The DOI matches its Crossref record; 111 of the 111 references it cites were found in a registry or an index; 100 of the 160 sources its claims cite were checked for support.
Quantifying atherogenic lipoproteins for lipid-lowering strategies: Consensus-based recommendations from EAS and EFLM
Open accessAbstract
The joint consensus panel of the European Atherosclerosis Society (EAS) and the European Federation of Clinical Chemistry and Laboratory Medicine (EFLM) recently addressed present and future challenges in the laboratory diagnostics of atherogenic lipoproteins. Total cholesterol, triglycerides, HDL cholesterol, LDL cholesterol, and calculated non-HDL cholesterol (=total - HDL cholesterol) constitute the primary lipid panel for estimating risk of atherosclerotic cardiovascular disease (ASCVD) and can be measured in the nonfasting state. LDL cholesterol is the primary target of lipid-lowering therapies. For on-treatment follow-up, LDL cholesterol shall be measured or calculated by the same method to attenuate errors in treatment decisions due to marked between-method variations. Lipoprotein(a)-cholesterol is part of measured or calculated LDL cholesterol and should be estimated at least once in all patients at risk of ASCVD, especially in those whose LDL cholesterol decline poorly upon statin treatment. Residual risk of ASCVD even under optimal LDL-lowering treatment should be also assessed by non-HDL cholesterol or apolipoprotein B, especially in patients with mild-to-moderate hypertriglyceridemia (2-10 mmol/L). Non-HDL cholesterol includes the assessment of remnant lipoprotein cholesterol and shall be reported in all standard lipid panels. Additional apolipoprotein B measurement can detect elevated LDL particle numbers often unidentified on the basis of LDL cholesterol alone. Reference intervals of lipids, lipoproteins, and apolipoproteins are reported for European men and women aged 20-100 years. However, laboratories shall flag abnormal lipid values with reference to therapeutic decision thresholds.
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Claims the paper makes
44 Partly supported · 35 Supported · 32 No full text of the sources · 11 Sources not found · 8 Own interpretation · 3 Supported so far · 1 Not supported · 1 Couldn’t confirm · 1 Not checked yet · 1 No basis given · accuracy not yet measured
At least one cited source doesn’t support this claim or points to a different paper, and none confirmed it — see the verdicts below.
In the paper
“suggesting that replacing LDLC by apoB would identify more individuals with increased risk of ASCVD [74]”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 8.1. Clinical performance -risk estimation
What the sources say
- Disputedcites [74] Welsh, 2019, Comparison of conventional lipoprotein tests and apolipoproteins in the prediction of cardiovascular disease. Data from UK biobank, Circulation sourceExperimental — accuracy not yet measured
The Discussion (page unavailable) concludes that replacing standard cholesterol measures with apolipoproteins does not improve CVD risk prediction. The Results likewise report no improvement in risk classification from adding an apolipoprotein measure to a model containing total cholesterol and HDL-C. The paper therefore does not support the claim that substituting apoB for LDL-C would identify more people at increased risk. (LLM, conf=0.88)
Checked by a reasoning model — may be wrong.
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Disputed
Every source the paper cites for this claim was checked and supports it.
In the paper
“While earlier studies emphasized the atherogenicity of small LDL particles, it is now recognized that all LDL particles are atherogenic, regardless of size [10].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 2.1. LDL particles
What the sources say
- Supportedcites [10] Mora, 2009, Advanced lipoprotein testing and subfractionation are not (yet) ready for routine clinical use, Circulation source
Section 1.B states that both small and large LDL particles are similarly atherogenic. It reports that, after accounting for correlations between particle types, both subclasses showed similar associations with atherosclerosis and CVD events. (LLM, conf=0.93)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Nonfasting lipid profiles, therefore, can potentially be more relevant to the estimation of an individual's cardiovascular risk than fasting lipids since in real life the postprandial state predominates most of our 24-h cycle [15,16].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 2.2. Remnant particles
What the sources say
- Partly supportedcites [15] Mora, 2008, Fasting compared with nonfasting lipids and apolipoproteins for predicting incident cardiovascular events, Circulation sourceExperimental — accuracy not yet measured
The Discussion (page unavailable) reports that several lipids predict cardiovascular events when measured nonfasting, supporting the possibility that nonfasting measurements are useful. It also says total, LDL, and non-HDL cholesterol may provide less useful risk information when measured nonfasting. The paper does not establish that nonfasting lipid profiles are generally more relevant because the postprandial state predominates over a 24-hour cycle. (LLM, conf=0.86)
- Supportedcites [16] Nordestgaard, 2017, A test in context: lipid profile, fasting versus non-fasting, J. Am. Coll. Cardiol. source
The paper’s discussion of fasting and nonfasting profiles (page not supplied) says fasting for more than eight hours occupies only a few hours of the day for most people. It also reports a stronger association with coronary heart disease for non-HDL cholesterol measured in nonfasting studies than in fasting studies, supporting the claim’s cautious suggestion that nonfasting profiles may be more relevant to cardiovascular risk estimation. (LLM, conf=0.88)
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In patients with mild-to-moderate hypertriglyceridemia, defined as 2-10 mmol/L [33], elevated baseline and on-treatment apoB helps identify the atherogenic dyslipidemia related to remnant lipoproteins combined with small dense LDL particles that is not reflected by LDLC and non-HDLC.”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 3. What is the standard lipid profile?
What the sources say
- Supportedcites [33] Hegele, 2014, European Atherosclerosis Society Consensus Panel. The polygenic nature of hypertriglyceridaemia: implications for definition, diagnosis, and management, Lancet Diabetes Endocrinol. source
Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Monogenic disorders such as familial hypercholesterolemia (FH) can be easily recognized from the standard lipid panel without the need to measure apoB [31,32].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 3. What is the standard lipid profile?
