Low-Density Lipoprotein Cholesterol

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Carl J Lavie - One of the best experts on this subject based on the ideXlab platform.

  • statins ezetimibe and proprotein convertase subtilisin kexin type 9 inhibitors to reduce low density Lipoprotein Cholesterol and cardiovascular events
    American Journal of Cardiology, 2017
    Co-Authors: James H Okeefe, James J Dinicolantonio, Carl J Lavie
    Abstract:

    Multiple lines of evidence suggest that the physiologically normal levels of Low-Density Lipoprotein Cholesterol (LDL-C) and the thresholds for development of atherosclerosis and adverse coronary events are in the 30- to 70-mg/dl range. More patients have been studied in randomized controlled trials assessing the effects of statins on outcomes than any other drug class in the history of medicine. This cumulative body of evidence documents that atherosclerosis progression is halted and coronary heart disease events are minimized when statin therapy with or without ezetimibe, and possibly proprotein convertase subtilisin–kexin type 9 (PCSK9) inhibitors, is used to drive down the LDL-C to a range of about 30 to 50 mg/dl. Thus far, these agents appear to be safe even when LDL-C is lowered to about 50 mg/dl, although more robust outcome and safety data are required, particularly for the PCSK9 inhibitors and very low LDL-C levels (e.g., down to 25 mg/dl). In conclusion, the current national guidelines specifying only the use of a high-potency statin without specific LDL-C goals may lead to substantial undertreatment of high-risk patients, leaving them vulnerable to future adverse cardiovascular events.

Michael D Shapiro - One of the best experts on this subject based on the ideXlab platform.

Nicola Ferri - One of the best experts on this subject based on the ideXlab platform.

  • from Lipoprotein apheresis to proprotein convertase subtilisin kexin type 9 inhibitors impact on low density Lipoprotein Cholesterol and c reactive protein levels in cardiovascular disease patients
    European Journal of Preventive Cardiology, 2018
    Co-Authors: M G Zenti, Anna Altomari, Maria Giovanna Lupo, Margherita Botta, Enzo Bonora, Alberto Corsini, Massimiliano Ruscica, Nicola Ferri
    Abstract:

    In this observational study, we compared the effect of Lipoprotein apheresis and evolocumab or alirocumab on levels of Lipoprotein Cholesterol, triglycerides and inflammatory markers (C reactive protein and interleukin 6) in cardiovascular patients ( n = 9). Patients were monitored during the last year of Lipoprotein apheresis followed by six months of treatment with proprotein convertase subtilisin/kexin type 9 inhibitors. The biochemical parameters were determined pre- and post- every apheresis procedure for 12 months and then after one, three and six months of treatment with evolocumab (140 mg every two weeks [Q2W]) or alirocumab (75 mg or 150 mg every two weeks [Q2W]). Lipoprotein apheresis significantly reduced Low-Density Lipoprotein Cholesterol levels from 138 ± 32 mg/dl to 46 ± 16 mg/dl ( p < 0.001), with an inter-apheresis level of 114 ± 26 mg/dl. Lipoprotein(a) was also reduced from a median of 42 mg/dl to 17 mg/dl ( p < 0.01). Upon anti-proprotein convertase subtilisin/kexin type 9 therapy, Low-Density Lipoprotein Cholesterol levels were similar to post-apheresis (59 ± 25, 41 ± 22 and 42 ± 21mg/dl at one, three and six months, respectively) as well as those of Lipoprotein(a) (18 mg/dl). However, an opposite effect was observed on high-density Lipoprotein Cholesterol levels: -16.0% from pre- to post-apheresis and +34.0% between pre-apheresis and proprotein convertase subtilisin/kexin type 9 inhibitors. Apheresis significantly reduced high-sensitivity C-reactive protein levels (1.5 ± 1.2 mg/l pre-apheresis to 0.6 ± 0.6 mg/l post-apheresis), while no changes were found upon proprotein convertase subtilisin/kexin type 9 mAbs administration. In conclusion, our study demonstrated that, by switching from Lipoprotein apheresis to anti-proprotein convertase subtilisin/kexin type 9 therapies, patients reached similar Low-Density Lipoprotein Cholesterol and Lipoprotein(a) levels, increased those of high-density Lipoprotein Cholesterol, and showed no changes on high-sensitivity C-reactive protein.

Sergio Fazio - One of the best experts on this subject based on the ideXlab platform.

Borge G Nordestgaard - One of the best experts on this subject based on the ideXlab platform.

  • cardiovascular disease risk associated with elevated Lipoprotein a attenuates at low low density Lipoprotein Cholesterol levels in a primary prevention setting
    European Heart Journal, 2018
    Co-Authors: Rutger Verbeek, Matthijs S Boekholdt, Kees G Hovingh, Renate M Hoogeveen, Anne Langsted, Lotte C A Stiekema, Simone L Verweij, Nicholas J Wareham, Kaytee Khaw, Borge G Nordestgaard
    Abstract:

