[The role of neovascularization in the formation of an unstable human atherosclerotic plaque]. / Rol' neovaskulyarizatsii v formirovanii nestabil'noi ateroskleroticheskoi blyashki u cheloveka.

MATERIAL AND METHODS: The study material was 20 autopsy samples obtained from males aged 65 to 72 years who died from acute atherosclerotic cardiovascular insufficiency. Aortic segments (from the arch, thoracic and abdominal regions), coronary arteries and the arteries of the base of the brain (a. basilaris) were investigated; these totaled 45 tissue segments. Neovessels and cellular responses in the arterial wall were examined by hematoxylin and eosin staining. VEGF was immunohistochemically detected using a highly sensitive two-stage streptavidin-biotin method. RESULTS: In unstable atherosclerotic lesions, there were active neovascularization processes in both the fibrous cap and the underlying parts of the adventitia. These changes are usually combined with a pronounced cellular inflammatory response that can contribute to their development. Endothelial growth factor may be one of the causes of neovascularization in unstable atherosclerotic lesions. CONCLUSION: A comparative immunomorphological study in the human aorta, coronary arteries, and a. basilaris revealed active neovascularization processes in the cap and the underlying parts of the adventitia in unstable atherosclerotic lesions. The cause of this neovascularization is probably endothelial growth factor and cellular inflammatory responses.

[Macrophages and Their Role in Destabilization of an Atherosclerotic Plaque].

The modern data on structure and the functional activity of macrophages are presented in the review. It is shown that they are the nonhomogeneous cell population. Two of their main subpopulations are presented as M1 and M2 phenotypes which perform opposite functions at inflammation development. The main attention in the review is paid to a role of macrophages in pathogenesis of atherosclerosis and, first, in formation of unstable atherosclerotic plaques which are the cause of the most severe complications of the disease. It is shown that main subpopulations of macrophages play different roles in formation of unstable and stable atherosclerotic plaques. Macrophages of M1 phenotype in the vascular wall carry out pro-atherogenic role and influence destabilization of an atherosclerotic plaque, while M2 macrophages perform atheroprotective function.

Chlamydia Pneumoniae and Immunoinflammatory Reactions in an Unstable Atherosclerotic Plaque in Humans.

Comparative study of the walls of the aorta, coronary artery, and a. basilaris detected for the first time intra- and extracellular depositions of Chlamydia pneumoniae in unstable atherosclerotic plaques. No chlamydia were detected in the intima of normal sites of the vascular wall and just negligible levels thereof in stable atherosclerotic plaques. An unstable plaque with intra- and extracellular colonies was characterized by infiltration of the cap and intima adjacent to the atheromatous core with mononuclear cells, primarily T cells. These data suggested that Chlamydia pneumoniae could play an important role in the development of immunoinflammatory processes in the vascular wall and promote destabilization and progressive development of atherosclerotic plaques in humans.

Role of interleukin-18 in destabilization of the atherosclerotic plaque in humans.

Precise location of IL-18 in cell and tissue elements of the atherosclerotic lesions in humans and its role in destabilization of the atherosclerotic plaque were detected. The data suggested a hypothesis on indirect involvement of IL-18 in destruction of the elastic and collagen fibers in an unstable plaque due to this cytokine capacity to induce the production of IFN-γ in T cells and macrophages, this eventually leading to inhibition of collagen and elastin synthesis in smooth muscle cells of the vascular wall and to loosening of the plaque cap.