Abstract
Coronary stents belong to the most commonly implanted devices worldwide. A number of different types of stent exist, with very different mechanical and biochemical characteristics that influence their interactions with vascular tissues. Inappropriate inflammatory reactions are the major cause of the two major complications that follow implantation of stents in a percentage as high as 5–20%. It is therefore important to understand these reactions and how different they are among different generations of stents.
Highlights
In-stent thrombosis was not a new phenomenon, characterrestenosis, an increase in the incidence of late in-stent thrombosis due to delayed its arterial healing and adverse reactions compromised the safety of these devices istics in patients who hypersensitivity had received implantation of bare metal stents (BMS) where completely different
The immunosuppressive action of the drug eluted might have paradoxically negative effects, inhibiting tissue repair reaction and fibrin removal. These processes might explain the acute presentation of restenosis, as the activation of the thrombotic cascade ensuing from incomplete thrombin removal, not causing occlusive thrombus, activates the recruitment of inflammatory cells such as monocytes, T cells, neutrophils via expression of adhesion molecules (ICAM, VCAM, intercellular, and vascular adhesion molecules), production of chemoattractant molecules (MCP-1 or monocyte chemoattractant protein-1, Interleukin (IL)-8) by endothelial, and smooth muscle cells and the production of growth factor such as PDGF, bFGF, TGF-beta, IGF, VEGF (vascular endothelial growth factor, and thrombin (Table 1, Figure 3)
Given the high mortality associlipid neointima was shown in 40% of the cases of in-stent restenosis, calcific lesions were ated with stent thrombosis, further understanding itsobserved mechanisms its reported in a similar incidence, andprogress thin-cap in fibroatheromas was in upand to 15%
Summary
With several million implantations per year, coronary artery stents are among the most commonly used devices for the treatment of a disease that still represents the major cause of mortality and morbidity worldwide [1]. DES failure remains a problem that affects, depending on a number of factors, up to 20% of the devices implanted [1]. Procedural and plaque factors obviously play an important role in stent failure [9]; it is clear from observations in both BMS and early-generation DES that the biological reactions induced by the implantation trauma and by the exposure to the stent components are crucial. While the multifactorial nature of stent failure is acknowledged [13], the present review will focus on the biological responses that follow stent implantation, and how these may lead to stent failure across the different generations of stents
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