RESUMO
This study sought to investigate the interplay between antibody and T cell responses triggered by an acute myocardial infarction (MI) and their possible role in the progress of this disease. Serum samples were collected from two groups of patients, group A (n = 26) within the first week of MI, and group B (n = 28) at 2 weeks and 2 months after MI. Patients in group A were older and had higher prevalence of hypertension and previous attack of MI than patients in group B. The levels of anti-myosin immunoglobulin M and immunoglobulin G antibodies in the serum samples from group A were significantly higher than those in normal control subjects. In group B, the levels of both antibodies were lower than those in group A but remained significantly higher than those in normal control subjects at both 2 weeks and 2 months. The levels of intercellular adhesion molecule-1 (sICAM-1) and vascular cell adhesion molecule-1 (sVCAM-1) in the serum samples from group A patients were significantly higher than those in normal control subjects. At 2 weeks after MI (group B), only the level of sVCAM-1, but not that of sICAM-1, was significantly higher than that in normal control subjects, and there were no significant changes in the levels of these two molecules from 2 weeks to 2 months after MI. We conclude that the higher levels of anti-myosin antibodies and adhesion molecules in group A patients as compared with group B patients may be due to higher or more frequent exposures of their immune systems to heart antigens. Furthermore, the immunoglobulin M antibody response during the first week of MI had an inverse relationship with the level of interleukin-2R (sIL-2R), which suggested a possible suppressive or regulatory role of this antibody on the cellular immune response during this time.
