Hi Robert,

One would assume so. Aspirin effects on cyclooxigenase 1 dramatically reduce the production of prostaglandin H2 and further Thromboxane A2. Both of these mediators increase platelet calcium levels leading to platelet activation and the release of ADP granules.

In a single-clopidogrel regimen, ADP receptors are blocked. Therapeutically approved doses, however, consider the optimal dosage for maintaining a minimal activity of those receptors to treat thrombotic disorders, while still keeping coagulation responses under healthy levels. Traces of ADP are therefore still allowed to enact their effect on a certain number of receptors in order to avoid bleeding.

In a co-aspirin-clopidogrel regimen. Aspirin would further reduce the levels of ADP made available in a single-clopidogrel regimen, therefore increasing the antithrombotic effects, while also enhancing the chances of bleeding events to occur.

Aspirin exerts its effects on platelets by means of COX-related action. It is not able to activate the ADP receptor.

Despite it has been hypothesised in the past that ASA would be able to modulate release of alpha granules, there is solid evidence that aspirin has no direct ADP-related platelet effects.

Andreé and Salvatore - many thanks for your contribution. It would be nice to see some laboratory evidence and platelet aggregation studies to prove or disapprove whether aspirin modulates ADP-mediated aggregation. I appreciate your thoughts on this; Cheers R.

I see you're getting itchy fingers, Robert...

Very good!

Looking forward to seeing new experimental evidence from your lab in the next future!

Keep going!