This study sought to investigate the interplay between antibody and T cell
responses triggered by an acute myocardial infarction (MI) and their possib
le 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 g
roup 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 t
han patients in group B. The levels of antimyosin immunoglobulin M and immu
noglobulin G antibodies in the serum samples from group A were significantl
y higher than those in normal control subjects. In group B, the levels of b
oth 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 w
ere 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 antib
odies and adhesion molecules in group A patients as compared with group B p
atients may be due to higher or more frequent exposures of their immune sys
tems 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 regulato
ry role of this antibody on the cellular immune response during this time.