Brain Ischemia Clinical Trial
Official title:
Evaluation of the Biological Response to Clopidogrel in Patients With Ischemic Stroke : Role of Platelet alpha2-adrenergic Receptors
Ischemic stroke (AIC) is the leading cause of non-traumatic disability in adults, the second
leading cause of dementia and the third leading cause of death in France.
Clopidogrel is one of the recommended first line in the secondary prevention of AIC non
cardioembolic origin. However recurrences occur in approximately 9% of patients receiving
clopidogrel. Some studies in patients with coronary artery disease have made the connection
between these treatment failures and non-biological response to clopidogrel. This
non-biological response is found for approximately 30% to 50% of patients. Several
mechanisms may explain this non-response. The most accepted mechanism is pharmacokinetic.
Indeed, clopidogrel is a prodrug that requires intestinal absorption by P-glycoprotein (PGP)
and a transformation by hepatic cytochrome into active metabolites. The genetic polymorphism
of proteins involved in these two steps explain the low plasma concentration of active
metabolites and thus the low efficacy of clopidogrel in some patients.
A new pharmacodynamic hypothesis suggests the involvement of platelet alpha 2-adrenergic
receptors. The activation of these receptors potentiates signaling pathway P2Y12 receptor
(channel inhibited by clopidogrel) and helps reduce platelet aggregation inhibiting response
to clopidogrel.
Interest in the biological response to clopidogrel in the AIC is innovative because few data are available in this area. In addition to testing a new pharmacodynamic hypothesis, we also wish to study and compare other measures of platelet function methods in order to be able to use commonly in treatment decisions. ;
Observational Model: Case-Only, Time Perspective: Prospective
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