We studied the effect of VEGF-A in experimental myocardial infarction on attraction of progenitor cells into the regeneration zone. The appearance of CD34(+)CD45(+) cells known as low-differentiated progenitor cells was observed in the damaged myocardial tissue in the presence of a considerable excess of VEGF-A. These cells can act as precursors of mesenchymal tissues depending on the direction of differentiation.

The relationship between vascular endothelium growth factor (VEGF) and cardiomyocyte oxidative phosphorylation level in experimental myocardial infarction, caused by diathermocoagulation of the periconical ventricular artery, was studied by immunofluorescent microscopy. Staining showed uneven distribution of cytochrome c in the mitochondria in the focus of myocardial infarction 2 h after the operation. After 24 h uneven staining of cardiomyocytes was found in the peri-infarction zone and no staining in the zone of myocardial infarction. This indicated a significant decrease in the level of redox enzymes. This picture persisted till day 14. Intraventricular injection of VEGF to animals led to a significant increase of the immunohistochemical reaction intensity, which reached the peak by day 7. The distribution of immunohistochemical reaction products under conditions of VEGF blocking was about the same as in spontaneous postinfarction reparative restitution. Our data indicated that increase of VEGF concentration in the myocardium maintained and stimulated oxidative phosphorylation in cardiomyocytes during the postinfarction period.

The aim of the investigation was to develop a simple and available for practical application method of pathomorphological assessment of myocardial infarction age with a wide range of registered terms.Materials and Methods. Specimens of the experimental myocardial infarction zone (a model of diathermocoagulation of the rat periconical interventricular artery; n=50) in the period from 2 h to 30 days, and post-mortem specimens of 30 men died of transmural myocardial infarction and post-infarction cardiosclerosis in the period from 6 h to 30 days were immunohistochemically investigated using antibodies to the matrix metalloproteinase 9 (MMP9).Results. It has been established that localization of MMP9 in the infarction zone enables determining with a sufficiently high precision the time that passed from infarction onset. In fatal outcomes developed during several hours after infarction, the neutrophil cytoplasm in the infarction zone had intensive color. On day 1-2 a bright color of the extracellular matrix was noted. In later terms (days 3-21) staining of the fibroblastic cell line in the border zone (with maximum on days 7-14) was observed. The dynamics of MMP9 content and its localization in the myocardium of the dead patients corresponds to the data obtained in the experimental investigations.Conclusion. The proposed method allows pathologists to clearly differentiate myocardial infarction age using pathomorphological investigations.

Cardiac involvement is the most important prognostic factor in eosinophilic granulomatosis with polyangiitis (Churg–Strauss syndrome). We report a case of Churg–Strauss syndrome in 65-year-old women masquerading as a non-ST elevation myocardial infarction. She had chest discomfort, dyspnea and ST depression, high troponin level and so myocardial infarction was diagnosed. She had had asthma for 4 years but had no eosinophilia in peripheral blood and lesions in the lungs at the time of the first hospitalization. Her skin was clean without rashes. 3 months later she was hospitalized again having pulmonary infiltrates. Laboratory tests revealed that eosinophil was significantly increased. Cardiac involvement in a pathological process led to death. Histological examination of heart and lungs showed necrotic coronary vasculitis, granulomas and perivascular eosinophilic infiltrates in myocardium, endocardium, pericardium and pulmonary eosinophilic infiltrates.