Rosuvastatin attenuates angiotensin II-induced neointimal formation after stent implantation in the rat

Objective We investigated the efficacy of oral rosuvastatin treatment to reduce in-stent neointima formation, both in the absence and presence of high levels of the proproliferative substance angiotensin II (Ang II).

Background Drawbacks of current drug-eluting stents include inhibition of reendothelialization, induction of abnormal coronary endothelial function, and, most importantly, late in-stent thrombosis. Statin treatment might be a more subtle approach, with known beneficial vascular effects.

Methods Wistar rats were allocated to four treatment groups by two consecutive randomization steps: one to allocate rosuvastatin 0.047% (wt/wt) supplemented rat chow, and one to implant an osmotic minipump releasing Ang II (200 ng/kg). Stents were implanted in the abdominal aorta in all groups. After 4 weeks, in-stent neointima formation and vascular function in the thoracic aorta were determined.

Results In the absence of Ang II, rosuvastatin reduced neointima formation by 23% as compared with control (0.66 +/- 0.06 versus 0.51 +/- 0.02 mm(2); P

Conclusion Ang II infusion increases in-stent neointima formation and decreases endothelial function. We now provide evidence that rosuvastatin effectively inhibits in-stent neointima formation and in parallel improves endothelial dilator function, both in the presence and absence of high Ang 11 levels. Coron Artery Dis 19:47-53 (c) 2008 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.