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Effect of short-term aspirin use on C-reactive protein
D Feng1, R P Tracy, I Lipinska
1Institute for Prevention of Cardiovascular Disease, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA.
Insights
Short-term aspirin therapy did not significantly reduce C-reactive protein (CRP) levels in healthy men, even after strenuous exercise. Further research is needed to explore aspirin
Area of Science:
- Cardiovascular Disease Research
- Inflammation Biomarkers
- Pharmacology
Background:
- Inflammatory markers like C-reactive protein (CRP) predict cardiovascular disease risk.
- Aspirin's cardiovascular benefits might stem from anti-inflammatory effects beyond its antiplatelet action.
- Previous studies suggest a link between CRP levels and aspirin's efficacy in preventing myocardial infarction.
Purpose of the Study:
- To investigate whether short-term aspirin therapy reduces CRP levels in healthy men.
- To examine the effect of aspirin on CRP levels before and after strenuous exercise.
- To assess potential anti-inflammatory properties of aspirin in relation to CRP.
Main Methods:
- A randomized, double-blind, parallel study involving 32 healthy men.
- Blood samples collected at rest and post-maximal treadmill exercise.
- Participants received either 81 mg or 325 mg of aspirin daily for 7 days.
- CRP levels measured using ELISA at baseline and after aspirin treatment.
Main Results:
- Strenuous exercise significantly increased CRP levels by 13% (P < 0.0001).
- Aspirin therapy did not significantly alter resting or post-exercise CRP levels.
- Overall, aspirin resulted in a nonsignificant 6% reduction in CRP (P = 0.20).
Conclusions:
- Short-term aspirin therapy does not significantly reduce CRP levels in healthy male subjects.
- Current data suggest aspirin may not impact inflammatory marker levels.
- Further studies with longer duration, different populations (e.g., those with coronary heart disease), and additional inflammatory markers are warranted.
Abstract:
Markers of inflammation, such as C-reactive protein (CRP) and fibrinogen, have been shown to be predictive of cardiovascular disease. In the Physicians Health Study, the magnitude of reduction in the risk of myocardial infarction with aspirin therapy was related to baseline CRP levels, raising the possibility that the protective effect of aspirin may be due to antiinflammatory properties in addition to its antiplatelet effect. We therefore investigated whether aspirin therapy lowers CRP levels. Because heavy physical exertion is a well-known trigger of myocardial infarction, we also investigated the effect of aspirin on CRP levels before and after strenuous exercise. Thirty-two healthy men, aged 29 +/- 6 years, were enrolled in a randomized, double-blind, parallel study. Blood samples were obtained immediately before and after maximal treadmill exercise at baseline and following 7 days of aspirin therapy (81 or 325 mg). The levels of CRP, as measured by ELISA, increased by 13% following exercise (P < 0.0001). However, aspirin did not significantly alter CRP levels, either at rest (0.81 +/- 0.13 mg/L before aspirin vs. 0.78 +/- 0.13 mg/L on aspirin) or following exercise (0.92 +/- 0.13 mg/L before aspirin vs. 0.86 +/- 0. 13 mg/L on aspirin), P = 0.73. When the resting and postexercise data were combined, the levels were 0.87 +/- 0.13 mg/L before aspirin and 0.82 +/- 0.13 mg/L on aspirin (a nonsignificant 6% reduction, P = 0.20). In conclusion, in healthy male subjects CRP levels were not significantly reduced by short-term aspirin therapy. Our data, taking together with other reports, suggest that aspirin may not affect the levels of inflammatory markers. However, further studies are needed with a longer duration of therapy, among subjects with coronary heart disease, and using additional markers of inflammation besides CRP to determine the long-term effects of aspirin use.