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  • 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.
  • Effect of Darapladib on Major Coronary Events After an Acute Coronary Syndrome: The SOLID-TIMI 52 Randomized Clinical Trial

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    JAMA. 2014; 312(10):1006-1015. doi: 10.1001/jama.2014.11061

    The SOLID-TIMI 52 randomized clinical trial evaluated darapladib, a selective lipoprotein-associated phospholipase A2 inhibitor, in patients after ACS and found it did not reduce the risk of coronary events.

  • Trends in Lipids and Lipoproteins in US Adults, 1988-2010

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    JAMA. 2012; 308(15):1545-1554. doi: 10.1001/jama.2012.13260
    Carroll and coauthors used data from 3 cross-sectional National Health and Nutrition Examination Surveys to observe trends in serum lipid levels in adults between 1988 and 2010.
  • Use of Emerging Lipoprotein Risk Factors in Assessment of Cardiovascular Risk

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    JAMA. 2012; 307(23):2540-2542. doi: 10.1001/jama.2012.6896
  • Lipid-Related Markers and Cardiovascular Disease Prediction

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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.
  • JAMA June 20, 2012

    Figure 2: Changes in Cardiovascular Disease Risk Discrimination and Classification After Adding Lipid-Related Markers

    The model containing conventional risk factors include age, systolic blood pressure, smoking status, history of diabetes, total and high-density lipoprotein cholesterol (HDL-C), each included as individual linear terms. Models were stratified by sex.aNet reclassification improvement was calculated only for participants in studies with at least 10 years of follow-up. Change in C-index adding lipoprotein(a) greater than 30 mg/dL was 0.0001 (95% CI, −0.0001 to 0.0003).bTriglyceride values were log-transformed.cP < .05 for comparison against model containing conventional risk factors.dP < .001 for comparison against model containing conventional risk factors.eLipoprotein(a) was modeled nonlinearly by including linear and quadratic terms of log-transformed lipoprotein(a).
  • JAMA November 16, 2011

    Figure 2: Proposed Mechanism of Evacetrapib on Lipid Exchange Between Lipoprotein Particles

    The left panel illustrates exchange of cholesteryl ester and triglycerides (TG) between high-density lipoprotein (HDL), low-density lipoprotein (LDL), and very low-density lipoprotein (VLDL) particles. The right panel illustrates the proposed effects of evacetrapib, which inhibits lipid exchange via the CETP (cholesteryl ester transfer protein) pathway. This mechanism theoretically results in HDL particles that contain greater amounts of cholesterol, and LDL particles that contain lesser amounts of cholesterol, resulting in an increase in circulating levels of HDL cholesterol and a decrease in LDL cholesterol.
  • Lipoprotein(a) Concentration and the Risk of Coronary Heart Disease, Stroke, and Nonvascular Mortality

    Abstract Full Text
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    JAMA. 2009; 302(4):412-423. doi: 10.1001/jama.2009.1063
  • JAMA July 22, 2009

    Figure 1: Literature Search and Study Selection

    Lp(a) indicates lipoprotein(a).
  • JAMA July 22, 2009

    Figure 4. Risk Ratios for Coronary Heart Disease per 3.5-Fold (1-SD) Higher Usual Lp(a) Level, by Age and Thirds of Individual Characteristics

    Lp(a) indicates lipoprotein(a); HDL-C, high-density lipoprotein cholesterol; CI, confidence interval. Sizes of data markers are proportional to the inverse of the variance of the risk ratios. Risk ratios are adjusted for age, usual levels of systolic blood pressure, smoking status, history of diabetes, body mass index, and total cholesterol and are stratified, where appropriate, by sex and study group. Studies with fewer than 3 cases per stratum were excluded from analyses. aBody mass index is calculated as weight in kilograms divided by height in meters squared. bCorrection for the cholesterol content of Lp(a) was made by subtracting estimated Lp(a) cholesterol values from total cholesterol; Lp(a) cholesterol was estimated from Lp(a) total mass using the following equation: Lp(a) − cholesterol (mg/dL) = 0.15 × Lp(a) (mg/dL) + 1.24.
  • JAMA July 22, 2009

    Figure 2: Risk Ratios for Coronary Heart Disease, Ischemic Stroke, or Nonvascular Death by Quantile of Usual Lp(a) Level

    Lp(a) indicates lipoprotein(a); MI, myocardial infarction. Sizes of data markers are proportional to the inverse of the variance of the risk ratios. Confidence intervals (CIs) were calculated using a floating absolute risk technique. Studies involving fewer than 10 cases of any outcome were excluded from the analysis of that outcome. aFurther adjustment for usual levels of systolic blood pressure, smoking status, history of diabetes, body mass index, and total cholesterol. The x- and y-axes are shown on a log scale. Lowest quantiles are referents.
  • JAMA July 22, 2009

