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1 processes initiating excessive and prolonged neointimal proliferation.
2 g enough to explain persistent inhibition of neointimal proliferation.
3 ssociated with stent thrombosis or increased neointimal proliferation.
4 thrombotic occlusions, and thereby inhibited neointimal proliferation.
5 ial hypertrophy, adventitial thickening, and neointimal proliferation.
6                                  The risk of neointimal proliferation (1.8%) and restenosis (2%) is l
7                 There was a low incidence of neointimal proliferation (1.8%) and restenosis (2%).
8 nd repeat revascularization due to excessive neointimal proliferation, a process that may be blunted
9  effect of IPC instillation of paclitaxel on neointimal proliferation after balloon overstretch of po
10 ted the hypothesis that CaMKIIdelta mediates neointimal proliferation after carotid artery ligation b
11 arrest in the synthetic state with excessive neointimal proliferation after carotid injury, as well a
12 actors for the development of restenosis and neointimal proliferation after endovascular stent implan
13 ed Z2D3 F(ab')2 in a swine model of coronary neointimal proliferation after overexpansion coronary st
14 a beta-particle-emitting stent would inhibit neointimal proliferation after placement in porcine ilia
15 ortic adventitia, coincident with prominent, neointimal proliferation among cholesterol-fed, atherosc
16 (fluoropolymer-based versus polymer-free) on neointimal proliferation and healing response in the fam
17 uting stents (DES) are effective in reducing neointimal proliferation and in-stent restenosis.
18                                              Neointimal proliferation and intima to media ratios in M
19 ude local inflammation leading to aggressive neointimal proliferation and late neoatherosclerosis.
20 sential to the development of the concentric neointimal proliferation and luminal narrowing character
21 ly that simvastatin attenuates smooth muscle neointimal proliferation and pulmonary hypertension in p
22 PB-PES, PF-PES was associated with increased neointimal proliferation and subsequent clinical resteno
23 ion of an FP-PES resulted in lower levels of neointimal proliferation and sustained biological effect
24 Nogo-A/B-deficient mice promotes exaggerated neointimal proliferation, and adenoviral-mediated gene t
25 ilator actions, inhibition of thrombosis and neointimal proliferation, and both pro- and antiinflamma
26 ts of stents coated with agents that inhibit neointimal proliferation are extremely promising.
27 actors for the development of restenosis and neointimal proliferation are poorly understood.
28              This was accompanied by reduced neointimal proliferation, as monitored by intimal thickn
29  16 or 24 Gy exhibited marked suppression of neointimal proliferation at 28-day follow-up, with quant
30         (68)Ga positron radiation suppresses neointimal proliferation at doses of 16 and 24 Gy.
31           ISR mainly results from aggressive neointimal proliferation, but recent data also suggest t
32 t coronary angioplasty sites caused enhanced neointimal proliferation by 8 weeks.
33  but have retained the capability to inhibit neointimal proliferation by eluting immunosuppressive dr
34 he ACHIEVE paclitaxel-coated stent decreased neointimal proliferation compared with the bare-metal PE
35 ve demonstrated that ISR is mainly caused by neointimal proliferation; consequently, this pathologic
36      However, few animal models of pulmonary neointimal proliferation exist, thereby limiting a compl
37  coronary stents are effective at preventing neointimal proliferation in a porcine model of restenosi
38                 Drug elution by BVS prevents neointimal proliferation in a similar fashion to drug-el
39 or produces a marked localized inhibition of neointimal proliferation in balloon-injured arteries.
40 loading technique have been shown to inhibit neointimal proliferation in experimental models of reste
41 ted vascular disease and in the treatment of neointimal proliferation in other settings.
42 g ISR lesions is counteracted by exaggerated neointimal proliferation in placebo patients.
43                                              Neointimal proliferation in response to arterial injury
44 hy analysis showed significantly more global neointimal proliferation in the BMS+DEB group (15.7+/-7.
45 ic approaches for limiting atherogenesis and neointimal proliferation in the future.
46 sirolimus-coated balloons effectively reduce neointimal proliferation in the porcine coronary model b
47 ug-delivery stent showed a minimal amount of neointimal proliferation in the stented segment.
48 supplemented females correlated with reduced neointimal proliferation in this group.
49                                              Neointimal proliferation in vivo and platelet-derived gr
50 of peri-stent remodeling is less, intrastent neointimal proliferation is greater and accompanied by m
51 vasculopathy is characterized by progressive neointimal proliferation, leading to ischemic failure of
52        The mechanisms underlying the reduced neointimal proliferation (NP) by intracoronary brachythe
53                                              Neointimal proliferation occurring after vascular or end
54 In this randomized trial, strut coverage and neointimal proliferation of a therapy of bare metal sten
55 et-derived growth factors help stimulate the neointimal proliferation of restenosis after coronary in
56  serial dilation (n = 27) and development of neointimal proliferation or restenosis, or both (n = 9).
57 evious studies established that stents cause neointimal proliferation proportional to injury.
58  cross-sectional area of stenosis comprising neointimal proliferation ranged from 8% to 95%, with a m
59           Two patients developed significant neointimal proliferation requiring valve-in-valve treatm
60 es (intimal hyperplasia, atherosclerosis and neointimal proliferation, sclerosis of arterialized saph
61 is corresponds to a significant reduction in neointimal proliferation seen at 4 weeks without a signi
62 drug-eluting stents has reduced the in-stent neointimal proliferation that causes restenosis and redu
63 consistent with chronic rejection, including neointimal proliferation, transplant vasculopathy, vesse
64                                              Neointimal proliferation was similar between PP and non-
65                    The inhibitory effects on neointimal proliferation were localized to the site of a
66 balloon injury, there is marked reduction of neointimal proliferation when the injured vessel is irra
67 eptors and humoral antibody showed almost no neointimal proliferation, whereas those grafted into mic
68  In contrast, CsA therapy resulted in marked neointimal proliferation, without evidence of vascular a