Impact of blood circulation on reendothelialization, restenosis and atrovastatinʹs restenosis prevention effects

Background The independent effects of numerous circulating inflammatory cytokines and inflammatory associated blood cells on reendothelialization and restenosis after PCI has been elucidated, whereas the blood circulationʹs general effect on restenosis is still pending. Thereby, author investigated the impact of blood circulation on reendothelialization, restenosis and atrovastatinʹs restenosis prevention effects. Methods and results 70 SD rats were divided equally in 7 groups: sham operation group, deendothelialization group, atrovastatin treatment group, occlusion group, occlusion and deendothelialization group, atrovastatin treatment after occlusion and deendothelialization group, and immediate sacrifice (after deendothelialization) group. The carotid model of deendothelialization by balloon and (or) thromboembolism occlusion was established, and 4 weeks after balloon injury, the reendothelialization ratio and restenosis ratio of each subjects were observed. The outcomes revealed that there is a natural self-repair phenomenon, featured as low level reendothelialization and restenosis inhibition, which can be significantly augmented under atrovastatin treatment. Yet when the blood circulation discontinued, not only the self-repair process, but also atrovastatinʹs beneficial effects on reendothelialization and restenosis disappeared. SPSS analysis revealed that there was inverse correlation between reendothelialization and restenosis. Conclusions Blood circulation not only per se generally promote reendothelialization and inhibits restenosis, but also serves as a necessary pathway for atrovastatin exerting therapeutic effects on reendothelialization and restenosis; Accelerating reendothelialization is a promising approach of restenosis prevention.