2020
DOI: 10.5041/rmmj.10403
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Modern Stents: Where Are We Going?

Abstract: Coronary artery stenting is the treatment of choice for patients requiring coronary angioplasty. We describe the major advancements with this technology. There have been significant developments in the design of stents and adjunctive medical therapies. Newer-generation drug-eluting stents (DES) have almost negligible restenosis rates and, when combined with proper anti-platelet treatment and optimal deployment, a low risk of stent thrombosis. The introduction of newer-generation DES with thinner stent struts, … Show more

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Cited by 14 publications
(16 citation statements)
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References 50 publications
(48 reference statements)
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“…[ 6 ]. Efforts were made to change all three components (platform, coating, and drug) of previous-generation stents [ 49 ]. Other materials were proposed for the metallic platform, namely cobalt-chromium and platinum-chromium alloys, as they allowed a reduction in the strut thickness [ 6 ].…”
Section: Evolution Of Cardiovascular Stentsmentioning
confidence: 99%
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“…[ 6 ]. Efforts were made to change all three components (platform, coating, and drug) of previous-generation stents [ 49 ]. Other materials were proposed for the metallic platform, namely cobalt-chromium and platinum-chromium alloys, as they allowed a reduction in the strut thickness [ 6 ].…”
Section: Evolution Of Cardiovascular Stentsmentioning
confidence: 99%
“…Such devices are called drug-filled stents (DFSs) and provide controlled elution from an internal stent lumen, avoiding the inflammation associated with polymers from earlier generations of DESs [ 168 , 169 ]. Early trials were considered successful as DFSs presented promising results, such as minimal neointimal hyperplasia and a high degree of stent strut coverage at one month after implantation in optical coherence tomography [ 49 , 170 ].…”
Section: Stent Optimizationmentioning
confidence: 99%
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“…Zotarolimus is an analog of rapamycin. Sirolimus and its analog could inhibit the proliferation and migration of VSMCs by blocking the cell cycle from the G 1 to S phase 21 , 22 through suppressing rapamycin mammalian targets. These drugs reduce the proliferation of VSMCs but harm the endothelialization of scaffold strut support.…”
Section: Main Textmentioning
confidence: 99%