Reducing Stent Restenosis with Nanosurface Engineering of Bare Metal Coronary Stents
- Indbinding:
- Paperback
- Udgivet:
- 1. marts 2024
- Størrelse:
- 216x279x9 mm.
- Vægt:
- 417 g.
- 2-4 uger.
- 18. december 2024
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Beskrivelse af Reducing Stent Restenosis with Nanosurface Engineering of Bare Metal Coronary Stents
Coronary artery disease is a largely prevalent category of heart disease, which is responsible for maximum number of mortalities worldwide. Coronary heart diseases mainly atherosclerosis occur when the coronary arteries become hardened and constricted due to the build-up of cholesterol and fatty residues forming a plaque on the vessel wall hampering normal arterial blood flow. Percutaneous coronary angioplasty is usually performed to eliminate stenosis that obstruct blood flow in arteries. During angioplasty, endothelial lining is denuded and the underlying vascular smooth muscle layer gets exposed thereafter. The outcome of this is a highly thrombogenic surface that could lead to formation of clots and re-occlusion of the artery.
Metallic coronary stents are implanted within an atherosclerotic artery to overcome the complications following percutaneous coronary intervention and to restore blood flow. The usage of bare metal coronary stents in angioplasty prevents elastic recoil but is complicated during angioplasty by the problem of restenosis. Restenosis occurs as a response to the endothelial injury, characterized by the recruitment of vascular SMCs to the injured area. These cells proliferate in the intimal space and generate an extracellular matrix that develops over a period of a few months, resulting in in-stent restenosis.
Metallic coronary stents are implanted within an atherosclerotic artery to overcome the complications following percutaneous coronary intervention and to restore blood flow. The usage of bare metal coronary stents in angioplasty prevents elastic recoil but is complicated during angioplasty by the problem of restenosis. Restenosis occurs as a response to the endothelial injury, characterized by the recruitment of vascular SMCs to the injured area. These cells proliferate in the intimal space and generate an extracellular matrix that develops over a period of a few months, resulting in in-stent restenosis.
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