The mechanism of in-stent restenosis in radius stent: an experimental porcine study.
BACKGROUND
We investigated the mechanism of in-stent restenosis in radius stents in comparison to balloon-expandable stent (NIR stent) in pigs, with a focus on extracellular matrix (ECM).


RESULTS
Radius (n = 4) or NIR (n = 4) stents were implanted in the left coronary arteries of miniature pigs. Quantitative coronary ultrasound (QCU) was performed before, immediately after, and at 1 and 4 weeks after the implantation. The stented-coronary arteries were harvested at 4 weeks after the implantation followed by immunohistochemical, histological, reverse transcription-polymerase chain reaction (RT-PCR) and real-time PCR studies. In QCU, mean luminal areas at 4 weeks did not differ between both groups, whereas the mean stent area and neointimal area were significantly greater in the radius (p < 0.01). The immunohistochemical study revealed a significantly decreased number of neointimal macrophages and neovascularizations (p < 0.05, p < 0.01, respectively), and a stronger expression of tenascin-C in the radius. The histological study showed a larger ECM area and less neointimal cell density in the radius than in the NIR. The RT-PCR and real-time PCR analysis revealed an enhanced expression of tanascin-C mRNA in the radius than in the NIR.


CONCLUSIONS
Increased production of ECM, especially tenascin-C, played a greater role in the neointimal formation in the radius stent than inflammation.
Iso
Yoshitaka
Y
Third Department of Internal Medicine, Showa University School of Medicine, Tokyo, Japan.
Suzuki
Hiroshi
H
Sato
Takatoshi
T
Shoji
Makoto
M
Shibata
Masayuki
M
Shimizu
Nobuyuki
N
Koba
Shinji
S
Geshi
Eiichi
E
Katagiri
Takashi
T
D000818:Animals; D023903:Coronary Restenosis / Q000209:etiology / Q000473:pathology; D003331:Coronary Vessels / Q000473:pathology; D005109:Extracellular Matrix / Q000235:genetics / Q000473:pathology*; D006083:Graft Occlusion, Vascular / Q000209:etiology / Q000473:pathology*; D007150:Immunohistochemistry; D008264:Macrophages; D009389:Neovascularization, Pathologic / Q000209:etiology; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000032:analysis; D015607:Stents / Q000009:adverse effects*; D013552:Swine; D019063:Tenascin / Q000235:genetics / Q000502:physiology; D017539:Tunica Intima / Q000473:pathology; D015854:Up-Regulation / Q000502:physiology
D012333:RNA, Messenger; D019063:Tenascin