Multiple Approaches to Inhibit Restenosis After Percutaneous Coronary Interventions
This is a Ph.D. dissertation. Restenosis occurs in 10-50% of patients after PCI, thus remaining a major challenge. Restenosis after PCI is a complex, multifactorial, overlapping wound healing process involving a cascade of cellular and molecular events including platelet activation, inflammatory cell infiltration, smooth muscle cell proliferation, migration and extracellular matrix production. Recent evidence shows that inflammation, matrix metalloproteinases and free oxygen radicals all play a critical role in the restenosis process. Different approaches to prevent restenosis after PCI were studied in this work. Restenosis has been remarkably reduced in the last decade with the introduction of stents. Stents have been optimized regarding their mechanical features, allowing for scaffolding of the plaque and producing an optimal coronary lumen at the end of the procedure. By their metallic nature however, they cause prolonged and chronic inflammation in the vessel wall. Therefore, the long term efficacy remains a concern. In the first study, the author evaluated the long-term follow-up of patients that underwent bare metal stent implantation. The long-term efficacy of this stent was established, and the major adverse cardiac events (MACE) during the long-term follow-up were mainly caused by progression of lesions in other vessels. This study confirmed that implantation of a bare metal stent in an effective treatment modality of atherosclerotic coronary disease. However, in-stent restenosis still results in a failure of this treatment in about 30% of the patients, mostly occurring within the first 6 months.
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The effect of reduced blood flow on the coronary wall temperature A study
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Acute gain adverse cardiac events angiographic angiographic follow-up antioxidant arterial injury arterial wall temperature atherosclerotic balloon angioplasty balloon injury batimastat binary restenosis rate biocompatibility blood CABG Cardiovasc Circulation clinical follow-up coronary angioplasty coronary artery disease coronary stent coronary wall temperature dexamethasone diameter stenosis direct stenting drug delivery drug eluting stents effect endothelial evaluate extracellular matrix flow in-stent restenosis inflammation inflammatory cells inflammatory response inhibit intravascular late loss lesion long-term Loss index lumen macrophages major adverse cardiac matrix metalloproteinases minimal luminal diameter MMPs months follow-up myocardial infarction neointimal formation neointimal hyperplasia oxygen paclitaxel patients PC coated percutaneous coronary interventions pigs pilot trial plaque Probucol procedure proliferation PTCA QCA data reduced reference vessel diameter restenosis role Scheerder segment sensors smooth muscle cells stenosis stent coating stent filament stent group stent implantation Table Tempamine coated stents thermography thermography catheter thrombosis unstable angina vascular vessel wall vivo