2002
DOI: 10.2165/00129784-200202030-00001
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Can Angiotensin Receptor Antagonists Prevent Restenosis After Stent Placement?

Abstract: Restenosis rates after coronary stent implantation in complex lesions are between 30 and 50%. Neointimal hyperplasia promoted by complex interaction between cellular and acellular elements, such as cytokines and growth factors, is thought to be the primary process responsible for restenosis. The risk of in-stent restenosis is increased in patients with a history of restenosis after percutaneous transluminal coronary angioplasty, in long lesions, in total occlusions, in patients with diabetes mellitus, in small… Show more

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Cited by 9 publications
(1 citation statement)
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“…In-stent restenosis results from proliferation and migration of smooth muscle cells that cause an increase in extracellular matrix production and neo-intimal hyperplasia [8][9][10][11]. Neointimal hyperplasia and in-stent restenosis involves complex interactions between cellular and acellular elements, such as cytokines and growth factors [6,[12][13][14][15]. Compared with bare metal stents (BMS) [16], the time frame to restenosis after implantation of drug-eluting stents (DES) may be longer as the antiproliferative drugs delay the biologic response to injury [17].…”
Section: Introductionmentioning
confidence: 99%
“…In-stent restenosis results from proliferation and migration of smooth muscle cells that cause an increase in extracellular matrix production and neo-intimal hyperplasia [8][9][10][11]. Neointimal hyperplasia and in-stent restenosis involves complex interactions between cellular and acellular elements, such as cytokines and growth factors [6,[12][13][14][15]. Compared with bare metal stents (BMS) [16], the time frame to restenosis after implantation of drug-eluting stents (DES) may be longer as the antiproliferative drugs delay the biologic response to injury [17].…”
Section: Introductionmentioning
confidence: 99%