[Detection of Antigens of Cardiotropic Viruses in Atherosclerotic Plaques in Patients with Fatal Myocardial Infarction].

AIM: To assess the frequency of detection of cardiotropic virus antigens in coronary artery atherosclerotic plaques in patients with fatal myocardial infarction (MI). MATERIALS AND METHODS: We examined fragments of coronary plaques of 12 patients with fatal type 1 MI. Immunohistochemistry (IHC) of plaques was performed with the paraffin blocks using antibodies to Herpes simplex virus (HSV)-1, HSV-2, HSV-6, cytomegalovirus (CMV), parvovirus B19, adenovirus, Epstein-Barr virus and enteroviruses. RESULTS: According to the IHC all patients had virus antigens. The most common virus agents in fragments of coronary plaques were HSV-6 (10 patients) and enteroviruses (5 patients). Antigens of CMV, parvovirus B19, adenovirus, Epstein-Barr virus were not detected in any case. CONCLUSIONS: In this study viral antigens in coronary artery atherosclerotic plaques were found in all victims of fatal MI. There was no difference in the frequency of detection and type of viral agents between plaques in culprit arteries and uncomplicated atherosclerotic plaques.

[Inflammation as a universal pathogenetic link between injury, repair and regeneration, in acute coronary syndrome. From experiment to clinic].

Theory of atherogenesis and its complications underwent numerous changes. Today we observe that inflammation is a universal pathogenetic link between various processes such as atherosclerosis, rupture of atherosclerotic plaques and following myocardial infarction, post-infarction cardiac repair and heart failure. This review discusses examples, difficulties, and prospects of implementation of anti-inflammatory therapies in management of acute coronary syndrome and its complications.

[Dynamics of brain CD68+ and stabilin-1+ macrophage infiltration in patients with myocardial infarction].

Te aim of the study was to evaluate the temporal dynamics of brain CD68+ and stabilin-1+ macrophage infltration in patients with fatal myocardial infarction (MI) type 1. MATERIALS AND METHODS: Te study included 31 patients with fatal MI type I. Te control group comprised 10 patients of 18-40 age group who died from injuries incompatible with life. Patients with MI were divided into two groups. Group 1 comprised patients who died during the frst 72 hours of MI, group 2 comprised patients who died on days 4‒28. Macrophage infltration in the brain was assessed by immunohistochemical analysis. We used CD68 as a marker for the cells of the macrophage lineage and stabilin-1 as an M2-like macrophage biomarker. RESULTS: In group 1 the number of brain CD68+ macrophages was signifcantly higher than in the control group. In group 2 the intensity of brain CD68+ cells infltration was lower than in group 1 and higher than in the control group. Tere was a small amount of stabilin-1+ macrophages in the brain of healthy people, as well as of patients who died from MI. Tere were no signifcant differences in the number of stabilin-1+ cells between group 1 and group 2. Correlation analysis revealed the presence of positive correlation between the number of CD68 + macrophages in the infarct, peri-infarct, and non-infarct areas of the myocardium and the number of CD68+ macrophages in the brain in patients with MI. Tere were not correlations between the number of CD68 + and stabilin-1+ cells and the presence of diabetes mellitus, history of stroke, history of MI, and pre-infarction angina. CONCLUSION: Te number of brain CD68+ macrophages signifcantly increased during the frst three days of MI. Te number of brain stabilin-1+ macrophages did not increase and did not differ from the control values. We observed a positive correlation between the number of CD68+ macrophages in the brain and myocardium.