THE INVOLVEMENT OF IMMUNE-REACTIONS IN CARDIAC DAMAGE DURING ACUTE MYOCARDIAL-INFARCTION - ROLE OF CELL-MEDIATED IMMUNE-RESPONSE

This study was undertaken with the aim of investigating humoral and ce ll-mediated immune response in acute myocardial infarction (AMI) as po ssible mechanisms involved in the infarction enlargement. Twenty three patients with first AMI and 15 healthy volunteers were examined. Of t he AMI patients, 14 had extensive infarction (group A), while 9 patien ts had small infarction (group B). Immunologic analyses were performed at admission, and repeated after 3, 7, 14 and 21 days of the acute ev ent. Following parameters were tested: number of CD3(+), CD4(+), CD8() and CD20(+) cells; serum IgG, IgA, IgM, C3, C4, immune complex acid anticardiac antibody levels; polymorphonuclear cell (PMN) function (ch emotaxis, phagocytosis, metabolic activity); leukocyte migration in vi tro in the presence of water-soluble homologous heart extract. It was demonstrated that the number of B cells, serum IgG, C3, immune complex and anticardiac antibody levels were elevated from 7th-14th days afte r AMI. Concerning these parameters, however, no significant difference s were obtained between group A and group B of AMI patients. Chemotaxi s and metabolic activity of peripheral blood PMN, but not phagocytosis , were enhanced during AMI, again changes of PMN did not correlate wit h the extension of infarction. In contrast, leukocyte migration inhibi tion in vitro revealed that only patients with extensive AMI have deve loped positive reaction during the first 14 days after the onset of th e disease, while leukocyte inhibition reaction appeared in patients wi th nonextensive AMI not earlier than the 21st day after the infarction , These findings demonstrate generation of immune reactivity during AM I and indicate that humoral immune response seems more likely to be an epiphenomenon related to tissue necrosis, while cell-mediated immune reactions could influence the extensiveness of cardiac damage.