Association of Apolipoprotein B–Containing Lipoproteins and Risk of Myocardial Infarction in Individuals With and Without Atherosclerosis
Open accessAbstract
IMPORTANCE: Lipid management typically focuses on levels of low-density lipoprotein cholesterol (LDL-C) and, to a lesser extent, triglycerides (TG). However, animal models and genetic studies suggest that the atherogenic particle subpopulations (LDL and very-low-density lipoprotein [VLDL]) are both important and that the number of particles is more predictive of cardiac events than their lipid content. OBJECTIVE: To determine whether common measures of cholesterol concentration, TG concentration, or their ratio are associated with cardiovascular risk beyond the number of apolipoprotein B (apoB)-containing lipoproteins. DESIGN, SETTING, AND PARTICIPANTS: This prospective cohort analysis included individuals from the population-based UK Biobank and from 2 large international clinical trials, FOURIER and IMPROVE-IT. The median (IQR) follow-up was 11.1 (10.4-11.8) years in UK Biobank and 2.5 (2.0-4.7) years in the clinical trials. Two populations were studied in this analysis: 389 529 individuals in the primary prevention group who were not taking lipid-lowering therapy and 40 430 patients with established atherosclerosis who were receiving statin treatment. EXPOSURES: ApoB, non-high-density lipoprotein cholesterol (HDL-C), LDL-C, and TG. MAIN OUTCOME AND MEASURES: The primary study outcome was incident myocardial infarction (MI). RESULTS: Of the 389 529 individuals in the primary prevention group, 224 097 (58%) were female, and the median (IQR) age was 56.0 (49.5-62.5) years. Of the 40 430 patients with established atherosclerosis, 9647 (24%) were female, and the median (IQR) age was 63 (56.2-69.0) years. In the primary prevention cohort, apoB, non-HDL-C, and TG each individually were associated with incident MI. However, when assessed together, only apoB was associated (adjusted hazard ratio [aHR] per 1 SD, 1.27; 95% CI, 1.15-1.40; P < .001). Similarly, only apoB was associated with MI in the secondary prevention cohort. Adjusting for apoB, there was no association between the ratio of TG to LDL-C (a surrogate for the ratio of TG-rich lipoproteins to LDL) and risk of MI, implying that for a given concentration of apoB-containing lipoproteins, the relative proportions of particle subpopulations may no longer be a predictor of risk. CONCLUSIONS AND RELEVANCE: In this cohort study, risk of MI was best captured by the number of apoB-containing lipoproteins, independent from lipid content (cholesterol or TG) or type of lipoprotein (LDL or TG-rich). This suggests that apoB may be the primary driver of atherosclerosis and that lowering the concentration of all apoB-containing lipoproteins should be the focus of therapeutic strategies.
AI snapshot
Written from the paper’s full text.
TL;DR
In a large primary-prevention cohort and two secondary-prevention trial cohorts, apolipoprotein B (apoB) was the only lipid parameter independently associated with myocardial infarction after full adjustment. Neither lipid content nor lipoprotein type added risk beyond the number of apoB-containing particles.
Key findings
In 389,529 primary-prevention individuals not on lipid-lowering therapy, apoB, non–HDL-C, and TG were each individually associated with incident MI, but after full adjustment only apoB remained associated (aHR per 1 SD, 1.27; 95% CI, 1.15-1.40; P < .001).
- In the same cohort, TG was associated with MI in clinically adjusted models (aHR per 1 SD, 1.16; 95% CI, 1.13-1.19; P < .001), but not after full clinical and lipid adjustment (aHR per 1 SD, 1.00; 95% CI, 0.96-1.04; P = .71).
- In 40,430 patients with established atherosclerosis receiving statin treatment, only apoB was associated with MI; TG was not associated in clinically adjusted (aHR per 1 SD, 1.03; 95% CI, 0.99-1.07) or clinically and lipid-adjusted models (aHR per 1 SD, 0.94; 95% CI, 0.89-1.00).
- Adjusting for apoB, the TG/LDL-C ratio was not associated with MI (aHR per 1 SD, 1.04; 95% CI, 0.99-1.09; P = .12), suggesting that for a given concentration of apoB-containing lipoproteins, particle type did not confer additional risk.
Methods
Prospective cohort analysis using UK Biobank primary-prevention individuals without lipid-lowering therapy (n = 389,529) and pooled secondary-prevention patients with established atherosclerosis from FOURIER and IMPROVE-IT receiving lipid-lowering therapy (n = 40,430). Median follow-up was 11.1 years in UK Biobank and 2.5 years in the clinical trials.
- Exposures were apoB, non–HDL-C, LDL-C, and TG; the primary outcome was fatal or nonfatal MI.
- Cox proportional hazards models estimated adjusted hazard ratios per 1 SD higher lipid parameter, with clinical adjustment and further adjustment for HDL-C, TG, non–HDL-C, and apoB; the TG/LDL-C ratio was evaluated with adjustment for apoB.
Limitations
The paper states that lipid values were measured using conventional lipid profiles rather than nuclear magnetic resonance spectroscopy, which would more accurately determine the VLDL-to-LDL ratio than the TG/LDL-C surrogate used.
- The paper states that UK Biobank lipid values and lipid-lowering therapy data were collected at baseline and may have changed during follow-up; because individuals with higher lipid values would be most likely to start lipid-lowering therapy, this may have attenuated associations. The study was also not enriched for severe hypertriglyceridemia.
- Evident from the text: the analysis is observational, limiting causal inference; the trial cohorts excluded patients with TG ≥400 mg/dL in FOURIER and ≥350 mg/dL in IMPROVE-IT, so severe hypertriglyceridemia is not represented.
Model-written summary. Check it against the paper before relying on it.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
10 of 13 cited sources checked · 6 supported · 0 flagged · accuracy not yet measured
- Premisecitation§ Introduction
Mendelian randomization studies have shown that apoB is a better predictor of coronary artery disease risk than serum LDL-C or triglyceride concentration.
“Mendelian randomization studies have shown that apoB is a better predictor of coronary artery disease risk than serum LDL-C or TG concentration”
Quote in the paperSubstantial claim2 of 2 sources checked- cites [4] Ference, 2019, Association of triglyceride-lowering LPL variants and LDL-C–lowering LDLR variants with risk of coronary heart disease., JAMA source
- cites [5] Richardson, 2020, Evaluating the relationship between circulating lipoprotein lipids and apolipoproteins with risk of coronary heart disease: a multivariable mendelian randomisation analysis., PLoS Med source
- Premisecitation§ Discussion
Prior work shows that apoB concentration is the most predictive parameter of CV risk.
“This study builds on prior work showing that apoB concentration is the most predictive parameter of CV risk,13,14,15”
Quote in the paperSubstantial claim3 of 3 sources checked- cites [13] Lawler, 2017, Discordance between circulating atherogenic cholesterol mass and lipoprotein particle concentration in relation to future coronary events in women., Clin Chem source
The Discussion (page not supplied) reports that, among women whose apoB and non-HDL cholesterol measurements were discordant, coronary heart disease risk tracked more closely with lipoprotein particle concentration, particularly apoB. It does not establish that apoB is the most predictive parameter of cardiovascular risk generally, across populations and risk measures. (LLM, conf=0.88)
Experimental — accuracy not yet measured - cites [14] Johannesen, 2021, Apolipoprotein B and non-HDL Cholesterol better reflect residual risk than LDL cholesterol in statin-treated patients., J Am Coll Cardiol source
The Conclusions report that apoB was a more accurate marker of all-cause mortality risk than LDL or non-HDL cholesterol in statin-treated patients, and of myocardial infarction risk than LDL cholesterol. The claim broadens those comparisons to call apoB the most predictive parameter of cardiovascular risk generally; the cited paper does not establish that broader ranking. (LLM, conf=0.87)
Experimental — accuracy not yet measured - cites [15] Sniderman, 2019, Apolipoprotein B particles and cardiovascular disease: a narrative review., JAMA Cardiol source
The Introduction reports that discordance analyses found apoB more accurate than LDL-C and non-HDL-C for predicting cardiovascular risk attributable to apoB lipoprotein particles. It does not establish apoB as the most predictive parameter of cardiovascular risk overall; it also notes studies finding apoB and non-HDL-C equivalent predictors. (LLM, conf=0.84)
Experimental — accuracy not yet measured
- Findingown data§ Results
In the primary prevention cohort (UK Biobank, no lipid-lowering therapy), apoB individually was associated with incident myocardial infarction.
“In the primary prevention cohort, apoB, non–HDL-C, and TG each individually were associated with incident MI.”
Quote in the paperSubstantial claim - Findingown data§ Results
Non-HDL-C association with MI was maintained after adding TG to the model.
“and while this was maintained after adding TG to the model”
Quote in the paperNot a substantial claim - Findingown data§ Results
The positive association between apoB and MI in primary prevention was maintained after full adjustment for lipid parameters, including TG, non-HDL-C, and HDL-C (HR, 1.27; 95% CI, 1.15-1.40; P < .001).
“This significant positive association was maintained after full adjustment for lipid parameters, including TG, non–HDL-C, and HDL-C (HR, 1.27; 95% CI, 1.15-1.40; P < .001) (Figure 1B).”
Quote in the paperSubstantial claim
- Findingown data§ Results
In primary prevention individuals without lipid-lowering therapy, apoB, LDL-C, and non-HDL-C were correlated (ρ ≥ 0.95).
“ApoB, LDL-C, and non–HDL-C were correlated (ρ ≥ 0.95).”
Quote in the paperNot a substantial claim - Findingown data§ Results
In the primary prevention cohort, triglycerides individually were associated with incident myocardial infarction.
“In the primary prevention cohort, apoB, non–HDL-C, and TG each individually were associated with incident MI.”
