The aim – the investigation of immune status properties and structural changes of myocardium in patients with myocarditis and dilated cardiomyopathy (DCM).
Materials and methods. We performed the examination of 82 patients: 54 with myocarditis (1st group) and 28 with DCM (2nd group). Control group included 20 healthy subjects. The average age in all groups had no reliable differences. We studied serum levels of CD8+, CD16+, CD19+ cells, immunoglobulins (Ig) G and M, antimyocardial antibody (ATm) titers and blast transformation lymphocyte activity for myocardium (BTLAm). By means of 2D echocardiography we measured left ventricular (LV) end-diastolic and end-systolic volume indices (iEDV and iESV), as well as LV ejection fraction (EF). The presence of myocardial edema, hyperemia and fibrosis was evaluated with cardiac magnetic resonance (CMR).
Results. In patients of the 2nd group, compared to the 1st one, we observed more pronounced LV dilatation by parameters of LV iEDV value – 118.1±6.0 and 87.1±5.5 ml/m2 respectively (P<0.05) and more significant impairment of LV systolic function by LV EF value – 32.9±1.8 and 40.2±1.9 %, respectively (P<0.01). All patients had left ventricular (LV) systolic dysfunction – LV ejection fraction (EF) ≤ 45 %. At CMR in the 1st group hyperemia was detected in 58.8 %, edema in 38.3 % and fibrotic/necrotic changes in 52.9 % patients, in the 2nd group we observed only diffuse fibrosis in 90.9 % cases. We also found a more pronounced activation of cellular and humoral autoimmune activity in the 1st group, characterized by the higher value of ATm titer by 27.2 % (P<0.05) and BTLAm by 76.9 % (P<0.01) in comparison to the 2nd group. Reliable direct correlation was established in the 1st group of BTLAm and edema with hyperemia – (r=0.82; Р<0.02 and r=0.74; Р<0.01), respectively. Furthermore, in the 1st group we found correlation of ATm titer with presence of edema and hyperemia – (r=0.62 and r=0.70), respectively (P<0.05). At the same time, we didn’t observe any correlation between immunologic markers and MRI changes in patients with DCM. Conclusion. We may suppose that LV dilatation and systolic dysfunction in patients with myocarditis was a sequence of inflammation in the myocardium, characterized by pronounced activation of both cellular and humoral immune response and confirmed at CMR by myocardial edema and hyperemia. Dilatation and LV systolic dysfunction in patients with DCM was not associated with intensity of immune pathologic reactions and was caused by diffuse fibrosis of myocardial tissue observed at CMR.