Immunological changes in acute myocardial infarction

Objective: This study was undertaken to investigate troponin and lymphocyte subset changes in acute myocardial infarctions (AMI) and to correlate these changes with disease variables. Methods: Forty-five patients with AMI admitted to the Coronary Care Unit, Jordan University Hospital and Queen Alia Heart Institute at King Hussein Medical Center, Amman, Jordan during the period November 1999 through to April 2000 were included in the study. Forty-five patients with non cardiac conditions were selected as a control group. Tests performed include; determination of the percentages of B-lymphocytes, T-lymphocytes and T-lymphocyte subsets by flow cytometry, measurements of serum cardiac troponin I (cTnI) by microparticle enzyme immunoassay and determination of minor blood groups by the gel test. Results: A significant increase in the percentages of CD8(+) and CD19(+) cells combined with a significant decrease in the percentages of CD3(+) and CD4(+) cells as well as a decrease of CD4(+)/CD8(+) ratio were documented in patients with AMI 24 hours after admission to the hospital. Except for CD19(+) cells, all of cell types assayed for returned to their normal percentages before discharge of patients. Very low CD4(+) cell percentages and CD4(+)/CD8(+) ratio were found to be poor prognostic signs of AMI. Serum cTnI levels which were elevated in all patients correlate very well with the decreased CD4(+) cell percentages, and the decreased CD4(+)/CD8(+) cell ratio and they seem to correlate with the extensiveness of infarction. Troponin and lymphocyte subset changes, on the other hand, did not correlate with the number of vessels diseased or the risk factors for AMI. Finally, a statistically significant association was observed between the Le (a(-)b(-)) phenotype and AMI. Conclusion: Immunologic change seem to accompany or follow AMI and changes in T-lymphocyte subsets and cTnI can be regarded as prognostic markers in AMI but these changes are independent of risk factors and the number of vessels diseased.