Evaluation of the Biological Response to Clopidogrel in Patients With Ischemic Stroke
NCT01955642 · Status: COMPLETED · Type: OBSERVATIONAL · Enrollment: 91
Last updated 2015-12-31
Summary
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.
Conditions
- Brain Ischemia
- Ischemic Attack
Interventions
- DRUG
-
Clopidogrel
75 mg milligrams per days of PLAVIX
Sponsors & Collaborators
-
Groupe de Recherche sur la Thrombose
collaborator OTHER -
Centre Hospitalier Universitaire de Saint Etienne
lead OTHER
Principal Investigators
-
Jerome VARVAT, MD · CHU de Saint-Etienne
Eligibility
- Min Age
- 18 Years
- Sex
- ALL
- Healthy Volunteers
- No
Timeline & Regulatory
- Start
- 2013-09-30
- Primary Completion
- 2015-12-31
- Completion
- 2015-12-31
Countries
- France
Study Locations
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