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  • Association of Genetic Variants Related to CETP Inhibitors and Statins With Lipoprotein Levels and Cardiovascular Risk

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    JAMA. 2017; 318(10):947-956. doi: 10.1001/jama.2017.11467

    This mendelian randomization analysis of individual-participant data estimated the association between changes in levels of low-density lipoprotein cholesterol (and other lipoproteins) and risk of cardiovascular events due to CETP variants, alone and in combination with HMGCR variants.

  • JAMA September 12, 2017

    Figure 2: Association of CETP Score With Risk of Major Cardiovascular Events Among 102 837 Participants From 14 Cohort or Case-Control Studies

    All information derived from the individual-participant data. A total of 102 837 participants who experienced a total of 13 821 first major cardiovascular events were included in the analysis. Among all participants, median cholesteryl ester transfer protein (CETP) genetic score was 34.8 (interquartile range [IQR], 28.3-41.1; range, 0-54.3). For participants in the group with CETP scores below the median, median CETP score was 28.2 (IQR, 23.3-32.0; range, 0-34.7). For participants in the group with CETP scores equal to or above the median, median CETP score was 41.1 (IQR, 37.9-44.8; range, 34.8-54.3). Higher scores indicate a greater number of high-density lipoprotein cholesterol (HDL-C)–raising alleles (weighted by the effect of each allele on HDL-C level) and is analogous to treatment with increasingly potent CETP inhibitors. Lipid and lipoprotein values are presented in mg/dL (to convert HDL-C and low-density lipoprotein cholesterol [LDL-C] values to mmol/L, multiply by 0.0259) as the difference in mean value for each group compared with the reference group, with 95% confidence intervals. Associations with major cardiovascular events were calculated using an inverse variance–weighted fixed-effects meta-analysis of the study-specific estimates of effect. In panels B and C, the association between the CETP score and risk of major cardiovascular events is compared with the association between the risk of major cardiovascular events and genetic scores consisting of variants in the 3-hydroxy-3-methyl-glutaryl-CoA reductase (HMGCR) gene (encodes the target of statins), proprotein convertase subtilisin/kexin type 9 (PCSK9) gene (encodes target of PCSK9 inhibitors), and Niemann-Pick C1-Like 1 intracellular cholesterol transporter 1 (NPC1L1) gene (encodes target of ezetimibe). All associations between the genetic scores and risk of major cardiovascular events are standardized per 10-mg/dL lower level of LDL-C (panel B) or 10-mg/dL lower level of apolipoprotein B (apoB) (panel C) and measured in the overall sample of studies that contributed individual-participant data. Data markers indicate point estimates of effect and are of equal size because the analysis compared approximately equal-sized groups divided by the median CETP score value or quartiles of the CETP score (panel A). OR indicates odds ratio.
  • Genetic Studies Help Clarify the Complexities of Lipid Biology and Treatment

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    JAMA. 2017; 318(10):915-917. doi: 10.1001/jama.2017.11750
  • Nocebo Effect May Account for Statin Adverse Events

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    JAMA. 2017; 317(24):2476-2476. doi: 10.1001/jama.2017.7582
  • High-Intensity Statins: Guideline Expectations and Clinical Application

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    JAMA. 2017; 317(24):2543-2544. doi: 10.1001/jama.2017.5781

    This commentary discusses a study published in JAMA Cardiology that examined the association between intensity of statin therapy in patients with atherosclerotic cardiovascular disease and all-cause mortality among patients in the Veterans Affairs health care system.

  • JAMA May 23, 2017

    Figure: Therapies That Target PCSK9 Effective at Reducing LDL Cholesterol

    In patients with high LDL cholesterol despite statin therapy, targeting PCSK9 effectively reduces LDL.
  • Comparison of Recommended Eligibility for Primary Prevention Statin Therapy Based on the US Preventive Services Task Force Recommendations vs the ACC/AHA Guidelines

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    JAMA. 2017; 317(15):1563-1567. doi: 10.1001/jama.2017.3416

    This study uses NHANES data to compare the numbers of US adults eligible for primary prevention statin treatment under USPSTF vs ACC/AHA guideline criteria.

  • Effect of Evolocumab on Progression of Coronary Disease in Statin-Treated Patients: The GLAGOV Randomized Clinical Trial

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    JAMA. 2016; 316(22):2373-2384. doi: 10.1001/jama.2016.16951

    This randomized clinical trial compares the effects of evolocumab vs placebo on change in percent atheroma volume among adult patients with angiographic coronary disease despite treatment with statins.

  • Statins for Prevention of Cardiovascular Disease in Adults: Evidence Report and Systematic Review for the US Preventive Services Task Force

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    JAMA. 2016; 316(19):2008-2024. doi: 10.1001/jama.2015.15629

    This Evidence Report and systematic review to support the 2016 US Preventive Services Task Force Recommendation Statement on use of statins for prevention of cardiovascular disease (CVD) summarizes published trial evidence about the benefits and harms of statins for primary CVD prevention.