Quote in the paperNot a substantial claim - Findingown data§ Results
In the primary prevention cohort, non-HDL-C individually was associated with incident myocardial infarction.
“In the primary prevention cohort, apoB, non–HDL-C, and TG each individually were associated with incident MI.”
Quote in the paperNot a substantial claim - Findingown data§ Results
In the secondary prevention cohort, only apoB was associated with myocardial infarction.
“Similarly, only apoB was associated with MI in the secondary prevention cohort.”
Quote in the paperSubstantial claim - Findingown data§ Results
Non-HDL-C was no longer associated with MI when adjusted for apoB.
“non–HDL-C was no longer associated with MI when adjusted for apoB (Table 2).”
Quote in the paperSubstantial claim - Findingown data§ Results
In the primary prevention cohort, each 1 SD higher apoB was associated with a 38% increase in risk of MI (aHR, 1.38; 95% CI, 1.34-1.42; P < .001).
“In the primary prevention cohort, each 1 SD higher apoB was associated with a 38% increase in risk of MI (aHR, 1.38; 95% CI, 1.34-1.42; P < .001) (Figure 1A).”
Quote in the paperSubstantial claim - Findingown data§ Results
The association between TG and MI in primary prevention was no longer apparent when adjusting for all clinical and lipid parameters (aHR per 1 SD, 1.00; 95% CI, 0.96-1.04; P = .71).
“However, this association was no longer apparent when adjusting for all clinical and lipid parameters (aHR per 1 SD, 1.00; 95% CI, 0.96-1.04; P = .71) (Figure 1B).”
Quote in the paperSubstantial claim - Findingown data§ Results
In the primary prevention cohort, each 1-SD increase in TG was associated with a 16% greater risk of MI (aHR per 1 SD, 1.16; 95% CI, 1.13-1.19; P < .001).
“In the primary prevention cohort, with each 1-SD increase, TG was associated with a 16% greater risk of MI (aHR per 1 SD, 1.16; 95% CI, 1.13-1.19; P < .001) (Figure 1A).”
Quote in the paperNot a substantial claim - Findingown data§ Results
Non-HDL-C had similar MI association with clinical adjustment.
“Non–HDL-C had similar MI association with clinical adjustment”
Quote in the paperSubstantial claim - Findingown data§ Results
Similar associations between lipid parameters were seen in the statin-treated secondary prevention cohort.
“Similar associations between lipid parameters were seen in the statin-treated secondary prevention cohort (eTable 2 in the Supplement).”
Quote in the paperNot a substantial claim - Findingown data§ Results
When apoB, non-HDL-C, and triglycerides were assessed together in the primary prevention cohort, only apoB was associated with incident myocardial infarction (adjusted hazard ratio per 1 SD, 1.27; 95% CI, 1.15-1.40; P < .001).
“However, when assessed together, only apoB was associated (adjusted hazard ratio [aHR] per 1 SD, 1.27; 95% CI, 1.15-1.40; P < .001).”
Quote in the paperSubstantial claim - Findingown data§ Results
The same pattern of associations for apoB and non-HDL-C was seen in secondary prevention.
“This same pattern was seen in secondary prevention (Figure 1C and D).”
Quote in the paperSubstantial claim - Findingown data§ Results
After adjustment for apoB, there was no association between the ratio of triglycerides to LDL-C and risk of myocardial infarction.
“Adjusting for apoB, there was no association between the ratio of TG to LDL-C (a surrogate for the ratio of TG-rich lipoproteins to LDL) and risk of MI”
Quote in the paperSubstantial claim- Rests on an assumption: The ratio of triglycerides to LDL-C is a surrogate for the ratio of triglyceride-rich lipoproteins to LDL.
- Findingown data§ Results
The flat association between TG/LDL-C ratio and MI was also seen in sensitivity analyses in the subset of individuals with TG levels greater than 200 mg/dL.
“This flat association was also seen in sensitivity analyses in the subset of individuals with TG levels greater than 200 mg/dL.”
Quote in the paperNot a substantial claim - Findingown data§ Results
In the secondary prevention group of patients treated with statin, TG was not associated with risk of MI in the clinically and lipid-adjusted model (aHR per 1 SD, 0.94; 95% CI, 0.89-1.00).
“or clinically and lipid-adjusted models (aHR per 1 SD, 0.94; 95% CI, 0.89-1.00) (Figure 1C, D).”
Quote in the paperSubstantial claim - Findingown data§ Results
The patterns for apoB and TG were consistent in sensitivity analyses performed in the subset of individuals with TG greater than 200 mg/dL and in the placebo and additional lipid-lowering therapy arms separate from both clinical trials.
“The patterns for apoB and TG were consistent in sensitivity analyses performed in the subset of individuals with TG greater than 200 mg/dL and in the placebo and additional lipid-lowering therapy arms separate from both clinical trials.”
Quote in the paperNot a substantial claim - Findingown data§ Results
Variance inflation factor values greater than 10 were obtained for apoB and non-HDL-C when the 2 lipids appeared in the same model.
“We obtained variant inflation factor values greater than 10 for apoB and non–HDL-C when the 2 lipids appeared in the same model”
Quote in the paperSubstantial claim - Findingown data§ Discussion
The amount of lipid (cholesterol or TG) carried on the apoB-containing lipoprotein particles did not confer additional risk beyond apoB concentration.
“Second, the amount of lipid (cholesterol or TG) carried on the apoB-containing lipoprotein particles did not confer additional risk beyond apoB concentration.”
Quote in the paperSubstantial claim - Findingreasoning§ Discussion
Both these prior studies and our work suggest that a TG-rich lipoprotein is just as important a risk factor for MI as an LDL particle.
“Of note, though, both these prior studies and our work suggest that a TG-rich lipoprotein is just as important a risk factor for MI as an LDL particle.”
Quote in the paperSubstantial claim- Rests on an assumption: TG estimates TG-rich lipoproteins (VLDL and IDL) and LDL-C estimates LDL particles.
- Findingown data§ Results
In the bootstrapped Cox models, despite an expected larger SD for apoB and non-HDL-C compared with TG, the mean estimates are consistent with the general findings.
“despite an expected larger SD for apoB and non–HDL-C compared with TG, the mean estimates are consistent with our general findings.”
Quote in the paperNot a substantial claim - Findingown data§ Results
In the secondary prevention group of patients treated with statin, TG was not associated with risk of MI in the clinically adjusted model (aHR per 1 SD, 1.03; 95% CI, 0.99-1.07).
“In the secondary prevention group of patients treated with statin, TG was not associated with risk of MI in either clinically adjusted (aHR per 1 SD, 1.03; 95% CI, 0.99-1.07)”
Quote in the paperSubstantial claim - Findingown data§ Results
The association between the ratio of lipoprotein types and MI was flat (aHR per 1 SD, 1.04; 95% CI, 0.99-1.09; P = .12).
“The association between the ratio of lipoprotein types and MI was flat (aHR per 1 SD, 1.04; 95% CI, 0.99-1.09; P = .12)”
Quote in the paperSubstantial claim - Findingown data§ Results
The findings were all consistent when a broader atherosclerotic cardiovascular disease composite end point was evaluated.
“The findings were all consistent when a broader atherosclerotic cardiovascular disease composite end point was evaluated (eTables 3 and 4 in the Supplement).”
Quote in the paperNot a substantial claim - Findingown data§ Conclusions
In this cohort study, association with MI was best captured by the number of apoB-containing lipoproteins, independent from lipid content (cholesterol or TG) or type of lipoprotein (LDL or TG-rich).
“In this cohort study, association with MI was best captured by the number of apoB-containing lipoproteins, independent from lipid content (cholesterol or TG) or type of lipoprotein (LDL or TG-rich).”
Quote in the paperSubstantial claim - Findingown data§ Discussion
The type of apoB-containing lipoprotein particle, either TG-rich lipoproteins or LDL particle, did not confer additional risk beyond particle concentration.
“Third, the type of apoB-containing lipoprotein particle, either TG-rich lipoproteins or LDL particle, did not confer additional risk beyond particle concentration.”
Quote in the paperSubstantial claim- Rests on an assumption: TG estimates TG-rich lipoproteins (VLDL and IDL) and LDL-C estimates LDL particles.
- Interpretationown data§ Results
For a given concentration of apoB-containing lipoproteins, the relative proportions of particle subpopulations may no longer be a predictor of risk.
“implying that for a given concentration of apoB-containing lipoproteins, the relative proportions of particle subpopulations may no longer be a predictor of risk.”
Quote in the paperSubstantial claim - Premisereasoning§ Introduction
ApoB measurement can be used as a surrogate for the concentration or number of atherogenic lipoprotein particles.
“As there is exactly 1 apoB-100 on each of the atherogenic apoB-containing particles (ie, LDL, IDL, and VLDL), its measurement can be used as a surrogate for the concentration or number of atherogenic lipoprotein particles.”
Quote in the paperSubstantial claim- Rests on an assumption: There is exactly one apoB-100 molecule on each atherogenic apoB-containing particle (LDL, IDL, and VLDL).
- Interpretationown data§ Results
In this cohort study, risk of myocardial infarction was best captured by the number of apoB-containing lipoproteins, independent from lipid content (cholesterol or triglycerides) or type of lipoprotein (LDL or triglyceride-rich).
“In this cohort study, risk of MI was best captured by the number of apoB-containing lipoproteins, independent from lipid content (cholesterol or TG) or type of lipoprotein (LDL or TG-rich).”
Quote in the paperSubstantial claim - Interpretationown data§ Results
ApoB may be the primary driver of atherosclerosis.
