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.

Hdl Handle:
http://hdl.handle.net/10147/207888
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.
Authors:
Tobin, William Oliver; Kinsella, Justin A; Collins, Daniel Ronan; Coughlan, Tara; O'Neill, Desmond; Egan, Bridget; Tierney, Sean; Feeley, Thomas Martin; Murphy, Raymond P; McCabe, Dominick J H
Affiliation:
Department of Neurology, The Adelaide and Meath Hospital/National Children's, Hospital, Tallaght, Dublin, UK.
Citation:
Br J Haematol. 2011 Mar;152(5):640-7. doi: 10.1111/j.1365-2141.2010.08539.x. Epub, 2011 Jan 12.
Journal:
British journal of haematology
Issue Date:
1-Feb-2012
URI:
http://hdl.handle.net/10147/207888
DOI:
10.1111/j.1365-2141.2010.08539.x
PubMed ID:
21223254
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.
Language:
eng
MeSH:
Adult; Aged; Aspirin/*pharmacology/therapeutic use; Blood Platelets/*drug effects/physiology; Blood Specimen Collection/methods; Dipyridamole/*pharmacology/therapeutic use; Drug Therapy, Combination; Female; Humans; Ischemic Attack, Transient/*blood/drug therapy; Longitudinal Studies; Male; Middle Aged; Platelet Activation/drug effects; Platelet Aggregation Inhibitors/*pharmacology/therapeutic use; Platelet Function Tests; Stroke/*blood/drug therapy
ISSN:
1365-2141 (Electronic); 0007-1048 (Linking)

Full metadata record

DC FieldValue Language
dc.contributor.authorTobin, William Oliveren_GB
dc.contributor.authorKinsella, Justin Aen_GB
dc.contributor.authorCollins, Daniel Ronanen_GB
dc.contributor.authorCoughlan, Taraen_GB
dc.contributor.authorO'Neill, Desmonden_GB
dc.contributor.authorEgan, Bridgeten_GB
dc.contributor.authorTierney, Seanen_GB
dc.contributor.authorFeeley, Thomas Martinen_GB
dc.contributor.authorMurphy, Raymond Pen_GB
dc.contributor.authorMcCabe, Dominick J Hen_GB
dc.date.accessioned2012-02-01T10:49:11Z-
dc.date.available2012-02-01T10:49:11Z-
dc.date.issued2012-02-01T10:49:11Z-
dc.identifier.citationBr 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.issn1365-2141 (Electronic)en_GB
dc.identifier.issn0007-1048 (Linking)en_GB
dc.identifier.pmid21223254en_GB
dc.identifier.doi10.1111/j.1365-2141.2010.08539.xen_GB
dc.identifier.urihttp://hdl.handle.net/10147/207888-
dc.description.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 </= 0.03), 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.en_GB
dc.language.isoengen_GB
dc.subject.meshAdulten_GB
dc.subject.meshAgeden_GB
dc.subject.meshAspirin/*pharmacology/therapeutic useen_GB
dc.subject.meshBlood Platelets/*drug effects/physiologyen_GB
dc.subject.meshBlood Specimen Collection/methodsen_GB
dc.subject.meshDipyridamole/*pharmacology/therapeutic useen_GB
dc.subject.meshDrug Therapy, Combinationen_GB
dc.subject.meshFemaleen_GB
dc.subject.meshHumansen_GB
dc.subject.meshIschemic Attack, Transient/*blood/drug therapyen_GB
dc.subject.meshLongitudinal Studiesen_GB
dc.subject.meshMaleen_GB
dc.subject.meshMiddle Ageden_GB
dc.subject.meshPlatelet Activation/drug effectsen_GB
dc.subject.meshPlatelet Aggregation Inhibitors/*pharmacology/therapeutic useen_GB
dc.subject.meshPlatelet Function Testsen_GB
dc.subject.meshStroke/*blood/drug therapyen_GB
dc.titleEnhanced 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.departmentDepartment of Neurology, The Adelaide and Meath Hospital/National Children's, Hospital, Tallaght, Dublin, UK.en_GB
dc.identifier.journalBritish journal of haematologyen_GB
dc.description.provinceLeinster-

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