Mechanisms of restenosis after coronary intervention: difference between plain old balloon angioplasty and stenting.
BACKGROUND
Restenosis after coronary intervention remains an unsolved and important clinical problem. We histologically examined the mechanism of restenosis after both balloon injury and stenting.


METHODS
Coronary arteries of swine were subjected to balloon injury and stenting. Next, just after stenting or at 7, 14, or 28 days, the animals were sacrificed for the evaluation by morphometric analysis, histological observation, and immunostaining.


RESULTS
The neointimal area peaked at 14 days in the balloon injury group (BG) and increased linearly up to 28 days in the stent group (SG). At 28 days, the total vascular area in the BG was reduced to 78% of the control values. In the SG, the total vascular area remained enlarged. According to the phenotypic analysis, the vascular smooth muscle cells (VSMCs) in the neointimal area at 28 days were the contractile type in the BG and the synthetic type in the SG. Proliferating cell nuclear antigen (PCNA) and macrophage-positive cells were not observed in neointima in the BG at 28 days, whereas they were observed around the stent struts in the SG. In addition, numerous inflammatory cells, such as neutrophils and eosinophils, were also present in the SG.


CONCLUSIONS
Restenosis after balloon injury consisted of arterial remodeling and neointimal hyperplasia, whereas that after stenting consisted mostly of neointimal hyperplasia. The neointimal area in the SG lasted longer than that in the BG. Continuous inflammation may be an important factor in the restenosis of stenting.
Nakatani
Masaki
M
Third Department of Internal Medicine, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, 142-8666, Tokyo, Japan. masaki-n@ya2.so-net.ne.jp
Takeyama
Youichi
Y
Shibata
Masayuki
M
Yorozuya
Minoru
M
Suzuki
Hiroshi
H
Koba
Shinji
S
Katagiri
Takashi
T
D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects*; D000818:Animals; D023903:Coronary Restenosis; D003331:Coronary Vessels / Q000473:pathology* / Q000648:ultrastructure; D004804:Eosinophils / Q000276:immunology; D006965:Hyperplasia / Q000209:etiology; D007150:Immunohistochemistry; D008264:Macrophages / Q000276:immunology; D008297:Male; D008854:Microscopy, Electron; D009131:Muscle, Smooth, Vascular / Q000473:pathology / Q000502:physiology; D009504:Neutrophils / Q000276:immunology; D010641:Phenotype; D018809:Proliferating Cell Nuclear Antigen / Q000096:biosynthesis; D015607:Stents / Q000009:adverse effects*; D013552:Swine; D013997:Time Factors; D017539:Tunica Intima / Q000276:immunology / Q000473:pathology*
D018809:Proliferating Cell Nuclear Antigen