Neovascularization of Carotid Atherosclerotic Plaque and Quantitative Methods of Its Dynamic Assessment in Vivo.

The study demonstrates significant variety of neovascularization degree and vessel diameter in the carotid atherosclerotic plaque. It is suggested that the increase in the number of vessels with a diameter <20 µ can be indicative of increased atherosclerosis activity, while the increase in the number of vessels with a diameter ≥40 µ indicates "reparative potential" of plaques. Duplex contrast-enhanced ultrasound scanning allows characterization of the localization and number of vessels with a diameter of ≥30 µ in the plaque, while even slight elevation of plasma concentration of basic fibroblast growth factor attests, first of all, to increased content of small vessels <30 µ in the plaque. The level of fibroblast growth factor >1.5 pg/ml is a reliable marker of increased number of both small and large vessels in the plaque.

[Morphometric characteristics of neovascularization of carotid atherosclerotic plaques]. / Morfometricheskaia kharakteristika neovaskuliarizatsii ateroskleroticheskikh bliashek karotidnogo sinusa.

OBJECTIVE: to identify the relationship between the magnitude of neovascularization of an atherosclerotic plaque and its other processes, such as atheromatosis, macrophage responses, hemorrhages, and calcification. MATERIAL AND METHODS: 48 carotid atherosclerotic plaques all their way underwent morphopathological examination, by assessing the magnitude of neovascularization (total vessel density per plague cm2; density of vessels of different diameters; localization in section), atheromatosis (a volume fraction), foam cells (a score of 0 to 5), hemorrhages (a score of 0 to 4), and calcification (a score of 0 to 4). The Mann-Whitney U test and the Spearman correlation coefficient with p<0.05 were used in the statistical analysis. RESULTS: There was a substantial variability in vessel diameters and densities in the plaque with a drastic predominance of vessels smaller than 20 µm in diameter (69.8±14.3%). The vessels with a diameter as large as 20 µm were more frequently located in the area of accumulation of foam cells or organizing hemorrhages (p<0.03), unlike those with a diameter of more than 40 µm, which were more common in the areas of connective tissue, especially adjacent to large calcifications, and in the foci of organized hemorrhages (p<0.008). Intensified calcification was accompanied by the higher density of vessels having a diameter of more than 40 µm (p<0.038) and particularly of those with a diameter of more than 60 µm (p=0.006). The degree of hemorrhages and the number of foam cells were unrelated to the density of vessels, but these increased with their localization in the surface areas of a plaque (p=0.000342). With the increasing severity of atheromatosis, there was a decrease in the density of vessels larger than 20 µm in diameter (p=0.00042). CONCLUSION: The number, diameter, and location of vessels in the plaque serve as a dynamic reflection of its destructive and reparative processes; and a larger number of vessels having a diameter of more than 40 µm can be an indicator for the activation of reparative processes.

[The Role of Blood-Brain Barrier in the Development of Childhood Febrile Seizures and Temporal Lobe Epilepsy.]

Blood-brain barrier (BBB) of the central nervous system (CNS) is a physiological barrier that makes it possible to control the exchange of ions, molecules and cells between blood and tissue and to prevent their free inflow into the brain. BBB is crucial for maintenance of brain homeostasis. BBB damage accompanies many degenerative, neurological and inflammatory (infectious or noninfectious) diseases and pathological states. Current review reports about BBB role in development of childhood febrile seizures and temporal lobe epi- lepsy.