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

William Tobin, Justin A. Kinsella, Daniel Ronan Collins, Tara Coughlan, Desmond O'Neill, Bridget Egan, Sean Tierney, Thomas Martin Feeley, Raymond P. Murphy, Dominick J H McCabe

Research output: Contribution to journalArticle

16 Citations (Scopus)

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® Collagen-Adenosine-diphosphate (C-ADP) and Collagen-Epinephrine cartridges was assessed in 52 patients within 4weeks of transient ischaemic attack (TIA) or ischaemic stroke on aspirin, and then 14d (14d) and >90d (90d) 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 90d (P≤0·03), and was unaffected by aspirin dose. 59% at 14d and 56% at 90d were 'dipyridamole non-responders' on the PFA-100. The proportion of non-responders at 14 and 90d was similar (P=0·9). Compared with baseline (4·6%), median monocyte-platelet complexes increased at 14d (5·0%, P=0·03) and 90d (4·9%, P=0·04). Low C-ADP closure times were associated with increased monocyte-platelet complexes at 14d (r=-0·32, P=0·02) and 90d (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 90d 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.

Original languageEnglish (US)
Pages (from-to)640-647
Number of pages8
JournalBritish Journal of Haematology
Volume152
Issue number5
DOIs
StatePublished - Mar 2011
Externally publishedYes

Fingerprint

Dipyridamole
Transient Ischemic Attack
Aspirin
Blood Platelets
Stroke
Monocytes
Collagen
Adenosine Diphosphate
Cerebrovascular Disorders
Epinephrine
Leukocytes

Keywords

  • Antiplatelet non-responsivness
  • Dipyridamole
  • Flow cytometry
  • Platelet function analyser-100
  • Stroke

ASJC Scopus subject areas

  • Hematology

Cite this

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. / Tobin, William; 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.

In: British Journal of Haematology, Vol. 152, No. 5, 03.2011, p. 640-647.

Research output: Contribution to journalArticle

Tobin, William ; 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. / 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. In: British Journal of Haematology. 2011 ; Vol. 152, No. 5. pp. 640-647.
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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{\circledR} Collagen-Adenosine-diphosphate (C-ADP) and Collagen-Epinephrine cartridges was assessed in 52 patients within 4weeks of transient ischaemic attack (TIA) or ischaemic stroke on aspirin, and then 14d (14d) and >90d (90d) 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 90d (P≤0·03), and was unaffected by aspirin dose. 59{\%} at 14d and 56{\%} at 90d were 'dipyridamole non-responders' on the PFA-100. The proportion of non-responders at 14 and 90d was similar (P=0·9). Compared with baseline (4·6{\%}), median monocyte-platelet complexes increased at 14d (5·0{\%}, P=0·03) and 90d (4·9{\%}, P=0·04). Low C-ADP closure times were associated with increased monocyte-platelet complexes at 14d (r=-0·32, P=0·02) and 90d (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 90d 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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