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Published on: January 28, 2020
The effect of aspirin on C-reactive protein as a marker of risk in unstable angina
S Kennon1, C P Price, P G Mills
1Department of Cardiology, Bart's and the London NHS Trust, United Kingdom. srok@dircon.co.uk
Insights
Aspirin pretreatment alters the predictive value of C-reactive protein (CRP) for cardiac events in unstable angina. This interaction suggests aspirin modifies inflammatory responses to myocardial injury, impacting event prediction.
Area of Science:
- Cardiology
- Inflammation Research
- Pharmacology
Background:
- C-reactive protein (CRP) elevation in acute coronary syndromes may indicate myocardial necrosis or inflammation driving atherosclerosis.
- Aspirin's anti-inflammatory properties or reduction of myocardial necrosis could influence CRP release.
- The clinical significance of aspirin's effect on CRP in unstable angina requires investigation.
Purpose of the Study:
- To assess the interaction between aspirin and C-reactive protein (CRP) release in patients with unstable angina.
- To determine if aspirin pretreatment modifies the prognostic value of CRP for adverse cardiac events.
Main Methods:
- Prospective cohort study of 304 patients with non-ST-elevation acute coronary syndromes.
- Serial blood sampling for C-reactive protein (CRP) and troponin I assays.
- 12-month follow-up for cardiac death and nonfatal myocardial infarction.
Main Results:
- Patients on aspirin showed lower troponin I concentrations.
- Maximum CRP concentrations were lower in patients taking aspirin, though not significantly.
- Significant interaction found: aspirin pretreatment attenuated the predictive value of CRP for 12-month cardiac events.
Conclusions:
- Prior aspirin therapy significantly influences the association between CRP levels and cardiac events in unstable angina.
- Aspirin's effect on the acute-phase inflammatory response to myocardial injury is a key mechanism behind this interaction.
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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