An initial chemical, mechanical or immunological insult induces endothelial dysfunction. This triggers a cascade of inflammatory reactions, in which monocytes, macrophages, T lymphocytes and vascular smooth muscle cells participate. Leukocyte adhesion molecules, cytokines, growth factors and metalloproteinases participate in all stages of atherogenesis. Almost all of the traditional risk factors for atherosclerosis are associated with and participate in the inflammatory process. Many infectious agents, mainly Chlamydia pneumoniae, have been proposed as potential triggers of the cascade. The immune system has been implicated in plaque formation, through the activation of cellular and humoral immunity against innate or microbial heat shock protein 60. Methods of detection of systemic or local plaque inflammation have been developed and research is being conducted on the potential use of anti-inflammatory and antibiotic drugs in atherosclerosis.

conventional AAA surgery is durable so that surveillance, during the first 5 postoperative years, is not justified in terms of cost-effectiveness. The impact of such a dilatation on endovascular AAA repair requires further investigation.

The proposed classification accurately grades the magnitude of intimal hyperplasia after CAS and provides important prognostic information. Diffuse proliferative (type IV) ISR lesions and diabetes are important determinants of long-term outcome after CAS. This classification will facilitate a standardized description of recurrence after CAS and enable early identification of high-risk patients for additional monitoring, treatment, and investigation.

progression of internal carotid artery stenosis occurred in 19% of cases. The mean progression rate in these patients was 15% annually and was correlated with CAD and the ultrasonographic characteristics of the plaque.

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