title: Hyperlipoproteinaemia(a) - apheresis and emerging therapies.
abstract: A high level of lipoprotein(a) (Lp(a)) is recognized as an independent and additional cardiovascular risk factor contributing to the risk of early onset and progressive course of cardiovascular disease (CVD). All lipid lowering medications in use mainly lower low density lipoprotein-cholesterol (LDL-c) with no or limited effect on levels of Lp(a). Niacin, the only component lowering Lp(a), is firstly often poorly tolerated and secondly not available anymore in many countries. A level of <50 mg/dl was recommended recently as the cut off level for clinical use and decision making. Since lipoprotein apheresis (LA) lowers not only LDL-c but also Lp(a) significantly, its use is recommended in some countries in very high-risk patients with early or progressive CVD. Retrospective analyses show that regular LA improves the course of CVD. This is supported by a recent prospective observational trial and data of the German Lipoprotein Apheresis Registry. Despite many treatment options, all too often it is not possible to reduce LDL-c levels to target and to reduce Lp(a) levels sustainably at all. Therefore, new drug therapies are awaited. Some of the lipid modifying drugs in development lower Lp(a) to some extent in addition to LDL-c; the only specific approach is the apoprotein(a) antisense oligonucleotide. Currently LA is the standard of care as a last resort treatment in high-risk patients with elevated Lp(a) and severe CVD despite optimal control of all other cardiovascular risk factors.
authors.affiliation: Medizinische Klinik und Poliklinik IV, Klinikum der Universität München, Ziemssenstrasse 1, 80336, München, Germany. anja.vogt@med.uni-muenchen.de.
authors.forename: Anja
authors.initials: A
authors.lastname: Vogt
mesh_terms: D000818:Animals; D015415:Biomarkers / Q000097:blood; D001781:Blood Component Removal; D002318:Cardiovascular Diseases / Q000517:prevention & control*; D008078:Cholesterol, LDL / Q000097:blood; D015316:Genetic Therapy / Q000379:methods*; D006801:Humans; D006951:Hyperlipoproteinemias / Q000097:blood / Q000175:diagnosis / Q000235:genetics / Q000628:therapy*; D000960:Hypolipidemic Agents / Q000627:therapeutic use*; D017270:Lipoprotein(a) / Q000097:blood*; D058990:Molecular Targeted Therapy; D016376:Oligonucleotides, Antisense / Q000627:therapeutic use*; D000091362:PCSK9 Inhibitors; D000071449:Proprotein Convertase 9 / Q000378:metabolism; D012307:Risk Factors; D015842:Serine Proteinase Inhibitors / Q000627:therapeutic use; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers; D008078:Cholesterol, LDL; D000960:Hypolipidemic Agents; D017270:Lipoprotein(a); D016376:Oligonucleotides, Antisense; D000091362:PCSK9 Inhibitors; D015842:Serine Proteinase Inhibitors; C472125:PCSK9 protein, human; D000071449:Proprotein Convertase 9
keywords: Acute coronary syndrome; Apheresis; Atherosclerosis; LDL-cholesterol; Lipoprotein(a); New lipid-lowering therapies