Coronary Stent Evolution – from Pathology to Clinic

Coronary artery disease (CAD) is the leading cause of morbidity and mortality worldwide. The pathogenesis of CAD relates to the presence of atherosclerotic plaques in coronary arteries, which are today most frequently treated by percutaneous coronary intervention. Initially, plain old balloon angioplasty demonstrated feasibility of dilating atherosclerotic coronary lesions; however, the high rate of acute-vessel recoil, restenosis, and dissection resulted in high acute closure rates and restenosis, which lead to the introduction of coronary stents, improving clinical outcome. However, in-stent restenosis (ISR) became the Achilles heel of bare metal stents owing to sustained neointimal (NI) growth. Drug-eluting stents (DES) were developed to reduce ISR, improving clinical outcomes and reducing the need for target vessel revascularisation. However, late and very late stent thrombosis emerged as a new problem compromising long-term results of DES, along with late catch-up of NI growth. Better materials, especially more biocompatible polymers, contributed to the refinement of DES technology, which substantially reduced stent thrombosis rates in second-generation DES. The idea of eliminating the foreign material after temporary scaffolding using fully bioresorbable scaffolds may hold great potential to revisit the interventional approach of treating CAD. This article will review the evolution of coronary artery intervention from clinical application to pathology, and will discuss current status and potential future directions of the newer therapeutic approaches.