The long-term efficacy of percutaneous coronary interventions is still hampered by restenosis. Restenosis is the result of a complex pathophysiological process, which is thought to be caused by an exaggerated healing response induced by the vascular injury caused by the percutaneous coronary interventions and the implantation of a foreign body (the stent). There is increasing evidence that inflammation plays an important role in the initiation and development of neointimal hyperplasia and subsequent restenosis. Dexamethasone (Decadron, Merck Sharpe and Dohme Ltd) is a glucocorticoid with well-known potent anti-inflammatory and antiproliferative properties. Early studies using either systemic or local delivery of dexamethasone have shown limited beneficial effects on restenosis. The dexamethasone-eluting stent (Dexamet, Abbott Vascular Devices Ltd) is one of the first generation of drug-eluting stents for local drug delivery to prevent restenosis. Preclinical studies demonstrated that implantation of dexamethasone-loaded coronary stents was safe and had a beneficial effect on stent implantation-related inflammation. A pilot trial suggested a beneficial effect on restenosis. Large randomized trials are underway to confirm these findings. This article reviews the potential role of inflammation in the pathogenesis of restenosis and the efficacy of dexamethasone in the prevention of restenosis.
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http://dx.doi.org/10.1586/14779072.2.5.653 | DOI Listing |
EClinicalMedicine
January 2025
Department of Cardiology, Hospital Universitario de La Princesa, IIS-IP, CIBER-CV, Universidad Autónoma Madrid, Madrid, Spain.
ACS Biomater Sci Eng
January 2025
Institute of Biomedical Engineering, University of Toronto, Toronto, Ontario M5S 3E3, Canada.
Restenosis remains a long-standing limitation to effectively maintain functional blood flow after percutaneous transluminal angioplasty (PTA). While the use of drug-coated balloons (DCBs) containing antiproliferative drugs has improved patient outcomes, limited tissue transfer and poor therapeutic targeting capabilities contribute to off-target cytotoxicity, precluding adequate endothelial repair. In this work, a DCB system was designed and tested to achieve defined arterial delivery of an antirestenosis therapeutic candidate, cadherin-2 (N-cadherin) mimetic peptides (NCad), shown to selectively inhibit smooth muscle cell migration and limit intimal thickening in early animal PTA models.
View Article and Find Full Text PDFJ Soc Cardiovasc Angiogr Interv
December 2024
The University of Toledo, Toledo, Ohio.
Background: Atherosclerotic renal artery stenosis (ARAS) may provoke hypertension and/or impaired kidney function. Some patients develop uncontrolled hypertension and deteriorating kidney function despite optimal medical therapy. In these patients, endovascular treatment is an important therapeutic option.
View Article and Find Full Text PDFJACC Adv
January 2025
Lady Davis Institute for Medical Research, Jewish General Hospital/McGill University, Montreal, Quebec, Canada.
Percutaneous coronary intervention (PCI) is a mainstay procedure for the treatment of coronary artery disease. PCI techniques have evolved considerably since the advent of PCI in 1978, and with this evolution in techniques has come changes in the best practices for patient management following PCI. The objective of this review is to provide a comprehensive overview of key considerations in patient management following PCI.
View Article and Find Full Text PDFJ Mater Sci Mater Med
January 2025
Department of Neurology, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, PR China.
In-stent restenosis (ISR) following interventional therapy is a fatal clinical complication. Current evidence indicates that neointimal hyperplasia driven by uncontrolled proliferation of vascular smooth muscle cells (VSMC) is a major cause of restenosis. This implies that inhibiting VSMC proliferation may be an attractive approach for preventing in-stent restenosis.
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