Clopidogrel discontinuation and platelet reactivity following coronary stenting

Hdl Handle:
http://hdl.handle.net/10147/229114
Title:
Clopidogrel discontinuation and platelet reactivity following coronary stenting
Authors:
MYLOTTE, D.; PEACE, A. J.; TEDESCO, A. T.; MANGIACAPRA, F.; DICKER, P.; KENNY, D.; FOLEY, D. P.
Citation:
Clopidogrel discontinuation and platelet reactivity following coronary stenting 2011, 9 (1):24 Journal of Thrombosis and Haemostasis
Journal:
Journal of Thrombosis and Haemostasis
Issue Date:
Jan-2011
URI:
http://hdl.handle.net/10147/229114
DOI:
10.1111/j.1538-7836.2010.04121.x
Additional Links:
http://doi.wiley.com/10.1111/j.1538-7836.2010.04121.x
Abstract:
Summary. Aims: Antiplatelet therapy with aspirin and clopidogrel is recommended for 1 year after drug-eluting stent (DES) implantation or myocardial infarction. However, the discontinuation of antiplatelet therapy has become an important issue as recent studies have suggested a clustering of ischemic events within 90 days of clopidogrel withdrawal. The objective of this investigation was to explore the hypothesis that there is a transient ‘rebound’ increase in platelet reactivity within 3 months of clopidogrel discontinuation. Methods and Results: In this prospective study, platelet function was assessed in patients taking aspirin and clopidogrel for at least 1 year following DES implantation. Platelet aggregation was measured using a modification of light transmission aggregometry in response to multiple concentrations of adenosine diphosphate (ADP), epinephrine, arachidonic acid, thrombin receptor activating peptide and collagen. Clopidogrel was stopped and platelet function was reassessed 1 week, 1 month and 3 months later. Thirty-two patients on dual antiplatelet therapy were recruited. Discontinuation of clopidogrel increased platelet aggregation to all agonists, except arachidonic acid. Platelet aggregation in response to ADP (2.5, 5, 10, and 20 μm) and epinephrine (5 and 20 μm) was significantly increased at 1 month compared with 3 months following clopidogrel withdrawal. Thus, a transient period of increased platelet reactivity to both ADP and epinephrine was observed 1 month after clopidogrel discontinuation. Conclusions: This study demonstrates a transient increase in platelet reactivity 1 month after clopidogrel withdrawal. This phenomenon may, in part, explain the known clustering of thrombotic events observed after clopidogrel discontinuation. This observation requires confirmation in larger populations.
Item Type:
Article
Language:
en
ISSN:
15387933

Full metadata record

DC FieldValue Language
dc.contributor.authorMYLOTTE, D.en_GB
dc.contributor.authorPEACE, A. J.en_GB
dc.contributor.authorTEDESCO, A. T.en_GB
dc.contributor.authorMANGIACAPRA, F.en_GB
dc.contributor.authorDICKER, P.en_GB
dc.contributor.authorKENNY, D.en_GB
dc.contributor.authorFOLEY, D. P.en_GB
dc.date.accessioned2012-06-15T13:34:50Z-
dc.date.available2012-06-15T13:34:50Z-
dc.date.issued2011-01-
dc.identifier.citationClopidogrel discontinuation and platelet reactivity following coronary stenting 2011, 9 (1):24 Journal of Thrombosis and Haemostasisen_GB
dc.identifier.issn15387933-
dc.identifier.doi10.1111/j.1538-7836.2010.04121.x-
dc.identifier.urihttp://hdl.handle.net/10147/229114-
dc.description.abstractSummary. Aims: Antiplatelet therapy with aspirin and clopidogrel is recommended for 1 year after drug-eluting stent (DES) implantation or myocardial infarction. However, the discontinuation of antiplatelet therapy has become an important issue as recent studies have suggested a clustering of ischemic events within 90 days of clopidogrel withdrawal. The objective of this investigation was to explore the hypothesis that there is a transient ‘rebound’ increase in platelet reactivity within 3 months of clopidogrel discontinuation. Methods and Results: In this prospective study, platelet function was assessed in patients taking aspirin and clopidogrel for at least 1 year following DES implantation. Platelet aggregation was measured using a modification of light transmission aggregometry in response to multiple concentrations of adenosine diphosphate (ADP), epinephrine, arachidonic acid, thrombin receptor activating peptide and collagen. Clopidogrel was stopped and platelet function was reassessed 1 week, 1 month and 3 months later. Thirty-two patients on dual antiplatelet therapy were recruited. Discontinuation of clopidogrel increased platelet aggregation to all agonists, except arachidonic acid. Platelet aggregation in response to ADP (2.5, 5, 10, and 20 μm) and epinephrine (5 and 20 μm) was significantly increased at 1 month compared with 3 months following clopidogrel withdrawal. Thus, a transient period of increased platelet reactivity to both ADP and epinephrine was observed 1 month after clopidogrel discontinuation. Conclusions: This study demonstrates a transient increase in platelet reactivity 1 month after clopidogrel withdrawal. This phenomenon may, in part, explain the known clustering of thrombotic events observed after clopidogrel discontinuation. This observation requires confirmation in larger populations.en_GB
dc.language.isoenen
dc.relation.urlhttp://doi.wiley.com/10.1111/j.1538-7836.2010.04121.xen_GB
dc.rightsArchived with thanks to Journal of Thrombosis and Haemostasisen_GB
dc.titleClopidogrel discontinuation and platelet reactivity following coronary stentingen_GB
dc.typeArticleen
dc.identifier.journalJournal of Thrombosis and Haemostasisen_GB
dc.description.provinceLeinsteren
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