Neoatherosclerosis after Drug‐Eluting Stent Implantation: Roles and Mechanisms

Abstract

In-stent neoatherosclerosis (NA), characterized by a relatively thin fibrous cap and large volume of yellow-lipid accumulation after drug-eluting stents (DES) implantation, has attracted much attention owing to its close relationship with late complications, such as revascularization and late stent thrombosis (ST). Accumulating evidence has demonstrated that more than one-third of patients with first-generation DES present with NA. Even in the advent of second-generation DES, NA still occurs. It is indicated that endothelial dysfunction induced by DES plays a critical role in neoatherosclerotic development. Upregulation of reactive oxygen species (ROS) induced by DES implantation significantly affects endothelial cells healing and functioning, therefore rendering NA formation. In light of the role of ROS in suppression of endothelial healing, combining antioxidant therapies with stenting technology may facilitate reestablishing a functioning endothelium to improve clinical outcome for patients with stenting.

<p>The Predictive Value of Monocyte Count to High-Density Lipoprotein Cholesterol Ratio in Restenosis After Drug-Eluting Stent Implantation</p>

“… 31 After DES implantation, endothelial dysfunction would cause reduced antithrombotic molecule expression and decreased production of nitric oxide, resulting in the penetration of high levels of lipoprotein and proteoglycans into the subendothelial space, which initializes the development of atherosclerosis. 38 Increased MHR was associated with endothelial dysfunction. This could partially explain the predictive value of MHR in restenosis after DES implantation.…”

Comparison of drug-eluting stents vs. drug-coated balloon after rotational atherectomy for severely calcified lesions of nonsmall vessels

“…In addition, when the stent is not well expanded because of insufficient lesion preparation, the risk for stent thrombosis increases [27]. Another issue would be the possibility of DES inducing chronic vessel wall inflammation because of the existence of the polymer and the delayed intimal healing, which can lead to neoatherosclerosis [28][29][30]. Neoatherosclerosis has been reported to be associated with subacute stent thrombosis, late stent thrombosis, and very late stent thrombosis.…”

Vascular Wall Reactions to Coronary Stents—Clinical Implications for Stent Failure

“…In terms of prevention, statins have been shown in small studies to stabilize neointima and prevent the appearance of neoatherosclerosis [ 74 ]. In contrast, although promising, an effect of antioxidants has been proposed but remains to be demonstrated [ 75 ].…”