    Aims: Lipoprotein(a) (Lp(a)) elevation is a causal risk factor for cardiovascular disease (CVD). It has however been suggested that elevated Lp(a) causes CVD mainly in individuals with high Low-Density Lipoprotein Cholesterol (LDL-C) levels. We hypothesized that the risk associated with high Lp(a) levels would largely be attenuated at low LDL-C levels. Methods and results: In 16 654 individuals from the EPIC-Norfolk prospective population study, and in 9448 individuals from the Copenhagen City Heart Study (CCHS) parallel statistical analyses were performed. Individuals were categorized according to their Lp(a) and LDL-C levels. Cut-offs were set at the 80th cohort percentile for Lp(a). Low-Density Lipoprotein Cholesterol cut-offs were set at 2.5, 3.5, 4.5, and 5.5 mmol/L. Low-Density Lipoprotein Cholesterol levels in the primary analyses were corrected for Lp(a)-derived LDL-C (LDL-Ccorr). Multivariable-adjusted hazard ratios were calculated for each category. The category with LDL-Ccorr <2.5 mmol/L and Lp(a) <80th cohort percentile was used as reference category. In the EPIC-Norfolk and CCHS cohorts, individuals with an Lp(a) ≥80th percentile were at increased CVD risk compared with those with Lp(a) <80th percentile for any LDL-Ccorr levels ≥2.5 mmol/L. In contrast, for LDL-Ccorr <2.5 mmol/L, the risk associated with elevated Lp(a) attenuated. However, there was no interaction between LDL-Ccorr and Lp(a) levels on CVD risk in either cohort. Conclusion: Lipoprotein(a) and LDL-C are independently associated with CVD risk. At LDL-C levels below <2.5 mmol/L, the risk associated with elevated Lp(a) attenuates in a primary prevention setting.

  • remnant Cholesterol low density Lipoprotein Cholesterol and blood pressure as mediators from obesity to ischemic heart disease
    Circulation Research, 2015
    Co-Authors: Anette Varbo, Marianne Benn, George Davey Smith, Nicholas J Timpson, Anne Tybjaerghansen, Borge G Nordestgaard
    Abstract:

    Rationale:Obesity leads to increased ischemic heart disease (IHD) risk, but the risk is thought to be mediated through intermediate variables and may not be caused by increased weight per se. Objective:To test the hypothesis that the increased IHD risk because of obesity is mediated through Lipoproteins, blood pressure, glucose, and C-reactive protein. Methods and Results:Approximately 90 000 participants from Copenhagen were included in a Mendelian randomization design with mediation analyses. Associations were examined using conventional measurements of body mass index and intermediate variables and using genetic variants associated with these. During ≤22 years of follow-up 13 945 participants developed IHD. The increased IHD risk caused by obesity was partly mediated through elevated levels of nonfasting remnant Cholesterol and Low-Density Lipoprotein Cholesterol, through elevated blood pressure, and possibly also through elevated nonfasting glucose levels; however, reduced high-density Lipoprotein cho...

  • pcsk9 r46l low density Lipoprotein Cholesterol levels and risk of ischemic heart disease 3 independent studies and meta analyses
    Journal of the American College of Cardiology, 2010
    Co-Authors: Marianne Benn, Borge G Nordestgaard, Peer Grande, Peter Schnohr, Anne Tybjaerghansen
    Abstract:

    Objectives The aim of this study was to examine the effect of PCSK9R46L on Low-Density Lipoprotein Cholesterol (LDL-C), risk of ischemic heart disease (IHD), and mortality. Background The 46L allele has been associated with reductions in LDL-C and risk of IHD, but results vary between studies. Methods We determined the association of R46L genotype with LDL-C, risk of IHD, myocardial infarction (MI), and mortality in the prospective CCHS (Copenhagen City Heart Study) (n = 10,032) and validated the results in: 1) the cross-sectional CGPS (Copenhagen General Population Study) (n = 26,013); and 2) the case-control CIHDS (Copenhagen Ischemic Heart Disease Study) (n = 9,654). We also performed meta-analyses of present and previous studies (n = 66,698). Results In carriers (2.6%) versus noncarriers, the 46L allele was associated with reductions in LDL-C of 0.35 to 0.55 mmol/l (11% to 16%) from 20 to 80+ years in the general population (CCHS and CGPS; p values Conclusions The PCSK946L allele was associated with reductions in LDL-C from 20 to 80+ years in the general population. The reduction in risk of IHD was larger than predicted by the observed reduction in LDL-C alone. This could be because genotype is a better predictor of lifelong exposure to LDL-C than LDL-C measured in adult life.

  • number needed to treat with rosuvastatin to prevent first cardiovascular events and death among men and women with low low density Lipoprotein Cholesterol and elevated high sensitivity c reactive protein justification for the use of statins in prevention an intervention trial evaluating rosuvastatin jupiter
    Circulation-cardiovascular Quality and Outcomes, 2009
    Co-Authors: Paul M. Ridker, John J P Kastelein, Jean G Macfadyen, Alberto J Lorenzatti, Francisco Antonio Helfenstein Fonseca, Jacques Genest, Antonio M Gotto, Wolfgang Koenig, Peter Libby, Borge G Nordestgaard
    Abstract:

    Background— As recently demonstrated, random allocation to rosuvastatin results in large relative risk reductions for first cardiovascular events among apparently healthy men and women with low levels of Low-Density Lipoprotein Cholesterol but elevated levels of high-sensitivity C-reactive protein. However, whether the absolute risk reduction among such individuals justifies wide application of statin therapy in primary prevention is a controversial issue with broad policy and public health implications. Methods and Results— Absolute risk reductions and consequent number needed to treat (NNT) values were calculated across a range of end points, timeframes, and subgroups using data from Justification for the Use of statins in Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER), a randomized evaluation of rosuvastatin 20 mg versus placebo conducted among 17 802 apparently healthy men and women with Low-Density Lipoprotein Cholesterol <130 mg/dL and high-sensitivity C-reactive protein ≥2 mg/L...

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