The role of neovascularization in the formation of an unstable human atherosclerotic plaque

Abstract

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. 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. 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.