The Effects of Local Delivery of Paclitaxel Nanoparticle on Porcine Coronary Stent Restenosis

Cha, Kwang Soo; Jeong, Myung Ho; Lee, Seung Uk; Cho, Chong Su; Joo, Shin Bae; Kim, Nam Ho; Kim, Kun Hyung; Cho, Jang Hyun; Kim, Sung Hee; Ahn, Young Keun; Cho, Jeong Gwan; Lee, Jae Hyuk; Park, Chang Soo; Park, Jong Chun; Kang, Jung Chaee

Abstract

BACKGROUND AND OBJECTIVES: Late coronary in-stent restenosis remains an important clinical problem in coronary intervention. The effects of Paclitaxel (Taxol), an antimicrotubule agent, on neointimal proliferation within porcine coronary arteries were evaluated. METHOD: Stent overdilation injury was performed in porcine coronary arteries without local delivery of paclitaxel (n=10, Group I). Stent overdilation injury was also performed after local delivery of paclitaxel nanoparticle using the Dispatch Catheter(TM) in other coronary arteries (n=10, Group II). Coronary angiography and histopathologic examinations, which were performed 4 weeks after stenting, and complete blood counts and blood chemistry before and 4 weeks after the local delivery were compared. RESULT: 1) Reference vessel diameter, stented artery diameter, and diameter stenosis were not different between two groups. 2) Histopathologic injury score, external elastic lamina area, internal elastic lamina area, and luminal area were not different between two groups. 3) Neointimal area and histopathologic area stenosis were smaller significantly in the group II than in group I (2.3+/-0.33 vs 3.7+/-1.40 mm2, 22.2+/-19.26 vs 31.1+/-7.15%: p=0.04, 0.03, respectively). 3) Proliferating cell nuclear antigen index was lower in the stent overdilation injury with local paclitaxel delivery group than in the stent overdilation injury alone (31.10+/-3.70 vs 46.80+/-5.20%, p=0.04). 4) No significant laboratory changes were observed before and 4 weeks after the local delivery.
CONCLUSION
Local delivery of paclitaxel nanoparticle inhibits neointima formation after stent overdilation injury in porcine coronary arteries without systemic toxicity.