Michael B Boffa1. 1. Department of Biochemistry, Room 4245A Robarts Research Institute, University of Western Ontario, 1151 Richmond Street North, London, ON, Canada, N6A 5B7. mboffa@uwo.ca.
Abstract
PURPOSE OF REVIEW: 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). RECENT FINDINGS: 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.
PURPOSE OF REVIEW: 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). RECENT FINDINGS: 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: Gregor Leibundgut; Corey Scipione; Huiyong Yin; Matthias Schneider; Michael B Boffa; Simone Green; Xiaohong Yang; Edward Dennis; Joseph L Witztum; Marlys L Koschinsky; Sotirios Tsimikas Journal: J Lipid Res Date: 2013-07-04 Impact factor: 5.922
Authors: James M McKenney; Michael J Koren; Dean J Kereiakes; Corinne Hanotin; Anne-Catherine Ferrand; Evan A Stein Journal: J Am Coll Cardiol Date: 2012-03-28 Impact factor: 24.094
Authors: W März; A Beckmann; H Scharnagl; R Siekmeier; U Mondorf; I Held; W Schneider; K T Preissner; L K Curtiss; W Gross Journal: FEBS Lett Date: 1993-07-05 Impact factor: 4.124
Authors: Wei-Qi Wei; Xiaohui Li; Qiping Feng; Michiaki Kubo; Iftikhar J Kullo; Peggy L Peissig; Elizabeth W Karlson; Gail P Jarvik; Ming Ta Michael Lee; Ning Shang; Eric A Larson; Todd Edwards; Christian M Shaffer; Jonathan D Mosley; Shiro Maeda; Momoko Horikoshi; Marylyn Ritchie; Marc S Williams; Eric B Larson; David R Crosslin; Sarah T Bland; Jennifer A Pacheco; Laura J Rasmussen-Torvik; David Cronkite; George Hripcsak; Nancy J Cox; Russell A Wilke; C Michael Stein; Jerome I Rotter; Yukihide Momozawa; Dan M Roden; Ronald M Krauss; Joshua C Denny Journal: Circulation Date: 2018-10-23 Impact factor: 29.690