“This suggests that apoB may be the primary driver of atherosclerosis”
- Also stated in: § Conclusions · hedged
“This suggests that apoB may be the primary driver of atherosclerosis”
Quote in the paperSubstantial claim - Also stated in: § Conclusions · hedged
- Study design and conductnone given§ Discussion
In this study, all lipid-adjusted analyses included adjustment for apoB, thereby accounting for lipoprotein particle concentration in the risk assessment.
“In this study, all lipid-adjusted analyses included adjustment for apoB, thereby accounting for lipoprotein particle concentration in the risk assessment.”
Quote in the paperSubstantial claim - Interpretationreasoning§ Discussion
Standard measurements of TG and cholesterol can be misleading as they measure overall serum concentrations without directly addressing the number and type of particles.
“Standard measurements of TG and cholesterol can be misleading as they measure overall serum concentrations without directly addressing the number and type of particles.”
Quote in the paperSubstantial claim - Interpretationown data§ Results
For a given number of apoB-containing lipoproteins, one type is not associated with significantly greater risk than the other.
“indicating that, for a given number of apoB-containing lipoproteins, one type is not associated with significantly greater risk than the other (Figure 2).”
Quote in the paperSubstantial claim- Rests on an assumption: TG estimates TG-rich lipoproteins (VLDL and IDL) and LDL-C estimates LDL particles.
- Interpretationown data§ Discussion
For two individuals with the same LDL-C levels, if one has twice the number of LDL particles but half the cholesterol content on each, that individual will have a higher risk of MI than the other.
“For example, 2 individuals can have the same LDL-C levels, but if one has twice the number of LDL particles but half the cholesterol content on each, our data suggest that that individual will have a higher risk of MI than the other.”
Quote in the paperSubstantial claim- Rests on an assumption: ApoB is in a 1:1 association with atherogenic lipoprotein particles.
- Classified as probably not a substantial claim. 19
- May combine two claims. 14
Classified as probably not a substantial claim.
Premisecitation§ IntroductionThe number of atherogenic particles may be the driver of cardiovascular risk, rather than cholesterol or triglyceride content per se.
“suggesting that the number of atherogenic particles may be the driver of cardiovascular risk, rather than cholesterol or TG content per se.4,5”
Quote in the paperSubstantial claim2 of 2 sources checked- cites [4] Ference, 2019, Association of triglyceride-lowering LPL variants and LDL-C–lowering LDLR variants with risk of coronary heart disease., JAMA source
- cites [5] Richardson, 2020, Evaluating the relationship between circulating lipoprotein lipids and apolipoproteins with risk of coronary heart disease: a multivariable mendelian randomisation analysis., PLoS Med source
Classified as probably not a substantial claim.
Premisecitation§ IntroductionRecent studies have suggested that triglycerides and remnant cholesterol may be more potent risk factors for myocardial infarction than LDL-C is.
“These studies have suggested that TG and remnant cholesterol may be more potent risk factors for myocardial infarction (MI) than LDL-C is.2,3”
Quote in the paperSubstantial claim1 of 2 sources checked- cites [2] Castañer, 2020, Remnant cholesterol, not LDL cholesterol, is associated with incident cardiovascular disease., J Am Coll Cardiol source
- cites [3] Balling, 2020, VLDL cholesterol accounts for one-half of the risk of myocardial infarction associated with apoB-containing lipoproteins., J Am Coll Cardiol source
The paper’s Abstract (page unavailable) reports that VLDL cholesterol explained 50% of the myocardial-infarction risk associated with apoB-containing lipoproteins, compared with 29% for IDL plus LDL cholesterol. This supports the remnant-cholesterol portion of the claim. It does not support the triglyceride portion: the same passage says VLDL triglycerides did not explain that risk. (LLM, conf=0.88)
Experimental — accuracy not yet measured
May combine two claims.
Premisecitation§ DiscussionThese measures do not identify the number of apoB-containing lipoprotein particles as reliably and have been shown to not always accurately predict CV risk.
“However, it should be recognized that these measures do not identify the number of apoB-containing lipoprotein particles as reliably and have been shown to not always accurately predict CV risk.17”
Quote in the paperSubstantial claim1 of 1 sources checked- cites [17] Mora, 2014, Discordance of low-density lipoprotein (LDL) cholesterol with alternative LDL-related measures and future coronary events., Circulation source
Probably not a substantial claim: may not pass S3 (load-bearing).
Premisecitation§ DiscussionPrior studies have shown that nuclear magnetic resonance spectroscopy is not superior to conventional lipid profiles.
“While such an approach can specifically measure the number and particle size of lipoprotein particles, prior studies have shown that they are not superior to conventional lipid profiles.22”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites [22] Mora, 2009, Lipoprotein particle profiles by nuclear magnetic resonance compared with standard lipids and apolipoproteins in predicting incident cardiovascular disease in women., Circulation source
Probably not a substantial claim: may not pass S3 (load-bearing).
Findingown data§ ResultsIn primary prevention individuals without lipid-lowering therapy, TG was positively correlated with apoB, LDL-C, and non-HDL-C (ρ = 0.38-0.52).
“TG was positively correlated with these 3 parameters (ρ = 0.38-0.52).”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Findingown data§ ResultsIn primary prevention individuals without lipid-lowering therapy, HDL-C was negatively correlated with TG (ρ = −0.49).
“and negatively correlated with TG (ρ = −0.49).”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Findingown data§ ResultsIn primary prevention individuals without lipid-lowering therapy, HDL-C was correlated with apoB, LDL-C, and non-HDL-C (ρ ≤ |0.12|).
“HDL-C was correlated with apoB, LDL-C, and non–HDL-C (ρ ≤ |0.12|)”
Quote in the paperNot a substantial claimMay combine two claims.
Findingown data§ DiscussionApoB was the only independent driver of lipid-associated MI risk, confirming the importance of particle concentration.
“First, apoB was the only independent driver of lipid-associated MI risk, confirming the importance of particle concentration.”
Quote in the paperSubstantial claim- Rests on an assumption: ApoB is in a 1:1 association with atherogenic lipoprotein particles.
Probably not a substantial claim: may not pass S3 (load-bearing).
Findingown data§ ResultsIn individuals not receiving lipid-lowering therapy, the median (IQR) TG/LDL-C ratio was 0.39 (0.29-0.55).
“In individuals not receiving lipid-lowering therapy, the median (IQR) TG/LDL-C ratio was 0.39 (0.29-0.55).”
Quote in the paperNot a substantial claimMay combine two claims.
Findingnone given§ DiscussionEach of these findings was consistent across both primary and secondary populations and in those receiving and not receiving lipid lowering therapy.
“Each of these findings was consistent across both primary and secondary populations and in those receiving and not receiving lipid lowering therapy.”
Quote in the paperSubstantial claimMay combine two claims.
Findingown data§ ResultsThe flat association between TG/LDL-C ratio and MI was seen up to TG/LDL-C ratios of 2 in the clinical trials, where LDL-C lowering therapies lowered LDL-C, resulting in much higher TG/LDL-C ratios.
“This flat association was seen up to TG/LDL-C ratios of 2 in the clinical trials, where LDL-C lowering therapies lowered LDL-C, resulting in much higher TG/LDL-C ratios (eFigure 2 in the Supplement).”
Quote in the paperSubstantial claimMay combine two claims.
Findingown data§ DiscussionThis study demonstrates that LDL-C and TG levels do not have predictive value beyond apoB.
“and further advances our understanding by demonstrating that LDL-C and TG levels do not have predictive value beyond apoB.”
Quote in the paperSubstantial claimMay combine two claims.
Findingown data§ DiscussionLDL-C and non-HDL-C are correlated with apoB, and therefore can be used to approximate lipoprotein particle concentration and CV risk when apoB is not available.
“LDL-C and non–HDL-C are correlated with apoB, and therefore can be used to approximate lipoprotein particle concentration and CV risk when apoB is not available.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductnone given§ MethodsA sensitivity analysis using a broader composite atherosclerotic cardiovascular disease end point was performed in each cohort.
“A sensitivity analysis using a broader composite atherosclerotic cardiovascular disease end point was performed in each cohort.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
Study design and conductreasoning§ MethodsIn FOURIER and IMPROVE-IT, myocardial infarction was adjudicated by the TIMI central clinical end points committee, and adjudicators were blinded to lipid levels and treatment arm.
“In FOURIER and IMPROVE-IT, MI was a component of the trials’ primary end points and was therefore adjudicated by the Thrombolysis in Myocardial Infarction (TIMI) central clinical end points committee. Adjudicators were blinded to lipid levels and treatment arm.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductnone given§ DiscussionNuclear magnetic resonance spectroscopy would offer a more accurate method for determining the VLDL-to-LDL ratio compared with the surrogate of TG to LDL-C used in this study.
“Nonetheless, nuclear magnetic resonance spectroscopy would offer a more accurate method for determining the VLDL-to-LDL ratio compared with the surrogate of TG to LDL-C used in this study.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Interpretationreasoning§ DiscussionBecause individuals with higher lipid values would be most likely to start lipid-lowering therapy, this may have attenuated the association for each lipid parameter.
“Because individuals with higher lipid values would be most likely to start lipid-lowering therapy, we anticipate this may have attenuated the association for each lipid parameter.”
Quote in the paperNot a substantial claim- Rests on an assumption: Individuals with higher lipid values are most likely to start lipid-lowering therapy.
Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
Premisecitation§ DiscussionThe American Association of Clinical Chemistry has stated that apoB is standardized and can be measured with more accuracy than LDL-C and non-HDL-C.
“but the American Association of Clinical Chemistry has stated that apoB is standardized and can be measured with more accuracy than LDL-C and non–HDL-C.21”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [21] Cole, 2013, Association of apolipoprotein B and nuclear magnetic resonance spectroscopy-derived LDL particle number with outcomes in 25 clinical studies: assessment by the AACC Lipoprotein and Vascular Diseases Division Working Group on Best Practices., Clin Chem source
Probably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductnone given§ DiscussionLipid values in these cohorts were measured using conventional lipid profiles rather than nuclear magnetic resonance spectroscopy.
