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1 group included 68 patients with 74 in-stent restenotic lesions.
2 ographic restenosis after gamma radiation of restenotic lesions.
3 nd myocardial infarctions than nonaggressive restenotic lesions.
4 mal formation in atherosclerotic plaques and restenotic lesions.
5 e-tissue-containing myxoid region typical of restenotic lesions.
6 en more striking in (nonstented and stented) restenotic lesions.
7 expression of these factors in VSMCs within restenotic lesions.
8 is increased and MMP-1 is decreased in early restenotic lesions.
9 atheromatous plaques and the development of restenotic lesions.
10 he femoral-popliteal segment in de- novo and restenotic lesions.
11 rominent component in stented and nonstented restenotic lesions.
12 ectable with immunohistochemistry in 4 of 13 restenotic lesions (31%) and in 3 of 37 de novo lesions
14 ative angiographic location of the recurrent restenotic lesion, after treatment of in-stent restenosi
16 lasty such as renal aorto-ostial lesions and restenotic lesions, as well as after a suboptimal balloo
17 oronary artery lesions (HR 1.46, p < 0.001), restenotic lesions at baseline (HR 1.58, p = 0.006), and
22 atients undergoing optimal DCA of de novo or restenotic lesions in 3.0- to 4.5-mm native coronary art
23 novo atherosclerotic or post-endarterectomy restenotic lesions in native carotid arteries were enrol
26 hese results suggest that the development of restenotic lesions involves localized deposits of specif
27 ar de novo atherosclerotic and, potentially, restenotic lesions) is fueled by more effective second-g
28 ultivessel disease, treatment of an in-stent restenotic lesion), laboratory findings (low baseline he
31 bute to the progression and development of a restenotic lesion, many signaling through a common pathw
33 to stain atherectomy specimens from 29 human restenotic lesions (mean restenosis interval, 6.0+/-4.4
35 ergoing percutaneous treatment of de novo or restenotic lesions of the superficial femoral or proxima
36 larly, final IVUS lumen CSA (p = 0.0001) and restenotic lesions (p = 0.006) were found to predict TLR
38 t multivariate predictors for late MACE were restenotic lesion (relative risk [RR] 1.33, p = 0.02), P