Inflammation-Induced Atherosclerosis as a Target for Prevention of Cardiovascular Diseases from Early Life

Atherogenesis starts from the fetal life, and its natural course consists of interrelations between traditional risk factors and inflammatory, immune, and endothelial biomarkers. Even the early-stages of atherosclerotic lesions, i.e. fatty streaks present the features of chronic inflammation. Markers of inflammation are associated with insulin resistance and major atherosclerosis risk factors. Several studies have confirmed a relationship between surrogate markers of future cardiovascular disease with childhood obesity, notably abdominal obesity, as well as with the degree of obesity. Moreover, functional and structural changes are documented in arteries of children with a familial predisposition to atherosclerotic diseases; these changes are associated with clusters of inflammatory factors and markers of oxidation. In addition to the development of atheromatous plaques, inflammation also plays an essential role in the destabilization of artery plaques, and in turn in the occurrence of acute thrombo-embolic disorders. Markers of inflammation can provide predictive clinical information about outcomes of patients with acute coronary syndromes, independent of the extent of myocardial damage. Moreover, serum levels of the inflammatory markers might add prognostic information provided by traditional risk factors. Platelets have an important role in vascular inflammation and atherosclerosis and in the formation of mural thrombi. As lifestyle modification trials have been successful in decreasing endothelial dysfunction and the level of markers of inflammation among children and adolescents, it is suggested that in addition to expanding pharmacological therapies considered for secondary prevention of atherosclerotic diseases aiming to control the inflammatory process, the importance of primordial/primary prevention of atherosclerosis should be underscored.