“Lipid values in these cohorts were measured using conventional lipid profiles rather than nuclear magnetic resonance spectroscopy.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
Study design and conductown data§ DiscussionOur study was not enriched for patients with severe hypertriglyceridemia, so we cannot comment on risk associations in such individuals.
“Moreover, our study was not enriched for patients with severe hypertriglyceridemia, so we cannot comment on risk associations in such individuals.”
Quote in the paperNot a substantial claimMay combine two claims.
Interpretationreasoning§ DiscussionFor two individuals with the same apoB levels, an individual with lower LDL-C may be perceived as being at lower risk, but that is not necessarily the case.
“Conversely, 2 individuals can have the same apoB levels (and hence the same number of atherogenic lipoproteins). An individual with lower LDL-C, the metric on which the field currently focuses, may be perceived as being at lower risk, but that is not necessarily the case.”
Quote in the paperSubstantial claim- Rests on an assumption: ApoB is in a 1:1 association with atherogenic lipoprotein particles.
Classified as probably not a substantial claim. May combine two claims.
Premisenone given§ DiscussionThese prior studies have limitations that include incomplete model adjustment, residual confounding, and not accounting for the concentration of lipoprotein particles as measured by apoB.
“However, these studies have limitations that include incomplete model adjustment, residual confounding, and not accounting for the concentration of lipoprotein particles as measured by apoB.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Premisecitation§ DiscussionRecent publications have reported that TG, rather than LDL-C, most strongly predict CV risk.
“These findings are of increased relevance as recent publications have reported that TG, rather than LDL-C, most strongly predict CV risk.2”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [2] Castañer, 2020, Remnant cholesterol, not LDL cholesterol, is associated with incident cardiovascular disease., J Am Coll Cardiol source
May combine two claims.
Interpretationreasoning§ DiscussionApoB allows for accurate assessment of particle concentration, and when it is held constant, the measurements of TG and LDL-C reflect particle type and content.
“ApoB allows for accurate assessment of particle concentration, and when it is held constant, the measurements of TG and LDL-C reflect particle type and content.”
Quote in the paperSubstantial claim- Rests on an assumption: ApoB is in a 1:1 association with atherogenic lipoprotein particles.
Classified as probably not a substantial claim. May combine two claims.
Study design and conductown data§ DiscussionLipid values and lipid-lowering therapy data were collected at baseline in UK Biobank, but may have changed in some individuals during the follow-up period.
“Additionally, lipid values and lipid-lowering therapy data were collected at baseline in UK Biobank, but may have changed in some individuals during the follow-up period.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
Premisereasoning§ DiscussionLDL-C is often calculated by laboratories rather than directly measured, which may contribute to less accurate measurements compared with those for apoB.
“Indeed, LDL-C is often calculated by laboratories rather than directly measured, which may contribute to less accurate measurements compared with those for apoB and support more widespread use of apoB.”
Quote in the paperNot a substantial claimClassified as probably not a substantial claim.
Study design and conductown data§ ResultsThe collinearity issue was addressed by running a bootstrapped version of an adjusted Cox regression for the risk of MI, including all the lipids under examination (apoB, TG, non-HDL-C, and HDL).
“we addressed the issue by running a bootstrapped version of an adjusted Cox regression for the risk of MI, including all the lipids under examination (apoB, TG, non–HDL-C, and HDL).”
Quote in the paperSubstantial claim
The paper relies on this without support.
There is exactly one apoB-100 molecule on each atherogenic apoB-containing particle (LDL, IDL, and VLDL).
“As there is exactly 1 apoB-100 on each of the atherogenic apoB-containing particles (ie, LDL, IDL, and VLDL)”
The paper relies on this without support.
Measures of cholesterol and triglycerides provide information on the lipids in the blood and thus only indirectly on the types of lipoproteins and their composition, and not on the number of lipoproteins.
“However, measures of cholesterol and TG provide information on the lipids in the blood and thus only indirectly on the types of lipoproteins and their composition, and not on the number of lipoproteins.”
The paper relies on this without support.
Fatal or nonfatal myocardial infarction can be known with high precision and is strongly associated with dyslipidemia.
“The end point of interest in both cohorts was fatal or nonfatal MI, a cardiovascular outcome that can be known with high precision and is strongly associated with dyslipidemia.”
The paper relies on this without support.
The ratio of triglycerides to LDL-C is a surrogate for the ratio of triglyceride-rich lipoproteins to LDL.
“the ratio of TG to LDL-C (a surrogate for the ratio of TG-rich lipoproteins to LDL)”
The paper relies on this without support.
ApoB is in a 1:1 association with atherogenic lipoprotein particles.
“given the 1:1 association between apoB and atherogenic lipoprotein particles.”
The paper relies on this without support.
TG estimates TG-rich lipoproteins (VLDL and IDL) and LDL-C estimates LDL particles.
“TG-rich lipoproteins (ie, VLDL and IDL, estimated by TG) or LDL particle (estimated by LDL-C).”
The paper relies on this without support.
Individuals with higher lipid values are most likely to start lipid-lowering therapy.
“Because individuals with higher lipid values would be most likely to start lipid-lowering therapy”
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Supplement labels the secondary cohort as untreated
MinorThe supplementary-table title describes the secondary-prevention cohort as receiving no lipid-lowering therapy, whereas the Methods describe that cohort as receiving lipid-lowering therapy.
“eTable 4. Baseline lipid parameters and adjusted hazard ratios for the composite endpoint myocardial infarction, stroke or cv death in the secondary prevention cohort without lipid lowering therapy”
“The second group included 40 430 patients with established atherosclerosis disease who were receiving lipid-lowering therapy”
Not every lipid-adjusted analysis adjusted for apoB
MinorThe discussion says all lipid-adjusted analyses included apoB adjustment. The results also describe a model that adds TG to the non-HDL-C analysis before separately adjusting for apoB, consistent with the partial-adjustment models in Table 2.
“In this study, all lipid-adjusted analyses included adjustment for apoB, thereby accounting for lipoprotein particle concentration in the risk assessment.”
“Non–HDL-C had similar MI association with clinical adjustment, and while this was maintained after adding TG to the model, non–HDL-C was no longer associated with MI when adjusted for apoB (Table 2).”
Cites
Sudlow, C., Gallacher, J., Allen, N., Beral, V., Burton, P., Danesh, J., Downey, P., Elliott, P., Green, J., Landray, M., et al. (2015) · PLOS Medicine · doi:10.1371/journal.pmed.1001779 · Cited by 12,728 · see citing works
Mach, F., Baigent, C., Catapano, A. L., Koskinas, K. C., Casula, M., Badimon, L., Chapman, M. J., De Backer, G. G., Delgado, V., Ference, B. A., et al. (2020) · European Heart Journal · doi:10.1093/eurheartj/ehz455 · Cited by 8,961 · see citing works
Self-citationThe UK Biobank resource with deep phenotyping and genomic data
Bycroft, C., Freeman, C., Petkova, D., Band, G., Elliott, L. T., Sharp, K., Motyer, A., Vukcevic, D., Delaneau, O., O’Connell, J., et al. (2018) · Nature · doi:10.1038/s41586-018-0579-z · Cited by 8,876 · see citing works
Evolocumab and Clinical Outcomes in Patients with Cardiovascular Disease
Sabatine, M. S., Giugliano, R. P., Keech, A. C., Honarpour, N., Wiviott, S. D., Murphy, S. A., Kuder, J. F., Wang, H., Liu, T., Wasserman, S. M., et al. (2017) · New England Journal of Medicine · doi:10.1056/nejmoa1615664 · Cited by 6,138 · see citing works
Self-citationMach, F., Baigent, C., Catapano, A. L., Koskinas, K. C., Casula, M., Badimon, L., Chapman, M. J., De Backer, G. G., Delgado, V., Ference, B. A., et al. (2019) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2019.08.014 · Cited by 4,854 · see citing works
Self-citationEzetimibe Added to Statin Therapy after Acute Coronary Syndromes
