Ceruloplasmin (CP) is an essential plasma α2-globulin that participates in the inflammatory acute-phase reaction, and is also involved in oxidative stress. It has been acknowledged that during acute coronary ischemic episodes there is a lack of balance between the production of reactive oxygen species and the development of antioxidant systems, resulting in oxidative stress. At the same time, a proinflammatory status is also known to be involved in acute coronary ischemic episodes as a risk factor that acts independently from the activation of coagulation or the endothelial dysfunction. It is thus reasonable to assume that CP might be a key player in the acute coronary ischemic syndrome. The objectives of the present paper focused on the determination of plasma CP and its correlation with plasma oxidative stress and acute-phase reaction markers on patients with acute myocardial infarction. A group of patients with acute myocardial infarction (N = 28) and a control group were included in our study. All patients agreed to participate in the study and the protocol was in compliance with the Declaration of Helsinki. We assayed the plasma concentrations of malondialdehyde (MDA), CP, uric acid, as well as the concentrations of plasma α2-globulin and fibrinogen, at four intervals post infarction (1, 3, 7, 10 days p.i.). The results indicated a progressive increase of the MDA concentration in the acute myocardial infarction group reaching a maximum during the third day p.i. (from 3.1 mM/ml on day 1 p.i. to 4.75 ± 1.02 mM/ml on day 3 p.i., p < 0.001 compared to controls, Student's t test). The concentrations of CP and uric acid, taken here as indicative of the antioxidant reaction, also progressively increased (CP: from 57.78 mg% on day 3 p.i. to 60.61 ± 2.16 mg% on day 7 p.i., p < 0.01 compared to controls; uric acid: from 5.4 mg% on day 3 p.i. to 6.38 ± 0.92 mg% on day 7 p.i., p < 0.01 compared to controls), but this increase was observed with a 4 day delay relative to the peak of MDA, being synchronized with the increase of inflammatory markers, that is, α2-globulin (from 11% on day 3 p.i. to 12% on day 7 p.i., p < 0.001 compared to controls) and fibrinogen (from 490 mg% on day 3 p.i. to 520 ± 91 mg% on day 7 p.i., p < 0.05 compared to controls). We concluded that there was an increase of the oxidative stress in acute myocardial infarction. However, future studies should try to specifically determine in what way the increase of plasma CP in acute coronary syndromes relates to inflammatory and antioxidant processes in acute coronary syndromes.