Carotid stenosis: aspects on progression, stabilization and follow-up
Abstract: Cardiovascular (CV) atherosclerotic diseases are the leading cause of death in Western nations. The presence of a carotid plaque, the degree of carotid stenosis as well as the rate of progression of carotid disease has been shown to be independent predictive factors for future ischemic events. The aim of this thesis was to detect clinical, sonographic and serologic patterns that could aid in identifying patients at risk of progression of atherosclerosis and the development of symptoms; the thesis also focuses on the role of current medical treatments in atherogenesis and plaque composition. In this thesis we demonstrate a high incidence of symptoms and disease progression contralateral to the carotid artery treated by endarterectomy, particularly in the presence of a moderate (i.e. >60%) stenosis degree at baseline. As evidence of possible protective effects on atherogenesis by beta-blockers grows, we decided to analyse plaque content of two factors involved in regulating the inflammatory process leading to the atherogenesis. Focusing on the soluble urokinase plasminogen activator receptor and the lipoprotein associated phospholipase A2 we detected a lower level of inflammation in patients on long-term treatment with beta-blockers. These findings were in line with a higher echogenicity of carotid plaques as evaluated using grey-scale median (GSM) analysis in patients on long-term treatment with beta-blockers. Finally, assessing possible preoperative plaque and serological markers we observed higher risk for postoperative stroke in patients with lower elastin plaque content and a higher risk of CV death in patients with lower circulating titers of antibodies of type IgG against the epitope p210 of the apolipoprotein B100 of LDL In conclusion, this thesis underlines that progression of contralateral disease after unilateral CEA occurs frequently. Moreover, it reinforces the possible atheroprotective effects of beta-blockers beyond the purely hemodynamic and the need to monitor the effects with non-invasive diagnostic tools. It also supports the concept that ECM proteins are important for plaque stability and suggest the potential of the assessment of Ab against oxLDL as a supplemental marker of generalised atherosclerosis. Further studies are needed to better identify high risk populations that are in need of more intensive secondary prevention
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