15289-s-bos

7 113 | Latest developments in the treatment of lipoprotein (a) Because the length of the kringle IV repeat can interfere with Lp(a) measurements, it is difficult to compare studies using different assays for Lp(a) measurement, and this may explain some of the contradictory results between studies. For reliable reproducible studies a gold standard for measuring Lp(a) is needed as is recently discussed by Jacobson[41]. Presently the most evidence based strategy for CVD prevention in patients with increased Lp(a) levels is to lower LDL-C by statin therapy, and for patients with progressive CVD combined with Lp(a)-hyperlipoproteinemia lipoprotein apheresis has proven to reduce CVD events. Key Points: (3-5 bullets in 1 sentence) • Lp(a) is a risk factor of CVD. • It is not clear if lowering Lp(a) lowers CVD risk. • First line treatment of Lp(a)-hyperlipoproteinemia should be statin therapy to decrease CVD risk. Figure 7.2 | Known and proposed mechanisms of compounds that lower Lp(a). ASO Apo-B, anti-sense oligonucleotide for apolipoprotein B (mipomersen); ASO apo(a), anti-sense oligonucleotide for apolipoprotein (a) (ISIS APO(a)Rx); MTP-inhibitors, microsomal triglyceride transport protein inhibitor (Lomitapide); CETP, cholesterol ester transfer protein; PCSK-9, proprotein convertase subtilisin/kexin type 9; Lp(a), lipoprotein (a); TRβ, the β isoform of the thyroid hormone receptor.