The different stages of hemostasis (i.e., primary hemostasis, coagulation and fibrinolysis) are involved in the early atherothrombosis steps. The aim of this study was to investigate the effect of epicatechin, a major flavonoid compound, on the hemostasis phenotype using clinically relevant in vitro global assays that mimic the complexity of the in vivo hemostasis systems. Plasma samples from 10 healthy volunteers were spiked with increasing concentrations of epicatechin (1 to 100 μM). Epicatechin effect on primary hemostasis, coagulation and fibrinolysis was assessed by measuring platelet aggregation using light transmission aggregometry, thrombin generation and clot lysis time (CLT), respectively. Epicatechin (100 μM) significantly decreased the maximal platelet aggregation induced by adenosine diphosphate (−39%), thrombin receptor activating peptide (−48%), epinephrine (−30%), and collagen (−30%). The endogenous thrombin potential was significantly reduced starting from 1 μM epicatechin (1332 ± 230 versus 1548 ± 241 nM min for control) (p < 0.01). Fibrinolysis was promoted by epicatechin, as indicated by CLT decrease by 16 and 33% with 10 and 100 μM epicatechin respectively, compared with control (1271 ± 775 s). These findings show that epicatechin reduces platelet function and leads to an anticoagulant and pro-fibrinolytic profile, providing new evidence of its interest for cardiovascular disease prevention.

Background: Anti-factor Xa assays and activated partial thromboplastin time (aPTT) are mainly employed to monitor patients treated with heparins. According to the Clinical and Laboratory Standards Institute and the French Working Group on Haemostasis and Thrombosis, anti-factor Xa activity and aPTT should be tested within 2 h of blood sampling for unfractionated heparin (UFH) monitoring. However, discrepancies exist depending on the used reagents and collecting tubes. The study aim was to determine the stability of aPTT and anti-factor Xa measurements using blood samples collected in citrate-containing or citrate-theophylline-adenosine-dipyridamole (CTAD) tubes and stored for up to 6 h. Methods: Patients receiving UFH or low molecular weight heparin (LMWH) were enrolled; aPTT and anti-factor Xa activity were tested using two different analyser/reagent pairs (Stago and reagent without dextran sulfate; Siemens and reagent with dextran sulfate) after 1, 4 and 6 h of sample storage as whole blood or as plasma. Results: For UFH monitoring, comparable anti-factor Xa activity and aPTT results were obtained with both analyser/reagent pairs when samples were stored as whole blood before plasma isolation. With samples stored as plasma, anti-factor Xa activity and aPTT were not affected up to 6 h after sampling when using the Stago/no-dextran sulfate reagent pair. With the Siemens/dextran sulfate-containing reagent, aPTT was significantly altered after 4 h of storage. For LMWH monitoring, anti-factor Xa activity remained stable (whole blood and plasma) for at least 6 h. Results were comparable with citrate-containing and CTAD tubes. Conclusions: Anti-factor Xa activity in samples stored as whole blood or plasma was stable for up to 6 h, regardless of the reagent (with/without dextran sulfate)/collection tube. Conversely, aPTT was more variable because other plasma parameters can influence its measure and complicate the interpretation of its variations after 4 h.