Coronary thrombosis, platelet-dependent

New small molecule FXa inhibitors currently in development are able to enter the clot/prothrombinase complex and inhibit free and bound factor Xa regarded as the key enzyme in ACS. Although direct FXa inhibitors do not inhibit platelet aggregation, they abolish platelet-dependent thrombus formation in canine coronary thrombosis. Thus, direct inhibition of FXa may have higher efficacy and better risk/benefit profile than existing antithrombotic therapies in the treatment and prevention of ACS. 

ReoPro) coronary cyclic flow reduction (Folts et al. 1991) inhibition of platelet-dependent thrombosis et al. 1986 coronary angioplasty in death, myocardial infarction, refractory ischemia, or unplanned revascularization Investigators, 1994... 

Coronary thrombosis is largely platelet-dependent, through platelet adhesion, activation and aggregation. Aspirin and ticlopidine predominantly target platelet activation pathways but because of the variety of means through which platelet can be activated, the blockade of any single platelet activation pathway can have limited efficacy. 

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