Evolution in metallic coronary stent design has been associated with a progressive decline in major adverse cardiovascular events, including stent thrombosis.1 Novel metal alloy composition, reduced strut thickness, enhanced platform flexibility and conformability, and improved polymer biocompatibility and/or bioresorption have contributed to improved outcomes. However, concerns regarding incomplete stent healing, neoatherosclerosis, and stent fracture persist, because beyond 1 year after implantation, even the “best-in-class” second-generation drug-eluting stents (DESs) have been associated with a 2% to 4% annual incidence of target lesion failure (TLF) events (ie, a composite of cardiac death, target vessel myocardial infarction, or ischemia-driven target lesion revascularization), which is similar to rates observed after implantation of bare metal stents or first-generation DESs in published2-9 and ongoing studies (Phil Zhang, MD, MS; written communication; November 17, 2016) (Figure). The pathogenesis of these very late events may relate to the common presence of a metallic prosthesis and/or permanent polymer that physically distorts the vessel and serves as a nidus for chronic inflammation, neoatherosclerosis, thrombosis, and strut fracture.
Kereiakes DJ. The TWENTE Trial in Perspective: Stents and Stent Trials in Evolution. JAMA Cardiol. 2017;2(3):235–237. doi:10.1001/jamacardio.2016.5208
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