Atherosclerosis Supplements (Atherosclerosis Suppl)

Publisher: Elsevier

Journal description

Supplement to Atherosclerosis.

Current impact factor: 2.29

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 2.293
2013 Impact Factor 9.667
2012 Impact Factor 4.333
2011 Impact Factor 1.702
2010 Impact Factor 2.064
2008 Impact Factor 6.559
2007 Impact Factor 4.935
2006 Impact Factor 5.875
2005 Impact Factor 8.963
2004 Impact Factor 4.14
2003 Impact Factor 4.457
2002 Impact Factor 8.3
2001 Impact Factor 16.25

Impact factor over time

Impact factor

Additional details

5-year impact 2.38
Cited half-life 9.10
Immediacy index 1.00
Eigenfactor 0.00
Article influence 0.74
Website Atherosclerosis Supplements website
Other titles Atherosclerosis., Atherosclerosis supplements
ISSN 1567-5688
OCLC 45218519
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details


  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Authors pre-print on any website, including arXiv and RePEC
    • Author's post-print on author's personal website immediately
    • Author's post-print on open access repository after an embargo period of between 12 months and 48 months
    • Permitted deposit due to Funding Body, Institutional and Governmental policy or mandate, may be required to comply with embargo periods of 12 months to 48 months
    • Author's post-print may be used to update arXiv and RepEC
    • Publisher's version/PDF cannot be used
    • Must link to publisher version with DOI
    • Author's post-print must be released with a Creative Commons Attribution Non-Commercial No Derivatives License
    • Publisher last reviewed on 03/06/2015
  • Classification

