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

Cedercrantz-Borna, Catharina LU ; Lazarowski, Eduardo; van Heusden, Catharina; Öhlin, Hans LU and Erlinge, David LU (2005) In Thrombosis Journal 3(10).
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:... (More)
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 <193 sec in EPI-COLL was 9.7 % in NCD, and increased to 26.0 % (n.s.) in NSTEMI and 83.3 % (p < 0.001) in STEMI. Chronic aspirin treatment significantly reduced platelet aggregation in NCD and NSTEMI, but it had no effect in STEMI. Plasma levels of ADP were markedly increased in STEMI (905 +/- 721 nmol/l, p < 0.01), but not in NSTEMI (317 +/- 245), compared to NCD (334 +/- 271, mean +/- SD). ADP levels correlated with increased platelet activity measured with ADP-COLL (r = -0.30, p < 0.05). Aspirin resistant patients (EPI-COLL < 193 sec) had higher ADP levels compared to aspirin responders (734 +/- 807 vs. 282 +/- 187 nmol/l, mean +/- SD, p < 0.05). 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. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
aspirin, acute coronary syndromes, platelets, ADP
in
Thrombosis Journal
volume
3
issue
10
publisher
BioMed Central
external identifiers
  • pmid:16045804
  • scopus:27444431936
ISSN
1477-9560
DOI
10.1186/1477-9560-3-10
language
English
LU publication?
yes
id
2e26b42a-2b1e-492f-839b-ab533d52264c (old id 1132746)
date added to LUP
2008-06-27 09:27:26
date last changed
2017-07-30 04:32:56
@article{2e26b42a-2b1e-492f-839b-ab533d52264c,
  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 &lt;193 sec in EPI-COLL was 9.7 % in NCD, and increased to 26.0 % (n.s.) in NSTEMI and 83.3 % (p &lt; 0.001) in STEMI. Chronic aspirin treatment significantly reduced platelet aggregation in NCD and NSTEMI, but it had no effect in STEMI. Plasma levels of ADP were markedly increased in STEMI (905 +/- 721 nmol/l, p &lt; 0.01), but not in NSTEMI (317 +/- 245), compared to NCD (334 +/- 271, mean +/- SD). ADP levels correlated with increased platelet activity measured with ADP-COLL (r = -0.30, p &lt; 0.05). Aspirin resistant patients (EPI-COLL &lt; 193 sec) had higher ADP levels compared to aspirin responders (734 +/- 807 vs. 282 +/- 187 nmol/l, mean +/- SD, p &lt; 0.05). 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.},
  author       = {Cedercrantz-Borna, Catharina and Lazarowski, Eduardo and van Heusden, Catharina and Öhlin, Hans and Erlinge, David},
  issn         = {1477-9560},
  keyword      = {aspirin,acute coronary syndromes,platelets,ADP},
  language     = {eng},
  number       = {10},
  publisher    = {BioMed Central},
  series       = {Thrombosis Journal},
  title        = {Resistance to aspirin is increased by ST-elevation myocardial infarction and correlates with adenosine diphosphate levels},
  url          = {http://dx.doi.org/10.1186/1477-9560-3-10},
  volume       = {3},
  year         = {2005},
}