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Association between inflammatory biomarkers and platelet aggregation in patients under chronic clopidogrel treatment

Academic Article
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Overview

authors

  • Bernlochner, I.
  • Steinhubl, Steven
  • Braun, S.
  • Morath, T.
  • Jaitner, J.
  • Stegherr, J.
  • Mehilli, J.
  • von Beckerath, N.
  • Schomig, A.
  • Kastrati, A.
  • Sibbing, D.

publication date

  • December 2010

journal

  • Thrombosis and Haemostasis  Journal

abstract

  • Inflammatory processes in the vessel wall are associated with progression of atherosclerosis and myocardial infarction. Both high levels of C-reactive protein (CRP)and high on-clopidogrel treatment platelet reactivity (HPR) have been linked to an increased risk of ischaemic events after percutaneous coronary intervention (PCI). The aim of this study was to explore the association between biomarker levels of inflammation and platelet reactivity. Stable patients (n=1,223) eligible for this study were under chronic antiplatelet treatment with aspirin and clopidogrel due to prior coronary stent placement. ADP-induced platelet aggregation (in AU*min) was measured on a Multiplate analyser. The primary outcome measure of this retrospective study was the ADP-induced platelet aggregation in patients with versus those without elevated CRP levels. Of the patients 15.5% (n=189) showed elevated CRP levels (≥5 mg/l). Platelet aggregation (median [interquartile range]) was significantly higher in patients with elevated CRP levels compared to patients with normal (<5 mg/l) CRP levels (305 [202-504] AU*min vs. 218 [144-384] AU*min; p<0.001).A multivariable linear regression model that adjusted for known predictors of HPR confirmed a significant independent association between elevated CRP levels and high ADP-induced platelet aggregation values (p=0.0002).Elevated WBC count and fibrinogen levels were also associated with higher platelet aggregation values (p<0.001 for both). In conclusion, elevated levels of CRP, WBC count and fibrinogen were significantly associated with high platelet reactivity in patients under chronic clopidogrel treatment. Whether a direct relation between platelets and inflammation exists, as well as the clinical impact of our results, warrants further investigations.

subject areas

  • Adenosine Diphosphate
  • Aged
  • Angioplasty, Balloon, Coronary
  • Aspirin
  • C-Reactive Protein
  • Cardiovascular Diseases
  • Chi-Square Distribution
  • Drug Administration Schedule
  • Drug Therapy, Combination
  • Female
  • Fibrinogen
  • Germany
  • Humans
  • Inflammation Mediators
  • Leukocyte Count
  • Linear Models
  • Logistic Models
  • Male
  • Middle Aged
  • Platelet Aggregation
  • Platelet Aggregation Inhibitors
  • Platelet Function Tests
  • Retrospective Studies
  • Risk Assessment
  • Risk Factors
  • Stents
  • Ticlopidine
  • Time Factors
  • Treatment Outcome
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Research

keywords

  • C-reactive protein
  • high on-clopidogrel treatment platelet reactivity
  • inflammation
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Identity

International Standard Serial Number (ISSN)

  • 0340-6245

Digital Object Identifier (DOI)

  • 10.1160/th10-05-0266

PubMed ID

  • 20838744
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Additional Document Info

start page

  • 1193

end page

  • 1200

volume

  • 104

issue

  • 6

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