title: Circulating endothelial cells, von Willebrand factor, interleukin-6, and prognosis in patients with acute coronary syndromes.
abstract: Markers of inflammation (eg, interleukin-6 [IL-6]), and endothelial perturbation (von Willebrand factor [VWF], circulating endothelial cells [CECs]) are altered in acute coronary syndromes (ACS). We hypothesized that CECs and IL-6 levels during the first 48 hours of ACS would predict 30-day and 1-year major cardiovascular end points (MACE). A total of 156 patients with ACS were included. Blood was drawn on admission (baseline) and 48 hours later for plasma VWF, IL-6 (both enzyme-linked immunosorbent assay [ELISA]), and CECs (CD146 immunomagnetic separation). CEC phenotyping was performed by indirect immunoperoxidase staining. At 30 days, 48 patients had a MACE, a predicted by baseline and 48-hour CECs and IL-6 levels, 48-hour VWF levels, and by the "admission-48 hour change" (Delta) in CECs, VWF, and IL-6 (all P = .002). On multivariate analysis, 48-hour CECs (P < .001) were the strongest predictor of MACE, followed by DeltaIL-6 (P = .01) and DeltaVWF (P = .048); 48-hour CECs were the only predictor of death (P = .007). At 1 year, 65 patients had MACE, predicted by 48-hour CECs and DeltaIL-6 levels (P < .001); age (P = .046) and 48-hour CECs (P < .001) were the only predictors of death. CECs stained 93% positive for endothelial nitric oxide synthase (eNOS) but were less than 1% positive for CD34, CD36, and CD45 and less than 3% for CD31. Like raised VWF, abnormal CECs and IL-6 levels during the first 48 hours of ACS were strongly associated with 30-day MACE. CECs at 48 hours were the only independent predictor of both death and MACE at 30 days and 1 year, indicating the crucial role of endothelial/vascular damage in ACS pathophysiology.
authors.affiliation: Haemostasis Thrombosis and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, United Kingdom.
authors.forename: Kaeng W
authors.initials: KW
authors.lastname: Lee
authors.forename: Gregory Y H
authors.initials: GY
authors.lastname: Lip
authors.forename: Muzahir
authors.initials: M
authors.lastname: Tayebjee
authors.forename: William
authors.initials: W
authors.lastname: Foster
authors.forename: Andrew D
authors.initials: AD
authors.lastname: Blann
mesh_terms: D000208:Acute Disease; D000368:Aged; D015415:Biomarkers; D003324:Coronary Artery Disease / Q000097:blood* / Q000175:diagnosis / Q000276:immunology*; D003430:Cross-Sectional Studies; D042783:Endothelial Cells / Q000276:immunology*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D016130:Immunophenotyping; D015850:Interleukin-6 / Q000097:blood* / Q000276:immunology; D007962:Leukocytes / Q000276:immunology; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D013234:Stem Cells / Q000276:immunology; D014841:von Willebrand Factor / Q000276:immunology / Q000378:metabolism*
chemical_list: D015415:Biomarkers; D015850:Interleukin-6; D014841:von Willebrand Factor