title: Biology and treatment of recurrent carotid stenosis.
abstract: The benefit of carotid revascularization in long term stroke prevention is hampered by the occurrence of restenosis at the site of surgery, which is associated with a modestly increased risk of stroke. Preventing restenosis is an important part in the overall treatment and prevention of stroke in patients with carotid artery disease. The site of recurrent stenosis is primarily situated at the ends of, or within the confines of the original endarterectomy site and the suture lines. Several etiological factors but also surgical technique play a key role in the development of carotid recurrent stenosis. However, the exact pathophysiology of recurrent disease is not fully understood. The morphogenesis of recurrent lesions is a process of ongoing thrombogenesis beginning immediately after blood flow is restored across the endarterectomized surface. The early lesion is subsequently formed as the thrombus organizes and smooth muscle cell ingrow occurs, creating a supposed morphologic distinction between early (within 2 years of CEA) and late (over 2 years) recurrent carotid disease. Further, plaque composition at primary CEA is an independent predictor of restenosis after CEA and dissection of a lipid-rich and macrophage infiltrated plaque is associated with a reduced risk of stenosis. CEA of stable atherosclerotic plaques has been associated with an increased risk for restenosis. In addition, stable atherosclerotic plaque characteristics with low macrophage content and small lipid core size are associated with an increased incidence of restenosis compared with unstable inflammatory lesions. The implication of these findings is that macrophage infiltration and lipid core size are the plaque characteristics that should be targeted with noninvasive plaque imaging to assess the risk of patients with recurrent carotid stenosis to become symptomatic. Furthermore, the longer the delay from stroke until revascularization, the more the lesion stabilizes and the higher the risk for restenosis. Thus, operating on symptomatic patients within a few weeks after the index event could potentially reduce the risk of restenosis. The optimal treatment strategy for restenosis has yet to be defined. Optimally, one would strive to a "tailor-made" treatment comprising of best medical therapy, surgery or CAS including regular follow-up. With the ongoing developments and insights in histological plaque characterization this tailor-made treatment might be available in the near future, thereby reducing the risk of, or maybe even avoiding the development of restenosis.
authors.affiliation: Department of Vascular Surgery, University Medical Center Utrecht, Utrecht, The Netherlands. G.J.deBorst-2@umcutrecht.nl
authors.forename: G J
authors.initials: GJ
authors.lastname: De Borst
authors.forename: F
authors.initials: F
authors.lastname: Moll
mesh_terms: D050197:Atherosclerosis / Q000150:complications*; D016893:Carotid Stenosis / Q000209:etiology / Q000473:pathology / Q000601:surgery; D016894:Endarterectomy, Carotid / Q000379:methods*; D006801:Humans; D008264:Macrophages / Q000473:pathology; D012008:Recurrence; D012307:Risk Factors