In-Stent Restenosis: Contributions of Inflammatory Responses and Arterial Injury to Neointimal Hyperplasia
- 1 January 1998
- journal article
- Published by Elsevier in Journal of the American College of Cardiology
- Vol. 31 (1), 224-230
- https://doi.org/10.1016/s0735-1097(97)00450-6
Abstract
No abstract availableKeywords
This publication has 26 references indexed in Scilit:
- Acute and chronic effects of self-expanding nitinol stents in porcine coronary arteriesCoronary Artery Disease, 1997
- Small stent size and intimal hyperplasia contribute to restenosis: A volumetric intravascular ultrasound analysisJournal of the American College of Cardiology, 1995
- Luminal loss and site of restenosis after Palmaz-Schatz coronary stent implantationThe American Journal of Cardiology, 1995
- Morphologic characteristics of lesion formation and time course of smooth muscle cell proliferation in a porcine proliferative restenosis modelJournal of the American College of Cardiology, 1994
- Local delivery of dexamethasone for prevention of neointimal proliferation in a rat model of balloon angioplasty.JCI Insight, 1994
- Safety, success, and restenosis after elective coronary implantation of the Palmaz-Schatz stent in 100 patients at a single centerAmerican Heart Journal, 1993
- Coronary intimal proliferation after balloon injury and stenting in swing: An animal model of restenosisJournal of the American College of Cardiology, 1992
- Restenosis and the proportional neointimal response to coronary artery injury: Results in a porcine modelJournal of the American College of Cardiology, 1992
- Interleukin-1 Mitogenic Activity for Fibroblasts and Smooth Muscle Cells Is Due to PDGF-AAScience, 1989
- Interleukin 1: a mitogen for human vascular smooth muscle cells that induces the release of growth-inhibitory prostanoids.JCI Insight, 1988