Showing 1 – 20 of 1288
Relevance | Newest | Oldest |
  • JAMA March 7, 2017

    Figure 1: Association of Damaging Lipoprotein Lipase Gene (LPL) Mutations With Circulating Lipid Concentrations

    Beta coefficients reflective of the difference in lipid concentrations between carriers of a damaging LPL mutation and noncarriers were derived from linear regression models that included adjustment for age, age squared, sex, cohort, and the first 5 principal components of ancestry. Principal components of ancestry were based on observed genotypic differences across subpopulations (eg, race or ethnicity) in the overall study. Inclusion of principal components as covariates in linear regression analyses increases statistical power for true relationships and minimizes confounding by ancestry. Fixed-effects meta-analysis was used to combine results across cohorts (P for heterogeneity > .50 for each lipid phenotype). The number of participants from each study cohort with lipid fraction values available is displayed. HDL indicates high-density lipoprotein; IQR, interquartile range; and LDL, low-density lipoprotein. To convert cholesterol to millimoles per liter, multiply by 0.0259; triglycerides to millimoles per liter, multiply by 0.0113.
  • JAMA August 9, 2016

    Figure 2: RCTs Showing Effect of Statins on Mean Percent Change in LDL, Total, and HDL Cholesterol Levels (Key Question 6)

    LDL indicates low-density lipoprotein; HDL, high-density lipoprotein.
  • JAMA August 9, 2016

    Figure 1: Analytic Framework

    MI indicates myocardial infarction. Evidence reviews for the US Preventive Services Task Force (USPSTF) use an analytic framework to visually display the key questions that the review will address to allow the USPSTF to evaluate the effectiveness and safety of a preventive service. The questions are depicted by linkages that relate interventions and outcomes. Dashed line indicates an association between an intermediate outcome and a health outcome. Further details are available from the USPSTF procedure manual.aIntermediate outcomes include lipid levels (total, low-density lipoprotein, high-density lipoprotein, and non–high-density lipoprotein cholesterol; triglycerides) and atherosclerosis markers (carotid intima-medial thickness, calcium score, pathological findings).
  • JAMA January 20, 2015

    Figure 4: Risk of Cardiovascular Disease (CVD) Events After Hospitalization for All Pneumonia in the Atherosclerosis Risk in Communities Study

    The analysis included 2040 participants (680 pneumonia cases and 1360 controls). The number of participants at risk and those who developed an event over each time interval were estimated using a complete case approach and participants with missing data for covariates were excluded. The estimates were adjusted for age, sex, race, hypertension, diabetes mellitus, plasma total, high-density lipoprotein and low-density lipoprotein cholesterol, smoking, alcohol abuse, atrial fibrillation, chronic kidney disease, presence of diagnostic Q waves in electrocardiogram, peripheral arterial disease (defined by ankle brachial index <0.9), carotid artery wall thickness, presence of carotid atherosclerotic plaque by ultrasound, and percentage of predicted forced expiratory volume in first second of expiration (FEV1) measured by spirometry. Adjusted hazard ratios were calculated using baseline (at study entry) covariates measurements.
  • JAMA January 20, 2015

    Figure 2: Risk of Cardiovascular Disease Events After Hospitalization for Pneumonia in the Cardiovascular Health Study

    CVD indicates cardiovascular disease. The analysis included 1773 participants (591 pneumonia cases and 1182 controls). Stratified analyses by severity of pneumonia included 633 participants (211 pneumonia cases and 422 controls) for pneumonia with organ dysfunction and 1140 participants (380 pneumonia cases and 422 controls) for pneumonia without organ dysfunction. The number of participants at risk and those who developed an event over each time interval were estimated using a complete case approach and participants with missing data for covariates were excluded. The estimates were adjusted for age, sex, race, hypertension, diabetes mellitus, serum total, high-density lipoprotein and low-density lipoprotein cholesterol, smoking, alcohol abuse, atrial fibrillation, chronic kidney disease, serum C-reactive protein, presence of subclinical cardiovascular disease, percentage of predicted forced expiratory volume in first second of expiration (FEV1) measured by spirometry, trajectories of activities of daily living and independent activities of daily living over time, and trajectories of modified mini-mental status examination scores over time. Adjusted hazard ratios were calculated using the most recently available measurements before inclusion in the nested analysis cohort.
  • JAMA December 17, 2014

    Figure 3: Effect of Study Diets on Main Outcomes

    The primary outcomes were systolic blood pressure, insulin sensitivity, and levels of low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, and triglycerides. Diastolic blood pressure was a secondary outcome. Additional data related to these outcomes are presented in Table 3 and eTable 3 in Supplement 2. Apolipoproteins and other lipid outcomes are in eTable 4. Carb indicates carbohydrate; GI, glycemic index. To convert cholesterol to mmol/L, multiply by 0.0259; triglycerides to mmol/L, multiply by 0.0113.aFor the 5 primary outcomes on the primary diet contrast (insulin sensitivity, triglycerides, HDL cholesterol, LDL cholesterol, and systolic blood pressure), we plot and tabulate 99% CI to achieve nominal 95% coverage.
  • JAMA April 16, 2014

