Anwer Habib,1 Hiroyoshi Mori,2 Kazuyuki Yahagi,2 *Aloke V. Finn2,3
1. Parkview Heart Institute, Fort Wayne, Indiana, USA
2. CVPath Institute Inc., Gaithersburg, Maryland, USA
3. University of Maryland School of Medicine, Baltimore, Maryland, USA
*Correspondence to firstname.lastname@example.org
Disclosure: The authors have declared no conflicts of interest.
Received: 02.06.16 Accepted: 28.10.16
Citation: EMJ. 2017;2:60-68.
Cardiovascular disease is a leading cause of death and disability worldwide. Current treatment strategies aimed at treating the consequences of coronary artery disease have embraced both optimal medical therapy and catheter based percutaneous coronary intervention with drug-eluting stents (DES). Current-generation DES elute predominantly mammalian target of rapamycin (mTOR) inhibitors, which act primarily as a cytostatic agent that retards vascular smooth muscle cell proliferation and migration; this occurs in response to injury and thus prevents restenosis. While DES have reduced restenosis, the use of first-generation DES was associated with an increased risk of late stent thrombosis and accelerated neointimal atherosclerosis (i.e. neoatherosclerosis), both major contributors to late stent failure. The underlying substrate of late DES failure is likely related to vascular endothelial dysfunction, which occurs after DES implantation. Initial concerns with first-generation DES have led to improvements in stent design, polymer load and biocompatibility, and pharmacologic agents, all of which have helped to improve healing responses, lessen late stent failure, and result in an overall improved safety profile. The armamentarium of DES has expanded from the current-generation durable polymer DES to bioresorbable polymer DES, polymer-free DES, and lastly totally bioresorbable vascular scaffolds with a goal of improving vascular responses and endothelial function while preserving anti-restenotic efficacy. We will review these contemporary DES in relation to their short and long-term effects on vascular biocompatibility and healing responses.
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