HDL-cholesterol and cardiovascular disease: rethinking our approach
Abstract
PURPOSE OF REVIEW: A low level of plasma high density lipoprotein cholesterol (HDL-C) is a strong and independent risk factor for atherosclerotic cardiovascular disease (ASCVD). However, several large studies recently revealed that pharmacologic interventions that increase HDL-C concentration have not improved cardiovascular outcomes when added to standard therapy. In addition, specific genetic variants that raise HDL-C levels are not clearly associated with reduced risk of coronary heart disease. These observations have challenged the 'HDL hypothesis' that HDL-C is causally related to ASCVD and that intervention to raise HDL-C will reduce ASCVD events. This article will present the current data on the HDL hypothesis and provide a revised paradigm of considering HDL in the atherosclerotic pathway. RECENT FINDINGS: Recent evidence has shed light on the complex nature of HDL-C metabolism and function. There are compelling data that the ability of HDL to promote cholesterol efflux from macrophages, the first step in the 'reverse cholesterol transport' (RCT) pathway, is inversely associated with risk for ASCVD even after controlling for HDL-C. This has led to the 'HDL flux hypothesis' that therapeutic intervention that targets macrophage cholesterol efflux and RCT may reduce risk. Preclinical studies of such interventions show promise and early phase clinical studies, though small, are encouraging. SUMMARY: The role of HDL-C in modulating atherosclerotic disease is as yet uncertain. However, new findings and therapies targeting HDL-C show early promise and may provide an important intervention in attenuating the burden of ASCVD in the future.
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The determination of pathophysiologically relevant lipids or proteins associated with HDL may come to replace HDL-C in the future, but at present such assays are not yet available for routine clinical use.
“The determination of pathophysiologically relevant lipids or proteins associated with HDL may come to replace HDL-C in the future, but at present such assays are not yet available for routine clinical use [9, 115].”
From HDL cholesterol: reappraisal of its clinical relevance (2017) · cites this paper as [115]
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- Authors
- Siddiqi, H. K., Kiss, D., & Rader, D.
- Affiliations
- Hospital of the University of Pennsylvania (US)
- Corresponding author
- Siddiqi, Hasan K.
- Venue
- Current Opinion in Cardiology
- Published
- 2015-09
- Volume
- 30
- Issue
- 5
- Pages
- 536-542
- ISSN
- 0268-4705 (ISSN-L)
- OpenAlex
- W2416480748
- Cited by
- 77
- References
- 54
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 8 · 2023: 7 · 2022: 7 · 2021: 4 · 2020: 10 · 2019: 4 · 2018: 9 · 2017: 12 · 2016: 4 · 2015: 3
- FWCI
- 1.79
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Current Opinion in Cardiology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Paraoxonase enzyme and polymorphisms
- Keywords
- HDL cholesterol, atherosclerotic cardiovascular disease, reverse cholesterol transport, macrophage cholesterol efflux, HDL-targeted therapy, genetic variants, coronary heart disease risk
- MeSH terms
- Cardiovascular Diseases, Clinical Trials as Topic, Humans, Cholesterol, HDL, Risk Factors, Treatment Outcome, Risk Assessment, Lipid Metabolism, Lipid Regulating Agents
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