Introduction Heart failure (HF) is associated with coagulation activation, abnormal inflammation and endothelial dysfunction. High levels of von Willebrand factor (VWF) may manifest endothelial dysfunction and hypercoagulable state. The haemostatic activity of VWF is a function of multimers size; only large multimers of VWF are haemostatically active. Thrombospondin-1 (TSP-1) reduces the average multimer size of VWF. Patients with HF are in risk of thromboembolic events and oral anticoagulation therapy (OAT) has been shown to prevent it. This study was designed to evaluate whether VWF and TSP-1 levels are modified by OAT in stable HF patients. The effect of OAT on markers of inflammation and coagulation was also investigated. Materials and methods Fifty-nine patients with stable HF were studied and 33 of them received OAT. VWF, TSP-1, fibrinogen, prothrombin fragment 1 + 2 (F1 + 2), tissue factor (TF), D-dimer, endogenous thrombin generation (ETG), C reactive protein (CRP), tumour necrosis factor α (TNFα) and interleukin 6 (IL-6) were measured. Results Stable HF patients receiving OAT had higher VWF ( p = 0.02) and lower TSP-1 ( p = 0.02), ETG and F1 + 2 ( p = 0.003) than patients without OAT. However, there were no significant differences in the levels of fibrinogen, TF, D-dimer, CRP, IL6 and TNFα. The TSP-1/VWF ratio in patients receiving AOT was significantly lower than in patients without OAT ( p = 0.005). Conclusion OAT may have a dual effect on the haemostatic profile in stable HF by reducing thrombin generation and increasing the VWF. The decrease of TSP-1 induced by OAT may be clinically effective in neoangiogenesis. The increase of VWF in patients receiving anticoagulant treatment may also reflect an effect of OAT on endothelial dysfunction.
