| Budget Amount *help |
¥3,800,000 (Direct Cost: ¥3,800,000)
Fiscal Year 2000: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1999: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Research Abstract |
Restenosis after coronary stenting remains a significiant clinical problem. Previous experimental animal studies have shown that coronary stenting induces neointimal proliferation. However, the mechanisms that underlie restenosis after coronary stenting in humans are still unclear.
We have previonsly reported that the formation of a concentric layer of neovascularization and macrophage accumulation observed at in-stent restenosis in human coronary arteries could result from organization processes of thrombosis (Komatsu R, Ueda M, et al. Circulation 98 : 224-233, 1998.)
The present study demonstrates that glycoprotein (GP) IIb/IIIa positive platelet thrombus was present in the neointima at early stages after stenting (Circulation 100, I-691, 1999). The present study, moreover, revealed that platelet activation, P-selectin-positive platelet aggregation, and P-selectin-mediated neutrophil accumulation were prominent changes in the early stages of human coronary arteries after stenting. The observations also suggests that these phenomena trigger the repair process, eventually this may lead to neointimal formation.
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