Abstract
Purpose of Review
To review the interactions between statins and proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibition.
Recent Findings
Statins are highly effective for reducing low-density lipoprotein cholesterol (LDL-C) and cardiovascular disease (CVD). However, statins also raise levels of PCSK9, a protein that increases circulating LDL-C levels by increasing LDL-C receptor degradation. Increases in PCSK9 levels also reduce the LDL-C response to statin therapy.
Summary
The interactions between statins, PCSK9, LDL-C, and cardiovascular risk are multifaceted and are influenced by genetic, lifestyle, and environmental factors as well as lipid-lowering therapies.
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References
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Acknowledgments
The authors acknowledge the research personnel of the Hartford Hospital Department of Preventive Cardiology, especially Gregory Panza, M.S., and Amanda Zaleski, M.S. In addition, all studies by Beth A. Taylor (Parker) and Paul D. Thompson involving human subjects were performed after approval by the appropriate institutional review boards with written informed consent obtained from all participants.
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Conflict of Interest
Dr. Taylor served on the Pharmacovigilance Monitoring Board for Amgen, Inc. and has received research support from Regeneron Pharmaceuticals, Inc.
Dr. Thompson has received research support from Genomas, Roche, Sanofi, Regeneron, Esperion, Amarin, and Pfizer; has served as a consultant for Amgen, Regeneron, Merck, Genomas, Runners World, Sanofi, Esperion, and Amarin; has received speaker honoraria from Merck, Astra Zeneca, Kowa, and Amarin; owns stock in Abbvie, Abbott Labs, General Electric, J&J; and has provided expert legal testimony on exercise-related cardiac events and statin myopathy.
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This article does not contain any studies with human or animal subjects performed by any of the authors.
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This article is part of the Topical Collection on Statin Drugs
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Taylor, B.A., Thompson, P.D. Statins and Their Effect on PCSK9—Impact and Clinical Relevance. Curr Atheroscler Rep 18, 46 (2016). https://doi.org/10.1007/s11883-016-0604-3
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DOI: https://doi.org/10.1007/s11883-016-0604-3