What the sources say
- Partly supportedcites [31] Nordestgaard, 2013, Eur. Heart J. sourceExperimental — accuracy not yet measured
The Diagnosis section (page not provided) identifies very high LDL cholesterol on repeated measurements as a criterion for FH, and its diagnostic criteria do not require an apoB measurement. But it also calls for considering family and clinical history, physical findings, genetic testing, and secondary causes; it does not say FH can generally be easily recognized from a standard lipid panel alone. (LLM, conf=0.88)
- Partly supportedcites [32] Wiegman, 2015, European Atherosclerosis Society Consensus Panel. Familial hypercholesterolaemia in children and adolescents: gaining decades of life by optimizing detection and treatment, Eur. Heart J. sourceExperimental — accuracy not yet measured
The Diagnosis section and Table 2 support using LDL-C from cholesterol testing to identify probable paediatric FH without listing apoB measurement as a requirement. But they also call for family history, repeat LDL-C testing and evaluation of secondary causes; genetic testing establishes the diagnosis. The paper therefore does not support the broader claim that FH is easily recognized from a standard lipid panel alone. (LLM, conf=0.85)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“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].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 2.1. LDL particles
What the sources say
- Partly supportedcites [9] Mudd, 2007, Beyond low-density lipoprotein cholesterol: defining the role of low-density lipoprotein heterogeneity in coronary artery disease, J. Am. Coll. Cardiol. sourceExperimental — accuracy not yet measured
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)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“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].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 2.1. LDL particles
What the sources say
- Partly supportedcites [9] Mudd, 2007, Beyond low-density lipoprotein cholesterol: defining the role of low-density lipoprotein heterogeneity in coronary artery disease, J. Am. Coll. Cardiol. sourceExperimental — accuracy not yet measured
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)
- Partly supportedcites [10] Mora, 2009, Advanced lipoprotein testing and subfractionation are not (yet) ready for routine clinical use, Circulation sourceExperimental — accuracy not yet measured
Section 1.A says CVD risk is more closely associated with NMR LDL particle concentration than with LDL cholesterol. That supports the comparison, but the paper describes an association, not a stronger causal relationship to ASCVD; it also says the clinical value of particle testing remains uncertain. The indexed passages provide no page numbers. (LLM, conf=0.90)
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Mendelian randomization studies suggest that life-long high serum concentrations of TG-rich lipoproteins or their remnants are causally associated with increased risk of ASCVD and all-cause mortality [17,18].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 2.2. Remnant particles
What the sources say
- Supportedcites [17] Nordestgaard, 2016, Triglyceride-rich lipoproteins and atherosclerotic cardiovascular disease: new insights from epidemiology, genetics, and biology, Circ. Res. source
The Abstract states that Mendelian-randomization studies demonstrate a causal association between triglyceride-rich lipoproteins and both ASCVD and all-cause mortality. The Genetics section describes testing lifelong exposure to remnant cholesterol, while the all-cause-mortality discussion specifies that its genetic evidence came from a single study. (LLM, conf=0.92)
- Not checked — no full text of the sourcecites [18] Thomsen, 2014, Low nonfasting triglycerides and reduced all-cause mortality: a mendelian randomization study, Clin. Chem. source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“They are typically predominant in patients with moderately elevated triglyceride (TG) concentrations or related conditions, such as diabetes and the metabolic syndrome, without necessarily having high LDLC concentration [11].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 2.1. LDL particles
What the sources say
- Supportedcites [11] Miller, 2011, Triglycerides and cardiovascular disease: a scientific statement from the American Heart Association, Circulation source
Section 6.2.3 (page unavailable) says hypertriglyceridemia is associated with small, dense, cholesterol-ester-depleted LDL particles and that people with type 2 diabetes and mild-to-moderate hypertriglyceridemia exhibit the small-particle pattern B profile. It also notes that LDL particles in diabetes may be atherogenic even at normal LDL-C concentrations. Section 9.1.3 links the triglyceride-to-HDL-C pattern characteristic of metabolic syndrome to small, dense LDL particles. (LLM, conf=0.88)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Postprandial accumulation of TG-rich remnant particles in blood is an important factor in atherogenesis [13,14].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 2.2. Remnant particles
What the sources say
- Supportedcites [13] Chapman, 2011, Triglyceride-rich lipoproteins and high-density lipoprotein cholesterol in patients at high risk of cardiovascular disease: evidence and guidance for management, Eur. Heart J. source
The section on experimental evidence links acutely elevated triglyceride-rich lipoprotein remnants in the postprandial phase to mechanisms of accelerated atherogenesis. It also reports that these remnants can contribute directly to plaque formation and progression. Page numbers are not provided in our copy. (LLM, conf=0.93)
- Not checked — no full text of the sourcecites [14] Nordestgaard, 2014, Triglycerides and cardiovascular disease, Lancet source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
- It may state two separate claims as one. 41
- Probably not a substantial claim. 18
- The quote only partly states this claim. 1
Every source the paper cites for this claim was checked and supports it.
In the paper
“Measurement of apolipoprotein B (apoB), the major protein component of LDL, or advanced measurement of LDLP (not yet widely available) can also be used to assess the number of LDL particles [10,12].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 2.1. LDL particles
What the sources say
- Supportedcites [10] Mora, 2009, Advanced lipoprotein testing and subfractionation are not (yet) ready for routine clinical use, Circulation source
The Apolipoproteins section says apoB reflects atherogenic particle number, with most plasma apoB found in LDL. Section 1.B explicitly describes LDL particle concentration as measured by either NMR testing or an apoB immunoassay. (LLM, conf=0.92)
- Supportedcites [12] Contois, 2009, Apolipoprotein B and cardiovascular disease risk: position statement from the AACC lipoproteins and vascular disease working group on best practices, Clin. Chem. source
The introduction (p. 1) describes apoB as a measure of LDL particle concentration and NMR as another way to quantify LDL particle number (LDL-P). Measurement Issues (p. 9) says LDL-P testing had been used mainly in research rather than clinical laboratories, consistent with the availability qualifier. (LLM, conf=0.92)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“These cholesterol-enriched remnant particles may enter the arterial intima and contribute to atherosclerosis, whereas nascent chylomicrons and very large VLDL particles do not cross the endothelial layer [17].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 2.2. Remnant particles
What the sources say
- Partly supportedcites [17] Nordestgaard, 2016, Triglyceride-rich lipoproteins and atherosclerotic cardiovascular disease: new insights from epidemiology, genetics, and biology, Circ. Res. sourceExperimental — accuracy not yet measured
The Biology section (page unavailable) says medium-sized triglyceride-rich lipoproteins can enter the arterial intima and become trapped, while large chylomicrons are too large to cross the endothelial barrier. It does not establish the same exclusion for very large VLDL particles, so that part of the claim is unsupported. (LLM, conf=0.86)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Although recent studies with PCSK9 inhibitors were not designed to target patients with high Lp(a) concentrations, they nevertheless revealed that patients with higher baseline Lp(a) concentration experienced greater absolute reductions in Lp(a) and tended to derive greater clinical benefit from PCSK9 inhibition [27,28].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > Laboratory reports should flag abnormal concentrations based on decision thresholds.
