[The predictive value of apolipoproteins in atheroma]

During the last three decades studies on the pathogenesis of atheroma have highlighted successively lipids, lipoproteins and apolipoproteins. The undisputed role of cholesterol has been widened by taking into account the nature and composition of lipoproteins in addition to their plasma levels. The concept of relative atherogenicity of lipoproteins and a better understanding of the role played by apolipoproteins have thrown more light on the formation of atheromatous plaques in the absence of hyperlipidaemia. On this point must be mentioned studies that associate LDL apo-B with coronary risk, and apo-A1 abnormalities which predispose to atheromatosis. More recently, attention has been focused on apo-E as a genetic factor that may interact with the environment to modulate blood cholesterol and triglyceride levels and secondarily influence individual tendencies to develop atherosclerosis. The three major forms of apo-E (E2, E3, E4) are encoded by three alleles (E2, E3, E4) and act on the same locus of chromosome 19 to determine 6 apo-E phenotypes in the population. We now know that the E2 allele is associated with lower levels, and the E4 allele with higher levels, of LDL-cholesterol than the E3 allele. E4 is a risk factor which predisposes to coronary atherosclerosis. It follows that the E2 allele should have protective powers, provided no other factor, ecological or hereditary, intervenes to foster the development of an atherogenic hypertriglyceridaemia.