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Blood, 15 January 2005, Vol. 105, No. 2, pp. 526-532.
Prepublished online as a Blood First Edition Paper on September 16, 2004; DOI 10.1182/blood-2004-03-1106.
Previous Article | Next Article 
Submitted March 25, 2004
Accepted September 2, 2004
Circulating endothelial cells, Von Willebrand Factor, interleukin-6 and prognosis in patients with acute coronary syndromes
Kaeng W Lee, Gregory Y Lip*, Muzahir Tayebjee, William Foster, and Andrew D Blann
Haemostasis Thrombosis and Vascular Biology Unit, City Hospital, Birmingham, UK
* Corresponding author; email: g.y.h.lip{at}bham.ac.uk.
Background: Markers of inflammation (e.g. interleukin-6[IL-6]), and endothelial perturbation (von Willebrand factor[vWf], circulating endothelial cells[CECs]) are altered in acute coronary syndromes (ACS). We hypothesised that CECs and IL-6 levels during the first 48hrs of ACS would predict 30day and 1 year major cardiovascular endpoints (MACE).
Methods: 156 patients with ACS were included. Blood was drawn on admission (baseline) and 48hrs later for plasma vWf, IL-6 (both ELISA) and CECs (immunomagnetic separation). CEC phenotyping was performed by indirect immunoperoxidase staining.
Results: At 30days, 48 patients had 1 MACE, predicted by baseline and 48hr CECs and IL-6 levels, 48hr vWf levels, and by the 'admission to 48hr change'( ) in CECs, vWf and IL-6 (all p 0.002). On multivariate analysis, 48hr CECs (p<0.001) were the strongest predictor of MACE, followed by IL-6 (p=0.01) and vWf (p=0.048); 48hr CECs were the only predictor of death (p=0.007). At 1 year, 65 patients had 1 MACE, predicted by 48hr CECs and IL-6 levels (p<0.001); age (p=0.046) and 48hr CECs (p<0.001) were the only predictors of death. CECs stained 93% positive for eNOS, but were <1% positive for CD34, CD36 and CD45, and <3% for CD31.
Conclusions: Like raised vWf, abnormal CECs and IL-6 levels during the first 48hrs of ACS were strongly associated with 30day MACE. CECs at 48hrs were the only independent predictor of both death and MACE at 30days and 1 year, indicating the crucial role of endothelial/vascular damage in ACS pathophysiology.

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