Ignite Creation Date:
2024-05-06 @ 2:20 AM
Last Modification Date:
2024-10-26 @ 11:17 AM
Study NCT ID:
NCT02028234
Status:
UNKNOWN
Last Update Posted:
2014-01-08
First Post:
2014-01-02
Brief Title:
Pharmacodynamic Comparison of Omeprazole Versus Pantoprazole on Platelet Reactivity in Patients With Acute Coronary Syndromes on Dual Antiplatelet Therapy With New P2Y12 Inhibitors -Trial dOPPLER-
Sponsor:
University of Roma La Sapienza
Organization:
University of Roma La Sapienza
Study Overview
Official Title:
Pharmacodynamic Comparison of Omeprazole Versus Pantoprazole on Platelet Reactivity in Patients With Acute Coronary Syndromes on Dual Antiplatelet Therapy With New P2Y12 Inhibitors
Status:
UNKNOWN
Status Verified Date:
2014-01
Last Known Status:
NOT_YET_RECRUITING
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:
dOPPLER
Brief Summary:
Clopidogrel and Prasugrel are pro-drug necessitating conversion in active metabolites through CYP 450 system CYP particularly CYP3A and CYP2C19 isoforms
These drugs are platelet purinergic receptor antagonists known as P2Y12 The link between active metabolite of Clopidogrel and Prasugrel to P2Y12 receptor prevents ADP receptor activation and inhibits several events leading to conformational change of platelets therefore facilitating their activation and aggregation that is the basis of acute coronary syndromes Proton pump inhibitors PPI are actually considered principal agents reducing gastroenteric bleeding risk associated to antiplatelet therapy Nevertheless the interaction between PPI and antiplatelet therapy has been object of interest Several studies demonstrated PPI reduce efficacy of clopidogrel on platelet reactivity Only few data about Prasugrel are available showing a minor effect of PPI on its antiplatelet activity than clopidogrel Differing from prasugrel and clopidogrel ticagrelor is a direct inhibitor of P2Y12 not necessitating biotransformation in the liver therefore its interaction with PPI remains unclear Interaction between omeprazole and clopidogrel seems related to high inhibitory activity of PPI on CYP2C19 interfering with the conversion of clopidogrel in its active metabolite
These drugs are platelet purinergic receptor antagonists known as P2Y12 The link between active metabolite of Clopidogrel and Prasugrel to P2Y12 receptor prevents ADP receptor activation and inhibits several events leading to conformational change of platelets therefore facilitating their activation and aggregation that is the basis of acute coronary syndromes Proton pump inhibitors PPI are actually considered principal agents reducing gastroenteric bleeding risk associated to antiplatelet therapy Nevertheless the interaction between PPI and antiplatelet therapy has been object of interest Several studies demonstrated PPI reduce efficacy of clopidogrel on platelet reactivity Only few data about Prasugrel are available showing a minor effect of PPI on its antiplatelet activity than clopidogrel Differing from prasugrel and clopidogrel ticagrelor is a direct inhibitor of P2Y12 not necessitating biotransformation in the liver therefore its interaction with PPI remains unclear Interaction between omeprazole and clopidogrel seems related to high inhibitory activity of PPI on CYP2C19 interfering with the conversion of clopidogrel in its active metabolite
Detailed Description:
Clopidogrel and Prasugrel are pro-drug necessitating conversion in active metabolites through CYP 450 system CYP particularly CYP3A and CYP2C19 isoforms
These drugs are platelet purinergic receptor antagonists known as P2Y12 The link between active metabolite of Clopidogrel and Prasugrel to P2Y12 receptor prevents ADP receptor activation and inhibits several events leading to conformational change of platelets therefore facilitating their activation and aggregation that is the basis of acute coronary syndromes
Despite double antiplatelet drugs are the principle therapy for the treatment and the prevention of atherothrombotic events in cardiovascular diseases they are the most important cause of bleeding peptic ulcer Proton pump inhibitors PPI are actually considered principal agents reducing gastroenteric bleeding risk associated to antiplatelet therapy Nevertheless the interaction between PPI and antiplatelet therapy has been object of interest Several studies demonstrated PPI reduce efficacy of clopidogrel on platelet reactivity probably through the inhibition of its metabolism increasing the risk of cardiovascular events Only few data about Prasugrel are available showing a minor effect of PPI on its antiplatelet activity than clopidogrel Differing from prasugrel and clopidogrel ticagrelor is a direct inhibitor of P2Y12 not necessitating biotransformation in the liver therefore its interaction with PPI remains unclear Nevertheless actual studies considered only clinical outcomes MACEs such as a subgroup analysis of the Platelet Inhibition and Patient Outcomes PLATO trial showing a higher rate of MACEs in clopidogrel and Ticagrelor patients undergone PPI therapy especially omeprazole treatment Interaction between omeprazole and clopidogrel seems related to high inhibitory activity of PPI on CYP2C19 interfering with the conversion of clopidogrel in its active metabolite It is yet unclear the higher rate of MACEs in the ticagrelor group similarly to clopidogrel despite it hasnt a hepatic metabolism
These drugs are platelet purinergic receptor antagonists known as P2Y12 The link between active metabolite of Clopidogrel and Prasugrel to P2Y12 receptor prevents ADP receptor activation and inhibits several events leading to conformational change of platelets therefore facilitating their activation and aggregation that is the basis of acute coronary syndromes
Despite double antiplatelet drugs are the principle therapy for the treatment and the prevention of atherothrombotic events in cardiovascular diseases they are the most important cause of bleeding peptic ulcer Proton pump inhibitors PPI are actually considered principal agents reducing gastroenteric bleeding risk associated to antiplatelet therapy Nevertheless the interaction between PPI and antiplatelet therapy has been object of interest Several studies demonstrated PPI reduce efficacy of clopidogrel on platelet reactivity probably through the inhibition of its metabolism increasing the risk of cardiovascular events Only few data about Prasugrel are available showing a minor effect of PPI on its antiplatelet activity than clopidogrel Differing from prasugrel and clopidogrel ticagrelor is a direct inhibitor of P2Y12 not necessitating biotransformation in the liver therefore its interaction with PPI remains unclear Nevertheless actual studies considered only clinical outcomes MACEs such as a subgroup analysis of the Platelet Inhibition and Patient Outcomes PLATO trial showing a higher rate of MACEs in clopidogrel and Ticagrelor patients undergone PPI therapy especially omeprazole treatment Interaction between omeprazole and clopidogrel seems related to high inhibitory activity of PPI on CYP2C19 interfering with the conversion of clopidogrel in its active metabolite It is yet unclear the higher rate of MACEs in the ticagrelor group similarly to clopidogrel despite it hasnt a hepatic metabolism
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