Serum soluble E-selectin and NT-proBNP levels additively predict mortality in diabetic patients with chronic heart failure
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Neuroendocrine activation with endothelial dysfunction is a key pathophysiological process in chronic heart failure (CHF). Although increased soluble E-selectin (sE-selectin) levels predict adverse events in several forms of cardiovascular disease, there are only scarce data on its predictive value in CHF. The aim of our study was to investigate whether sE-selectin is a useful predictor of mortality in CHF patients and whether its predictive power is additive to that of NT-proBNP.
Plasma levels of sE-selectin were measured by ELISA in 192 CHF patients with clinical systolic heart failure. The study population was followed up for 14.9 months on average; 46 patients died during this period.
Levels of sE-selectin were significantly higher in non-surviving patients than in survivors (p = 0.005) and significantly correlated with the following inflammatory markers: CRP (r = 0.242, p = 0.001), TNF-α (r = 0.201, p = 0.005), TNF-RII (r = 0.207, p = 0.004), and IL-6 (r = 0.339, p < 0.0001). According to Cox regression analysis of the prediction power of sE-selectin for all-cause mortality, high sE-selectin levels independently and significantly predicted short-term mortality in CHF (HR 1.47, 95% CI 1.103–1.956). Furthermore, sE-selectin predicted mortality in CHF patients with concomitant diabetes mellitus, as well as simultaneously elevated sE-selectin and NT-proBNP levels additively predicted mortality.
This study demonstrated a weak correlation of sE-selectin level with inflammatory markers and prediction of short-term mortality in diabetic CHF patients. Elevated serum sE-selectin levels and concomitantly increased NT-proBNP concentrations have additive predictive power in CHF. This suggests that parallel activation of various pathophysiological pathways confers increased risk of adverse outcome in CHF.
KeywordsHeart failure sE-selectin NT-proBNP Inflammation
We are grateful to our patients who consented to participate in this study. The authors appreciate the skillful technical assistance of Holeczky Rudolfné, Szigeti Antalné, Korponai Gézáné, Sturmann Piroska and Kókai Márta. This study was supported by the following grants: Hungarian Scientific Research Fund (OTKA T046837, NF72689, ZP), and National Development Agency TÁMOP 4.2.2-08/01/KMR-2008-0004 (Semmelweis Bridge Project).
Conflict of interest
No financial conflicts of interest are present with regard to this manuscript by the authors.
- 3.Chong AY, Blann AD, Patel J, Freestone B, Hughes E, Lip GYH (2004) Endothelial dysfunction and damage in congestive heart failure: relation of flow-mediated dilation to circulating endothelial cells, plasma indexes of endothelial damage, and brain natriuretic peptide. Circulation 110:1794–1798PubMedCrossRefGoogle Scholar
- 4.Gombos T, Makó V, Cervenak L, Papassotiriou J, Kunde J, Hársfalvi J, Förhécz Z, Pozsonyi Z, Borgulya G et al (2009) Levels of von Willebrand factor antigen and von Willebrand factor cleaving protease (ADAMTS13) activity predict clinical events in chronic heart failure. Thromb Haemost 102:573–580PubMedGoogle Scholar
- 5.Khan SQ, Dhillon O, Struck J, Quinn P, Morgenthaler NG, Squire IB, Davies JE, Bergmann A, Ng LL (2007) C-terminal pro-endothelin-1 offers additional prognostic information in patients after acute myocardial infarction: Leicester Acute Myocardial Infarction Peptide (LAMP) Study. Am Heart J 154:736–742PubMedCrossRefGoogle Scholar
- 13.White M, Ducharme A, Ibrahim R, Whittom L, Lavoie J, Guertin M-C, Racine N, He Y, Yao G et al (2006) Increased systemic inflammation and oxidative stress in patients with worsening congestive heart failure: improvement after short-term inotropic support. Clin Sci 110:483–489PubMedCrossRefGoogle Scholar
- 14.Kistorp C, Chong AY, Gustafsson F, Galatius S, Raymond I, Faber J, Lip GYH, Hildebrandt P (2008) Biomarkers of endothelial dysfunction are elevated and related to prognosis in chronic heart failure patients with diabetes but not in those without diabetes. Eur J Heart Fail 10:380–387PubMedCrossRefGoogle Scholar
- 16.Förhécz Z, Gombos T, Borgulya G, Pozsonyi Z, Prohászka Z, Jánoskuti L (2009) Red cell distribution width in heart failure: prediction of clinical events and relationship with markers of ineffective erythropoiesis, inflammation, renal function, and nutritional state. Am Heart J 158:659–666PubMedCrossRefGoogle Scholar