Non Invasive Assessment of Cardiovascular Risk Profile: The Role of the Ultrasound Markers

2012 
Recent studies showed the key role played by inflammation and immune responses in development, progression, and rupture of atherosclerotic plaque (2,3,4). The presence of an immune reaction and/or infective antigens as potential triggers of atherogenesis (5,6) makes atherosclerosis be considered as an autoimmune disease in which the adaptive immune system is targeted against self-antigens modified by biochemical factors such as oxidative stress and hypercholesterolemia (7). These give rise to plaque birth (8,9) and the inflammatory status of the plaque makes the lesions unstable, inducing their abruption and acute thrombotic obstruction. Therefore, it induces impairment in endothelial function in bioactive antiatherogenic or proatherogenic molecules production (10), although other factors could increase such an imbalance: age (11), sex (12), hypertension (13), obesity (14), smoking (15), dyslipidemia (16), diabetes (17), all able to increase oxidative stress and vascular inflammation (18), morphological wall alterations and subsequently progression of atheromatous lesions.
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