Cannon, C. P., Blazing, M. A., Giugliano, R. P., McCagg, A., White, J. A., Theroux, P., Darius, H., Lewis, B. S., Ophuis, T. O., Jukema, J. W., et al. (2015) · New England Journal of Medicine · doi:10.1056/nejmoa1410489 · Cited by 4,487 · see citing works
Self-citationKANNEL, W. B., DAWBER, T. R., KAGAN, A., REVOTSKIE, N., & STOKES, J. (1961) · Annals of Internal Medicine · doi:10.7326/0003-4819-55-1-33 · Cited by 1,837 · see citing works
Elliott, P., Peakman, T. C., & Biobank, O. B. O. U. (2008) · International Journal of Epidemiology · doi:10.1093/ije/dym276 · Cited by 996 · see citing works
Richardson, T. G., Sanderson, E., Palmer, T. M., Ala-Korpela, M., Ference, B. A., Davey Smith, G., & Holmes, M. V. (2020) · PLOS Medicine · doi:10.1371/journal.pmed.1003062 · Cited by 843 · see citing works
Self-citationBoekholdt, S. M., Arsenault, B. J., Mora, S., Pedersen, T. R., LaRosa, J. C., Nestel, P. J., Simes, R. J., Durrington, P., Hitman, G. A., Welch, K. M. A., et al. (2012) · JAMA · doi:10.1001/jama.2012.366 · Cited by 795 · see citing works
Ference, B. A., Kastelein, J. J. P., Ray, K. K., Ginsberg, H. N., Chapman, M. J., Packard, C. J., Laufs, U., Oliver-Williams, C., Wood, A. M., Butterworth, A. S., et al. (2019) · JAMA · doi:10.1001/jama.2018.20045 · Cited by 724 · see citing works
Self-citationSniderman, A. D., Williams, K., Contois, J. H., Monroe, H. M., McQueen, M. J., de Graaf, J., & Furberg, C. D. (2011) · Circulation: Cardiovascular Quality and Outcomes · doi:10.1161/circoutcomes.110.959247 · Cited by 659 · see citing works
Apolipoprotein B Particles and Cardiovascular Disease: A Narrative Review
Sniderman, A. D., Thanassoulis, G., Glavinovic, T., Navar, A. M., Pencina, M., Catapano, A., & Ference, B. A. (2019) · JAMA Cardiology · doi:10.1001/jamacardio.2019.3780 · Cited by 593 · see citing works
Self-citationRemnant Cholesterol, Not LDL Cholesterol, Is Associated With Incident Cardiovascular Disease
Castañer, O., Pintó, X., Subirana, I., Amor, A. J., Ros, E., Hernáez, Á., Martínez-González, M. Á., Corella, D., Salas-Salvadó, J., Estruch, R., et al. (2020) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2020.10.008 · Cited by 540 · see citing works
Mora, S., Otvos, J. D., Rifai, N., Rosenson, R. S., Buring, J. E., & Ridker, P. M. (2009) · Circulation · doi:10.1161/circulationaha.108.816181 · Cited by 490 · see citing works
Johannesen, C. D. L., Mortensen, M. B., Langsted, A., & Nordestgaard, B. G. (2021) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2021.01.027 · Cited by 359 · see citing works
Cannon, C. P., Giugliano, R. P., Blazing, M. A., Harrington, R. A., Peterson, J. L., Sisk, C. M., Strony, J. T., Musliner, T. A., McCabe, C. H., Veltri, E. P., et al. (2008) · American Heart Journal · doi:10.1016/j.ahj.2008.07.023 · Cited by 297 · see citing works
Self-citationMora, S., Buring, J. E., & Ridker, P. M. (2014) · Circulation · doi:10.1161/circulationaha.113.005873 · Cited by 255 · see citing works
Sabatine, M. S., Giugliano, R. P., Keech, A., Honarpour, N., Wang, H., Liu, T., Wasserman, S. M., Scott, R., Sever, P. S., & Pedersen, T. R. (2016) · American Heart Journal · doi:10.1016/j.ahj.2015.11.015 · Cited by 176 · see citing works
Self-citationBalling, M., Afzal, S., Varbo, A., Langsted, A., Davey Smith, G., & Nordestgaard, B. G. (2020) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2020.09.610 · Cited by 175 · see citing works
Wilson, P. W. F., Jacobson, T. A., Martin, S. S., Jackson, E. J., Le, N., Davidson, M. H., Vesper, H. W., Frikke‐Schmidt, R., Ballantyne, C. M., & Remaley, A. T. (2021) · Journal of clinical lipidology · doi:10.1016/j.jacl.2021.09.046 · Cited by 134 · see citing works
Cole, T. G., Contois, J. H., Csako, G., McConnell, J. P., Remaley, A. T., Devaraj, S., Hoefner, D. M., Mallory, T., Sethi, A. A., & Warnick, G. R. (2013) · Clinical Chemistry · doi:10.1373/clinchem.2012.196733 · Cited by 122 · see citing works
Lawler, P. R., Akinkuolie, A. O., Ridker, P. M., Sniderman, A. D., Buring, J. E., Glynn, R. J., Chasman, D. I., & Mora, S. (2017) · Clinical Chemistry · doi:10.1373/clinchem.2016.264515 · Cited by 104 · see citing works
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Palaniappan, L. P., Allen, N. B., Almarzooq, Z., Anderson, C. A. M., Arora, P. K., Avery, C. L., Baker-Smith, C. M., Bansal, N., Currie, M. E., Earlie, R. S., et al. (2026) · Circulation · doi:10.1161/cir.0000000000001412 · Cited by 312 · see citing works
2026 ACC/AHA/AACVPR/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Dyslipidemia
Blumenthal, R. S., Morris, P. B., Gaudino, M., Johnson, H. M., Anderson, T. S., Bittner, V. A., Blankstein, R., Brewer, L. C., Cho, L., de Ferranti, S. D., et al. (2026) · JACC · doi:10.1016/j.jacc.2025.11.016 · Cited by 304 · see citing works
Non-HDL-cholesterol in dyslipidemia: Review of the state-of-the-art literature and outlook
Raja, V., Aguíar, C., Al-Sayed, N., Chibber, Y. S., ElBadawi, H., Владиславович, Е. М., Hermans, M. P., Pandey, R. C., Ray, K. K., Tokgözoğlu, L. S., et al. (2023) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2023.117312 · Cited by 217 · see citing works
Friend or Foe? The Role of Animal-Source Foods in Healthy and Environmentally Sustainable Diets
Beal, T., Gardner, C. D., Herrero, M., Iannotti, L. L., Merbold, L., Nordhagen, S., & Mottet, A. (2023) · Journal of Nutrition · doi:10.1016/j.tjnut.2022.10.016 · Cited by 211 · see citing works
Björnson, E., Adiels, M., Taskinen, M.-R., Burgess, S., Rawshani, A., Borén, J., & Packard, C. J. (2023) · European Heart Journal · doi:10.1093/eurheartj/ehad337 · Cited by 183 · see citing works
Cheeley, M. K., Saseen, J. J., Agarwala, A., Ravilla, S., Ciffone, N., Jacobson, T. A., Dixon, D. L., & Maki, K. C. (2022) · Journal of Clinical Lipidology · doi:10.1016/j.jacl.2022.05.068 · Cited by 197 · see citing works
Glavinovic, T., Thanassoulis, G., Graaf, J. D., Couture, P., Hegele, R. A., & Sniderman, A. D. (2022) · Journal of the American Heart Association · doi:10.1161/jaha.122.025858 · Cited by 166 · see citing works
Burgess, S., Mason, A. M., Grant, A. J., Slob, E. A. W., Gkatzionis, A., Zuber, V., Patel, A. R., Tian, H., Liu, C., Haynes, W. G., et al. (2023) · The American Journal of Human Genetics · doi:10.1016/j.ajhg.2022.12.017 · Cited by 148 · see citing works
World Heart Federation Cholesterol Roadmap 2022
Ray, K. K., Ference, B. A., Séverin, T., Blom, D. J., Nicholls, S. J., Shiba, M. H., Almahmeed, W. A., Rodrigo Alonso, K., Daccord, M., Владиславович, Е. М., et al. (2022) · Global Heart · doi:10.5334/gh.1154 · Cited by 146 · see citing works
Self-citationWriting Committee Members, Blumenthal, R. S., Morris, P. B., Gaudino, M., Johnson, H. M., Anderson, T. S., Bittner, V. A., Blankstein, R., Brewer, L. C., Cho, L., et al. (2026) · Circulation · doi:10.1161/cir.0000000000001423 · Cited by 122 · see citing works
Kirkpatrick, C. F., Sikand, G., Petersen, K. S., Anderson, C. A. M., Aspry, K. E., Bolick, J. P., Kris‐Etherton, P. M., & Maki, K. C. (2023) · Journal of clinical lipidology · doi:10.1016/j.jacl.2023.05.099 · Cited by 128 · see citing works
Sniderman, A. D., Dufresne, L., Pencina, K. M., Bilgic, S., Thanassoulis, G., & Pencina, M. J. (2024) · European Heart Journal · doi:10.1093/eurheartj/ehae258 · Cited by 117 · see citing works
“26 However, given that apoB is a more accurate measure of the adequacy of lipid-lowering therapy than LDL-C or non-HDL-C, 1,3–13 , 27 there In summary, the present prospective discordance analysis adds to the evidence that apoB is a more accurate marker of cardiovascular risk than LDL-C, non-HDL-C,…”
BackgroundResultSoffer, D. E., Marston, N. A., Maki, K. C., Jacobson, T. A., Bittner, V. A., Peña, J. M., Thanassoulis, G., Martin, S. S., Kirkpatrick, C. F., Virani, S. S., et al. (2024) · Journal of Clinical Lipidology · doi:10.1016/j.jacl.2024.08.013 · Cited by 115 · see citing works
Self-citationHansen, C. D., Gram-Kampmann, E.-M., Hansen, J. K., Hugger, M. B., Madsen, B. S., Jensen, J. M., Olesen, S., Torp, N., Rasmussen, D. N., Kjærgaard, M., et al. (2023) · Annals of Internal Medicine · doi:10.7326/m22-1787 · Cited by 110 · see citing works
Hagström, E., Steg, P. G., Szarek, M., Bhatt, D. L., Bittner, V. A., Danchin, N., Diaz, R., Goodman, S. G., Harrington, R. A., Jukema, J. W., et al. (2022) · Circulation · doi:10.1161/circulationaha.121.057807 · Cited by 118 · see citing works
Emerging Evidence of Pathological Roles of Very-Low-Density Lipoprotein (VLDL)
Huang, J.-K., & Lee, H. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23084300 · Cited by 111 · see citing works
“Increased Apo C-III, Apo E-III, and E-IV of VLDL in MetS exhibit reduced LPL activity and function [8,27,104,105].”
