Objectives: The purpose of this research was to investigate the level of inflammation in patients with ST elevation myocardial infarction (STEMI) that underwent successful primary percutaneous intervention, and conservatively treated patients with myocardial infarction without ST elevation (NSTEMI) based on the changes in cell-mediated immunity, through the frequency of leukocyte subpopulations, expression of the activation molecule CD25, cytokines IL-4 and interferon gamma (IFN-), and through monitoring the concentration of IL-18, erythrocyte sedimentation rate, hs-CRP (high sensitivity C-reactive protein) and other laboratory parameters (urates, AST, ALT, GT, urea, creatinin, hemoglobin) during early stationary medical rehabilitation. Patients, material and methods: The patients with STEMI who underwent successful primary percutaneous intervention in KBC Rijeka following permanent drug therapy were included. Second group were patients with NSTEMI who were conservatively treated with drug therapy according to the guidelines of the European Society of Cardiology and were all included in the program of early stationary medical rehabilitation. Third group were healthy subjects of the appropriate age and sex who were subjected to systematic routine laboratory and clinical investigation in Thalassotherapia-Opatija. The sample of 20 ml of venous blood was taken form each patient on day 1, 7, 14, 21 and 28 after the acute coronary event and it was used for further immunological and biochemical investigations. Peripheral blood mononuclear cells were obtained after gradient centrifugation after which their phenotype and activation levels were analyzed by simultaneous multiple staining of surface antigens using direct immunoflourescency and flow cytometry analyzes. Cell samples that were scheduled for intracellular cytokines staining, interleukin (IL)-4 and IFN-, were previously stimulated with PMA (phorbol myristate acetat), ionomycine and monensim following previously established protocol to improve visualization of cytokine accumulation into the stimulated cells. Immunocytochemitstry was used to visualize CD3 molecules in the samples of freshly isolated peripheral blood mononuclear cells. We used immunohistochemistry to show cytokine IL-15, chemokine CXCL 10 and molecules CD3, CD56 in heart tissue of subjects who died from acute coronary event. ELISA (enzyme-linked immunosorbent assay) was used to visualize IL-18 in peripheral blood test groups. Results: In NSTEMI and STEMI patients a decrease in T cell percentages was shown in the middle of rehabilitation period and was followed by the decrease in mean fluorescence intensity (MFI) for CD3 molecule, reflecting the decrease in the percentage of CD3+CD8+ T lymphocyte subtypes with increased expression of CD25 molecules in NSTEMI subjects, and the ratio of IFN-+ /IL-4+ cells in the subpopulation of CD3+CD56- T cells. Percentage of CD3-CD56+ NK cells did not significantly differ in NSTEMI and STEMI patients during early medical rehabilitation period and in comparison with healthy subjects, although the proportion of CD56+dim NK subset significantly increased and CD56+bright NK subset significantly decreased on day 7 and 14 after the acute coronary event in NSTEMI patients when compared with healthy examinees at the end of the rehabilitation period. In patients with NSTEMI percentage of NK cells that express the activation marker CD25, including their CD56+dim and CD56+bright NK subset, was significantly higher on day 14 and 28 compared to healthy subjects and the proportion of activated CD25+ T cells was significantly higher during the entire duration of rehabilitation in relation to the control group. Total number of leukocytes in peripheral blood was significantly increased at the end of the rehabilitation period (21st day) only in NSTEMI patients, but percentage of monocytes in the peripheral blood is significantly reduced on day 7, 14, 21 and 28 in comparison with healthy examinees. In the sera of patients with NSTEMI we have shown higher levels of IL-18 compared to healthy examinees during the entire rehabilitation, unlike the concentration of IL-18 in patients with STEMI, which did not differ from healthy examinees. In patients who died in the first week after acute coronary event we have detected IL-15 expression within viable cardiomyocytes encircling the necrotic region and the presence of CD3+ and CD56+ cells were found in the vicinity of weakly APAF-1+ myocardial filaments with a reduced number of nucleuses. Conclusion: Decrease in number of cells with cytotoxic CD3+CD8+CD56- and CD3-CD56+ bright phenotype, and decreased percentage of monocytes in peripheral blood of patients with NSTEMI during early stationary medical rehabilitation is probably a consequence of their recruitment into the myocardium under the influence of pro-inflammatory environment in the peripheral blood and their recruitment by the IL-15, showing that NSTEMI patients have stronger and prolonged inflammatory reaction than STEMI patients who underwent successful primary percutaneous intervention.