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Published on: October 12, 2017
Lipoprotein(a): Evidence for Role as a Causal Risk Factor in Cardiovascular Disease and Emerging Therapies
Harpreet S Bhatia1, Michael J Wilkinson1
1Division of Cardiovascular Medicine, Department of Medicine, University of California San Diego, La Jolla, CA 92093, USA.
Insights
Lipoprotein(a) (Lp(a)) is a confirmed cause of cardiovascular diseases like atherosclerotic cardiovascular disease (ASCVD) and calcific aortic valve disease (CAVD). New therapies targeting Lp(a) are in development to manage this significant cardiovascular risk.
Area of Science:
- Cardiology
- Genetics
- Epidemiology
Background:
- Lipoprotein(a) (Lp(a)) is a recognized risk factor for cardiovascular diseases.
- Evidence from mechanistic, epidemiologic, and genetic studies confirms Lp(a)'s causal role.
Purpose of the Study:
- To review the evidence supporting Lp(a) as a causal risk factor for ASCVD and AS/CAVD.
- To discuss current and emerging strategies for managing Lp(a)-associated cardiovascular risk.
Main Methods:
- Review of mechanistic studies.
- Analysis of epidemiologic data.
- Examination of genetic evidence.
Main Results:
- Strong evidence supports Lp(a) as a causal factor in ASCVD.
- Lp(a) is also implicated as a causal factor in AS/CAVD.
- Limited therapeutic options currently exist for elevated Lp(a).
Conclusions:
- Lp(a) is a significant, modifiable risk factor for ASCVD and AS/CAVD.
- Several targeted therapies for Lp(a) are in clinical development.
- Management of Lp(a)-associated risk is an evolving area in cardiovascular medicine.
Abstract:
Lipoprotein(a) (Lp(a)) is an established risk factor for multiple cardiovascular diseases. Several lines of evidence including mechanistic, epidemiologic, and genetic studies support the role of Lp(a) as a causal risk factor for atherosclerotic cardiovascular disease (ASCVD) and aortic stenosis/calcific aortic valve disease (AS/CAVD). Limited therapies currently exist for the management of risk associated with elevated Lp(a), but several targeted therapies are currently in various stages of clinical development. In this review, we detail evidence supporting Lp(a) as a causal risk factor for ASCVD and AS/CAVD, and discuss approaches to managing Lp(a)-associated risk.
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