Abstract 15025: E-NTPDase Gene Eluting Stent Prevents In-stent Restenosis in Injured Artery; Optical Coherence Tomography Evaluation
Backgrounds Ectonucleoside triphosphate diphosphohydrolase (E-NTPDase) rapidly hydrolyzes ADP, which is well known to induce smooth muscle cell proliferation, to AMP at arterial wall. We had reported that human placental E-NTPDase (hE-NTPDase) gene eluting stent prevents in-stent thrombosis without the use of antiplatelet drugs. In the present study, we performed the further investigations about the effects of our hE-NTPDase gene eluting stent on the prevention of in-stent restenosis.
Methods and Results We generated hE-NTPDase gene eluting stent with pBS CAG vectors encoding hE-NTPDase. We performed balloon injury of right femoral artery (FA) and stent implantation into the injured FA in 20 male Japanese white rabbits. The rabbits were divided into two groups: the bare metal stent (BMS) group and the hE-NTPDase gene eluting stent (hE-NTPDase stent) group (n=10 in each group). The mRNA expression level of endogenous E-NTPDase, which is an isoform of placental E-NTPDase and expressed in normal vascular endothelial cells, was dramatically reduced in injured FA. However, in the hE-NTPDase stent group, E-NTPDase mRNA expression was preserved in the stent implanted FA on day 7. Angiography on day 28 demonstrated the remarkable stenosis (>50%) at the stent implanted site in 8 of 10 rabbits in the BMS group, but in only 1 of 10 rabbits in the hE-NTPDase stent group (p<0.05). Additionally, optical coherence tomography (OCT) evaluation in vivo on day 28 revealed that the mean neointima area of 15 slices of the stent implanted FA was significantly larger in the BMS group (2.51±0.77 mm2) than in the hE-NTPDase stent group (0.88±0.50 mm2) (p<0.05, figure), which was confirmed by histological examination. Additionally, OCT demonstrated the visible thrombus at the surface of neointima in the BMS group but not in the hE-NTPDase stent group.
Conclusion E-NTPDase gene eluting stent can inhibit excessive neointima growth, thereby prevents in-stent restenosis in the injured artery.
- © 2011 by American Heart Association, Inc.