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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 4: Association of Genetic Variants With Naturally Occurring Discordance Between Changes in Concentrations of LDL-C and apoB and the Risk of CHD Among CARDIoGRAMplusC4D Consortium Participants

    Analyses are based on summary data from up to 62 240 participants with coronary heart disease (CHD) and 127 299 control participants from the Coronary Artery DIsease Genome Wide Replication and Meta-analysis plus the Coronary Artery Disease Genetics (CARDIoGRAMplusC4D) Consortium. Effect sizes are standardized per 10-mg/dL lower level of low-density lipoprotein cholesterol (LDL-C) or 10-mg/dL lower level of apolipoprotein B (apoB). MR-Egger regression estimates are presented for sensitivity analyses. Data markers indicate point estimates of effect; error bars, 95% confidence intervals.
  • JAMA September 12, 2017

    Figure 3: Separate and Combined Effects of the CETP and HMGCR Scores on 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, the median cholesteryl ester transfer protein (CETP) genetic score was 34.8 (interquartile range [IQR], 28.3-41.1; range, 0-54.3). The median CETP and 3-hydroxy-3-methyl-glutaryl-CoA reductase (HMGCR) score, IQR, and range of values for each group is presented in Table 2. Lipid and lipoprotein values are presented in mg/dL (to convert high-density lipoprotein cholesterol [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 panel B, the study population was first divided into 2 groups based on whether the HMGCR score was below or equal to or greater than the median value. The association between the CETP score and the risk of major cardiovascular events was then estimated modeling the CETP score as a continuous variable scaled to the lipid effects in the dichotomous score analysis. There was evidence for effect modification of the HMGCR score on the association between the CETP genetic score and the risk of major cardiovascular events (P = .04). Data markers indicate point estimates of effect and are of equal size because the analysis compared approximately equal-sized groups divided into a factorial analysis (panel A) or the median HMGCR score value (panel B). Error bars represent 95% confidence intervals. apoB indicates apolipoprotein B; OR, odds ratio.
  • 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

    Abstract Full Text
    JAMA. 2017; 318(10):915-917. doi: 10.1001/jama.2017.11750
  • Lipid-Related Markers and Cardiovascular Disease Prediction

    Abstract Full Text
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    JAMA. 2012; 307(23):2499-2506. doi: 10.1001/jama.2012.6571
    To determine whether adding lipid markers to the panel of current cardiovascular disease (CVD) risk markers would enhance CVD risk assessment, the Emerging Risk Factors Collaboration reviewed available records from 165544 participants in 37 prospective cohort trials, in which 15126 had incident fatal or nonfatal CVD outcomes.
  • Association of LDL Cholesterol, Non–HDL Cholesterol, and Apolipoprotein B Levels With Risk of Cardiovascular Events Among Patients Treated With Statins: A Meta-analysis

    Abstract Full Text
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    JAMA. 2012; 307(12):1302-1309. doi: 10.1001/jama.2012.366
  • JAMA March 28, 2012

    Figure 2: Association Between on-Statin Lipid or Apolipoprotein Levels and Risk of Major Cardiovascular Events Stratified by Study

    Data markers indicate hazard ratios (HRs) for risk of major cardiovascular events per 1-SD increase of on-statin low-density lipoprotein cholesterol (LDL-C), non–high-density lipoprotein cholesterol (non–HDL-C), or apolipoprotein B (apoB) and 95% CIs. For placebo-controlled trials, data from the placebo group were not used in this analysis. Dashed line indicates point estimate for all participants combined. All interaction terms by study were nonsignificant.
  • JAMA November 11, 2009

    Figure 3: Hazard Ratios for Coronary Heart Disease Across Fifths of Usual Lipids or Apolipoproteins

    Analyses were based on 91 307 participants (involving 4499 cases) from 22 studies. Regression analyses were stratified, where appropriate, by sex and trial group and adjusted for age, systolic blood pressure, smoking status, history of diabetes mellitus, and body mass index; furthermore, analyses of non–HDL-C were adjusted for HDL-C and loge triglyceride, analyses of apolipoprotein B (apo B) were adjusted for apolipoprotein AI (apo AI) and loge triglyceride, analyses of HDL-C were adjusted for non–HDL-C and loge triglyceride, and analyses of apo AI were adjusted for apo B and loge triglyceride. Studies with fewer than 10 cases were excluded from analysis. Sizes of data markers are proportional to the inverse of the variance of the hazard ratios. Referent groups are lowest fifths. Lines are fitted by first-degree fractional polynomial regression of log hazard ratios on mean SD score. Error bars indicate 95% confidence intervals. The y-axis is shown on a log scale. The x-axis is shown on a Z-transformed scale.
  • JAMA June 18, 2008

