1999
DOI: 10.1097/00045415-199907000-00014
|View full text |Cite
|
Sign up to set email alerts
|

Prevention of Coronary Restenosis

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1
1

Citation Types

1
42
0
3

Year Published

2002
2002
2007
2007

Publication Types

Select...
9

Relationship

0
9

Authors

Journals

citations
Cited by 57 publications
(46 citation statements)
references
References 0 publications
1
42
0
3
Order By: Relevance
“…8 Furthermore, inflammatory and immune responses, as well as apoptotic processes have also been implicated [9][10][11] in the underlying disease mechanism. Our findings represent the first direct clinical-epidemiological evidence for the actual relevance of these mechanisms by highlighting molecular variants of seven genes that belong to the postulated pathogenic pathways (apolipoprotein CIII, cystathionine beta-synthase, monocyte differentiation antigen CD14, endothelial nitric oxide synthase 3, tumor suppressor protein p53, p53-associated protein, and tumor necrosis factor receptor type 1) and that we found to be significantly associated with the incidence of restenosis.…”
Section: Discussionmentioning
confidence: 99%
“…8 Furthermore, inflammatory and immune responses, as well as apoptotic processes have also been implicated [9][10][11] in the underlying disease mechanism. Our findings represent the first direct clinical-epidemiological evidence for the actual relevance of these mechanisms by highlighting molecular variants of seven genes that belong to the postulated pathogenic pathways (apolipoprotein CIII, cystathionine beta-synthase, monocyte differentiation antigen CD14, endothelial nitric oxide synthase 3, tumor suppressor protein p53, p53-associated protein, and tumor necrosis factor receptor type 1) and that we found to be significantly associated with the incidence of restenosis.…”
Section: Discussionmentioning
confidence: 99%
“…In light of our finding that patients with the II genotype did not have a beneficial effect of the quinapril treatment, this favorable effect on restenosis was achieved by inhibition of the renin-angiotensin system. Given that multiple factors are associated with the development of neointimal hyperplasia, 6 sufficient protection from restenosis could not be obtained by the administration of an ACE inhibitor only. To our knowledge, the PARIS Study by Meurice et al is the only other published study on the effect of quinapril on in-stent restenosis.…”
Section: Control Groupmentioning
confidence: 99%
“…The mechanism by which restenosis occurs after coronary artery intervention may differ between conventional balloon angioplasty and intracoronary stent implantation. 12 In-stent restenosis results predominantly from neointimal hyperplasia consisting of smooth muscle cell migration and extracellular matrix formation, 6 not from late recoil. The present study was designed to evaluate the relationship between the effect of quinapril, a tissue-specific ACE inhibitor with high affinity 13 and an insertion/deletion (I/D) polymorphism of the ACE gene on the prevention of restenosis after coronary stent implantation.…”
mentioning
confidence: 99%
“…Placement of 32 P wires markedly reduced subsequent restenosis rates in a recently reported randomised controlled trial, and extensive investigation continues in this field. 1,2 In ophthalmology, the role of both external beam radiation and brachytherapy in the management of age-related macular degeneration (ARMD) and the role of beta radiation in trabeculectomy are currently under evaluation. It is therefore appropriate to revisit the role of beta radiation in ophthalmology.…”
Section: Introductionmentioning
confidence: 99%