinical Pharmacology Department, Zaporozhye, Ukraine. The objective of this study was toevaluate the prognostic value of circulating VE-catherin for cumulative survival in patients with ischemic chronic heart failure. Predictive Value of Circulatingve-catherin in Coronary Artery Disease JM Vol 16, No 2
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