Elevated Lipoprotein(a): Background, Current Insights and Future Potential Therapies.
PCSK9
antisense therapy
aortic stenosis
apheresis
cardiovascular disease
genetics
lipoprotein (a)
lipoprotein turnover
statin
Journal
Vascular health and risk management
ISSN: 1178-2048
Titre abrégé: Vasc Health Risk Manag
Pays: New Zealand
ID NLM: 101273479
Informations de publication
Date de publication:
2021
2021
Historique:
received:
17
06
2021
accepted:
13
08
2021
entrez:
16
9
2021
pubmed:
17
9
2021
medline:
25
12
2021
Statut:
epublish
Résumé
Lipoprotein(a) forms a subfraction of the lipid profile and is characterized by the addition of apolipprotein(a) (apo(a)) to apoB100 derived particles. Its levels are mostly genetically determined inversely related to the number of protein domain (kringle) repeats in apo(a). In epidemiological studies, it shows consistent association with cardiovascular disease (CVD) and most recently with extent of aortic stenosis. Issues with standardizing the measurement of Lp(a) are being resolved and consensus statements favor its measurement in patients at high risk of, or with family histories of CVD events. Major lipid-lowering therapies such as statin, fibrates, and ezetimibe have little effect on Lp(a) levels. Therapies such as niacin or cholesterol ester transfer protein (CETP) inhibitors lower Lp(a) as well as reducing other lipid-related risk factors but have failed to clearly reduce CVD events. Proprotein convertase subtilisin kexin-9 (PCSK9) inhibitors reduce cholesterol and Lp(a) as well as reducing CVD events. New antisense therapies specifically targeting apo(a) and hence Lp(a) have greater and more specific effects and will help clarify the extent to which intervention in Lp(a) levels will reduce CVD events.
Identifiants
pubmed: 34526771
doi: 10.2147/VHRM.S266244
pii: 266244
pmc: PMC8436116
doi:
Substances chimiques
Hydroxymethylglutaryl-CoA Reductase Inhibitors
0
Lipoprotein(a)
0
PCSK9 protein, human
EC 3.4.21.-
Proprotein Convertase 9
EC 3.4.21.-
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
527-542Informations de copyright
© 2021 Handhle et al.
Déclaration de conflit d'intérêts
Dr Adie Viljoen reports personal fees, non-financial support from Novo Nordisk, personal fees from Novartis, non-financial support from Lilly, personal fees from Boehringer Ingelheim, grants, personal fees from Sanofi, personal fees from Napp, personal fees from Novartis, personal fees from Pfizer, personal fees, non-financial support from Astra Zeneca, outside the submitted work. Professor Anthony S Wierzbicki is: Site clinical trial investigator: volanesorsen for Akcea, Site clinical trial investigator: Evinacumab for Regeneron, Site clinical trial investigator: Evolocumab for Amgen, outside the submitted work. The authors report no other conflicts in this work.
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