[Ischemic cardiopathy: risk factors and their biological role]

Atherosclerosis is a slowly progressive process, involving the intima and media of large and medium sized arteries and leading to the formation of focal lesions (plaques), containing lipid and fibrous tissue. A classification of atherosclerotic lesions includes: isolated foam cells, fatty streaks, preatheroma, atheroma, and fibroatheroma. Fibroatheroma is an unstable lesion, which might be complicated by intraplaque hemorrhage, rupture and overimposed thrombosis, leading to ischemia. This is the main mechanism responsible for myocardial infarction, stroke, and intermittent claudication. A widely accepted hypothesis for the pathogenesis of atherosclerosis is the response to the injury hypothesis. Endothelial damage or dysfunction is associated with increased arterial wall permeability to plasma constituents and with adhesion of platelets and monocytes, releasing growth factors and chemoattractant molecules. Several factors, in particular hyperlipidemia, arterial hypertension, diabetes mellitus, produce endothelial damage, which is followed by other cellular reactions involved in the atherosclerotic process. Since long time it has been reported that atherosclerosis has some features of the inflammatory processes. The inflammatory response in the arterial system is to some extent different from that occurring in other tissues and organs, such as the liver, kidney, lung or joints. The measurement of metabolic markers of coronary risk (cholesterolemia, homocysteinemia, glycosylated hemoglobin) is useful to estimate the global coronary risk in the individual patient. The demonstration of atherosclerotic plaques by noninvasive ultrasounds provides a sensitive marker of early arterial disease, allowing an objective evaluation of the response of the arterial system to different treatments.