Feng D, Tracy R P, Lipinska I, Murillo J, McKenna C, Tofler G H
Institute for Prevention of Cardiovascular Disease, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA.
J Thromb Thrombolysis. 2000 Jan;9(1):37-41. doi: 10.1023/a:1018644212794.
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.
炎症标志物，如C反应蛋白（CRP）和纤维蛋白原，已被证明可预测心血管疾病。在医师健康研究中，阿司匹林治疗降低心肌梗死风险的程度与基线CRP水平有关，这增加了阿司匹林的保护作用可能除了其抗血小板作用外还归因于抗炎特性的可能性。因此，我们研究了阿司匹林治疗是否会降低CRP水平。由于剧烈体力活动是心肌梗死的一个众所周知的诱因，我们还研究了阿司匹林对剧烈运动前后CRP水平的影响。32名年龄在29±6岁的健康男性参加了一项随机、双盲、平行研究。在基线时以及阿司匹林治疗7天（81毫克或325毫克）后，在最大跑步机运动前后立即采集血样。通过酶联免疫吸附测定法（ELISA）测量，运动后CRP水平升高了13%（P<0.0001）。然而，阿司匹林并未显著改变CRP水平，无论是在静息状态下（阿司匹林治疗前为0.81±0.13毫克/升，阿司匹林治疗时为0.78±0.13毫克/升）还是运动后（阿司匹林治疗前为0.92±0.13毫克/升，阿司匹林治疗时为0.86±0.13毫克/升），P=0.73。当将静息和运动后的数据合并时，阿司匹林治疗前的水平为0.87±0.13毫克/升，阿司匹林治疗时为0.82±0.13毫克/升（非显著降低6%，P=0.20）。总之，在健康男性受试者中，短期阿司匹林治疗并未显著降低CRP水平。我们的数据与其他报告一起表明，阿司匹林可能不会影响炎症标志物的水平。然而，需要在冠心病患者中进行更长疗程的治疗研究，并使用除CRP之外的其他炎症标志物来确定阿司匹林使用的长期影响。