    Figure 3: Mean Change in Glycated Hemoglobin, High- and Low-Density Lipoprotein Cholesterol, and Triglyceride Levels From Baseline Through 36 Months

    Mean value at baseline: A, 7.8% for both placebo and aleglitazar; B, 41.8 mg/dL for placebo and 42.2 mg/dL for aleglitazar; C, 154 mg/dL for placebo and 152 mg/dL for aleglitazar; and D, 79.7 mg/dL for placebo and 78.9 mg/dL for aleglitazar. To convert high-density lipoprotein and low-density lipoprotein to millimoles per liter, multiply by 0.0259; triglycerides to millimoles per liter, multiply by 0.0113. Error bars indicate 95% CIs.
  • Dysfunctional HDL May Increase Heart Disease Risk

    Abstract Full Text
    JAMA. 2014; 311(9):894-894. doi: 10.1001/jama.2014.1872
  • JAMA November 23, 2011

    Figure 1: Estimated 24-Hour Urinary Excretion of Sodium and Composite of Cardiovascular Death, Stroke, Myocardial Infarction, and Hospitalization for Congestive Heart Failure

    Spline plot for adjusted Cox models. Median intake is reference standard. Salt approximates 2.5 × sodium g per day. Model was adjusted for age, sex, race/ethnicity (white vs nonwhite); prior history of stroke or myocardial infarction; creatinine, body mass index; comorbid vascular risk factors (hypertension, diabetes mellitus, atrial fibrillation, smoking, low- and high-density lipoprotein); treatment allocation (ramipril, telmisartan, neither, or both); treatment with statins, β-blockers, diuretic therapy, calcium antagonist, and antithrombotic therapy; fruit and vegetable consumption, level of exercise; baseline blood pressure and change in systolic blood pressure from baseline to last follow-up; and urinary potassium. Dashed lines indicate 95% CIs. Events and numbers at risk are shown between values on x-axis because they indicate the numeric range between these values.aSpline curve truncated at 12 g per day (63 participants had sodium excretion >12 g/d, event rate 21/63).
  • JAMA November 23, 2011

    Figure 2: Estimated 24-Hour Urinary Excretion of Sodium and Cardiovascular Death, Myocardial Infarction, Hospitalization for Congestive Heart Failure, and Stroke

    Spline plot for adjusted Cox models. Median intake is reference standard. Salt approximates 2.5 × sodium g per day. Model was adjusted for age, sex, race/ethnicity (white vs nonwhite); prior history of stroke or myocardial infarction; creatinine, body mass index; comorbid vascular risk factors (hypertension, diabetes mellitus, atrial fibrillation, smoking, low- and high-density lipoprotein); treatment allocation (ramipril, telmisartan, neither, or both); treatment with statins, β-blockers, diuretic therapy, calcium antagonist, and antithrombotic therapy; fruit and vegetable consumption, level of exercise; baseline blood pressure and change in systolic blood pressure from baseline to last follow-up; and urinary potassium. Dashed lines indicate 95% CIs. Events and numbers at risk are shown between values on x-axis because they indicate the numeric range between these values.aSpline curve truncated at 12 g per day (63 participants had sodium excretion >12 g/d; event rate, 8/63 for cardiovascular death and for myocardial infarction, 7/63 for congestive heart failure, and 4/63 for stroke).
  • JAMA November 23, 2011

    Figure 3: Estimated 24-Hour Urinary Excretion of Potassium and Stroke

    Spline plot for adjusted Cox models. Median excretion is the reference standard. Model adjusted for age, sex, race/ethnicity (white vs nonwhite); prior history of stroke or myocardial infarction; creatinine, body mass index; comorbid vascular risk factors (hypertension, diabetes mellitus, atrial fibrillation, smoking, low- and high-density lipoprotein); treatment allocation (ramipril, telmisartan, neither, or both); treatment with statins, β-blockers, diuretic therapy, calcium antagonist, and antithrombotic therapy; fruit and vegetable consumption, level of exercise; baseline blood pressure and change in systolic blood pressure from baseline to last follow-up, and urinary sodium. Dashed lines indicate 95% CIs. Events and numbers at risk are shown between values on x-axis because they indicate the numeric range between these values.aSpline curve truncated at 5 g per day (29 participants had potassium excretion >5 g/d, event rate 1/29).
  • Effects of the CETP Inhibitor Evacetrapib Administered as Monotherapy or in Combination With Statins on HDL and LDL Cholesterol: A Randomized Controlled Trial

    Abstract Full Text
    free access has multimedia
    JAMA. 2011; 306(19):2099-2109. doi: 10.1001/jama.2011.1649
  • 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.
  • JAMA June 22, 2011

