Genetics of Lipoprotein(a): Cardiovascular Disease and Future Therapy

Publikation: Bidrag til tidsskriftReviewForskningfagfællebedømt

Standard

Genetics of Lipoprotein(a) : Cardiovascular Disease and Future Therapy. / Langsted, Anne; Nordestgaard, Børge G.

I: Current Atherosclerosis Reports, Bind 23, Nr. 8, 46, 2021.

Publikation: Bidrag til tidsskriftReviewForskningfagfællebedømt

Harvard

Langsted, A & Nordestgaard, BG 2021, 'Genetics of Lipoprotein(a): Cardiovascular Disease and Future Therapy', Current Atherosclerosis Reports, bind 23, nr. 8, 46. https://doi.org/10.1007/s11883-021-00937-0

APA

Langsted, A., & Nordestgaard, B. G. (2021). Genetics of Lipoprotein(a): Cardiovascular Disease and Future Therapy. Current Atherosclerosis Reports, 23(8), [46]. https://doi.org/10.1007/s11883-021-00937-0

Vancouver

Langsted A, Nordestgaard BG. Genetics of Lipoprotein(a): Cardiovascular Disease and Future Therapy. Current Atherosclerosis Reports. 2021;23(8). 46. https://doi.org/10.1007/s11883-021-00937-0

Author

Langsted, Anne ; Nordestgaard, Børge G. / Genetics of Lipoprotein(a) : Cardiovascular Disease and Future Therapy. I: Current Atherosclerosis Reports. 2021 ; Bind 23, Nr. 8.

Bibtex

@article{1303f20700e1491e99262b87550bbc0d,
title = "Genetics of Lipoprotein(a): Cardiovascular Disease and Future Therapy",
abstract = "Purpose of Review: Lipoprotein(a) levels are determined 80–90% by genetics and differ by up to 1000-fold between individuals. This review discusses the most recent literature on lipoprotein(a) as a risk factor for cardiovascular disease, as well as future lipoprotein(a)lowering therapies. Recent Findings: Over the past few decades, numerous studies have observed that high lipoprotein(a) levels are associated observationally and causally through human genetics with increased risk of cardiovascular disease. Also, the development of safe and effective therapies to lower lipoprotein(a) is ongoing, most importantly using antisense oligonucleotides to prevent production of lipoprotein(a). Finally, both observational and genetic studies have estimated the extent to which lowering of lipoprotein(a) is needed to obtain a clinically meaningful reduction in the risk of cardiovascular disease. Summary: Lipoprotein(a) is a causal risk factor for cardiovascular disease; however, currently no approved safe and effective therapy is available to lower lipoprotein(a) levels. That said, promising randomized studies using antisense oligonucleotides show up to 80% reductions in lipoprotein(a), reductions that hopefully will result in lowering the risk of cardiovascular disease as presently tested in the ongoing HORIZON phase 3 trial.",
keywords = "Aortic stenosis, Atherosclerosis, Epidemiology, Genetics, KIV-2, Lp(a), Mendelian randomization, Myocardial infarction, Stroke",
author = "Anne Langsted and Nordestgaard, {B{\o}rge G.}",
note = "Publisher Copyright: {\textcopyright} 2021, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.",
year = "2021",
doi = "10.1007/s11883-021-00937-0",
language = "English",
volume = "23",
journal = "Current Atherosclerosis Reports",
issn = "1523-3804",
publisher = "Springer Healthcare",
number = "8",

}

RIS

TY - JOUR

T1 - Genetics of Lipoprotein(a)

T2 - Cardiovascular Disease and Future Therapy

AU - Langsted, Anne

AU - Nordestgaard, Børge G.

N1 - Publisher Copyright: © 2021, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

PY - 2021

Y1 - 2021

N2 - Purpose of Review: Lipoprotein(a) levels are determined 80–90% by genetics and differ by up to 1000-fold between individuals. This review discusses the most recent literature on lipoprotein(a) as a risk factor for cardiovascular disease, as well as future lipoprotein(a)lowering therapies. Recent Findings: Over the past few decades, numerous studies have observed that high lipoprotein(a) levels are associated observationally and causally through human genetics with increased risk of cardiovascular disease. Also, the development of safe and effective therapies to lower lipoprotein(a) is ongoing, most importantly using antisense oligonucleotides to prevent production of lipoprotein(a). Finally, both observational and genetic studies have estimated the extent to which lowering of lipoprotein(a) is needed to obtain a clinically meaningful reduction in the risk of cardiovascular disease. Summary: Lipoprotein(a) is a causal risk factor for cardiovascular disease; however, currently no approved safe and effective therapy is available to lower lipoprotein(a) levels. That said, promising randomized studies using antisense oligonucleotides show up to 80% reductions in lipoprotein(a), reductions that hopefully will result in lowering the risk of cardiovascular disease as presently tested in the ongoing HORIZON phase 3 trial.

AB - Purpose of Review: Lipoprotein(a) levels are determined 80–90% by genetics and differ by up to 1000-fold between individuals. This review discusses the most recent literature on lipoprotein(a) as a risk factor for cardiovascular disease, as well as future lipoprotein(a)lowering therapies. Recent Findings: Over the past few decades, numerous studies have observed that high lipoprotein(a) levels are associated observationally and causally through human genetics with increased risk of cardiovascular disease. Also, the development of safe and effective therapies to lower lipoprotein(a) is ongoing, most importantly using antisense oligonucleotides to prevent production of lipoprotein(a). Finally, both observational and genetic studies have estimated the extent to which lowering of lipoprotein(a) is needed to obtain a clinically meaningful reduction in the risk of cardiovascular disease. Summary: Lipoprotein(a) is a causal risk factor for cardiovascular disease; however, currently no approved safe and effective therapy is available to lower lipoprotein(a) levels. That said, promising randomized studies using antisense oligonucleotides show up to 80% reductions in lipoprotein(a), reductions that hopefully will result in lowering the risk of cardiovascular disease as presently tested in the ongoing HORIZON phase 3 trial.

KW - Aortic stenosis

KW - Atherosclerosis

KW - Epidemiology

KW - Genetics

KW - KIV-2

KW - Lp(a)

KW - Mendelian randomization

KW - Myocardial infarction

KW - Stroke

U2 - 10.1007/s11883-021-00937-0

DO - 10.1007/s11883-021-00937-0

M3 - Review

C2 - 34148150

AN - SCOPUS:85108508383

VL - 23

JO - Current Atherosclerosis Reports

JF - Current Atherosclerosis Reports

SN - 1523-3804

IS - 8

M1 - 46

ER -

ID: 273643662