الفهرس 
Introduction and aim of workOnly 14 pages are availabe for public view
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Abstract
Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by a systemic inflammatory state , involving several organs. Immune cell and soluble inflammatory mediators play a crucial role in RA pathogenesis. These inflammatory processes resemble those in other chronic inflammatory diseases, such as atherosclerosis, depending on a growing body of evidence that atherosclerosis is a chronic inflammatory disease rather than a cholesterol storage disease. Some authers consider atherosclerosis as an extra-articular manifestation of RA.
RA is recognized as an independent risk factor for accelerated atherosclerosis.There are some common features in their pathophysiology.In both, there is vascular inflammation of the vessel wall as manifested by mononuclear cell infiltration, elevated levels of cytokines, C-reactive protein (CRP), tumor necrosis factor a (TNF-α), interleukin (IL)-1, and IL-6 and increased cellular adhesion molecules.
Cigarette smoking, diabetes mellitus, hypertension, dyslipidaemia, obesity and physical inactivity are important risk factors for atherosclerosis which could, if prevalent in RA patients, explain the excess cardiovascular burden in these patients. Antirheumatic treatment utilized in RA , as well as in other inflammatory diseases may be either pro- or antiatherogenic.
Risk assessment for atherosclerosis should begin during childhood through Screening for risk factors. Carotid atherosclerosis can be determined by the assessment of carotid IMT using high-resolution B-mode ultrasound. Great advances have been made in imaging techniques that enable visualization and characterization of plaques.