Sex functions as a modifier of thrombosis and response to antithrombotic therapy, driven by differences in procoagulant protein expression and platelet function.
How does sex modify the mechanisms of thrombosis and the response to antithrombotic therapy?
This review highlights critical sex-based differences in thrombosis mechanisms and emphasizes that men and women may not derive equal benefit from standard antithrombotic therapies.
Sex-based differences in the prevalence and presentation of arterial and venous thrombosis exist, and emerging data indicate that men and women do not accrue equal benefit from antithrombotic therapy. Sex hormones alter procoagulant protein expression and the function of blood and vascular cells. Sex-based differences in platelet function have been reported, and in animal models, sex-based differences in thrombosis have been noted. Here we review plausible mechanisms that may explain how sex functions as a modifier of thrombosis and summarize clinical data on the interaction between sex and response to antithrombotic therapy.
Bailey et al. (Tue,) conducted a review in Arterial and venous thrombosis. Sex (female vs male) was evaluated. Sex functions as a modifier of thrombosis and response to antithrombotic therapy, driven by differences in procoagulant protein expression and platelet function.