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).
