Atherothrombosis is associated with the presence of a microinflammatory response, usually monitored by the use of C-reactive protein (CRP) measurements. In the Physician Health Study it was suggested that individuals who benefit most from the treatment are those who have enhanced concentrations of this biomarker. The possibility was suggested that one of the mechanisms of action of aspirin in thrombotic prevention is through its anti-inflammatory properties in terms of reducing the concentration of CRP. We conducted a regression analysis in a cohort of 3888 apparently healthy individuals and those with atherothrombotic risk factors and vascular events, 370 of whom were under the treatment of low doses (<or= 325 mg/day) of aspirin. The significant determinants of CRP concentrations included body mass index, oral contraceptives, hormonal replacement therapy, gender, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides, physical activity, age, smoking status and the presence of diabetes mellitus but not the use of low dose of aspirin. We conclude that the use of low doses (<or= 325 mg/day) of aspirin does not have a significant role in the modulation of CRP concentrations in apparently healthy individuals and those with atherothrombotic risk factors and vascular events. The anti-atherothrombotic activity of this drug is probably not mediated through a significant reduction of the concentration of this protein.