Beth A Taylor1,2,3, Paul D Thompson4,5. 1. Department of Kinesiology, University of Connecticut, Gampel Pavilion Room 207, 2095 Hillside Rd, U-1110, Storrs, CT, 06269-1110, USA. Beth.Taylor@uconn.edu. 2. Division of Cardiology, Henry Low Heart Center, Hartford Hospital, Hartford, CT, USA. Beth.Taylor@uconn.edu. 3. University of Connecticut School of Medicine, Farmington, CT, USA. Beth.Taylor@uconn.edu. 4. Division of Cardiology, Henry Low Heart Center, Hartford Hospital, Hartford, CT, USA. Paul.Thompson@hhchealth.org. 5. University of Connecticut School of Medicine, Farmington, CT, USA. Paul.Thompson@hhchealth.org.
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. 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.
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. 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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