Ignite Creation Date:
2024-05-06 @ 2:02 AM
Last Modification Date:
2024-10-26 @ 11:13 AM
Study NCT ID:
NCT01955642
Status:
COMPLETED
Last Update Posted:
2015-12-31
First Post:
2013-09-27
Brief Title:
Evaluation of the Biological Response to Clopidogrel in Patients With Ischemic Stroke
Sponsor:
Centre Hospitalier Universitaire de Saint Etienne
Organization:
Centre Hospitalier Universitaire de Saint Etienne
Study Overview
Official Title:
Evaluation of the Biological Response to Clopidogrel in Patients With Ischemic Stroke Role of Platelet alpha2-adrenergic Receptors
Status:
COMPLETED
Status Verified Date:
2015-12
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
AAPIX
Brief 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
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
Detailed Description:
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
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None
Secondary IDs
| Secondary ID | Type | Domain | Link |
|---|---|---|---|
| 2013-000313-20 | EUDRACT_NUMBER | None | None |