Related Experiment Video
Updated: Aug 15, 2026
Catheter Ablation in Combination With Left Atrial Appendage Closure for Atrial Fibrillation
Published on: February 26, 2013
Circulating endothelial cells in atrial fibrillation with and without acute cardiovascular disease
Bethan Freestone1, Gregory Y H Lip, Aun Yeong Chong
1Haemostasis, Thrombosis, and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, UK.
Insights
Patients with atrial fibrillation (AF) show elevated von Willebrand factor, indicating endothelial dysfunction. Complications like stroke reveal further endothelial damage, marked by increased circulating endothelial cells (CECs) and soluble thrombomodulin (sTM).
Area of Science:
- Cardiovascular Medicine
- Hematology
- Cell Biology
Background:
- Normal adults have minimal circulating endothelial cells (CECs).
- Elevated CECs are linked to endothelial damage in conditions like myocardial infarction and stroke.
- Atrial fibrillation (AF) is associated with a hypercoagulable state and endothelial dysfunction markers.
Purpose of the Study:
- To investigate if CECs are elevated in patients with AF.
- To determine if CEC levels correlate with plasma markers of endothelial damage/dysfunction.
- To compare endothelial markers in stable AF, complicated AF, and healthy controls.
Main Methods:
- Measured CECs using immunofluorescence.
- Quantified plasma levels of von Willebrand factor (vWf), soluble E-selectin (sEsel), and soluble thrombomodulin (sTM) via ELISA.
- Included 28 chronic stable AF patients, 63 AF patients with acute events, and 20 healthy controls.
Main Results:
- Chronic stable AF patients had higher plasma vWf but similar CEC counts compared to healthy controls.
- AF patients with acute cardiovascular/cerebrovascular events showed significantly increased CECs and sTM compared to stable AF patients.
- vWf and sEsel levels did not significantly differ between stable AF and complicated AF groups.
Conclusions:
- Uncomplicated AF exhibits endothelial dysfunction (increased vWf) but not frank endothelial damage (normal CECs).
- Clinical complications in AF, such as stroke, are associated with additional endothelial damage, indicated by elevated CECs and sTM.
- These findings highlight distinct mechanisms of endothelial perturbation in AF, differentiating between underlying dysfunction and acute damage.
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.