Increased circulating endothelial cells in acute heart failure: comparison with von Willebrand factor and soluble
Aun Yeong Chong1, Gregory Y H Lip, Bethan Freestone
1Haemostasis Thrombosis and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham B18 7QH, United Kingdom.
Insights
Circulating endothelial cells (CECs) indicate endothelial damage in heart failure. Elevated CECs, von Willebrand factor, and soluble E-selectin levels were observed in heart failure patients, suggesting their use as a novel measure.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Cell Biology
Background:
- Circulating endothelial cells (CECs) are markers of endothelial damage in cardiovascular conditions.
- Endothelial dysfunction is implicated in chronic heart failure.
- This study investigated CECs in acute heart failure.
Purpose of the Study:
- To determine if CECs are elevated in acute heart failure.
- To assess the correlation between CECs and plasma markers of endothelial perturbation, specifically von Willebrand factor (vWf) and soluble E-selectin.
- To evaluate CECs as a potential indicator of endothelial damage in heart failure.
Main Methods:
- Studied 30 acute heart failure patients, 30 chronic stable heart failure patients, and 20 healthy controls.
- Quantified CECs using epifluorescence microscopy and CD146-immunomagnetic separation.
- Measured plasma vWf and soluble E-selectin using ELISA.
Main Results:
- CECs, vWf, and soluble E-selectin were significantly higher in heart failure patients compared to controls (p<0.01).
- No significant difference in CECs between acute and chronic heart failure.
- CECs correlated with plasma vWf (p<0.0001) and soluble E-selectin (p=0.022).
Conclusions:
- CECs may serve as a novel measure of endothelial damage in acute heart failure.
- Elevated CECs have implications for thrombotic risk and prognosis in acute and chronic heart failure.
- CECs represent a potentially valuable biomarker in heart failure management.
Background:
Circulating endothelial cells (CECs) in the peripheral blood, probably representing the most direct evidence of endothelial cell damage, are increased in myocardial infarction, unstable angina and critical limb ischaemia. As chronic heart failure is also associated with endothelial abnormalities, we hypothesised that CECs are raised in acute heart failure and that they would correlate with plasma indices of endothelial perturbation, that is, von Willebrand factor (vWf) and soluble E-selectin.
Methods:
We studied 30 patients with acute heart failure (venesected within 24 h of emergency hospital admission), 30 patients with chronic stable heart failure (venesected as out-patients, all patients in sinus rhythm with ejection fraction < or = 40%) and 20 healthy controls. CECs were quantified using epifluorescence microscopy after CD146-immunomagnetic separation and phenotyped by streptavidin/biotin immunocytochemistry. Citrated plasma was analysed for soluble E-selectin and vWf by ELISA.
Results:
Levels of CECs, vWf and soluble E-selectin were significantly higher (all p<0.01) in patients with heart failure compared to controls, with no significant differences between acute and chronic heart failure. CECs correlated with plasma vWf (p<0.0001) and soluble E-selectin (p = 0.022) but not ejection fraction or NYHA class. In multiple regression analysis, heart failure was the only independent predictor of raised CECs (p<0.0001). Immunoperoxidase-defined surface expression of CD34, CD45 and CD36 by CECs was <2%, 0% and 8%, respectively.
Conclusion:
CECs, a possibly heterologous population, may be used as a novel measure of endothelial damage in acute heart failure and may have implications for the thrombotic risk associated with acute and chronic heart failure and prognosis in this condition.
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