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.
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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