Abstract
With the development of drug-eluting stents, intimal re-endothelialisation is significantly inhibited by antiproliferative drugs, and stent restenosis transforms from smooth muscle cell proliferation to neoatherosclerosis (NA). As a result of the development of intravascular imaging technology, the incidence and characteristics of NA can be explored in vivo, with some progress made in illustrating the mechanisms of NA. Experimental studies have shed light on the molecular characteristics of NA. More critically, sufficient evidence proves NA as a significant cause of late stent failure. Treatments for NA are still being explored. In this review, we summarise the histopathological characteristics of different types of stent NA, explore the potential relationship of NA with native atherosclerosis and discuss the clinical significance of NA in late stent failure and the promising present and future prevention and treatment strategies.