    Figure 2: Associations of CETP Genotypes With CETP Phenotypes and Lipid Levels

    CETP indicates cholesteryl ester transfer protein; CI, confidence interval; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol. To convert apolipoproteins A-I and B to mg/dL, divide by 0.01; to convert HDL-C and LDL-C to mg/dL, divide by 0.0259; and to convert triglyercides to mg/dL, divide by 0.0113. Assessment of heterogeneity: I2 (95% CI) for CETP mass, CETP activity, HDL-C, apolipoprotein A-I, LDL-C, apolipoprotein B, and triglycerides, respectively, were 66% (39%-81%), 71% (44%-86%), 75% (69%-80%), 66% (46%-78%), 51% (32%-65%), 14% (0%-51%), and 49% (30%-62%) for TaqIB; 0% (0%-71%), NA*, 56% (33%-71%), 0% (0%-68%), 24% (0%-58%), 16% (0%-60%), and 0% (0%-49%) for I405V; and 71% (17%-90%), NA*, 37% (0%-61%), 36% (0%-78%), 29% (0%-63%), 0% (0%-90%), and 0% (0%-57%) for −629C>A. NA* indicates I2 statistics were not calculated when there were only 2 studies. aPooled estimates calculated by random-effects models. Estimates calculated by fixed-effect models are shown in eTable 3. bStandardized mean differences. cCalculated with reference to the weighted mean level of each marker in common homozygotes.
  • Clinical Utility of Different Lipid Measures for Prediction of Coronary Heart Disease in Men and Women

    Abstract Full Text
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    JAMA. 2007; 298(7):776-785. doi: 10.1001/jama.298.7.776
  • Fasting Insulin and Apolipoprotein B Levels and Low-Density Lipoprotein Particle Size as Risk Factors for Ischemic Heart Disease

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    JAMA. 1998; 279(24):1955-1961. doi: 10.1001/jama.279.24.1955
  • JAMA June 24, 1998

    Figure: Fasting Insulin and Apolipoprotein B Levels and Low-Density Lipoprotein Particle Size as Risk Factors for Ischemic Heart Disease

    Prevalence of cumulative number of risk factors in 85 pairs of ischemic heart disease (IHD) cases and controls. The upper panel shows the proportion of IHD cases and controls with 1 or more of the nontraditional metabolic risk factors (elevated fasting plasma insulin levels, elevated apolipoprotein B levels, and small, dense low-density lipoprotein [LDL] particles) compared with subjects having none of these risk factors. The lower panel presents the frequency of cases and controls with 1 or more of the traditional risk factors (elevated low-density lipoprotein cholesterol [LDL-C] and triglyceride levels and reduced high-density lipoprotein cholesterol [HDL-C] levels) compared with subjects having none of these risk factors. The presence or absence of risk factors is based on the 50th percentile value of controls for each variable (fasting insulin, 72 pmol/L [10 µU/mL]; apolipoprotein B, 1.1 g/L [110 mg/dL]; LDL particle diameter, 25.82 nm; LDL-C, 3.7 mmol/L [143 mg/dL]; triglycerides, 1.52 mmol/L [135 mg/dL]; and HDL-C, 1.01 mmol/L [39 mg/dL]).
  • Why Is She Away? The Problem of Sickness Among Women in Industry

    Abstract Full Text
    JAMA. 1946; 131(12):1030-1030. doi: 10.1001/jama.1946.02870290080027
  • Apolipoprotein B-100 Hopkins (Arginine4019 [unk] Tryptophan): A New Apolipoprotein B-100 Variant in a Family With Premature Atherosclerosis and Hyperapobetalipoproteinemia

    Abstract Full Text
    JAMA. 1989; 262(14):1980-1988. doi: 10.1001/jama.1989.03430140098032
  • Insulin-like Growth Factor and Apolipoprotein B

    Abstract Full Text
    JAMA. 1991; 266(14):1937-1938. doi: 10.1001/jama.1991.03470140049019
  • Primary Hypertriglyceridemia With Borderline High Cholesterol and Elevated Apolipoprotein B Concentrations: Comparison of Gemfibrozil vs Lovastatin Therapy

    Abstract Full Text
    JAMA. 1990; 264(21):2759-2763. doi: 10.1001/jama.1990.03450210059033
  • Coffee Intake and Elevated Cholesterol and Apolipoprotein B Levels in Men

    Abstract Full Text
    JAMA. 1985; 253(10):1407-1411. doi: 10.1001/jama.1985.03350340059017