title: Circulating endothelial cells in atrial fibrillation with and without acute cardiovascular disease.
abstract: Normal adults have very few circulating endothelial cells (CECs) in their blood, but increased levels have been shown in association with conditions associated with endothelial damage such as myocardial infarction and stroke. As atrial fibrillation (AF) is associated with a hypercoagulable state and abnormalities of plasma indices of endothelial damage/dysfunction, we hypothesised that CECs would also be raised in this condition, and would correlate with these plasma markers. We measured CECs (by immunofluoresence) as an indicator of frank endothelial damage, alongside 3 plasma indices of endothelial perturbation: von Willebrand factor (vWf), soluble E-selectin and soluble thrombomodulin (sTM) (all ELISA) in 28 patients with chronic 'stable' AF, 63 patients with AF plus an acute cardiovascular or cerebrovascular event as positive controls, and 20 healthy subjects in sinus rhythm as negative controls. Chronic 'stable' AF patients had significantly higher levels of plasma vWf (p<0.001 ), but comparable numbers of CECs (p=0.1638) in comparison to healthy controls. In patients with AF associated with an acute cardiovascular or cerebrovascular event, levels of CECs (p<0.0001) and sTM (p=0.004), but not vWf or sEsel, were significantly increased in comparison to chronic 'stable' AF patients. Patients with uncomplicated AF have abnormal systemic endothelial damage/dysfunction, as evident by increased plasma vWf levels, but normal numbers of CECs, compared to subjects in sinus rhythm. However, following clinical complications, such as stroke or significant haemodynamic compromise, further endothelial disturbance (as indicated by high levels of sTM and CECs) suggests additional endothelial damage.
authors.affiliation: Haemostasis, Thrombosis, and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, UK.
authors.forename: Bethan
authors.initials: B
authors.lastname: Freestone
authors.forename: Gregory Y H
authors.initials: GY
authors.lastname: Lip
authors.forename: Aun Yeong
authors.initials: AY
authors.lastname: Chong
authors.forename: Sunil
authors.initials: S
authors.lastname: Nadar
authors.forename: Kaeng W
authors.initials: KW
authors.lastname: Lee
authors.forename: Andrew D
authors.initials: AD
authors.lastname: Blann
mesh_terms: D000208:Acute Disease; D000368:Aged; D001281:Atrial Fibrillation / Q000097:blood* / Q000473:pathology*; D015415:Biomarkers; D002908:Chronic Disease; D019040:E-Selectin / Q000097:blood; D042783:Endothelial Cells / Q000473:pathology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000473:pathology*; D020521:Stroke / Q000097:blood / Q000473:pathology; D018180:Thrombomodulin / Q000097:blood; D013927:Thrombosis / Q000097:blood / Q000473:pathology; D014841:von Willebrand Factor / Q000378:metabolism
chemical_list: D015415:Biomarkers; D019040:E-Selectin; D018180:Thrombomodulin; D014841:von Willebrand Factor