Impatto del profilo lipidico sulla malattia aterosclerotica in due differenti coorti di pazienti ad alto rischio cardiovascolare

Dyslipidemias are one of the most important cardiovascular risk factors, especially in middle-age subjects and represent a variety of quantitative and/or qualitative lipoprotein abnormalities. According to etiology, dyslipidemias have been identified as primitive and secondary diseases; while primitive dyslipidemias firstly recognize a genetic origin and so called inherited dyslipidemias, secondary dyslipidemias recognize several pathological conditions that affect lipid metabolism (1). According to clinical presentation, we classically recognize five different phenotype based on Fredrickson classification; however, in clinical practice we recognize three principle pathogenic phenotypes: pure hypercholesterolemia [a very increased amount of low-density lipoprotein (LDL) cholesterol], atherogenic dyslipidemia [combined increased amount of LDL cholesterol and tryglicerides (TG)] and pure hypertrygliceridemia (a very increased amount of TG) (2). As previously mentioned, lipid abnormalities are strongly associated with cardiovascular diseases; in particular, several studies have shown that cholesterol-rich apolipoprotein-B-containing lipoprotein have a central role in the pathogenesis of atherosclerosis. Of note, ApoB-lipoproteins up to only approximately 70 nm in diameter [i.e., chylomicron remnants, smaller very low-density lipoproteins (VLDL), intermediate-density lipoproteins (IDL), LDL, and lipoprotein(a)] can efficiently cross an intact endothelium, and among these, the smaller ones pass more readily than the larger ones (3). Moreover, studies in-vivo of the influx and egress of apoB-lipoproteins into and out of the arterial intima have shown that, although the endothelial layer remains intact over most atherosclerotic lesions, its permeability to apoB-lipoproteins becomes abnormally high (4).