BackgroundYang, X. H., Zhang, B. L., Cheng, Y., Fu, S. K., & Jin, H. M. (2023) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2023.03.012 · Cited by 81 · see citing works
Sniderman, A. D., Návar, A. M., & Thanassoulis, G. (2021) · JAMA Cardiology · doi:10.1001/jamacardio.2021.5080 · Cited by 78 · see citing works
Apolipoprotein B: Bridging the Gap Between Evidence and Clinical Practice
Oliveira-Gomes, D. D., Joshi, P. H., Peterson, E. D., Rohatgi, A. K., Khera, A., & Návar, A. M. (2024) · Circulation · doi:10.1161/circulationaha.124.068885 · Cited by 80 · see citing works
Excess Apolipoprotein B and Cardiovascular Risk in Women and Men
Johannesen, C. D. L., Langsted, A., Nordestgaard, B. G., & Mortensen, M. B. (2024) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2024.03.423 · Cited by 76 · see citing works
Nelson, A. J., Sniderman, A. D., Ditmarsch, M., Dicklin, M. R., Nicholls, S. J., Davidson, M. H., & Kastelein, J. J. P. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23169417 · Cited by 71 · see citing works
Dai, H., Hou, T., Wang, Q., Hou, Y., Wang, T., Zheng, J., Lin, H., Zhao, Z., Li, M., Wang, S., et al. (2023) · European Journal of Preventive Cardiology · doi:10.1093/eurjpc/zwad171 · Cited by 64 · see citing works
Best practice for LDL-cholesterol: when and how to calculate
Martins, J., Steyn, N., Rossouw, H. M., & Pillay, T. S. (2023) · Journal of Clinical Pathology · doi:10.1136/jcp-2022-208480 · Cited by 61 · see citing works
“In a recent cohort study by Marston et al , 48 association with MI was best captured by the number of apoB-containing lipoproteins, independent from lipid content (cholesterol or TG) or type of lipoprotein (LDL or TG-rich).”
BackgroundSarraju, A., Brennan, D. M., Hayden, K., Stronczek, A., Goldberg, A. C., Michos, E. D., McGuire, D. K., Mason, D., Tercek, G., Nicholls, S. J., et al. (2025) · The Lancet · doi:10.1016/s0140-6736(25)00721-4 · Cited by 63 · see citing works
Standardization of Apolipoprotein B, LDL‐Cholesterol, and Non‐HDL‐Cholesterol
Contois, J. H., Langlois, M. R., Cobbaert, C. M., & Sniderman, A. D. (2023) · Journal of the American Heart Association · doi:10.1161/jaha.123.030405 · Cited by 57 · see citing works
Hansen, M. K., Mortensen, M. B., Warnakula Olesen, K. K., Thrane, P. G., & Maeng, M. (2024) · The Lancet Regional Health - Europe · doi:10.1016/j.lanepe.2023.100774 · Cited by 57 · see citing works
Galimberti, F., Casula, M., & Olmastroni, E. (2023) · Pharmacological Research · doi:10.1016/j.phrs.2023.106873 · Cited by 63 · see citing works
“More recently, Marston et al. [36] conducted a prospective cohort study that included 389,529 participants in the primary prevention group and 40,430 participants in the secondary prevention group.”
Role of Treg cell subsets in cardiovascular disease pathogenesis and potential therapeutic targets
Xia, Y., Gao, D., Wang, X., Liu, B., Shan, X., Sun, Y., & Ma, D. (2024) · Frontiers in Immunology · doi:10.3389/fimmu.2024.1331609 · Cited by 57 · see citing works
Karwatowska‐Prokopczuk, E., Tardif, J., Gaudet, D., Ballantyne, C. M., Shapiro, M. D., Moriarty, P. M., Baum, S. J., Amour, E. S., Alexander, V. J., Xia, S., et al. (2022) · Journal of clinical lipidology · doi:10.1016/j.jacl.2022.06.005 · Cited by 51 · see citing works
Elliott, P. S., Kharaty, S. S., & Phillips, C. M. (2022) · Nutrients · doi:10.3390/nu14245371 · Cited by 51 · see citing works
Intracellular tPA–PAI-1 interaction determines VLDL assembly in hepatocytes
Dai, W., Zhang, H., Lund, H., Zhang, Z., Castleberry, M., Rodriguez, M., Kuriakose, G., Gupta, S. K., Lewandowska, M., Powers, H. R., et al. (2023) · Science · doi:10.1126/science.adh5207 · Cited by 47 · see citing works
Brunham, L. R., Lonn, E., & Mehta, S. R. (2024) · Canadian Journal of Cardiology · doi:10.1016/j.cjca.2024.04.017 · Cited by 50 · see citing works
Nicholls, S. J., Nelson, A. J., Ditmarsch, M., Kastelein, J. J. P., Ballantyne, C. M., Ray, K. K., Návar, A. M., Nissen, S. E., Goldberg, A. C., Brunham, L. R., et al. (2024) · American Heart Journal · doi:10.1016/j.ahj.2024.05.002 · Cited by 46 · see citing works
Self-citationApoB100 and Atherosclerosis: What’s New in the 21st Century?
Kounatidis, D. C., Vallianou, N. G., Poulaki, A., Evangelopoulos, A. A., Panagopoulos, F., Stratigou, T., Geladari, E. V., Karampela, Ι., & Dalamaga, Μ. (2024) · Metabolites · doi:10.3390/metabo14020123 · Cited by 45 · see citing works
“The authors concluded that the number of ApoB-containing lipoproteins may be superior in reflecting MI risk, independent of the type of lipoprotein or lipid content [41].”
BackgroundApoB-containing lipoproteins: count, type, size, and risk of coronary artery disease
Morze, J., Melloni, G. E. M., Wittenbecher, C., Ala‐Korpela, M., Rynkiewicz, A., Guasch‐Ferré, M., Ruff, C. T., Hu, F. B., Sabatine, M. S., & Marston, N. (2025) · European Heart Journal · doi:10.1093/eurheartj/ehaf207 · Cited by 41 · see citing works
“4 Similarly, Mendelian randomization studies have demonstrated equivalent atherogenicity of VLDL and LDL. 5,6 However, this view was challenged by a recent gen-etic analysis suggesting that the per-particle risk of VLDL carries twice the atherogenic risk compared with LDL particles.”
Self-citationWilliams, K. J. (2023) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.123.320065 · Cited by 41 · see citing works
“44,86 Post hoc analyses of PCSK9i trials have implicated residual circulating apoB-lipoproteins in residual ASCVD event risk, 90,91 as would be expected.”
BackgroundRuscica, M., Macchi, C., Giuliani, A., Rizzuto, A. S., Ramini, D., Sbriscia, M., Carugo, S., Bonfigli, A. R., Corsini, A., Olivieri, F., et al. (2023) · Cardiovascular Diabetology · doi:10.1186/s12933-023-01948-8 · Cited by 38 · see citing works
Tybjærg‐Hansen, A., Nordestgaard, B. G., & Christoffersen, M. (2023) · European Heart Journal · doi:10.1093/eurheartj/ehad419 · Cited by 35 · see citing works
Khan, S. S., Greenland, P., Hayman, L. L., Khera, R., Návar, A. M., Pencina, M. J., Reza, N., Shah, S. H., Shanbhag, S. M., Weber, B., et al. (2026) · Circulation · doi:10.1161/cir.0000000000001401 · Cited by 42 · see citing works
Menopausal hormone therapy in women with dyslipidemia and nonalcoholic fatty liver disease
Pοlyzos, S. A., Lambrinoudaki, I. V., & Goulis, D. G. (2022) · HORMONES · doi:10.1007/s42000-022-00369-8 · Cited by 31 · see citing works
European guidelines for the treatment of dyslipidaemias: New concepts and future challenges
Pirillo, A., Casula, M., & Catapano, A. L. (2023) · Pharmacological Research · doi:10.1016/j.phrs.2023.106936 · Cited by 31 · see citing works
Risk factors for clonal hematopoiesis of indeterminate potential and mosaic chromosomal alterations
Jakubek, Y. A., Reiner, A. P., & Honigberg, M. C. (2022) · Translational research · doi:10.1016/j.trsl.2022.11.009 · Cited by 30 · see citing works
Sayed, A., Peterson, E. D., Virani, S. S., Sniderman, A. D., & Návar, A. M. (2024) · JAMA Cardiology · doi:10.1001/jamacardio.2024.1310 · Cited by 30 · see citing works
Sampson, M. L., Wolska, A. T., Meeusen, J. W., Donato, L. J., Jaffe, A. S., & Remaley, A. T. (2022) · Frontiers in Genetics · doi:10.3389/fgene.2022.935257 · Cited by 29 · see citing works
Kristensen, F., Christensen, D. H., Mortensen, M. B., Mæng, M., Kahlert, J. A., Sørensen, H. T., & Thomsen, R. W. (2023) · Cardiovascular Diabetology · doi:10.1186/s12933-023-01921-5 · Cited by 28 · see citing works
Liang, X., Zhang, J., Yu, J., Zhao, J., & Yang, S.-S. (2025) · European journal of medical research · doi:10.1186/s40001-025-02562-y · Cited by 29 · see citing works
“When occurring in the coronary arteries, it may lead to local clots that thoroughly block the blood flow, causing myocardial infarction [6, 7].”
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Shnayder, N. A., Владимировна, Г. В., Trefilova, V. V., Efremov, I. S., Dontceva, E. A., Narodova, E. A., Петрова, М. М., Soloveva, I. A., Tepnadze, L. E., Reznichenko, P. A., et al. (2023) · Biomedicines · doi:10.3390/biomedicines11051499 · Cited by 25 · see citing works
Zimerman, A., Wiviott, S. D., Park, J., Murphy, S. A., Ran, X., Bramson, C., Curto, M., Ramos, V., Jevne, A., Kuder, J., et al. (2024) · European Journal of Preventive Cardiology · doi:10.1093/eurjpc/zwae090 · Cited by 26 · see citing works
Self-citationUse of Apolipoprotein B in the Era of Precision Medicine: Time for a Paradigm Change?
