Thrombosis Journal (Jul 2005)

Resistance to aspirin is increased by ST-elevation myocardial infarction and correlates with adenosine diphosphate levels

  • Öhlin Hans,
  • van Heusden Catharina,
  • Lazarowski Eduardo,
  • Borna Catharina,
  • Erlinge David

DOI
https://doi.org/10.1186/1477-9560-3-10
Journal volume & issue
Vol. 3, no. 1
p. 10

Abstract

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Abstract Background To be fully activated platelets are dependent on two positive feedback loops; the formation of thromboxane A2 by cyclooxygenase in the platelets and the release of ADP. We wanted to evaluate the effect of aspirin on platelet function in patients with acute coronary syndromes and we hypothesized that increased levels of ADP in patients with acute coronary syndromes could contribute to aspirin resistance. Methods Platelet activity in 135 patients admitted for chest pain was assessed with PFA-100. An epinephrine-collagen cartridge (EPI-COLL) was used for the detection of aspirin resistance together with an ADP-collagen cartridge (ADP-COLL). ADP was measured with hplc from antecubital vein samples. Three subgroups were compared: chest pain with no sign of cardiac disease (NCD), NonST-elevation myocardial infarction (NSTEMI) and STEMI. Results Platelet activation was increased for the STEMI group compared NCD. Aspirin resistance defined as Conclusion Platelets are activated and aspirin resistance is more frequent in STEMI, probably due to a general activation of platelets. ADP levels are increased in STEMI and correlates with platelet activation. Increased levels of ADP could be one reason for increased platelet activity and aspirin resistance.

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