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Irinotecan‐eluting stents inhibited neointimal proliferation in hypercholesterolemic rabbit aortas
Author(s) -
Berrocal Daniel H.,
González Germán E.,
Morales Celina,
Gelpi Ricardo J.,
Grinfeld Liliana R.
Publication year - 2006
Publication title -
catheterization and cardiovascular interventions
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.988
H-Index - 116
eISSN - 1522-726X
pISSN - 1522-1946
DOI - 10.1002/ccd.20694
Subject(s) - medicine , necrosis , irinotecan , restenosis , urology , fibrin , pathology , gastroenterology , stent , cancer , immunology , colorectal cancer
Objective: To assess the effect of irinotecan‐eluting stents (IS) on neointimal growth in the aortas of hypercholesterolemic rabbits and to determine other local histopathological effects such as necrosis, fibrin, and inflammatory reaction.Methods : Phosphorylcholine‐coated stents were deployed in the aortas of hypercholesterolemic rabbits. Group 1 (control; n = 8) received unloaded stents, group 2 ( n = 7) and group 3 ( n = 9) received IS with 0.046 mg and 1.29 mg of irinotecan, respectively. Eight weeks after implantation the rabbits were killed. Neointimal thickness (NT) was assessed by morphometry. Semiquantitative injury score (from 0 to 3+) was used to analyze inflammatory infiltrate, fibrin deposits, and necrosis in the stented segments.Results : NT was reduced only in high‐doses IS (G1, 167.4 ± 20.8 μ; G2, 170.24 ± 21.2 μ; G3, 111.56 ± 12.7 μ; P < 0.05, G3 vs G1 and G2). Necrosis decreased significantly with IS [1.00 ± 0.10 in G1 to 0.33 ± 0.07 and 0.02 ± 0.01 in G2 and G3, respectively] only in the media layer. The inflammatory infiltrate was present in the three layers of aortas from G1, but only decreased significantly in the intimae layer of the high‐dose group [1.50 ± 0.15 in G1 vs 1.00 ± 0.18 in G3, P < 0.05].Conclusion : Stents loaded with high‐dose irinotecan inhibit NT in the aortas of hypercholesterolemic rabbits. This effect was accompanied by decreased inflammatory infiltrate and media necrosis. © 2006 Wiley‐Liss, Inc.