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Cited by 336Lipoproteins and Cardiovascular HealthCholesterol and Lipid MetabolismParaoxonase enzyme and polymorphisms

The DOI matches its Crossref record; 279 of the 282 references it cites were found in a registry or an index.

High-density lipoproteins: A consensus statement from the National Lipid Association

Toth, Peter P., Barter, Philip J., Rosenson, Robert S., Boden, William E., Chapman, M. John, Cuchel, Marina, D'Agostino, Ralph B., Davidson, Michael H., Davidson, W. Sean, Heinecke, Jay W., Karas, Richard H., Kontush, Anatol, Krauss, Ronald M., Miller, Michael, Rader, Daniel J.·2013·Journal of Clinical Lipidology
DOI 10.1016/j.jacl.2013.08.001
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Abstract

For >4 decades it has been recognized that elevated serum levels of high-density lipoprotein cholesterol (HDL-C) are associated with reduced risk of cardiovascular disease (CVD) and its sequelae. Many prospective observational studies performed around the world have confirmed an inverse relationship between HDL-C and cardiovascular risk in people irrespective of sex, race, or ethnicity. Consequently, it was assumed that, by extension, raising HDL-C through lifestyle modification and pharmacologic intervention would reduce risk of CVD. Animal studies are consistent with this assumption. Lipid treatment guidelines around the world promoted the recognition of HDL-C as a therapeutic target, especially in high-risk patients. Some post hoc analyses from randomized controlled trials also suggest that raising HDL-C beneficially affects the risk of CVD. However, a number of recent randomized studies putatively designed to test the "HDL hypothesis" have failed to show benefit. The results of these trials have caused many clinicians to question whether HDL-C is a legitimate therapeutic target. In response to the many questions and uncertainties raised by the results of these trials, the National Lipid Association convened an expert panel to evaluate the current status of HDL-C as a therapeutic target; to review the current state of knowledge of HDL particle structure, composition, and function; and to identify the salient questions yet to be answered about the role of HDL in either preventing or contributing to atherosclerotic disease. The expert panel's conclusions and clinical recommendations are summarized herein. The panel concludes that, although low HDL-C identifies patients at elevated risk, and much investigation suggests that HDL may play a variety of antiatherogenic roles, HDL-C is not a therapeutic target at the present time. Risk stratified atherogenic lipoprotein burden (low-density lipoprotein cholesterol and non-HDL-C) should remain the primary and secondary targets of therapy in patients at risk, as described by established guidelines. The National Lipid Association emphasizes that rigorous research into the biology and clinical significance of low HDL-C should continue. The development of novel drugs designed to modulate the serum levels and functionality of HDL particles should also continue. On the basis of an enormous amount of basic scientific and clinical investigation, a considerable number of reasons support the need to continue to investigate the therapeutic effect of modulating HDL structure and function.

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Crossref · 10.1016/j.jacl.2013.08.001

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Research works printed but not linked: 3

  1. Voight, 2012, Plasma HDL cholesterol and risk of myocardial infarction: a mendelian randomisation study, Lancet, 380, 572, 10.1016/S0140-6736(12)60312-2 · DOI · Paper page
  2. Morse, 2001, Niacin plus simvastatin protect against atherosclerosis progression and clinical events in CAD patients with low HDL-C and diabetes mellitus or impaired fasting glucose, J Am Coll Cardiol, 37, 262A
  3. Kannel, 1992, Efficacy of lipid profiles in prediction of coronary disease, Am Heart J, 124, 768, 10.1016/0002-8703(92)90288-7 · DOI

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Metadata

Authors
Toth, P. P., Barter, P. J., Rosenson, R. S., Boden, W. E., Chapman, M. J., Cuchel, M., D'Agostino, R. B., Davidson, M. H., Davidson, W. S., Heinecke, J. W., Karas, R. H., Kontush, A., Krauss, R. M., Miller, M., & Rader, D. J.
Affiliations
  • CGH Medical Center (US)
  • The Heart Research Institute (AU)
  • Icahn School of Medicine at Mount Sinai (US)
  • Albany Medical College (US)
  • Inserm (FR)
  • University of Pennsylvania (US)
  • University of Chicago (US)
  • University of Cincinnati (US)
  • University of Washington (US)
  • Tufts University (US)
  • University of California, San Francisco (US)
  • University of Maryland, Baltimore (US)
Corresponding author
Toth, Peter P.
ORCID
Venue
Journal of Clinical Lipidology
Publisher
Elsevier BV
Published
2013-09
Volume
7
Issue
5
Pages
484-525
ISSN
  • 1876-4789 (ISSN-L)
  • 1933-2874
DOI
10.1016/j.jacl.2013.08.001
OpenAlex
W2106601510
Cited by
336
References
282
Citations by year
2026: 6 · 2025: 21 · 2024: 10 · 2023: 21 · 2022: 34 · 2021: 24 · 2020: 38 · 2019: 25 · 2018: 28 · 2017: 26 · 2016: 19 · 2015: 41 · 2014: 41 · 2013: 2
FWCI
33.82
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Journal of clinical lipidology (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Heart, Lung, and Blood Institute (R01HL112625)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Paraoxonase enzyme and polymorphisms
Keywords
HDL cholesterol, cardiovascular risk, atherosclerosis, LDL cholesterol, non-HDL cholesterol, risk stratification
MeSH terms
Animals, Cardiovascular Diseases, Humans, Lipoproteins, HDL, Risk Factors, Societies, Scientific, Consensus, Molecular Targeted Therapy

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