Abstract
Several randomized and observational studies have reported steady increase in cumulative incidence of late and very late ST (LST/VLST) following first-generation drug-eluting stents (DES: sirolimus-(SES) and paclitaxel-(PES)) up to 5 years. Pathologic studies have identified uncovered struts as the primary substrate responsible for LST/VLST following DES, where delayed arterial healing is associated with stent struts penetrating into the necrotic core, long/overlapping stents, and bifurcation stenting especially in flow divider region. Grade V stent fracture also induces LST/VLST and restenosis. Hypersensitivity reaction is exclusive to SES as an etiology of LST/VLST, whereas malapposition secondary to excessive fibrin deposition is associated with PES. Uncovered struts can be identified in SES and PES with duration of implant beyond 12 months, particularly in stents placed for “off-label” indications. Neoatherosclerosis is another important contributing factor for VLST in DES and bare metal stents (BMS); however, DES shows rapid and more frequent development of neoatherosclerosis than BMS. Future pathologic studies should address the long-term safety of newer generation DES including zotarolimus- and everolimus-eluting stents in terms of the improvement in reendothelialization, decreased inflammation and fibrin deposition as well as a lower incidence of stent fracture-related adverse events, and reduced neoatherosclerosis, which likely contribute to the decreased risk of LST/VLST and better patient outcomes.
Highlights
Percutaneous coronary interventions (PCI) involving stenting are the most widely performed procedures for the treatment of symptomatic coronary disease [1]
Concern still exists about the long-term safety of Drugeluting stents (DES) technology since several randomized and observational studies have shown a steady increase in cumulative incidence of very late stent thrombosis (ST) associated with first-generation DES (sirolimus-(SES) and paclitaxel-eluting stents (PES)) up to 5 years [5,6,7,8,9], while pathologic studies have suggested delayed re-endothelialization as an important substrate [10, 11]
Because dramatic hemodynamic alternations occur at branch points within the arterial tree, coronary bifurcations are extraordinarily susceptible to atherosclerosis
Summary
Percutaneous coronary interventions (PCI) involving stenting are the most widely performed procedures for the treatment of symptomatic coronary disease [1]. Drugeluting stents (DES) have dramatically reduced restenosis rates and have become the standard of care for the treatment of atherosclerotic coronary artery disease [2,3,4]. The development of atherosclerotic changes within the neointima (neoatherosclerosis) has been identified as another important mechanism of very late ST [12]. This paper will focus on the pathologic mechanisms of late and very late ST following first-generation DES implantation, the differential vascular response between SES and PES, and characteristics of neoatherosclerosis following first-generation DES as compared to bare metal stents (BMS) in human coronary arteries
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