Edge vascular response after percutaneous coronary intervention

The concept of edge vascular response (EVR) was first introduced with bare-metal stents and later with radioactive stents of various activity levels. Although radioactive stents reduced intra-stent neointimal hyperplasia and thereby the incidence of in-stent restenosis in a dose-dependent manner, tissue proliferation at the non-irradiated proximal and distal stent edges resulted in the failure of this invasive treatment. The advent of first- and second-generation drug-eluting stents (DES) reduced in-stent restenosis to approximately 5% to 10%, depending on the lesion subset and DES type. When in-segment restenosis (stent and 5-mm proximal and distal margins) occurred, it was most commonly focal and located at the proximal edge. In addition, stent thrombosis, the other main contributing factor for DES failure, seemed in part to be associated with residual plaque presence and underlying tissue composition at the landing zone of the implanted device, particularly if landed in a necrotic core rich milieu. More recently, the introduction of bioresorbable scaffolds for the treatment of coronary artery disease has prompted the re-evaluation of the EVR. This has recently been assessed up to 2-years after implantation of the Absorb bioresorbable vascular scaffold (Abbott Vascular, Santa Clara, California). In general, the EVR consists of a focal but significant proximal lumen loss that in a few instances necessitates target lesion revascularization of a flow-limiting edge stenosis. Herein, we provide an overview of the in vivo evaluation of the EVR with intravascular ultrasound, virtual histology intravascular ultrasound, and the more recently developed optical coherence tomography. Our objective is to highlight the clinical importance of the EVR as a predisposing and contributing factor to device failure with either baremetal stents, DES, or bioresorbable scaffolds.

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