    Figure 3. Risk Ratios for Vascular and Nonvascular Outcomes per 3.5-Fold (1-SD) Higher Usual Lp(a) Level, Adjusted for Cardiovascular Risk Factors

    Lp(a) indicates lipoprotein(a); MI, myocardial infarction; CI, confidence interval. Sizes of data markers are proportional to the inverse of the variance of the risk ratios. Risk ratios are adjusted for age, usual levels of systolic blood pressure, smoking status, history of diabetes, body mass index, and total cholesterol and are stratified, where appropriate, by sex and study group. Studies involving fewer than 10 cases of any outcome were excluded from the analysis of that outcome. aSubtotals do not add to the total number of coronary heart disease outcomes because some nested case-control studies did not subdivide outcomes into coronary death or nonfatal MI.
  • Genetically Elevated Lipoprotein(a) and Increased Risk of Myocardial Infarction

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    JAMA. 2009; 301(22):2331-2339. doi: 10.1001/jama.2009.801
  • JAMA June 10, 2009

    Figure 1: Risk of Myocardial Infarction by Extreme Levels of Lipoprotein(a) in the General Population

    Hazard ratios (HRs) were multivariable adjusted for age, sex, total cholesterol (corrected for the lipoprotein[a] contribution), triglycerides, body mass index, hypertension, diabetes mellitus, smoking, and use of lipid-lowering therapy and for women also for menopause and hormone therapy or for all of these variables as well as kringle IV type 2 (KIV-2) genotype. P values are test for trend of hazard ratios where lipoprotein(a) groups with increasing levels were coded 1, 2, 3, 4, and 5. Values are from the 1991-1994 examination of the Copenhagen City Heart Study with up to 16 years of follow-up (n = 7524). Controls used in the Copenhagen Ischemic Heart Disease Study (n = 1200) were excluded from analysis. CI indicates confidence interval.
  • JAMA June 10, 2009

    Figure 2: Mean Lipoprotein(a) Levels in the CCHS as a Function of Octiles or Quartiles of Apolipoprotein(a) KIV-2 Repeats

    P values are for Cuzick nonparametric test for trend of mean lipoprotein(a) levels. Participants in the 1991-1994 or 2001-2003 examination were included (n = 9867). CCHS indicates Copenhagen City Heart Study; KIV-2, kringle IV type 2. Error bars indicate 95% confidence intervals.
  • JAMA June 10, 2009

    Figure 4: Risk of Myocardial Infarction for Doubling in Lipoprotein(a) Levels in the CCHS

    The risk estimate for a doubling in plasma lipoprotein(a) was calculated using Cox regression while that for genetically elevated lipoprotein(a) was derived from an instrumental variable analysis. Hazard ratios (HRs) were multifactorially adjusted for age, sex, total cholesterol (corrected for the lipoprotein[a] contribution), triglycerides, body mass index, hypertension, diabetes mellitus, smoking, and use of lipid-lowering therapy and for women also for menopause and hormone therapy. CCHS indicates Copenhagen City Heart Study; CI, confidence interval.
  • Mendelian Randomization: Nature's Randomized Trial in the Post–Genome Era

    Abstract Full Text
    JAMA. 2009; 301(22):2386-2388. doi: 10.1001/jama.2009.812
  • JAMA June 10, 2009

    Figure 3: Risk of Myocardial Infarction by Quartiles of Apolipoprotein(a) KIV-2 Repeats in the CCHS, CGPS, and CIHDS

    In the Copenhagen City Heart Study (CCHS), risk estimates were adjusted for age and sex or multivariably for age, sex, total cholesterol (corrected for the lipoprotein[a] contribution), triglycerides, body mass index, hypertension, diabetes mellitus, smoking, and use of lipid-lowering therapy and for women also for menopause and hormone therapy. In the Copenhagen General Population Study (CGPS) and Copenhagen Ischemic Heart Disease Study (CIHDS), odds ratios (ORs) were adjusted for age and sex or multivariably for age, sex, and diabetes mellitus. P values are test for trend of risk estimates (hazard ratios [HRs] or ORs) where kringle IV type 2 (KIV-2) groups with decreasing numbers of KIV-2 repeats were coded 1, 2, 3, and 4. There was no overlap of individuals between studies. Participants in the CGPS with incomplete information on covariates were dropped from analysis (n = 151); otherwise, numbers of individuals included are as shown in Table 1. CI indicates confidence interval (shown as error bars).
  • ACAT Inhibition and Progression of Carotid Atherosclerosis in Patients With Familial Hypercholesterolemia: The CAPTIVATE Randomized Trial

    Abstract Full Text
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    JAMA. 2009; 301(11):1131-1139. doi: 10.1001/jama.301.11.1131