Steffel J Lüscher TF Ruschitzka F Tanner FC 2006 Selective inhibitors of cyclooxygenase-2 (COX-2) have come under scrutiny because of a possibly increased thrombotic risk observed in retrospective studies and comparatively small cancer trials. Indeed, inhibition of COX-2 may favor a prothrombotic environment by suppressing endothelial prostacyclin synthesis while leaving COX-1-dependent platelet thromboxane (TX) A2 synthesis unopposed. However, in vitro studies have shown that the effect of coxibs on coagulation is dependent on several variables; for example, the coxib celecoxib reduces endothelial tissue factor expression, a key initiator of the coagulation cascade. Furthermore, animal studies are inconclusive as some studies investigating the effect of COX-2 inhibition in atherosclerosis imply a detrimental effect of coxibs, whereas others suggest a beneficial effect on plaque progression and stability. In healthy human subjects and in patients with atherosclerotic vascular diseases, the effect of COX-2 inhibition on coagulation is equally unclear as no prospective, randomized, double-blinded studies sufficiently powered to investigate cardiovascular endpoints have been performed to directly investigate a potentially cardiotoxic effect of coxibs. Here, we review the effect of COX-2 inhibition on the coagulation system; we discuss the molecular mechanisms involved and summarize important clinical trials in which an increased frequency of thrombotic complications coxibs was observed. https://sonar.ch/global/documents/104325 eng info:eu-repo/semantics/altIdentifier/doi/10.1097/00005344-200605001-00004 info:eu-repo/semantics/altIdentifier/pmid/16785824 Journal of cardiovascular pharmacology. - 2006 Animals Blood Coagulation Cyclooxygenase 2 Cyclooxygenase Inhibitors Endothelial Cells Humans Macrophages Models, Animal Cyclooxygenase-2 inhibition and coagulation. http://purl.org/coar/resource_type/c_6501