INTRODUCTION: Chronic obstructive pulmonary disease (COPD) patients have increased risk for cardiovascular mortality and venous thromboembolism. Tissue factor (TF) is the physiological initiating mechanism for blood coagulation and is pro-inflammatory. METHODS: We have studied circulating blood-borne TF-procoagulant activity (TF-PCA), plasma coagulation factors (F) VIIa and FVIII, and thrombin-antithrombin (TAT) complexes in 11 stable, moderate-severe COPD patients, 10 free of exacerbation for >3 weeks. RESULTS: TF-PCA was increased in COPD patients (52.3+/-5.6 U/ml, (SE)) compared to control subjects (20.7+/-1.5, n=45, p<0.0001). TAT levels were increased (COPD patients: 2.99+/-0.65 ug/l; control subjects: 1.31+/-0.13, n=53, p<0.0001), indicating enhanced thrombin generation. Plasma FVIIa (the activated form of FVII) was higher in COPD (83+/-11 mU/ml; controls, 64+/-5 mU/ml, n=20) but did not reach statistical significance. Plasma FVIIc and FVIII were not increased. TF-PCA levels were inversely related to plasma FVIIa (r=-0.80, p=0.003) and FVIIc (r=-0.76, p=0.007). CONCLUSIONS: Blood-borne TF-PCA is elevated and constitutes a prothrombotic and proinflammatory state in stable but moderate-severe COPD, and may contribute to the increased risk for vascular events.
INTRODUCTION:Chronic obstructive pulmonary disease (COPD) patients have increased risk for cardiovascular mortality and venous thromboembolism. Tissue factor (TF) is the physiological initiating mechanism for blood coagulation and is pro-inflammatory. METHODS: We have studied circulating blood-borne TF-procoagulant activity (TF-PCA), plasma coagulation factors (F) VIIa and FVIII, and thrombin-antithrombin (TAT) complexes in 11 stable, moderate-severe COPDpatients, 10 free of exacerbation for >3 weeks. RESULTS:TF-PCA was increased in COPDpatients (52.3+/-5.6 U/ml, (SE)) compared to control subjects (20.7+/-1.5, n=45, p<0.0001). TAT levels were increased (COPDpatients: 2.99+/-0.65 ug/l; control subjects: 1.31+/-0.13, n=53, p<0.0001), indicating enhanced thrombin generation. Plasma FVIIa (the activated form of FVII) was higher in COPD (83+/-11 mU/ml; controls, 64+/-5 mU/ml, n=20) but did not reach statistical significance. Plasma FVIIc and FVIII were not increased. TF-PCA levels were inversely related to plasma FVIIa (r=-0.80, p=0.003) and FVIIc (r=-0.76, p=0.007). CONCLUSIONS: Blood-borne TF-PCA is elevated and constitutes a prothrombotic and proinflammatory state in stable but moderate-severe COPD, and may contribute to the increased risk for vascular events.
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