Shedding light on scaffold vascular response.

SEE PAGE 1361 A rterial healing or vascular response after percutaneous coronary interventions (PCIs) describes a reparative mechanism to acute procedural injury attributed to balloon barotrauma and/or stent deployment itself (2,3). Early vascular responses after bare metal stent or drug-eluting stent (DES) placement are driven by fibrinand plateletrich thrombi depositions and migration of smooth muscle cells. In contrast, late vascular responses to DES are primarily attributed to delayed strut healing subsequent to drug toxicity, polymer-induced inflammation followed by hypersensitivity reactions, and in-stent neoatherosclerosis leading to late target lesion revascularization (TLR) or late stent thrombosis. Further technological innovations in the quest for optimal coronary stenting (4) led to the development of bioresorbable scaffolds (BRSs) made of biodegradable polymers or biocorrodible metals. The property of transient vessel scaffolding (w6 months) and complete resorption over a period of 3 years with subsequent restoration of vessel anatomy (form), physiology (function), and local hemodynamic milieu promises to eliminate or reduce the risk of late vascular responses (5,6). Bench work in experimental porcine models after Absorb Bioresorbable Vascular Scaffold (BVS) (Abbott Vascular, Santa Clara, California) deployment has