Myocardial revascularization (CABG) surgery remains one of the main therapies for
coronary disease. However, vascular disease that follows CABG remains a challenge to
medicine. The mechanical, molecular and cellular changes undergone by the venous
vascular graft when inserted into the coronary artery flow culminate in thrombosis,
intimal hyperplasia, and atherosclerotic process, and end with restenosis.[1],[2]CABG experimental models were crucial to the understanding of mechanisms present in the
course of vascular disease. The vascular graft model with anastomosis of the external
jugular vein with the carotid artery represents an experimental model of vascular
disease similar to that occurring after CABG. Pigs, rabbits, and rats may be used in
this model because of protocol reproducibility, cost, and benefit.[3],[4]Strategies interfering with the mechanisms of vascular disease after CABG may reduce
venous graft restenosis. Rapamycin, an immunosuppressive, showed antiproliferative
effect of vascular smooth muscle cells in experimental models.[4],[5] Tianshu-Chu et al.,[6] in an experimental study in rats that reproduces vascular disease
after CABG, demonstrated that the combination of rapamycin and cyanoacrylate showed
synergy to prevent intimal thickening. The combination of rapamycin and cyanoacrylate
inhibited cell proliferation, primarily of dedifferentiated vascular smooth muscle cells
(myofibroblasts) and vascular cells, preventing intimal hyperplasia, extracellular
matrix deposition and neoangiogenesis. Thus, the combination of rapamycin with
cyanoacrylate shows synergy when compared to the isolated use.
Authors: Ivo Skalský; Ondrej Szárszoi; Elena Filová; Martin Pařízek; Andriy Lytvynets; Jana Malušková; Alena Lodererová; Eduard Brynda; Věra Lisá; Zuzana Burdíková; Martin Capek; Jan Pirk; Lucie Bačáková Journal: Int J Pharm Date: 2012-02-21 Impact factor: 5.875