CLINICAL STUDY
The effect of aspirin on C-reactive protein as a marker of risk in unstable angina
Simon Kennon, MB, MRCP*,
Christopher P. Price, PhD, FRCPath ,
Peter G. Mills, MA, FRCP*,
Kulasegaram Ranjadayalan, MPhil, MRCP ,
Jackie Cooper, MSc ,
Heather Clarke, PhD, MRCPath and
Adam D. Timmis, MD, FRCP*
* Department of Cardiology, Bart’s and the London NHS Trust, London, United Kingdom
Department of Clinical Biochemistry, Bart’s and the London NHS Trust, London, UK
Department of Cardiology, Newham Healthcare Trust, London, UK
MRC Epidemiology and Medical Care Unit, Charterhouse Square, London, UK
Manuscript received August 8, 2000;
revised manuscript received December 7, 2000,
accepted December 22, 2000.
Reprint requests and correspondence: Dr. Simon Kennon, Cardiology Department, London Chest Hopital, Bonner Rd, London E2 9JX, United Kingdom
srok{at}dircon.co.uk
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.
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Abbreviations and Acronyms
| | CRP | = C-reactive protein | | OR | = odds ratio |
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