Cole, J., Zubirán, R., Wolska, A. T., Jialal, I., & Remaley, A. T. (2023) · Journal of Clinical Medicine · doi:10.3390/jcm12175737 · Cited by 23 · see citing works
“[9] performed a similar analysis on 40,430 statin-treated patients from the FOURIER and IMPROVE-IT studies, who were followed up for a median of 2.”
BackgroundMethodInfluentialDyslipidemia: A Narrative Review on Pharmacotherapy
de Oliveira, L. D., de Assis, A. C. R., Giraldez, V. Z. R., Scudeler, T. L., & Soares, P. R. (2024) · Pharmaceuticals · doi:10.3390/ph17030289 · Cited by 26 · see citing works
“In recent years, the value of apoB (an essential structural component of LDL-C) as a marker of CV risk has increased through epidemiological studies, clinical trials, and Mendelian randomization analyses [154–161].”
BackgroundKraaijenhof, J. M., Kerkvliet, M., Nurmohamed, N. S., Grefhorst, A., Kroon, J., Wareham, N. J., Hovingh, G. K., Stroes, E. S. G., Boekholdt, S. M., & Reeskamp, L. F. (2025) · European Journal of Preventive Cardiology · doi:10.1093/eurjpc/zwaf037 · Cited by 27 · see citing works
Self-citationShen, Y., Gu, H.-M., Zhai, L., Wang, B., Qin, S., & Zhang, D. (2022) · Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids · doi:10.1016/j.bbalip.2022.159196 · Cited by 24 · see citing works
Ma, J., Joehanes, R., Liu, C., Keshawarz, A., Hwang, S., Bui, H., Tejada, B., Sooda, M., Munson, P. J., Demirkale, C. Y., et al. (2022) · Scientific Reports · doi:10.1038/s41598-022-24100-0 · Cited by 23 · see citing works
Chen, K.-S., Chan, H.-C., & Chan, C.-M. (2024) · International Journal of Retina and Vitreous · doi:10.1186/s40942-024-00606-9 · Cited by 22 · see citing works
“MI is often caused by the natural progression of coronary atherosclerosis, with coronary artery occlusion resulting from plaques prone to rupture or erosion being the most common cause of MI [49].”
Yun, S. Y., Rim, J. H., Kang, H., Lee, S., & Lim, J. (2022) · Annals of Laboratory Medicine · doi:10.3343/alm.2023.43.3.237 · Cited by 22 · see citing works
“Studies have compared these three lipid markers in ASCVD [10-12, 15-17 15-17]; however, identifying the most potent marker of ASCVD is challenging.”
Ballantyne, C. M., & Norata, G. D. (2025) · European Heart Journal · doi:10.1093/eurheartj/ehaf606 · Cited by 23 · see citing works
Triglyceride-Rich Lipoproteins and Atherosclerotic Cardiovascular Disease Risk
Duell, P. B. (2023) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2022.11.013 · Cited by 22 · see citing works
The Causal-Benefit Model to Prevent Cardiovascular Events
Kohli-Lynch, C. N., Thanassoulis, G., Pencina, M. J., Sehayek, D., Pencina, K. M., Moran, A. E., & Sniderman, A. D. (2024) · JACC Advances · doi:10.1016/j.jacadv.2023.100825 · Cited by 22 · see citing works
ApoB, LDL-C, and non-HDL-C as markers of cardiovascular risk
Sehayek, D., Cole, J., Björnson, E., Wilkins, J. T., Mortensen, M. B., Dufresne, L., Pencina, K. M., Pencina, M. J., Thanassoulis, G., & Sniderman, A. D. (2025) · Journal of Clinical Lipidology · doi:10.1016/j.jacl.2025.05.024 · Cited by 20 · see citing works
Koba, S., Satoh, N., Ito, Y., Yokota, Y., Tsunoda, F., Sakai, K., Nakamura, Y., Shoji, M., Hirano, T., & Shinke, T. (2024) · Clinical Chemistry · doi:10.1093/clinchem/hvae061 · Cited by 20 · see citing works
Zaheen, M., Pender, P., Dang, Q., Sinha, E., Chong, J. J. H., Chow, C. K., & Zaman, S. J. (2025) · Journal of Cardiovascular Development and Disease · doi:10.3390/jcdd12040148 · Cited by 22 · see citing works
“This suggests that apolipoprotein B may be a key factor in the development of atherosclerosis, but these findings were not specific to young MI patients [105].”
Lipoprotein(a), family history of cardiovascular disease, and incidence of heart failure
Wang, H., Zhang, N., Liu, Y., Xia, T.-L., Chen, G., Yang, J., & Li, F. (2023) · Journal of Lipid Research · doi:10.1016/j.jlr.2023.100398 · Cited by 20 · see citing works
“Sensitivity analysis was also performed by further adjusting for apolipoprotein B [(apo) B], as previous studies have reported that apoB may be the primary driver of atherosclerosis beyond other lipids (30, 31).”
MethodJin, D., Trichia, E., Islam, N., Bešević, J., Lewington, S., & Lacey, B. (2023) · Journal of the American Heart Association · doi:10.1161/jaha.123.029552 · Cited by 19 · see citing works
Doi, T., Langsted, A., & Nordestgaard, B. G. (2024) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2024.117556 · Cited by 22 · see citing works
Johannesen, C. D. L., Mortensen, M. B., Nordestgaard, B. G., & Langsted, A. (2025) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2025.119139 · Cited by 21 · see citing works
Sampson, M. L., Zubirán, R., Wolska, A. T., Meeusen, J. W., Donato, L. J., Jaffe, A. S., Melloni, G. E. M., Giugliano, R. P., Sabatine, M. S., Marston, N., et al. (2025) · Clinical Chemistry · doi:10.1093/clinchem/hvaf073 · Cited by 18 · see citing works
Self-citationCandás‐Estébanez, B., Fernández‐Cidón, B., Corbella, E., Tebé, C., Fanlo‐Maresma, M., Esteve-Luque, V., Salas‐Salvadó, J., Fitó, M., Riera‐Mestre, A., Ros, E., et al. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25021338 · Cited by 18 · see citing works
“The er-MedDiet+PA intervention also induced a decrease in VLDL-TG, and, as a consequence, lVLDL-P was also reduced, and LDL particle size increased—changes that are recognized as anti-atherogenic [21].”
BackgroundCascade testing for elevated lipoprotein(a) in relatives of probands with high lipoprotein(a)
Chakraborty, A., Chan, D. C., Ellis, K. L., Pang, J., Barnett, W., Woodward, A. M., Vorster, M., Norman, R., Moses, E. K., & Watts, G. F. (2022) · American Journal of Preventive Cardiology · doi:10.1016/j.ajpc.2022.100343 · Cited by 18 · see citing works
Kalra, D. K., Ray, K. K., Bajaj, A., Kushner, P. R., Wilcox, M. L., Dicklin, M. R., Kirkpatrick, C. F., & Maki, K. C. (2026) · Journal of clinical lipidology · doi:10.1016/j.jacl.2026.02.006 · Cited by 17 · see citing works
Residual lipid risk in atherosclerotic cardiovascular disease
Nordestgaard, B. G., & Hegele, R. A. (2026) · European Heart Journal · doi:10.1093/eurheartj/ehag087 · Cited by 24 · see citing works
Colesterol remanente, riesgo vascular y prevención de la arteriosclerosis
Pintó, X., Fanlo‐Maresma, M., Esteve, V., Millán, J., Blanco, A., Blasco, M., Díaz-Díaz, J. L., Rodríguez, Á. D., Mangas, A., Pascual, V., et al. (2023) · Clínica e Investigación en Arteriosclerosis · doi:10.1016/j.arteri.2023.02.001 · Cited by 18 · see citing works
Lipid profile and lipoprotein(a) testing
Parhofer, K. G., & Laufs, U. (2023) · Deutsches Ärzteblatt international · doi:10.3238/arztebl.m2023.0150 · Cited by 16 · see citing works
Apolipoprotein B in cardiovascular risk assessment
Ahmad, M., Sniderman, A. D., & Hegele, R. A. (2023) · Canadian Medical Association Journal · doi:10.1503/cmaj.230048 · Cited by 16 · see citing works
APOB is a potential prognostic biomarker in hepatocellular carcinoma
Lin, Z., Ji, X., Tian, N., Gan, Y., & Ke, L. (2024) · Discover Oncology · doi:10.1007/s12672-024-00877-6 · Cited by 15 · see citing works
“Among the apolipoprotein family members, APOB consists of tiny particles that carry dietary lipids through the blood-stream from the intestines to the liver [22, 23].”
BackgroundBlood-Based DNA Methylation Biomarkers to Identify Risk and Progression of Cardiovascular Disease
Willmer, T., Mabasa, L., Sharma, J. R., Muller, C. J. F., & Johnson, R. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26052355 · Cited by 15 · see citing works
“Some of these genes, including APOB , have been previously reported to be strong drivers of myocardial infarction risk [130].”
Li, J.-N., Wang, M., Tan, Y., & Wang, L.-L. (2024) · The American Journal of Chinese Medicine · doi:10.1142/s0192415x24500381 · Cited by 15 · see citing works
Cargo Receptor-Mediated ER Export in Lipoprotein Secretion and Lipid HomeostasisPreprint
Wang, X., & Chen, X. (2022) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a041260 · Cited by 14 · see citing works
Colchicine promotes atherosclerotic plaque stability independently of inflammationPreprint
Li, W., Lin, A., Hutton, M., Dhaliwal, H., Nadel, J., Rodor, J., Tumanov, S., Örd, T., Hadden, M. K., Mokrý, M., et al. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.10.03.560632 · Cited by 14 · see citing works
“low-density lipoproteins (LDLs), very low-density lipoproteins, and chylomicron remnants) (29, 30).”