What the sources say
- Supportedcites [27] O'Donoghue, 2019, Lipoprotein(a), PCSK9 inhibition and cardiovascular risk: insights from the FOURIER Trial, Circulation source
The Abstract reports that patients with higher baseline Lp(a) experienced greater absolute Lp(a) reductions and tended to derive greater coronary benefit from evolocumab. It describes FOURIER as a trial in patients with established atherosclerotic cardiovascular disease, rather than one designed to enroll patients with high Lp(a). (LLM, conf=0.95)
- Partly supportedcites [28] Ray, 2019, Lipoprotein(a) reductions from PCSK9 inhibition and major adverse cardiovascular events: pooled analysis of alirocumab phase 3 trials, Atherosclerosis sourceExperimental — accuracy not yet measured
Section 3.3 reports a stronger association between Lp(a) reduction and fewer major adverse cardiovascular events among patients with baseline Lp(a) ≥50 mg/dL; the Discussion describes greater benefit as a possibility, consistent with the claim’s 'tended to' wording. The Discussion says higher initial Lp(a) levels are likely to offer greater absolute reductions, but the cited text does not establish as an observed subgroup result that these patients experienced greater absolute reductions with PCSK9 inhibition. Page numbers were not available in our copy. (LLM, conf=0.78)
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Circulating LDL particles are highly atherogenic and there is a direct, graded relationship between LDLC concentration and the incidence of ASCVD observed in randomized controlled trials, prospective epidemiological cohort studies, and Mendelian randomization studies [7,8].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 2.1. LDL particles
What the sources say
- Supportedcites [7] Ference, 2017, Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel, Eur. Heart J. source
Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
- Partly supportedcites [8] Baigent, 2010, Cholesterol Treatment Trialists' (CTT) Collaboration. Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170 000 participants in 26 randomised trials, Lancet sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Direct LDLC measurement should preferably be used in the calculation of RemnantC; otherwise RemnantC simply equals TG/2.2 (in mmol/L) when Friedewald-calculated LDLC is used, i.e.TC -HDLC -(TC -HDLC -TG/2.2),and it does not add clinical information beyond TG concentration [1]”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 2.2. Remnant particles
What the sources say
- Supportedcites [1] Langlois, 2018, Clin. Chem. source
The REMNANT PARTICLES section (p. 5) explicitly states that when Friedewald-calculated LDLC is used, Remnant-C equals TG/2.2 in mmol/L and provides no clinical information beyond TG concentration. It contrasts this with using directly measured LDLC. (LLM, conf=0.95)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“RemnantC, measured or calculated, differs from non-HDLC in that non-HDLC contains RemnantC plus LDLC and does not differentiate between these two causal risk factors [1].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 2.2. Remnant particles
What the sources say
- Supportedcites [1] Langlois, 2018, Clin. Chem. source
The REMNANT PARTICLES section (p. 5) explicitly says that measured or calculated Remnant-C differs from non-HDLC because non-HDLC contains Remnant-C plus LDLC. It also explains that non-HDLC can mask high Remnant-C when LDLC is low, supporting the point that the combined measure does not distinguish the two components. (LLM, conf=0.93)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“All LDL particles are atherogenic, but their concentration is not always reflected by LDLC measurement because the cholesterol content in the particles can vary widely between individuals according to the continuous remodeling of lipoproteins in blood [10].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 2.1. LDL particles
What the sources say
- Partly supportedcites [10] Mora, 2009, Advanced lipoprotein testing and subfractionation are not (yet) ready for routine clinical use, Circulation sourceExperimental — accuracy not yet measured
In §1.B (page not supplied), the paper says small and large LDL particles are similarly atherogenic and illustrates that two people can have the same LDL cholesterol level but different LDL particle concentrations because smaller particles contain less cholesterol. The passage does not attribute this variation to continuous remodeling of lipoproteins in blood, so that causal explanation is unsupported. (LLM, conf=0.88)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Calculated by subtracting HDLC from TC, non-HDLC represents the cholesterol in all particles causing cardiovascular disease, that is, LDL, VLDL, IDL, and Lp(a); in the nonfasting state this additionally includes the cholesterol in chylomicrons and their remnant particles [1].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 7.1. Non-HDL cholesterol
What the sources say
- Partly supportedcites [1] Langlois, 2018, Clin. Chem. sourceExperimental — accuracy not yet measured
The CALCULATED NON-HDLC section (p. 12) defines non-HDLC as total cholesterol minus HDL cholesterol and lists LDL, VLDL, IDL, chylomicron remnants, and Lp(a) among the particles it covers. The LDL PARTICLES section (p. 5) specifies that chylomicron remnants contribute in the nonfasting state. The REMNANT PARTICLES section (p. 5) distinguishes these atherogenic remnants from nascent chylomicrons, which it says are initially too large to enter the arterial wall; the claim does not preserve that distinction when describing chylomicrons as particles causing cardiovascular disease. (LLM, conf=0.84)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Not uncommonly, changes in a patient's LDLC test result over time are within the range of uncertainty of laboratory method variation and may not be due to therapeutic intervention [1].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 6. LDLC test errors: are they clinically relevant?
What the sources say
- Supportedcites [1] Langlois, 2018, Clin. Chem. source
The source states the claim nearly verbatim in “LDLC TEST ERRORS: ARE THEY CLINICALLY RELEVANT?” (p. 11). It explains that differences between methods and laboratories can mimic or mask a treatment effect, while noting that this issue is less relevant when the same laboratory and method are used over time. (LLM, conf=0.95)
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Direct measurements of dLDLC and dHDLC in normolipidemic samples usually meet the National Cholesterol Education Program (NCEP) total error goals of ≤12% and ≤13%, respectively, but total error ranged from -26% to +32% for dLDLC and -20% to +36% for dHDLC in a comprehensive study of different assays in dyslipidemic samples [42].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 5.2. Direct LDLC and HDLC assays
What the sources say
- Partly supportedcites [42] Miller, 2010, Seven direct methods for measuring HDL and LDL cholesterol compared with ultracentrifugation reference measurement procedures, Clin. Chem. sourceExperimental — accuracy not yet measured
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Despite this limitation, non-HDLC yields more accurate cardiovascular risk classification than either Friedewald cLDLC or dLDLC, and also more consistent risk scores using different manufacturers' assays for dHDLC in the calculation [58].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 7.1. Non-HDL cholesterol
What the sources say
- Supportedcites [58] van Deventer, 2011, Non-HDL-cholesterol shows improved accuracy for cardiovascular risk score classification compared to direct or calculated LDL cholesterol in a dyslipidemic population, Clin. Chem. source
The Results (Non–HDL-C for CVD Risk Score Classification; page unavailable) report that non–HDL-C generally classified fewer patients incorrectly than direct or calculated LDL-C in the studied dyslipidemic population. The Discussion (page unavailable) says that non–HDL-C calculated using direct HDL-C results showed better harmonization of risk-score classification across methods. (LLM, conf=0.93)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Guideline-recommended therapeutic goals for non-HDLC are arbitrarily set typically at 0.8 mmol/L (30 mg/dL) higher than LDLC goals (Table 6); this value is based on the assumption that the”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 7.1. Non-HDL cholesterol
