The role of vascular inflammation in the development of in-stent restenosis is mostly triggered by an endothelial ­disruption and abrasion caused by balloon inflation and stent placement. This vascular injury initiates the release of ­several mediators leading to adhesion of thrombocytes, neutrophils, and monocytes. These cells, for their part, release vasoactive, thrombogenic, lymphocytic, and mitogenic substances, which lead to vasoconstriction, vascular remodeling, neointimal proliferation, thrombosis, and inflammation, finally resulting in in-stent restenosis [9, 10].

In their study on the mechanisms of carotid artery stent restenosis by intravascular ultrasound study, Clark et al. considered that procedural factors during carotid artery stenting could play an important role in the development of in-stent restenosis. They concluded that the wider the stent was, the less likely the occurrence of in-stent restenosis during follow-up because a stent with a larger diameter results in a reduced flow velocity, fewer turbulences, and thus less frequent in-stent restenosis [11].

Schillinger et al., analyzing the importance of periinterventional serum levels of acute-phase reactants in 6-month restenosis after stent implantation in the carotid artery, observed that within the first 48 h after intervention, a significant increase of C-reactive protein and serum amyloid A levels was found in patients with and without restenosis. However, patients with 6-month restenosis had significantly higher postintervention serum levels of acute-phase reactants compared with the levels in patients without restenosis, and they had a significantly higher relative increase of C-reactive protein and serum amyloid A levels during the first 48 h after intervention (Table 6.2) [12, 13].