15289-s-bos

12 | Chapter 1 Non-traditional risk factors CVD risk predictionmight be improvedbymeasuringnon-traditional risk factors. Among these is lipoprotein (a), or Lp(a). Lp(a) was discovered in 1963 by Kare Berg and is a LDL- like proteinwith an apo(a)moiety. Lp(a) levels are predominantly genetically determined (39), and inversely correlated with the length of the apo(a) moiety. The length of apo(a) is mainly determined by kringle IV type 2 repeats (figure 1). Lp(a) concentration and kringle IV type 2 repeat number are independent risk factors for CVD in the general population, and FH (12,40). In FH, women clearly have a lower CVD burden than men (41-43). but female FH patients, whose Lp(a) levels are elevated, might be susceptible of premature CVD (44). The relationship between Lp(a) and CVD risk may be effected true the binding of oxidized phospholipids which may cause instability of atherosclerotic plaques through increased inflammation (45). Other pathophysiological mechanisms in which Lp(a) could play a role are wound healing and fibrinolysis pathways, however how these pathways play a role in the atherosclerosis pathophysiology is unknown (39,46). Unfortunately, there is a poor Lp(a) lowering responds to statins and other lipid lowering medication. Novel therapeutic agents are currently being developed who are aimed to specifically lower Lp(a) levels but to date no therapy is registered that can exclusively lower Lp(a) levels. Figure 1 | Schematical structure of Lipoprotein (a).