Published: 2 August 2021
Author(s): Felicita Andreotti, Massimo Massetti, Aldo P Maggioni
Section: Commentary

Plasma or serum concentrations of lipoprotein(a) - Lp(a) - are an established marker of risk for atherothrombotic cardiovascular disease (CVD) and for degenerative aortic valve stenosis (1). Mechanistic experiments, prospective observations, and genetic studies strongly support a causal role of Lp(a) for CVD development (1–3). Apolipoprotein(a) is synthesised mostly in the liver and is exclusively bound to low-density lipoprotein (LDL) to form Lp(a). The latter contributes to arterial lipid deposits (4) and can inhibit endogenous fibrinolysis by competing with plasminogen for fibrin binding (3).


Stay informed on our latest news!


This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.