Multiple Approaches to Inhibit Restenosis
After Percutaneous Coronary Interventions
By Xiaoshun Liu
Leuven University Press
173 pages, Illustrated, 6 ¼" x 9 ½"
$110.00 Paper Original
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.
Acta Biomedica Lovaniensia, No. 330
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