Enhanced ex vivo inhibition of platelet function following addition of dipyridamole to aspirin after transient ischaemic attack or ischaemic stroke: first results from the TRinity AntiPlatelet responsiveness (TrAP) study.
AuthorsTobin, William Oliver
Kinsella, Justin A
Collins, Daniel Ronan
Feeley, Thomas Martin
Murphy, Raymond P
McCabe, Dominick J H
AffiliationDepartment of Neurology, The Adelaide and Meath Hospital/National Children's, Hospital, Tallaght, Dublin, UK.
Blood Platelets/*drug effects/physiology
Blood Specimen Collection/methods
Drug Therapy, Combination
Ischemic Attack, Transient/*blood/drug therapy
Platelet Activation/drug effects
Platelet Aggregation Inhibitors/*pharmacology/therapeutic use
Platelet Function Tests
MetadataShow full item record
CitationBr J Haematol. 2011 Mar;152(5):640-7. doi: 10.1111/j.1365-2141.2010.08539.x. Epub, 2011 Jan 12.
JournalBritish journal of haematology
AbstractEx vivo dipyridamole 'non-responsiveness' has not been extensively studied in ischaemic cerebrovascular disease. Platelet surface marker expression, leucocyte-platelet complex formation and inhibition of platelet function at high shear stress as detected by the PFA-100(R) Collagen-Adenosine-diphosphate (C-ADP) and Collagen-Epinephrine cartridges was assessed in 52 patients within 4 weeks of transient ischaemic attack (TIA) or ischaemic stroke on aspirin, and then 14 d (14 d) and >90 d (90 d) after adding dipyridamole. A novel definition of 'Dipyridamole non-responsiveness' was used. The median C-ADP closure time increased following addition of dipyridamole, remained elevated at 90 d (P /= 0.5), at 14 and 90 d versus baseline. Additional inhibition of platelet function has been detected with the PFA-100 when dipyridamole is added to aspirin. Elevated monocyte-platelet complexes may contribute to ex vivo dipyridamole non-responsiveness.
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