What the sources say
- Supportedcites [1] Langlois, 2018, Clin. Chem. source
Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
- Partly supportedcites [2] Nordestgaard, 2016, Eur. Heart J. sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- The authors state this as an assumption: The optimal VLDLC concentration associated with the fasting TG threshold 1.7 mmol/L is 0.8 mmol/L.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“It is the structural protein for all non-HDL lipoproteins and exists as 2 isoforms: apoB100, the major isoform in VLDL, IDL, LDL, and Lp(a), and apoB48 in chylomicrons and chylomicron remnants [12].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 7.2. Apolipoprotein B
What the sources say
- Partly supportedcites [12] Contois, 2009, Apolipoprotein B and cardiovascular disease risk: position statement from the AACC lipoproteins and vascular disease working group on best practices, Clin. Chem. sourceExperimental — accuracy not yet measured
The ‘apo B STRUCTURE AND FUNCTION’ section (p. 2) identifies two isoforms and calls apo B-48 the structural protein of chylomicrons. The ‘apo B-CONTAINING LIPOPROTEINS AND CVD RISK’ section (p. 2) lists VLDL, IDL, LDL, and Lp(a) as apo B-containing particles. Our copy does not explicitly assign apo B-100 to each of those particles or mention apo B-48 in chylomicron remnants. (LLM, conf=0.82)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Lowering LDLC to concentrations below a target of 1.8 mmol/L in patients at high cardiovascular risk or 1.4 mmol/L in patients at very high risk (or by ≥ 50% if these targets cannot be attained) is of critical importance [4].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > Table 7
What the sources say
- Partly supportedcites [4] Mach, 2019, 2019 ESC/EAS guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk. The Task force for the management of dyslipidaemias of the European society of cardiology (ESC) and European atherosclerosis society (EAS), Eur. Heart J. sourceExperimental — accuracy not yet measured
The treatment-goals passage recommends LDL-C below 1.8 mmol/L for high-risk patients and below 1.4 mmol/L for very-high-risk patients. It recommends a ≥50% reduction from baseline alongside each absolute goal, not only as an alternative if the goal cannot be attained. (LLM, conf=0.91)
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“ApoB can be measured in the nonfasting state because even at peak postprandial concentrations, the number of chylomicron-apoB48 particles in healthy individuals is usually < 1% and the number of VLDL-apoB100 particles is < 10% of the number of LDL-apoB100 particles [12].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 7.2. Apolipoprotein B
What the sources say
- Partly supportedcites [12] Contois, 2009, Apolipoprotein B and cardiovascular disease risk: position statement from the AACC lipoproteins and vascular disease working group on best practices, Clin. Chem. sourceExperimental — accuracy not yet measured
The MEASUREMENT ISSUES section (p. 9) says fasting is not required for apo B measurement, and the apo B-CONTAINING LIPOPROTEINS AND CVD RISK section (p. 2) says most plasma apo B is associated with LDL. Neither passage gives the claimed <1% chylomicron-apoB48 or <10% VLDL-apoB100 particle ratios at peak postprandial concentrations in healthy individuals. (LLM, conf=0.88)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“A major impediment to LDLP testing is its limited availability in the clinical laboratories, higher cost, and lack of standardization [63], although it does provide additional information on other lipoproteins VLDL and HDL, beyond LDLP.”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 7.2. Apolipoprotein B
What the sources say
- Supportedcites [63] Clouet-Foraison, 2017, Advanced lipoprotein testing for cardiovascular diseases risk assessment: a review of the novel approaches in lipoprotein profiling, Clin. Chem. Lab. Med. source
The Introduction (page unavailable) identifies LDL-P measurement as an advanced lipoprotein test and describes lack of standardization as a general issue for these methods. The Concluding remarks (page unavailable) say most advanced methods are not suitable for routine clinical-laboratory use because they are not cost-effective or readily automated for high throughput. Together, these passages support the stated impediments, though the review frames them as applying to most advanced methods rather than every LDL-P assay. (LLM, conf=0.86)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“ApoB is recommended for risk assessment and may be preferred over non-HDLC, if available, in persons with mild-to-moderate hypertriglyceridemia (2-10 mmol/L), diabetes, obesity or metabolic syndrome, or very low LDLC < 1.8 mmol/L [4].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 7.2. Apolipoprotein B
What the sources say
- Partly supportedcites [4] Mach, 2019, 2019 ESC/EAS guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk. The Task force for the management of dyslipidaemias of the European society of cardiology (ESC) and European atherosclerosis society (EAS), Eur. Heart J. sourceExperimental — accuracy not yet measured
The “Changes in recommendations” section recommends ApoB for risk assessment in people with high triglycerides, diabetes, obesity or metabolic syndrome, or very low LDL-C, and says it may be preferred over non-HDL-C in several of those groups. It does not give the claimed triglyceride range of 2–10 mmol/L or define very low LDL-C as <1.8 mmol/L; its preference-over-non-HDL-C statement also does not explicitly include metabolic syndrome. Page numbers are unavailable in our copy. (LLM, conf=0.88)
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Another advantage of LC-MSMS is that it enables the simultaneous (multiplexed) measurement of multiple apolipoproteins in addition to apoB100 in a single run of the assay, thus making it possible to achieve a complete apolipoprotein profile in the patient, including HDL-and VLDL-associated apolipoproteins for comprehensive characterization of dyslipidemias [68].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 7.2. Apolipoprotein B
What the sources say
- Partly supportedcites [68] van den Broek, 2016, Automated multiplex LC-MS/MS assay for quantifying serum apolipoproteins A-I, B, C-I, C-II, C-III, and E with qualitative apolipoprotein E phenotyping, Clin. Chem. sourceExperimental — accuracy not yet measured
The Discussion (page unavailable) says the assay expands the panel to six apolipoprotein quantities in one workflow, supporting multiplexed measurement alongside apoB-100. The paper does not establish that those six measurements constitute a complete patient apolipoprotein profile; it presents their clinical value for dyslipidemia as a potential benefit. (LLM, conf=0.86)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“However, apoB cannot substitute for NMRor ion mobility-based particle size measurements and does not differentiate between LDL and VLDL particle numbers [61,62].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 7.2. Apolipoprotein B
What the sources say
- Not checked — no full text of the sourcecites [61] 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
- Supportedcites [62] Mora, 2015, Circulation source
The paper states that apoB measures the total concentration of atherogenic particles—including VLDL, IDL and LDL—regardless of size, so it does not distinguish their numbers or sizes. It contrasts this with ion mobility, which separates particles by size and counts them across lipoprotein classes (introductory passages in our copy; page unavailable). (LLM, conf=0.88)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Addition of PCSK9 inhibition to statin therapy allows more patients to achieve non-HDLC and apoB goals and lower risk of ASCVD, with no attenuation of benefit at lower concentrations [88].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 9.3. Secondary treatment target: non-HDLC or apoB?
