The effect of aspirin on C-reactive protein as a marker of risk in unstable angina.
OBJECTIVE
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.
Kennon
S
S
Department of Cardiology, Bart's and the London NHS Trust, United Kingdom. srok@dircon.co.uk
Price
C P
CP
Mills
P G
PG
Ranjadayalan
K
K
Cooper
J
J
Clarke
H
H
Timmis
A D
AD
D000368:Aged; D000789:Angina, Unstable / Q000188:drug therapy* / Q000276:immunology / Q000401:mortality; D001241:Aspirin / Q000009:adverse effects / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism*; D015331:Cohort Studies; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000188:drug therapy / Q000276:immunology / Q000401:mortality; D011446:Prospective Studies; D012306:Risk; D015996:Survival Rate; D019210:Troponin I / Q000097:blood
D015415:Biomarkers; D019210:Troponin I; D002097:C-Reactive Protein; D001241:Aspirin