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

OBJECTIVES This study was designed to assess the interaction between aspiri n 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 tha t drives atherogenesis. Aspirin has the potential to influence CRP release, either by its anti-inflammatory activity or by reducing myocardial necrosi s. The clinical significance of this potential interaction has not previous ly been tested. METHODS We conducted a prospective cohort study of 304 consecutive patients admitted with non-ST-elevation acute coronary syndromes. Serial blood samp les were obtained for CRP and troponin I assay. End points were cardiac dea th 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 concent rations 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 interac tion (p = 0.04) between prior aspirin therapy and the predictive value of C RP concentrations for death and myocardial infarction at 12 months. Thus, o dds ratios (95% confidence intervals) for events associated with an increas e 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 o f the acute-phase inflammatory responses to myocardial injury is the major mechanism of this interaction. (J Am Cell Cardiol 2001;37:1266-70) (C) 2001 by the American College of Cardiology.