Girona, J., Guardiola, M., Barroso, E., García‐Altares, M., Ibarretxe, D., Plana, N., Ribalta, J., Amigó, N., Correig, X., Vázquez‐Carrera, M., et al. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26052039 · Cited by 13 · see citing works
“Although the mechanisms by which VLDL are related to the atherosclerosis physiopathology are still unclear, these lipoproteins have been proposed as a causal risk factor for atherosclerotic CV disease, showing a atherogenic risk per particle than LDL [11,12,37].”
Novel Biomarkers for Atherosclerotic Disease: Advances in Cardiovascular Risk Assessment
Jigoranu, A. R., Roca, M., Costache, A. D., Mitu, O., Oancea, A. F., Miftode, R.-Ş., Haba, M. Ș. C., Botnariu, G., Maștaleru, A., Gavril, R. S., et al. (2023) · Life · doi:10.3390/life13081639 · Cited by 13 · see citing works
“They evaluated the triglyceride/LDL-C ratio while adjusting for apoB and clinical risk factors and concluded that the type of apoB-containing lipoprotein brought no additional risk-assessment value [86].”
MethodAssociations between apolipoprotein B and bone mineral density: a population-based study
Zhao, X., Tan, N., Zhang, Y., et al. (2023) · BMC Musculoskeletal Disorders · doi:10.1186/s12891-023-06990-x · Cited by 13 · see citing works
Liao, K. P., Rist, P. M., Giles, J. T., Santacroce, L. M., Connelly, M. A., Glynn, R. J., Ridker, P. M., Tawakol, A. A., Bathon, J. M., & Solomon, D. H. (2024) · Arthritis Research & Therapy · doi:10.1186/s13075-024-03352-3 · Cited by 14 · see citing works
“Apolipoprotein B (apoB), a more direct measurement of atherogenic lipid particles has the strongest association with CV outcomes compared to other lipid and lipoprotein measurements [16].”
BackgroundBilgic, S., Pencina, K. M., Pencina, M. J., Cole, J., Dufresne, L., Thanassoulis, G., & Sniderman, A. D. (2024) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.124.321165 · Cited by 15 · see citing works
Anderson, J. L., Knight, S., May, H. T., Le, V. T., Almajed, J., Bair, T. L., Knowlton, K. U., & Muhlestein, J. B. (2022) · Journal of Clinical Medicine · doi:10.3390/jcm12010075 · Cited by 13 · see citing works
Papathanasiou, K. A., Roussos, C. E., Armylagos, S., Rallidis, S. L., & Rallidis, L. S. (2024) · Journal of Cardiovascular Development and Disease · doi:10.3390/jcdd11100316 · Cited by 12 · see citing works
“ApoB-containing lipoproteins are the main drivers for atherosclerosis progression among patients with established CAD and are predictive of new MI [26,27].”
BackgroundNacarelli, G. S., Fasolino, T. K., & Davis, S. C. (2023) · Nutrition Reviews · doi:10.1093/nutrit/nuad102 · Cited by 12 · see citing works
Roles of O-GlcNAcylation in Mitochondrial Homeostasis and Cardiovascular Diseases
Qiu, Z., Cui, J., Huang, Q., Qi, B., & Xia, Z. (2024) · Antioxidants · doi:10.3390/antiox13050571 · Cited by 13 · see citing works
“Atherosclerosis is a key predisposing factor in the development of CHD and leads to much morbidity and mortality worldwide, including most myocardial infarction and many strokes, as well as disabling peripheral artery disease [23,175,176].”
BackgroundTale of two systems: the intertwining duality of fibrinolysis and lipoprotein metabolism
Dai, W., Castleberry, M., & Zheng, Z. (2023) · Journal of Thrombosis and Haemostasis · doi:10.1016/j.jtha.2023.08.004 · Cited by 14 · see citing works
Wu, J., Fan, Q., He, Q., Zhong, Q., Zhu, X., Cai, H., He, X., Xu, Y., Huang, Y., & Di, X. (2023) · Medicine · doi:10.1097/md.0000000000036284 · Cited by 11 · see citing works
“[33] The enrichment analysis results revealed that the KEGG pathway primarily focuses on cholesterol metabolism, the PPAR signaling pathway, and vitamin digestion and absorption.”
BackgroundRemnant cholesterol, vascular risk, and prevention of atherosclerosis
Pintó, X., Fanlo‐Maresma, M., Esteve-Luque, V., & Millán, J. (2023) · Clínica e Investigación en Arteriosclerosis (English Edition) · doi:10.1016/j.artere.2023.07.005 · Cited by 12 · see citing works
Remnant cholesterol: a reliable prognostic marker?
Pirillo, A., & Catapano, A. L. (2023) · European Journal of Preventive Cardiology · doi:10.1093/eurjpc/zwad107 · Cited by 11 · see citing works
Rehman, M. B., Björnson, E., Adiels, M., Morze, J., Bergström, G. M. L., Gummesson, A., Erlinge, D., Fall, T., Matic, L. P., Söderberg, S., et al. (2026) · European Heart Journal · doi:10.1093/eurheartj/ehaf1124 · Cited by 11 · see citing works
“Early studies suggested that all apoB-containing lipoproteins had approximately equal atherogenicity, 28,29 but recent investigations have revealed this not to be the case.”
Li, T., Zhu, P., Song, Y., Tang, X., Gao, Z., Run-Lin, G. A. O., & Yuan, J. (2023) · 老年心脏病学杂志：英文版 · doi:10.26599/1671-5411.2023.12.001 · Cited by 12 · see citing works
Maidman, S. D., Hegele, R. A., & Rosenson, R. S. (2024) · Current Atherosclerosis Reports · doi:10.1007/s11883-024-01258-8 · Cited by 11 · see citing works
Fujino, M., Giovanni, G. D., Butters, J., Kataoka, Y., Hucko, T., Nelson, A. J., Nissen, S. E., Psaltis, P. J., & Nicholls, S. J. (2025) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2025.119145 · Cited by 10 · see citing works
Faquih, T. O., Aziz, N. A., Gardiner, S. L., Li‐Gao, R., de Mutsert, R., Milaneschi, Y., Trompet, S., Jukema, J. W., Rosendaal, F. R., Vlieg, A. V. H., et al. (2023) · Human Molecular Genetics · doi:10.1093/hmg/ddad020 · Cited by 10 · see citing works
Reijnders, E., van der Laarse, A., Ruhaak, L. R., & Cobbaert, C. M. (2024) · Clinical Proteomics · doi:10.1186/s12014-024-09465-w · Cited by 10 · see citing works
“In particular, apolipoprotein B (ApoB) has been identified as a strong independent predictor of CVD risk, with several studies demonstrating its superiority over traditional lipids such as LDL-c, and non-HDL-c [17–19].”
BackgroundVelilla, T. A., Guijarro, C., Ruíz, R. C., Piñero, M. R., Marcos, J. F. V., Pérez, A., López, M. A. B., López, A. M., Donaire, J. A. G., Obaya, J. C., et al. (2023) · Neurology Perspectives · doi:10.1016/j.neurop.2023.100126 · Cited by 10 · see citing works
Bilgic, S., & Sniderman, A. D. (2023) · Current Opinion in Cardiology · doi:10.1097/hco.0000000000001100 · Cited by 9 · see citing works
Pikkemaat, M., Woodward, M., af Geijerstam, P., Harrap, S. B., Hamet, P., Mancia, G., Marre, M., Poulter, N. R., Chalmers, J. P., & Harris, K. (2024) · Diabetes Obesity and Metabolism · doi:10.1111/dom.15935 · Cited by 9 · see citing works
- Authors
- Marston, N. A., Giugliano, R. P., Melloni, G. E. M., Park, J.-G., Morrill, V., Blazing, M. A., Ference, B., Stein, E., Stroes, E. S., Braunwald, E., Ellinor, P. T., Lubitz, S. A., Ruff, C. T., & Sabatine, M. S.
- Affiliations
- Brigham and Women's Hospital (US)
- Broad Institute (US)
- Duke University (US)
- University of Cambridge (GB)
- Metabolic and Atherosclerosis Research Center, Cincinnati, Ohio
- Amsterdam University Medical Centers (NL)
- Thrombolysis in Myocardial Infarction (TIMI) Study Group, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts
- Corresponding author
- Marston, Nicholas A.
- ORCID
- Venue
- JAMA Cardiology
- Publisher
- American Medical Association (AMA)
- Published
- 2022-03-01
- Volume
- 7
- Issue
- 3
- Pages
- 250
- ISSN
- 2380-6583 (ISSN-L)
- PMC
- PMC8590731
- OpenAlex
- W3213895219
- Semantic Scholar
- a8dd33ed82854a233b2e5383c88457332240ec72
- Cited by
- 262
- References
- 23
- Citations by year
- 2026: 43 · 2025: 50 · 2024: 67 · 2023: 68 · 2022: 32 · 2021: 2
- FWCI
- 35.66
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- JAMA Cardiology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Pure Amsterdam UMC (submittedVersion)
- Funders
- British Heart Foundation (CH/1996001/9454)
- Medical Research Council (MC_PC_17228)
- National Heart, Lung, and Blood Institute (K08HL153950)
- 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
- apolipoprotein B, apoB-containing lipoproteins, myocardial infarction, atherosclerosis, non-HDL cholesterol, triglycerides, LDL cholesterol, VLDL, cardiovascular risk, statin therapy, primary prevention, lipid control, FOURIER trial, IMPROVE-IT trial, UK Biobank
- MeSH terms
- Apolipoproteins B, Cholesterol, Female, Humans, Lipoproteins, Cholesterol, LDL, Male, Myocardial Infarction, Prospective Studies, Cohort Studies, Atherosclerosis
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Claims read by deepseek-v4.1-flash under definition version 3 (extract-v3) on 2026-10-19.
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