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Patients with diabetes represent a population at higher risk for cardiovascular disease. Diabetic dyslipidemia is characterized by the so-called atherogenic lipid triad, consisting of an increase in small dense low density lipoprotein particles and in triglyceride-rich lipoproteins, and a decrease in high-density lipoprotein cholesterol, with an increase in non-HDL cholesterol. Numerous trials have investigated the efficacy of add-on ezetimibe therapy for patients with type 2 diabetes and not controlled by statin therapy. The published data highly suggest that patients with type 2 diabetes may be more likely to benefit from ezetimibe/statin combination therapy. However, evidence specifically addressing hard clinical endpoints and prospective trials addressing differences in response between patients with or without diabetes are still needed.
    Atherosclerosis Supplements 02/2015; 17. DOI:10.1016/S1567-5688(15)50002-0
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    ABSTRACT: Proprotein convertase subtilisin/kexin type 9 (PCSK9) plays a major role in the regulation of lipoprotein metabolism, mostly through control of low-density lipoprotein receptor degradation. Depletion of cellular cholesterol causes a compensatory increase in plasma PCSK9 levels, which can diminish the cholesterol-lowering power of statins and may lead to the overproduction of intestinal lipoproteins, mainly thorough the up regulation of microsomal triglyceride transfer protein and the Niemann-Pick C1-like 1 protein, the target of ezetimibe. Thus, ezetimibe therapy may counter this unwanted effect of statins, providing an additional theoretical rationale for combining the effect of ezetimibe on intestinal cholesterol absorption and that of statins on cholesterol synthesis.
    Atherosclerosis Supplements 02/2015; 17. DOI:10.1016/S1567-5688(15)50006-8
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    ABSTRACT: Diabetes and metabolic syndrome are associated with abnormal postprandial lipoprotein metabolism, with a significant delay in the clearance of many lipid parameters, including triglycerides and chylomicrons. Abnormal concentrations of plasma lipids can result from changes in the production, conversion, or catabolism of lipoprotein particles. Whereas the liver is involved in controlling serum lipid levels through synthesis of liver derived triglyceride-rich lipoproteins and low-density lipoprotein metabolism, the intestine also has a major role in lipoprotein production. Postprandial lipemia results from increases in apoB-48 availability, lipogenesis, and the synthesis and absorption of cholesterol in the enterocytes. Increased intestinal lipoprotein production prolongs postprandial lipemia in patients with diabetes and MetS, and may contribute directly to atherogenesis in these patients. © 2015 Elsevier Ireland Ltd. All rights reserved.
    Atherosclerosis Supplements 02/2015; 17:12-6. DOI:10.1016/S1567-5688(15)50004-4
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    ABSTRACT: Ezetimibe exerts multiple favorable effects on the lipoprotein profile and reduces some inflammatory markers. Decreasing cholesterol synthesis with statin treatment can cause a compensatory increase in cholesterol absorption that reduces the efficacy of statin therapy, whereas addition of a cholesterol absorption inhibitor can improve outcomes. Recent evidence suggests a beneficial effect on atherosclerosis. In patients with diabetes, the effect of insulin resistance on low-density lipoprotein metabolism combined with the effect of hyperglycemia on cholesterol absorption may further diminish the favorable effects of statins. Further analysis is needed also to determine whether the stronger effects of ezetimibe seen in patients with diabetes are a consequence of an interaction of the drug with specific mechanisms. © 2015 Elsevier Ireland Ltd. All rights reserved.
    Atherosclerosis Supplements 02/2015; 17:17-22. DOI:10.1016/S1567-5688(15)50005-6
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    ABSTRACT: Nuclear receptors are involved in many important function and mediate signaling by factors including hormones, vitamins and a number of endogenous ligands and xenobiotics, several of which are involved in lipid metabolism. This review focuses on the liver X receptor (LXR), which is an important regulator of whole-body cholesterol, fatty acid, and glucose homeostasis that binds to LXR response elements as a heterodimer with retinoid X receptors, and the farnesoid X receptor (FXR), which is a bile acid receptor involved in feedback inhibition of bile acid synthesis, and thus cholesterol catabolism. These nuclear receptors regulate gene programs that control intestinal and hepatic lipid homeostasis through their effects on cholesterol transport and catabolism. © 2015 Elsevier Ireland Ltd. All rights reserved.
    Atherosclerosis Supplements 02/2015; 17:9-11. DOI:10.1016/S1567-5688(15)50003-2
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    ABSTRACT: NAFLD has become the most common liver disorder in countries, where obesity, type 2 diabetes mellitus, dyslipidemia, and metabolic syndrome are common. The strong association between these conditions and the risk of cardiovascular disease make treatment crucial. Possible interventions for NAFLD target excess body weight, insulin resistance, inflammation, oxidative stress or intestinal lipid absorption. Administration of combination therapy with a statin plus ezetimibe, associated with lifestyle changes, may represent an effective strategy because of the strong reduction in low-density lipoprotein cholesterol levels. Combination therapy is often more effective, especially when complementary mechanisms of action are involved. Ezetimibe is effective and well tolerated in combination with a number of lipid lowering therapies, including statins, orlistat, and insulin-sensitizing agents. There is strong evidence from preclinical models to supporting the use of ezetimibe in this setting. Larger controlled trials are needed to confirm its effectiveness in patients with NAFLD, to establish the most efficacious combinations and to determine whether treatment can reverse fibrosis. © 2015 Elsevier Ireland Ltd. All rights reserved.