    Figure 3: Subgroup Analyses for New-Onset Diabetes and First Major Cardiovascular Events

    Data were available for age, high-density lipoprotein (HDL) cholesterol levels, and triglyceride concentrations in all trials; for body mass index (BMI) in 4 trials; and for fasting plasma glucose levels in 3 trials. The medians of the variables are per-trial medians, which are provided in the eTable. P values apply to heterogeneity between groups. Data marker size indicates relative weight of the studies; OR, odds ratio; and CI, confidence interval.
  • JAMA January 12, 2011

    Figure: CETP Inhibition Shows Promise as Way to Reduce Cardiovascular Disease Risk

    A new drug may increase levels of high-density lipoprotein (HDL-C) cholesterol and lower low-density lipoprotein (LDL-C) cholesterol via cholesteryl ester transfer protein inhibition.
  • Vascular Abnormalities, Paraoxonase Activity, and Dysfunctional HDL in Primary Antiphospholipid Syndrome

    Abstract Full Text
    free access
    JAMA. 2009; 302(11):1210-1217. doi: 10.1001/jama.2009.1346
  • JAMA May 6, 2009

    Figure 3: Univariate and Sex- and Age-Adjusted Proportional Hazards Analysis of Association With the First Venous Thromboembolism

    eGFR indicates estimated glomerular filtration rate; MI, myocardial infarction; UAE, urinary albumin excretion; VTE, venous thromboembolism. To convert values for cholesterol, HDL, and LDL to mmol/L, multiply by 0.0259; to convert values for triglycerides to mmol/L, multiply by 0.0113; to convert CRP to nmol/L multiply by 9.524; to convert PAI-1 to pmol/L, multiply by 19.231. aSex- and age-adjusted hazard ratios (HRs) with corresponding 95% confidence intervals (95% CIs). Sex was adjusted for age only and age for sex only. Use of oral contraceptives was also adjusted for age only. bBody mass index (BMI [calculated as weight in kilograms divided by height in meters squared]), metabolic syndrome, cholesterol, high-density lipoprotein (HDL), low-density lipoprotein (LDL), and triglycerides were classified according to the Adult Treatment Panel III of the National Cholesterol Education Program.cC-reactive protein (CRP) was classified according to the Centers for Disease Control and Prevention and the American Heart Association.dSince normal ranges of tissue plasminogen activator (tPA) and plasminogen activator inhibitor-1 (PAI-1) in the general population are unknown, we dichotomized these variables using their medians as cutoffs.
  • JAMA November 12, 2008

    Figure 4: Levels of Nonfasting Triglycerides and Lipoprotein Cholesterol for Individuals With Previous Ischemic Stroke vs Controls

    Values were measured in 9637 individuals participating in the 1991-1994 examination of the Copenhagen City Heart Study; these individuals were not treated with lipid-lowering therapy. Boxes indicate interquartile range; horizontal lines, median; error bars, 95% confidence intervals. P values (triglycerides: P < .01 for ischemic stroke vs controls in men and P < .05 in women; remnant cholesterol: P < .01 for ischemic stroke vs controls in men and P < .05 in women) are from general linear models adjusting for age, total cholesterol level, alcohol consumption, smoking, hypertension, and atrial fibrillation, with further adjustment in women for postmenopausal status and hormone therapy. HDL indicates high-density lipoprotein; LDL, low-density lipoprotein.
  • JAMA November 12, 2008

    Figure 1: Hazard Ratios (HRs) for Ischemic Stroke by Increasing Levels of Nonfasting Triglycerides, Stratified by Adjustment

    Values are from 13 956 individuals from the Copenhagen City Heart Study with up to 31 years of follow-up, during which time 1529 developed ischemic stroke. Multivariate adjustment was for total cholesterol level, alcohol consumption, smoking, hypertension, atrial fibrillation, and lipid-lowering therapy, with further adjustment in women for postmenopausal status and hormone therapy. P values for trend examine whether increased levels of triglycerides are associated with increased HRs (triglyceride strata were coded 0, 1, 2, 3, 4, and 5 for increasing triglyceride levels). BMI indicates body mass index (calculated as weight in kilograms divided by height in meters squared); CI, confidence interval (shown as error bars in the plots); HDL, high-density lipoprotein.
  • JAMA June 4, 2008

    Figure 1: Hazard Ratio for Ischemic Heart Disease (IHD) as a Function of High-Density Lipoprotein (HDL) Cholesterol in Quintiles in the Copenhagen City Heart Study

    The HDL cholesterol values were from the second examination (1981-1983), and included a total number of 12 031 individuals. Hazard ratios were adjusted for age, sex, total cholesterol, hypertension, diabetes, and smoking. The highest quintile of HDL cholesterol (70-148 mg/dL) served as the reference group. To convert HDL cholesterol to mmol/L, multiply by 0.0259. Error bars indicate 95% confidence intervals.