What the sources say
- Partly supportedcites [88] Ray, 2016, Reductions in atherogenic lipids and major cardiovascular events: a pooled analysis of 10 ODYSSEY trials comparing alirocumab with control, Circulation sourceExperimental — accuracy not yet measured
The Results (Lipid Levels During Treatment; page unavailable) report that more alirocumab-treated patients achieved very low non–HDL-C and apoB levels, but do not establish that more patients met specified goals. The Discussion (page unavailable) finds lower non–HDL-C and apoB associated with lower MACE rates without discernible attenuation at lower levels. The Conclusions say outcomes trials were still assessing whether PCSK9 inhibition added to statins reduces MACE, so the claim overstates a demonstrated reduction in ASCVD risk. (LLM, conf=0.87)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Although apoB demonstrates competitive clinical performance compared with non-HDLC, there is no evidence yet of significant population healtheconomic benefit of intensifying pharmacological intervention aiming to further reduce apoB at very low concentrations of LDLC [1].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 9.3. Secondary treatment target: non-HDLC or apoB?
What the sources say
- Partly supportedcites [1] Langlois, 2018, Clin. Chem. sourceExperimental — accuracy not yet measured
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Guideline-based non-HDLC thresholds have been arbitrarily defined by consensus of expert groups, based on the assumption that a normal VLDLC concentration exists when TG are < 1.7 mmol/L, which is < 0.8 mmol/L as estimated by the Friedewald formula [1,2].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 9.1. Non-HDL cholesterol
What the sources say
- Supportedcites [1] Langlois, 2018, Clin. Chem. source
Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
- Partly supportedcites [2] Nordestgaard, 2016, Eur. Heart J. sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Diabetes and abdominal obesity, disorders that underlie the clinical expression of complex dyslipidemias without elevated LDLC, are attaining epidemic proportions [11].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 11. Conclusion and future research priorities
What the sources say
- Supportedcites [11] Miller, 2011, Triglycerides and cardiovascular disease: a scientific statement from the American Heart Association, Circulation source
The Introduction (page unavailable) describes a growing epidemic of obesity and type 2 diabetes alongside rising triglycerides and receding mean LDL-C levels. Section 5.2 links visceral abdominal fat to elevated triglycerides, while section 4.4 explains that LDL-C alone may not reliably reflect the atherogenic particles in these dyslipidemic states. Together, these passages support the citing sentence as a broad paraphrase. (LLM, conf=0.85)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In patients with mixed hyperlipidemias, routine genetic testing is not warranted [33].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 10.3. Alert values
What the sources say
- Supportedcites [33] Hegele, 2014, European Atherosclerosis Society Consensus Panel. The polygenic nature of hypertriglyceridaemia: implications for definition, diagnosis, and management, Lancet Diabetes Endocrinol. source
In “Redefinition of hypertriglyceridaemic states,” the paper includes familial combined hyperlipidaemia among patients with triglyceride concentrations of 2–10 mmol/L and explicitly advises against routine genetic testing in that group. It reserves testing in severe hypertriglyceridaemia for paediatric and adolescent patients. (LLM, conf=0.91)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“These novel technologies provide complementary diagnostic information regarding the complex molecular basis of dyslipidemias and, as such, can be used to explore and evaluate precision medicine approaches for identifying better and individualized treatment options for patients at high risk of ASCVD [99].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 11. Conclusion and future research priorities
What the sources say
- Supportedcites [99] Ruhaak, 2019, Apolipoprotein profiling as a personalized approach to the diagnosis and treatment of dyslipidaemia, Ann. Clin. Biochem. source
Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plainconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“This may compensate for the under-or overestimation of LDLC in terms of clinical decision making, given the uncertainty of dLDLC measurements or the Friedewald calculation in dyslipidemic samples when LDLC lowering approaches 1.4 mmol/L, and non-HDLC can be used at high TG ≥ 4.5 mmol/l.”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 9.1. Non-HDL cholesterol
What the sources say
- Partly supportedcites [1] Langlois, 2018, Clin. Chem. sourceExperimental — accuracy not yet measured
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“To improve patient comfort and compliance, there are practical advantages of this approach for follow-up without the need to fast [2].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 9.3. Secondary treatment target: non-HDLC or apoB?
What the sources say
- Supportedcites [2] Nordestgaard, 2016, Eur. Heart J. source
The Introduction (page unavailable) says non-fasting testing simplifies sampling and is likely to improve patient compliance. The Constituents of the plasma lipid profile section says calculated non-HDL cholesterol can be added to a standard report at no additional cost, and the Influence of food intake section describes non-fasting testing as practical for monitoring treatment responses. (LLM, conf=0.88)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In a pediatric setting, reporting age-and gender-specific reference intervals is relevant for early identification of children with hyperlipidemia associated with premature atherosclerosis, especially FH [32].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 10.2. Reference limits
What the sources say
- Partly supportedcites [32] Wiegman, 2015, European Atherosclerosis Society Consensus Panel. Familial hypercholesterolaemia in children and adolescents: gaining decades of life by optimizing detection and treatment, Eur. Heart J. sourceExperimental — accuracy not yet measured
The Screening section recommends using country-, age- and gender-specific LDL-C levels to screen children for FH when DNA testing is unavailable. The Conclusions link early FH identification to preventing atherosclerosis. The paper does not specifically recommend reporting laboratory reference intervals or extend that recommendation to pediatric hyperlipidemia generally. (LLM, conf=0.84)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“For nonfasting samples, laboratories should flag abnormal TG concentrations as ≥2 mmol/L according to the Women's Health Study, which found that this threshold was optimal for ASCVD prediction [91].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 10.1. Threshold values
What the sources say
- Partly supportedcites [91] White, 2015, Identifying an optimal cutpoint for the diagnosis of hypertriglyceridemia in the nonfasting state, Clin. Chem. sourceExperimental — accuracy not yet measured
The Results and Discussion identify 175 mg/dL (1.98 mmol/L, approximately 2 mmol/L) as the optimal nonfasting triglyceride cutpoint for predicting incident CVD in the Women’s Health Study. The paper proposes a diagnostic cutpoint, but does not specifically direct laboratories to flag results at that level; its measured outcome is a composite of CVD events rather than an outcome expressly defined as ASCVD. (LLM, conf=0.82)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“This necessarily results in on-treatment LDL and VLDL particle numbers that are higher than would be anticipated from the concurrent LDLC follow-up measurement and may explain part of residual risk among statin-treated patients [62,90].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 9.2. Apolipoprotein B
What the sources say
- Partly supportedcites [62] Mora, 2015, Circulation sourceExperimental — accuracy not yet measured
The Results report that rosuvastatin lowered LDL particle numbers less than LDL-c (27.8% versus 48.5%), and the Discussion links on-treatment atherogenic particles, including VLDL subfractions, to residual risk. The paper does not establish that LDL and VLDL particle numbers are necessarily higher than a concurrent LDL-c measurement would predict for every statin-treated patient. (LLM, conf=0.87)
- Partly supportedcites [90] Lawler, 2017, Atherogenic lipoprotein determinants of cardiovascular disease and residual risk among individuals with low low-density lipoprotein cholesterol, J. Am. Heart Assoc. sourceExperimental — accuracy not yet measured
The Results sections ‘Lipoprotein Subclass Response to Statin Therapy’ and ‘Residual Risk of CVD’ (page unavailable) report that LDL-c fell more than some LDL particle subclasses, VLDL particle responses were variable, and small VLDL particle levels were associated with residual risk. They do not establish that both LDL and VLDL particle numbers are necessarily higher than a concurrent LDL-c measurement would predict for every statin-treated patient. (LLM, conf=0.86)
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Guidelines propose using non-HDLC or apoB as a secondary treatment target in the management of patients with mild-to-moderate hypertriglyceridemia (2-10 mmol/L), including patients with diabetes [4,5].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 9.3. Secondary treatment target: non-HDLC or apoB?