  • Statin Use for the Primary Prevention of Cardiovascular Disease in Adults: US Preventive Services Task Force Recommendation Statement

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    JAMA. 2016; 316(19):1997-2007. doi: 10.1001/jama.2016.15450

    This Recommendation Statement from the US Preventive Services Task Force recommends use of low- to moderate-dose statins for primary prevention in adults aged 40 to 75 years who have 1 or more CVD risk factors and a calculated CVD event risk of 10% or greater (B recommendation).

  • Statins for Primary Prevention: The Debate Is Intense, but the Data Are Weak

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    JAMA. 2016; 316(19):1979-1981. doi: 10.1001/jama.2016.15085
  • Interpretation and Use of Another Statin Guideline

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    JAMA. 2016; 316(19):1977-1979. doi: 10.1001/jama.2016.15087
  • Evolving Approaches for Statins in Primary Prevention: Progress, but Questions Remain

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    JAMA. 2016; 316(19):1981-1983. doi: 10.1001/jama.2016.15094
  • Statins for Primary Prevention in Older Adults: Uncertainty and the Need for More Evidence

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    JAMA. 2016; 316(19):1971-1972. doi: 10.1001/jama.2016.15212

    This Viewpoint summarizes the findings and limitations of clinical trial evidence regarding the benefits and risks of statins for primary prevention of atherosclerotic cardiovascular disease in persons older than 75 years.

  • What to Believe and Do About Statin-Associated Adverse Effects

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    JAMA. 2016; 316(19):1969-1970. doi: 10.1001/jama.2016.16557

    This Viewpoint reviews the myths about and makes recommendations for statin treatment.

  • Cholesterol, Cardiovascular Risk, Statins, PCSK9 Inhibitors, and the Future of LDL-C Lowering

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    JAMA. 2016; 316(19):1967-1968. doi: 10.1001/jama.2016.16575

    This Viewpoint discusses the role of implementation and translational science and digital platforms for improving population cardiovascular risk and advancing precision treatments in an era of intensive statin therapy and PCSK9 inhibitors.

  • Association Between Lowering LDL-C and Cardiovascular Risk Reduction Among Different Therapeutic Interventions: A Systematic Review and Meta-analysis

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    JAMA. 2016; 316(12):1289-1297. doi: 10.1001/jama.2016.13985

    This meta-analysis compares the association between lowering low-density lipoprotein cholesterol (LDL-C) and cardiovascular risk reduction for statin vs nonstatin therapies that lower LDL-C.

  • Cost-effectiveness of PCSK9 Inhibitor Therapy in Patients With Heterozygous Familial Hypercholesterolemia or Atherosclerotic Cardiovascular Disease

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    JAMA. 2016; 316(7):743-753. doi: 10.1001/jama.2016.11004

    This study estimates the cost-effectiveness of adding proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors to statin therapy for patients with heterozygous familial hypercholesterolemia (FH) or atherosclerotic cardiovascular disease (ASCVD).

  • JAMA August 16, 2016

    Figure 2: Incremental Cost-effectiveness Ratio (ICER) of PCSK9 Inhibitor Therapy Among Patients With Heterozygous Familial Hypercholesterolemia or Atherosclerotic Cardiovascular Disease

    The ICER for proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor therapy increases with the annual cost of PCSK9 inhibitor therapy. Blue, orange, and black data markers indicate the price at which PCSK9 inhibitor therapy would become cost-effective in the United States at willingness-to-pay thresholds of $150 000 per quality-adjusted life-year (QALY) ($6810), $100 000 per QALY ($4536), and $50 000 per QALY ($2261), respectively. In the base case, status quo statin plus PCSK9 inhibitor therapy is compared with status quo statin plus ezetimibe (black line). When PCSK9 inhibitor therapy costs less than $7049 per year (inflection in the graph), ezetimibe is eliminated by extended dominance and status quo statin plus PCSK9 inhibitory therapy is compared directly with status quo statin therapy (gray line). For reference, vertical lines include the list price of a 1-year supply of evolocumab in the United States and 3 European countries.
  • Lipid Screening in Childhood and Adolescence for Detection of Familial Hypercholesterolemia: Evidence Report and Systematic Review for the US Preventive Services Task Force

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    JAMA. 2016; 316(6):645-655. doi: 10.1001/jama.2016.6176

    This systematic review to support the 2016 update of the US Preventive Services Task Force Recommendation Statement on screening for lipid disorders in children and adolescents summarizes published evidence about the effectiveness of routine screening, accuracy of screening tests and strategies, and potential screening harms.