Beyond Low-Density Lipoprotein Cholesterol
Open accessAbstract
Recent clinical trials in patients with coronary artery disease (CAD) provide evidence that low-density lipoprotein cholesterol (LDL-C) levels should be lowered even further to prevent recurrent CAD. However, despite more aggressive interventions for lowering LDL-C levels, the majority of CAD events go undeterred, perhaps related to the fact that intervention was not started earlier in life or that LDL-C levels represent an incomplete picture of atherogenic potential. Nevertheless, LDL-C remains the contemporary standard as the primary goal for aggressive LDL reduction. If triglycerides are >200 mg/dl, the measurement of non-high-density lipoprotein cholesterol (HDL-C) is recommended. Measurement of apolipoprotein (apo)B has been shown in nearly all studies to outperform LDL-C and non-HDL-C as a predictor of CAD events and as an index of residual CAD risk. This is because apoB reflects the total number of atherogenic apoB-containing lipoproteins and is a superior predictor of the number of low-density lipoprotein particles (LDL-P). Estimates of LDL-P and size can also be made by nuclear magnetic resonance spectroscopy, density gradient ultracentrifugation, and gradient gel electrophoresis. Although a number of studies show that such estimates predict CAD, LDL-P, and size often accompany low HDL-C and high triglyceride levels, and therefore such additional lipoprotein testing has not been recommended for routine screening and follow-up. Because apoB is a superior predictor of LDL-P, we recommend that apoB and the apoB/apoA-I ratio be determined after measurement of LDL-C, non-HDL-C, and the ratio of total cholesterol/HDL-C to better predict CAD and assess efficacy of treatment.
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The number of LDL particles (LDLP) measured by lipoprotein subfractionation techniques is more strongly causally related to ASCVD than the cholesterol content of the particles.
“This residual risk indicates that a focus solely on the measurement of LDLC is not an optimal strategy for all patients, in part explained by accumulating evidence that the number of LDL particles (LDLP) measured by lipoprotein subfractionation techniques is more strongly causally related to ASCVD than the cholesterol content of the particles [9,10].”
From Quantifying atherogenic lipoproteins for lipid-lowering strategies: Consensus-based recommendations from EAS and EFLM (2020) · cites this paper as [9]
The Abstract and “Beyond LDL-C and Non-HDL-C” sections say LDL-C can underrepresent particle number and that particle-number-related measures can better predict CAD risk. The “Other assessments of LDL particle number and size” section reports associations between LDL-P and atherosclerosis, but the paper does not establish the claim’s stronger causal comparison with cholesterol content. The “Treatment Implications” section says it remains unresolved whether CAD risk is related to LDL-P itself or also independently to particle size; page numbers were unavailable in our copy. (LLM, conf=0.87)
Experimental — accuracy not yet measuredMany individuals experience ASCVD-related events or progression of atherosclerosis despite not having elevated LDLC or even concentrations <1.8 mmol/L.
“Despite the overwhelming evidence that LDLC-targeted therapies effectively reduce ASCVD in the population, many individuals experience ASCVD-related events or progression of atherosclerosis despite not having elevated LDLC or even concentrations < 1.8 mmol/L [9].”
From Quantifying atherogenic lipoproteins for lipid-lowering strategies: Consensus-based recommendations from EAS and EFLM (2020) · cites this paper as [9]
The Abstract says that most CAD events were not prevented despite aggressive LDL-C lowering, and Treatment Implications of LDL Heterogeneity explains that patients can have elevated risk with low or normal LDL-C. The paper discusses a 70 mg/dL (approximately 1.8 mmol/L) treatment goal, but these passages do not establish that many people experienced events or atherosclerosis progression while their LDL-C was below that level. (LLM, conf=0.85)
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- Authors
- Mudd, J. O., Borlaug, B. A., Johnston, P. V., Kral, B. G., Rouf, R., Blumenthal, R. S., & Kwiterovich, P. O.
- Affiliations
- Johns Hopkins University (US)
- Corresponding author
- Kwiterovich, Peter O.
- Venue
- Journal of the American College of Cardiology
- Publisher
- Elsevier BV
- Published
- 2007-10
- Volume
- 50
- Issue
- 18
- Pages
- 1735-1741
- ISSN
- 0735-1097 (ISSN-L)
- OpenAlex
- W16445148
- Cited by
- 136
- References
- 60
- Citations by year
- 2026: 7 · 2025: 5 · 2024: 5 · 2023: 4 · 2022: 3 · 2021: 6 · 2020: 4 · 2019: 4 · 2018: 5 · 2017: 7 · 2016: 7 · 2015: 6 · 2014: 9 · 2013: 9 · 2012: 12
- FWCI
- 12.61
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Journal of the American College of Cardiology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Keywords
- LDL cholesterol, coronary artery disease, apolipoprotein B, non-HDL cholesterol, LDL particle number, LDL particle size, triglycerides, residual cardiovascular risk, atherogenic lipoproteins, cardiovascular risk prediction
- MeSH terms
- Apolipoproteins B, Coronary Artery Disease, Humans, Lipoproteins, LDL, Particle Size, Predictive Value of Tests, Risk Factors, Biomarkers, Apolipoprotein A-I
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