Abstract

Advances in basic and clinical sciences over the past decades have substantially improved our understanding of inflammatory and thrombotic pathways implicated in atherogenesis. It is now clear that multiple genetic and environmental factors interfere with the natural course of atherosclerosis in early life and lead toward premature clinical manifestations in the adolescence and in the middle age. Importantly, various molecular and cellular agents with pro-atherogenic properties have been identified, and similarities have been found between atherosclerotic vascular disease, chronic inflammatory disorders and cancer [1, 2], all of which can be viewed as diseases of premature aging. Identification of common pathways of aging, and premature morbidity and mortality in these disorders has prompted the search for therapeutic means with universal beneficial effects. In fact, over the past decade, we have witnessed a strong emphasis on anti-inflammatory effects of cardiovascular drugs, such as angiotensin converting enzyme inhibitors (ACE-I), statins, aspirin, which are believed to reduce incidence of vascular events by acting not only on their primary therapeutic targets but also on the inflammatory process [3].

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