Coronary healing after stenting: wounds, faith, and the quest for the perfect stent.

After coronary angioplasty, the arteries heal by a series of complex and dynamic mechanisms, which aim to restore vessel architecture and ensure laminar flow. With stent implantation, foreign material is introduced: an additional variable that significantly disturbs the healing process. Ideally, the stent struts should be covered by a perfectly functioning neo-endothelium, but this is not always the case. At different stages, peri-strut components induce inflammation with cell infiltration, fibrin, and clot formation. Patient and plaque factors play a role in healing, but we know from early-generation drug-eluting stents (DES) with permanent polymer (PP) that stent factors are crucial. The absence of strut coverage and increased fibrin formation were shown to be pathological correlates of delayed arterial healing in early-generation DES. Chronic inflammation, eosinophilic infiltrates suggesting a hypersensitivity reaction, strut malapposition, bifurcation stenting, or strut penetration of a necrotic core are other mechanisms of delayed arterial healing, precipitating stent thrombosis (ST). In particular, the lingering polymer has been held accountable for on-going inflammation and local hypersensitivity. The interventional community hoped to decrease chronic inflammation and hypersensitivity by creating more biocompatible and/or bioabsorbable materials.