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.
dc.contributor.author | Tobin, William Oliver | |
dc.contributor.author | Kinsella, Justin A | |
dc.contributor.author | Collins, Daniel Ronan | |
dc.contributor.author | Coughlan, Tara | |
dc.contributor.author | O'Neill, Desmond | |
dc.contributor.author | Egan, Bridget | |
dc.contributor.author | Tierney, Sean | |
dc.contributor.author | Feeley, Thomas Martin | |
dc.contributor.author | Murphy, Raymond P | |
dc.contributor.author | McCabe, Dominick J H | |
dc.date.accessioned | 2012-02-01T10:49:11Z | |
dc.date.available | 2012-02-01T10:49:11Z | |
dc.date.issued | 2012-02-01T10:49:11Z | |
dc.identifier.citation | Br J Haematol. 2011 Mar;152(5):640-7. doi: 10.1111/j.1365-2141.2010.08539.x. Epub, 2011 Jan 12. | en_GB |
dc.identifier.issn | 1365-2141 (Electronic) | en_GB |
dc.identifier.issn | 0007-1048 (Linking) | en_GB |
dc.identifier.pmid | 21223254 | en_GB |
dc.identifier.doi | 10.1111/j.1365-2141.2010.08539.x | en_GB |
dc.identifier.uri | http://hdl.handle.net/10147/207888 | |
dc.description.abstract | Ex 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. | |
dc.language.iso | eng | en_GB |
dc.subject.mesh | Adult | en_GB |
dc.subject.mesh | Aged | en_GB |
dc.subject.mesh | Aspirin/*pharmacology/therapeutic use | en_GB |
dc.subject.mesh | Blood Platelets/*drug effects/physiology | en_GB |
dc.subject.mesh | Blood Specimen Collection/methods | en_GB |
dc.subject.mesh | Dipyridamole/*pharmacology/therapeutic use | en_GB |
dc.subject.mesh | Drug Therapy, Combination | en_GB |
dc.subject.mesh | Female | en_GB |
dc.subject.mesh | Humans | en_GB |
dc.subject.mesh | Ischemic Attack, Transient/*blood/drug therapy | en_GB |
dc.subject.mesh | Longitudinal Studies | en_GB |
dc.subject.mesh | Male | en_GB |
dc.subject.mesh | Middle Aged | en_GB |
dc.subject.mesh | Platelet Activation/drug effects | en_GB |
dc.subject.mesh | Platelet Aggregation Inhibitors/*pharmacology/therapeutic use | en_GB |
dc.subject.mesh | Platelet Function Tests | en_GB |
dc.subject.mesh | Stroke/*blood/drug therapy | en_GB |
dc.title | 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. | en_GB |
dc.contributor.department | Department of Neurology, The Adelaide and Meath Hospital/National Children's, Hospital, Tallaght, Dublin, UK. | en_GB |
dc.identifier.journal | British journal of haematology | en_GB |
dc.description.province | Leinster | |
html.description.abstract | Ex 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 </= 0.03), and was unaffected by aspirin dose. 59% at 14 d and 56% at 90 d were 'dipyridamole non-responders' on the PFA-100. The proportion of non-responders at 14 and 90 d was similar (P= 0.9). Compared with baseline (4.6%), median monocyte-platelet complexes increased at 14 d (5.0%, P= 0.03) and 90 d (4.9%, P= 0.04). Low C-ADP closure times were associated with increased monocyte-platelet complexes at 14 d (r= -0.32, P= 0.02) and 90 d (r= -0.33, P = 0.02). Monocyte-platelet complexes increased in the subgroup of dipyridamole non-responders on the PFA-100 (P</= 0.045), but not in responders (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. |