Plasma Lp(a) profile in patients with familial hypercholesterolemia treated by dextransulfate cellulose LDL-apheresis and plasma-exchange

Lipoprotein (a) – Lp(a) – is a glycoprotein containing Apo B100 and Apo(a). It was suggested that plasma Lp(a) concentration is an independent predictor of vascular disease and coronary heart disease risk (1, 2). It is also demonstrated that LDL, the most atherogenic lipoprotein in plasma, contains Apo B100 and is associated with high incidence of coronary heart disease. Lp(a) shares a close structural homology with plasminogen, and is similarly involved in the fibrinolytic system. Both plasma Lp(a) and plasminogen levels are genetically controlled by gene loci located on chromosome 6. Thus, it was thought that Lp(a) may be both involved in thrombogenesis and atherogenesis on the basis of its structure and properties.Interestingly, a reduction of Lp(a) below 30 mg/dl - higher concentrations are considered to be pathologic -, is substantially not allowed by drugs. Thus, an alternative therapeutic option can be plasmapheresis, and in particular LDL apheresis / Lp(a) apheresis (8). The aim of this randomized, controlled, single-center study was to investigate whether LDL apheresis / Lp(a) apheresis and plasma-exchange can lower to the target plasma Lp(a) in patients with genetically determined hyperLp(a)lipoproteinemia associated to familial hypercholesterolemia in a combined form.