What the sources say
- Partly supportedcites [4] Mach, 2019, 2019 ESC/EAS guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk. The Task force for the management of dyslipidaemias of the European society of cardiology (ESC) and European atherosclerosis society (EAS), Eur. Heart J. sourceExperimental — accuracy not yet measured
Section 9.4.2.2 calls non-HDL-C or ApoB a secondary objective of therapy and discusses atherogenic dyslipidaemia in people with type 2 diabetes. The secondary-goals passage likewise recommends risk-based non-HDL-C and ApoB targets. Neither passage ties those targets specifically to the claimed triglyceride range of 2–10 mmol/L, so that qualifier is not supported by our copy. (LLM, conf=0.84)
- Not checked — no full text of the sourcecites [5] Anderson, 2016, Canadian cardiovascular society guidelines for the management of dyslipidemia for the prevention of cardiovascular disease in the adult, Can. J. Cardiol. source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“For the present purposes, the combination of non-HDLC with Martin-Hopkins cLDLC may be considered as an appropriate strategy to guide therapy and they can be calculated from the standard lipid profile [1].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 9.1. Non-HDL cholesterol
What the sources say
- Partly supportedcites [1] Langlois, 2018, Clin. Chem. sourceExperimental — accuracy not yet measured
The LDLC VS NON-HDLC section (p. 18) says combining non-HDLC with calculated LDL-C is an appropriate strategy to guide therapy, and ON-TREATMENT DISCORDANCES (p. 21) says these measures can be calculated from a standard lipid profile. The paper does not specifically recommend Martin-Hopkins calculated LDL-C for that combination; the VLDLC section (p. 9) says the clinical value of alternative LDL-C calculations remains to be determined. (LLM, conf=0.88)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“< 0.1 g/L (10 mg/dL): genetic abetalipoproteinemia”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > Financial support
What the sources say
- Supportedcites [2] Nordestgaard, 2016, Eur. Heart J. source
Table 8 in “Life-threatening plasma lipid concentrations—what to do?” associates apolipoprotein B below 10 mg/dL (equivalent to 0.1 g/L) with genetic abetalipoproteinaemia. The accompanying text recommends referral for further evaluation, so this is an indicator rather than a definitive diagnosis. No page number is available in our copy. (LLM, conf=0.88)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“< 0.1 g/L (10 mg/dL): genetic hypoalphalipoproteinemia”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > Financial support
What the sources say
- Supportedcites [2] Nordestgaard, 2016, Eur. Heart J. source
Table 8 in “Life-threatening plasma lipid concentrations—what to do?” associates apolipoprotein A1 below 10 mg/dL (equivalent to 0.1 g/L) with genetic hypoalphalipoproteinaemia. The paper recommends referral for further assessment, rather than treating the concentration as a diagnosis on its own. No page number is available in our copy. (LLM, conf=0.90)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
In the paper
“for conversion of Lp(a) concentrations in mg/dL to nmol/L, 13930 individuals from the Copenhagen General Population Study had measurements in both mg/dL and nmol/L by Denka Seiken assays distributed by Roche Diagnostics (Rotkreuz, Switzerland).The correlation was done by linear regression with an R 2 value of 0.996, and the conversion was done by the following equation: Lp(a), nmol/L = 2.18*Lp(a),”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 10.3. Alert values
What the sources say
- Not checked — no full text of the sourcecites [3] Langsted, 2019, High lipoprotein(a) and high risk of mortality, Eur. Heart J. source
plaincorrelationaln = 13,930- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one. The quote only partly states this claim.
In the paper
“One of the major differences between Lp(a) and LDL particles is that LDLs are effectively lowered by statins, whereas Lp(a) is typically resistant to this treatment [24].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > Laboratory reports should flag abnormal concentrations based on decision thresholds.
What the sources say
- Not checked — no full text of the sourcecites [24] Willeit, 2018, Baseline and on-statin treatment lipoprotein(a) levels for prediction of cardiovascular events: individual patient-data meta-analysis of statin outcome trials, Lancet source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Direct”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 2.1. LDL particles
What the sources say
- Not checked — no full text of the sourcecites [19] Varbo, 2017, Remnant lipoproteins, Curr. Opin. Lipidol. source
- Not checked — no full text of the sourcecites [20] Varbo, 2018, Remnant cholesterol and myocardial infarction in normal weight, overweight, and obese individuals from the copenhagen general population study, Clin. Chem. source
plaincorrelational- Asserted: fails — The authors may not put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The authors may not put it forward as true. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“Lp(a) concentrations do not change in response to normal food intake and are minimally increased in inflammation, although the influence of acute illness or acute phase reactions on Lp(a) concentration is discussed controversially [34].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 3. What is the standard lipid profile?
