Latest research on Clopidogrel

Clopidogrel, an antiplatelet agent structurally and pharmacologically similar to ticlopidine, is used to inhibit blood clots in a variety of conditions such as peripheral vascular disease, coronary artery disease, and cerebrovascular disease. Clopidogrel is sold under the name Plavix by Sanofi and Bristol-Myers Squibb. The drug is an irreversible inhibitor of the P2Y12 adenosine diphosphate receptor found on the membranes of platelet cells. Clopidogrel use is associated with several serious adverse drug reactions such as severe neutropenia, various forms of hemorrhage, and cardiovascular edema.

Latest findings

All patients received Aspirin 300 mg and Clopidogrel 300-600 mg, and 120 IU/kg of Unfractionated heparin intravenously before PCI. [source, 2016]
Clopidogrel is the most widely used P2Y12-antagonist. [source, 2016]
Clinical trials have demonstrated that high platelet reactivity (HPR) after Clopidogrel administration increases the risk of recurrent atherothrombotic events [1]. [source, 2016]
Recently, our group showed that the ratio of ADP- to TRAP-induced platelet aggregation (r- ADP-agg) is a valuable tool reflecting a patient’s individual degree of P2Y12–mediated platelet reactivity and that a high r-ADP-agg is associated with an increased mortality in patients after coronary stent-implantation on Clopidogrel [13, 14]. [source, 2016]
Data of this study were collected during an observational single centre study in which the anti-platelet effect of Clopidogrel in patients after coronary stent implantation had been investigated. [source, 2016]
All patients received 100 mg ASA per day and 75 mg Clopidogrel after a loading dose of 300 mg (at least 24 hours before platelet aggregation assay) or 600 mg (at least 12 hours before platelet aggregation assay). [source, 2016]
Furthermore, factors that might influence platelet reactivity after Clopidogrel treatment were analysed following the description of Siller-Matula [15, 16] according to availability as shown in Table 2. [source, 2016]
Numerous factors can influence the extent of platelet inhibition by Clopidogrel [15, 16]. [source, 2016]
For example, our group recently showed that a high r-ADP-agg is associated with an increased mortality in patients after coronary stent-implantation and Clopidogrel therapy [14]. [source, 2016]
Badr et al. recently observed that platelet activation via thrombin receptors PAR-1 and PAR-4 is preserved in the majority of patients after platelet inhibition with Clopidogrel. [source, 2016]