title: Emerging Therapeutic Options for Lowering of Lipoprotein(a): Implications for Prevention of Cardiovascular Disease.
abstract: OBJECTIVE
  Elevated plasma concentrations of lipoprotein(a) (Lp(a)) are an independent and causal risk factor for cardiovascular diseases including coronary artery disease, ischemic stroke, and calcific aortic valve stenosis. This review summarizes the rationale for Lp(a) lowering and surveys relevant clinical trial data using a variety of agents capable of lowering Lp(a).
  
  
  RESULTS
  Contemporary guidelines and recommendations outline populations of patients who should be screened for elevated Lp(a) and who might benefit from Lp(a) lowering. Therapies including drugs and apheresis have been described that lower Lp(a) levels modestly (∼20 %) to dramatically (∼80 %). Existing therapies that lower Lp(a) also have beneficial effects on other aspects of the lipid profile, with the exception of Lp(a)-specific apheresis and an antisense oligonucleotide that targets the mRNA encoding apolipoprotein(a). No clinical trials conducted to date have managed to answer the key question of whether Lp(a) lowering confers a benefit in terms of ameliorating cardiovascular risk, although additional outcome trials of therapies that lower Lp(a) are ongoing. It is more likely, however, that Lp(a)-specific agents will provide the most appropriate approach for addressing this question.
authors.affiliation: Department of Biochemistry, Room 4245A Robarts Research Institute, University of Western Ontario, 1151 Richmond Street North, London, ON, Canada, N6A 5B7. mboffa@uwo.ca.
authors.forename: Michael B
authors.initials: MB
authors.lastname: Boffa
mesh_terms: D000818:Animals; D001781:Blood Component Removal; D002318:Cardiovascular Diseases / Q000517:prevention & control*; D006801:Humans; D017270:Lipoprotein(a) / Q000235:genetics / Q000378:metabolism*; D016376:Oligonucleotides, Antisense / Q000627:therapeutic use; D012307:Risk Factors
chemical_list: D017270:Lipoprotein(a); D016376:Oligonucleotides, Antisense
keywords: Anacetrapib; Antisense oligonucleotides; Apolipoprotein(a); Cardiovascular disease; Drug therapy; Lipoprotein apheresis; Lipoprotein(a); Niacin; PCSK9