Copyright © 2003 by the European Society of Cardiology.
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Interleukin-6, endothelial activation and thrombogenesis in chronic atrial fibrillation
a Haemostasis, Thrombosis and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, UK
b Hematology Unit, Hospital San Vicente, Alicante, Spain
c Department of Cardiology, Hospital General, Alicante, Spain
d Department of Haematology, Hospital General, Alicante, Spain
* Correspondence to: Professor G.Y.H. Lip, University Department of Medicine, City Hospital, Birmingham B18 7QH, UK. Tel: 00 44 121 507 5080; fax 00 44 121 507 5907
E-mail address: G.Y.H.LIP{at}bham.ac.uk
Received 8 January 2003; revised 26 February 2003; accepted 15 April 2003
Background A prothrombotic or hypercoagulable state has been described in AF, which could increase the risk of thromboembolism. As inflammation has been related to thrombogenesis and endothelial activation, we hypothesised that the prothrombotic state in AF (as assessed by an index of thrombogenesis, prothrombin fragment 1+2 [F1+2]) and endothelial activation (soluble E-selectin (sEsel)) could be related to an index of inflammation (interleukin-6 (IL-6)).
Patients and methods We studied 191 consecutive patients (98 male; mean age 72.3±9.2years) with chronic non-rheumatic AF who were not on anticoagulant therapy. Plasma IL-6, sEsel and F1+2 were measured by ELISA. Research indices were compared to 74 controls in sinus rhythm matched for age and sex. In 43 patients with AF, the effects of introducing anticoagulation (INR 2.0–3.0) were also studied.
Results Patients with AF had elevated levels of F1+2 (p<0.001) and IL-6 (p=0.045), but not sEsel. There was no significant correlation between F1+2 and IL-6. In multivariate analysis, only F1+2 levels were independently associated with the presence of AF (p=0.001). After oral anticoagulation, plasma levels of F1+2 and sEsel were significantly decreased (both p<0.01).
Conclusion High levels of IL-6 in AF suggest an inflammatory state, which appears to be more related to clinical variables of the patients, rather than to the presence of AF per se. There was no association of inflammation with endothelial activation (sEsel) or the presence of abnormal thrombogenesis (high F1+2 levels) in AF. Moreover, no changes in IL-6 levels were found despite the reduction of the other markers by oral anticoagulant therapy.
Key Words: Atrial fibrillation • Hypercoagulable • Inflammation
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