    Atherosclerosis Supplements 02/2015; 17:27-34. DOI:10.1016/S1567-5688(15)50007-X
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    ABSTRACT: Statins represent the elective lipid-lowering strategy in hyperlipidemic and high cardiovascular-risk patients. Despite excellent safety and tolerability, reversible muscle-related and dose-dependent adverse events may decrease a patient's compliance. Large meta-analyses, post-hoc and genetic studies showed that statins might increase the risk of new-onset diabetes (NOD), particularly in insulin-resistant, obese, old patients. Race, gender, concomitant medication, dose and treatment duration may also contribute to this effect. Based on this evidence, to warn against the possibility of statin-induced NOD or worsening glycemic control in patients with already established diabetes, FDA and EMA changed the labels of all the available statins in the USA and Europe. Recent meta-analyses and retrospective studies demonstrated that statins' diabetogenicity is a dose-related class effect, but the mechanism(s) is not understood. Among statins, only pravastatin and pitavastatin do not deteriorate glycemic parameters in patients with and without type 2 diabetes mellitus. Interestingly, available data, obtained in small-scale, retrospective or single-center clinical studies, document that pitavastatin, while ameliorating lipid profile, seems protective against NOD. Beyond differences in pharmacokinetics between pitavastatin and the other statins (higher oral bioavailability, lower hepatic uptake), its consistent increases in plasma adiponectin documented in clinical studies may be causally connected with its effect on glucose metabolism. Adiponectin is a protein with antiatherosclerotic, anti-inflammatory and antidiabetogenic properties exerted on liver, skeletal muscle, adipose tissue and pancreatic beta cells. Further studies are required to confirm this unique property of pitavastatin and to understand the mechanism(s) leading to this effect.
    Atherosclerosis Supplements 01/2015; 16. DOI:10.1016/S1567-5688(14)70002-9
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    Atherosclerosis Supplements 09/2014; 15(2):52. DOI:10.1016/j.atherosclerosissup.2014.07.001
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    ABSTRACT: Homozygous familial hypercholesterolaemia (HoFH) is a rare and severe hereditary lipid disorder that is typically associated with high serum levels of low-density lipoprotein cholesterol (LDL-C). Excessive exposure to high levels of LDL-C puts affected individuals at very high risk of premature onset coronary heart disease, and this considerably limits life expectancy. Although the clinical features and treatment of HoFH have been extensively researched, societal and socio-psychological impacts of the disease have not been reported to date. The current study was conducted to investigate the burden of disease and treatment from the patient's perspective by means of semi-structured interviews with 24 HoFH patients. The findings of the survey indicate that HoFH represents a considerable burden for patients, not only due to physical signs and limitations caused by the disease but also a number of psychosocial factors, treatment-related issues and impact on their education and employment situation.
    Atherosclerosis Supplements 09/2014; 15(2):46–51. DOI:10.1016/j.atherosclerosissup.2014.07.006
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    ABSTRACT: Although homozygous familial hypercholesterolaemia (HoFH) is rare, patients with this disease have a poor prognosis, even when they receive the best available treatment, including pharmacotherapy and apheresis. The current therapeutic gap emphasizes the potential impact of new and developmental treatment options, which include lomitapide, mipomersen, anti-PCSK9 monoclonal antibodies and CETP inhibitors. It is imperative that patients with HoFH receive the most appropriate treatment as early as possible and clinical guidance is needed to provide clinicians with the information they require to expedite diagnosis and initiate effective treatment. Until now, however, guidance on the management of (HoFH) has generally been included as part of broader guidelines on dyslipidemia, FH or low-density lipoprotein (LDL)-apheresis and even in guidelines specifically on FH, HoFH has been under-represented. A consensus statement on recommendations for the management of HoFH has recently been published by a working group of the European Atherosclerosis Society. An outline of the content of the statement is presented in the current paper.
    Atherosclerosis Supplements 09/2014; 15(2):26–32. DOI:10.1016/j.atherosclerosissup.2014.07.004
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    Atherosclerosis Supplements 09/2014; 15(2):17–18. DOI:10.1016/j.atherosclerosissup.2014.07.002

  • Atherosclerosis Supplements 07/2014; 235(2):e136. DOI:10.1016/j.atherosclerosis.2014.05.381

  • Atherosclerosis Supplements 01/2013; 14(2):229. DOI:10.1016/S1567-5688(15)50001-9

  • Atherosclerosis Supplements 06/2011; 12(1):158. DOI:10.1016/S1567-5688(11)70758-9

  • Atherosclerosis Supplements 06/2011; 12(1):57. DOI:10.1016/S1567-5688(11)70262-8