[The mysteries of lipoprotein (a): a bridge between thrombosis and atheroma]

Nearly 30 years have elapsed since Berg discovered a genetic variant of low density lipoproteins (LDL) which he called lipoprotein (a), abbreviated Lp (a). Lp (a) rapidly appeared as an independent factor of atherosclerosis. Its physico-chemical characteristics are well-known, but this cannot be said of its function, its metabolism and the exact mechanism of its contribution to atherogenesis. The plasma Lp (a) concentration is determined genetically and its seems that few factors can lower it. Owing to its structural analogy with plasminogen, Lp (a) has been suspected to bind fibrin by a competitive mechanism, thereby facilitating thrombosis, a necessary step in the progression of atherosclerosis. However, these results remain controverted, and indeed there is some evidence of a possible interaction between Lp (a) and alpha-2-antiplasmin, a physiological inhibitor of fibrinolysis, an effect that would accentuate fibrinolysis. This paradoxical action of Lp (a) and the various mysteries which still shroud this lipoprotein are perhaps due to the diversity of its isotypes.