What the sources say
- Not checked — no full text of the sourcecites [34] Langsted, 2014, Lipoprotein(a): fasting and nonfasting levels, inflammation, and cardiovascular risk, Atherosclerosis source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“The equation uses a fixed TG:cholesterol ratio (TG/2.2 in mmol/L or TG/5 in mg/dL) to estimate VLDLC and assumes lack of chylomicrons which are more TGrich than VLDL [44].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 5.3. Calculated LDLC
What the sources say
- Not checked — no full text of the sourcecites [44] Nauck, 2002, Methods for measurement of LDL-cholesterol: a critical assessment of direct measurement by homogeneous assays versus calculation, Clin. Chem. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“The cLDLC equations and also most dLDLC assays include the cholesterol content of Lp(a) [52].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 5.4. Effect of Lp(a)-cholesterol on LDLC
What the sources say
- Not checked — no full text of the sourcecites [52] Yeang, 2015, ‘LDLC’ = LDL-C + Lp(a)-C: implications of achieved ultra-low LDL-C levels in the proprotein convertase subtilisin/kexin type 9 era of potent LDL-C lowering, Curr. Opin. Lipidol. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Considering that an Lp(a) particle is composed of about 30-45% of cholesterol by weight, a significant overestimation of LDLC concentration occurs in subjects with high and very high Lp(a) concentrations [52]”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 5.4. Effect of Lp(a)-cholesterol on LDLC
What the sources say
- Not checked — no full text of the sourcecites [52] Yeang, 2015, ‘LDLC’ = LDL-C + Lp(a)-C: implications of achieved ultra-low LDL-C levels in the proprotein convertase subtilisin/kexin type 9 era of potent LDL-C lowering, Curr. Opin. Lipidol. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“The biases noted in dLDLC and dHDLC assays when analyzing dyslipidemic samples suggest that non-specific cross-reaction takes place, reflecting difficulties in selectively measuring the cholesterol in LDL or HDL fractions when atypical lipoproteins are present.”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 5.2. Direct LDLC and HDLC assays
What the sources say
- Not checked — no full text of the sourcecites [40] Ramasamy, 2018, Update on the laboratory investigation of dyslipidemias, Clin. Chim. Acta source
- Not checked — no full text of the sourcecites [41] Contois, 2011, Reliability of low-density lipoprotein cholesterol, non-high density lipoprotein cholesterol, and apolipoprotein B measurement, J. Clin. Lipidol. source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Non-HDLC can be obtained in the nonfasting state and does not require TG to be less than 4.5 mmol/L, which is the limitation for calculation of cLDLC [44].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 7.1. Non-HDL cholesterol
What the sources say
- Not checked — no full text of the sourcecites [44] Nauck, 2002, Methods for measurement of LDL-cholesterol: a critical assessment of direct measurement by homogeneous assays versus calculation, Clin. Chem. source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Some individuals with high RemnantC have low LDLC and thus will have relatively low non-HDLC if Lp(a) is also low, and if interpreting non-HDLC instead of RemnantC, the high RemnantC will be masked in these individuals [30].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 7.1. Non-HDL cholesterol
What the sources say
- Not checked — no full text of the sourcecites [30] Langlois, 2018, Which lipids should be analyzed for diagnostic workup and follow-up of patients with hyperlipidemias?, Curr. Cardiol. Rep. source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“When compared to Martin-Hopkins cLDLC, non-HDLC translates to only modest improvement for risk classification that could change clinical management (in ~2% of individuals in a general population), although discordance of Martin-Hopkins cLDLC and, as a consequence, risk underestimation is still common (80-90%) in patients with TG ≥ 4.5 mmol/L [60].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 7.1. Non-HDL cholesterol
What the sources say
- Not checked — no full text of the sourcecites [60] Sathiyakumar, 2018, Impact of novel low-density lipoprotein-cholesterol assessment on the utility of secondary non-high-density lipoprotein-cholesterol and apolipoprotein B targets in selected worldwide dyslipidemia guidelines, Circulation source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“At this point of time, there is insufficient evidence of benefit from outcome studies to support the option to replace the standard lipid profile (with calculation of cLDLC and non-HDLC) by single followup measurement of apoB to guide lipid-lowering therapies.”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > Table 7
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The suggested use of apoB would be cost-effective if these tests guide therapy to reduce the healthcare costs of ASCVD to a greater extent than standard therapy guided by LDLC, yet the evidence base of this approach is still incomplete (Table 7).”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 8.3. Cost-effectiveness -health economic benefit
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Like non-HDLC, apoB can always be measured in the nonfasting state and is not affected by biological TG variability.”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 7.2. Apolipoprotein B
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Lowering non-HDLC thresholds leads to upward reclassification of patients (if the goal is to reduce undertreatment), higher thresholds lead to downward reclassification (if the goal is to reduce overtreatment).”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 9.1. Non-HDL cholesterol
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“If ≤ 2 of 20 values (≤10%) fall outside the reference interval then the interval can be adopted [96,97].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 10.2. Reference limits
What the sources say
- Not checked — no full text of the sourcecites [96] Ceriotti, 2009, Reference intervals: the way forward, Ann. Clin. Biochem. source
- Not checked — no full text of the sourcecites [97] Henny, 2016, Working Group Accreditation and ISO/CEN standards (WG-A/ISO) of the EFLM. Recommendation for the review of biological reference intervals in medical laboratories, Clin. Chem. Lab. Med. source
plainconditionaln = 20- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Data from concordance/discordance analyses suggest that calculation of non-HDLC is at least equally good at predicting ASCVD compared with measurement or calculation of LDLC in the overall population and statin-treated patients; it may also be superior to LDLC if discordantly high, especially at normal or low LDLC concentrations and in individuals with hypertriglyceridemia because it includes Rem”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 9.1. Non-HDL cholesterol
What the sources say
- Not matchedcites [81][82][83]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“At TG concentration ≥4.5 mmol/L, a condition wherein use of Friedewald cLDLC or Martin-Hopkins cLDLC is not recommended and also dLDLC is likely to be inaccurate, use of non-HDLC calculation may be considered instead of dLDLC measurement to evaluate therapeutic response.”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 9.3. Secondary treatment target: non-HDLC or apoB?
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may state two separate claims as one.
In the paper
“This situation is challenging for new generation assays to meet regulations for in vitro diagnostic medical devices, requiring evidence of clinical performance of the assays [70].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 10.1. Threshold values
What the sources say
- Not checked — no full text of the sourcecites [70] Horvath, 2014, From biomarkers to medical tests: the changing landscape of test evaluation, Clin. Chim. Acta source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“For decision thresholds it is unnecessary to validate them in the laboratory [97].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 10.2. Reference limits
What the sources say
- Not checked — no full text of the sourcecites [97] Henny, 2016, Working Group Accreditation and ISO/CEN standards (WG-A/ISO) of the EFLM. Recommendation for the review of biological reference intervals in medical laboratories, Clin. Chem. Lab. Med. source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
The paper relies on this without support.
ApoB assays currently provide the most accurate measurement of overall burden of atherogenic particles in the fasting and nonfasting state.
“ApoB assays currently provide the most accurate measurement of overall burden of atherogenic particles in the fasting and nonfasting state.”
The authors state this as an assumption.
The optimal VLDLC concentration associated with the fasting TG threshold 1.7 mmol/L is 0.8 mmol/L.
“this value is based on the assumption that the”
The paper relies on this without support.
dHDLC measurement errors in hypertriglyceridemic samples affect the calculation of non-HDLC.
