The effect of aspirin on C-reactive protein as a marker of risk in unstable angina

J Am Coll Cardiol. 2001 Apr;37(5):1266-70. doi: 10.1016/s0735-1097(01)01130-5.


Objectives: This study was designed to assess the interaction between aspirin and C-reactive protein (CRP) release in unstable angina.

Background: C-reactive protein release in acute coronary syndromes may be a response to myocardial necrosis or may reflect the inflammatory process that drives atherogenesis. Aspirin has the potential to influence CRP release, either by its anti-inflammatory activity or by reducing myocardial necrosis. The clinical significance of this potential interaction has not previously been tested.

Methods: We conducted a prospective cohort study of 304 consecutive patients admitted with non-ST-elevation acute coronary syndromes. Serial blood samples were obtained for CRP and troponin I assay. End points were cardiac death and nonfatal myocardial infarction during follow-up for 12 months.

Results: A total of 174 patients (57%) were taking aspirin before admission. Patients taking aspirin had lower troponin I concentrations throughout the sampling period, only 45 (26.0%) having concentrations >0.1 mg/l compared with 48 (37.8%) patients not taking aspirin (p = 0.03). Maximum CRP concentrations were also lower in patients taking aspirin (8.16 mg/l [3.24 to 24.5]) than in patients not taking aspirin (11.3 mg/l [4.15 to 26.1]), although the difference was not significant. However, there was significant interaction (p = 0.04) between prior aspirin therapy and the predictive value of CRP concentrations for death and myocardial infarction at 12 months. Thus, odds ratios (95% confidence intervals) for events associated with an increase of 1 standard deviation in maximum CRP concentration were 2.64 (1.22-5.72) in patients not pretreated with aspirin compared with 0.98 (0.60-1.62) in patients pretreated with aspirin.

Conclusions: The association between CRP and cardiac events in patients with unstable angina is influenced by pretreatment with aspirin. Modification of the acute-phase inflammatory responses to myocardial injury is the major mechanism of this interaction.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Angina, Unstable / drug therapy*
  • Angina, Unstable / immunology
  • Angina, Unstable / mortality
  • Aspirin / adverse effects
  • Aspirin / therapeutic use*
  • Biomarkers / blood
  • C-Reactive Protein / metabolism*
  • Cohort Studies
  • Female
  • Follow-Up Studies
  • Humans
  • Male
  • Middle Aged
  • Myocardial Infarction / drug therapy
  • Myocardial Infarction / immunology
  • Myocardial Infarction / mortality
  • Prospective Studies
  • Risk
  • Survival Rate
  • Troponin I / blood


  • Biomarkers
  • Troponin I
  • C-Reactive Protein
  • Aspirin