“However, dHDLC measurement errors in hypertriglyceridemic samples still affect the calculation of non-HDLC and most assays limit the measurement of dHDLC to TG < 10 mmol/L.”
The paper relies on this without support.
Most dHDLC assays limit the measurement of dHDLC to TG < 10 mmol/L.
“However, dHDLC measurement errors in hypertriglyceridemic samples still affect the calculation of non-HDLC and most assays limit the measurement of dHDLC to TG < 10 mmol/L.”
The paper relies on this without support.
ApoB is a clearly defined measurand in contrast to the heterogeneous LDLC fraction.
“In contrast to the heterogeneous LDLC fraction, apoB is a clearly defined measurand.”
The paper relies on this without support.
ApoB quantification by automated immunoassays such as immunonephelometry and immunoturbidimetry can be easily implemented in clinical laboratories.
“ApoB quantification by automated immunoassays such as immunonephelometry and immunoturbidimetry can be easily implemented in the clinical laboratories.”
The paper relies on this without support.
Most nephelometric and turbidimetric apoB measurements are limited to TG < 10 mmol/L due to interference of light scattering or absorption caused by chylomicrons and large VLDLs.
“Far higher than the maximum allowed TG concentration of 4.5 mmol/L for cLDLC, most nephelometric and turbidimetric apoB measurements are limited to TG < 10 mmol/L due to interference of light scattering or absorption caused by chylomicrons and large VLDLs;”
The paper relies on this without support.
Implementation of apoB assays in follow-up of lipid-lowering therapies would impose healthcare systems and patients with yearly extra cost.
“Implementation of apoB assays in follow-up of lipid-lowering therapies would impose healthcare systems and patients with yearly extra cost, although one might consider replacing the standard lipid profile (needed for calculation of LDLC and non-HDLC) by single follow-up measurement of apoB in order to attenuate the rise of expenses.”
The paper relies on this without support.
Guideline-recommended LDLC thresholds are based on observations with Friedewald cLDLC using older HDLC precipitation methods which differ from dHDLC assays used nowadays.
“Guideline-recommended LDLC thresholds are based on observations with Friedewald cLDLC using the older HDLC precipitation methods which differ from dHDLC assays used nowadays.”
The paper relies on this without support.
Increased baseline glycerol concentrations can be found in patients with diabetes and chronic kidney disease and during intravenous lipid infusion, and TG may be wrongly flagged in these patients unless a glycerol-corrected TG assay is used.
“Increased baseline glycerol concentrations can be found in patients with diabetes and chronic kidney disease and during intravenous lipid infusion, and TG may be wrongly flagged in these patients unless glycerol-corrected TG assay is used.”
The paper relies on this without support.
There is no consensus on which threshold value in mmol/L to be used for Lp(a).
“There is no consensus on which threshold value in mmol/L to be used for Lp(a); however, for conversion of Lp(a) concentrations in mg/dL to nmol/L, 13930 individuals from the Copenhagen General Population Study had measurements in both mg/dL and nmol/L by Denka Seiken assays distributed by Roche Diagnostics (Rotkreuz, Switzerland).”
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
“| 20-39 | 0.67 | 26 | 1.0 | 39 | 1.2 | 85 | 1.5 | 56 | 2.0 | 76 |”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > Financial support
Reported 85 · recomputed 46.32
Citations
Cites
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Self-citation2016 ESC/EAS Guidelines for the Management of Dyslipidaemias
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Self-citation
Cited by
Sorted by citations
Items 201–227 of 227
A step forward in the consensus on lipid profile characteristics for cardiovascular prevention
Pintó, X., & Pedro‐Botet, J. (2023) · Clínica e Investigación en Arteriosclerosis (English Edition) · doi:10.1016/j.artere.2023.05.004
Quo vadis, colesterol de las LDL?
Cobos, A., & Valdivielso, P. (2023) · Advances in Laboratory Medicine / Avances en Medicina de Laboratorio · doi:10.1515/almed-2023-0049
Consensus document for lipid profile testing and reporting in Spanish clinical laboratories
Velilla, T. A., Guijarro, C., Ruíz, R. C., Piñero, M. R., Marcos, J. F. V., López, A. M. B., López, A. M., Donaire, J. A. G., Obaya, J. C., Guerra, L. C., et al. (2023) · Endocrinología Diabetes y Nutrición (English ed ) · doi:10.1016/j.endien.2023.05.012
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Cobos, A., & Valdivielso, P. (2023) · Advances in Laboratory Medicine / Avances en Medicina de Laboratorio · doi:10.1515/almed-2023-0051
Velilla, 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) · Nefrología · doi:10.1016/j.nefro.2023.02.002 · Cited by 1
Velilla, 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) · Endocrinología Diabetes y Nutrición · doi:10.1016/j.endinu.2023.02.002
Labordiagnostik von Fettstoffwechselstörungen
März, W., Scharnagl, H., Kleber, M. E., Silbernagel, G., Nauck, M., Müller‐Wieland, D., & von Eckardstein, A. (2024) · Diabetes aktuell · doi:10.1055/a-2302-8505
Self-citationMétodo analítico y aplicación de fórmulas en la determinación de colesterol
Peralta, A. L. H., & Jara, A. G. P. (2024) · Revista Científica Arbitrada Multidisciplinaria PENTACIENCIAS · doi:10.59169/pentaciencias.v6i4.1092
Gómez-Barrado, J. J., Gómez-Turégano, P., Beltran-Moreno, M., Fernández-Chamorro, A. I., Rodríguez, B. R., & Kounka, Z. (2024) · Clínica e Investigación en Arteriosclerosis (English Edition) · doi:10.1016/j.artere.2024.09.002
In, J. W., Kim, J., & Chung, S. (2024) · Laboratory Medicine Online · doi:10.47429/lmo.2025.15.1.47
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Bril, F., Berg, G. A., Barchuk, M., & Nogueira, J. P. (2025) · Journal of Lipid and Atherosclerosis · doi:10.12997/jla.2025.14.1.69
Pilot study on laboratory sample exchange: Evaluation and key findings
Oprea, O. R., Handolescu, D. I., & Dobreanu, M. (2025) · Revista română de medicină de laborator · doi:10.2478/rrlm-2025-0012
Motevalli, M. S., Tanous, D., Drenowatz, C. J., Schauer, M., Mair, S., Kohlberger, M., Ruedl, G., & Wirnitzer, K. (2025) · Dietetics · doi:10.3390/dietetics4040045
韩, 晓. (2023) · Advances in Clinical Medicine · doi:10.12677/acm.2023.131103
Comparison of Lipid Measurements by Clinical Chemistry and NMR Spectroscopy
Tekin, N., Saral, N. Y., Toker, A., Şahin, F., Baykal, A. T., & Serteser, M. (2025) · Diagnostics · doi:10.3390/diagnostics16010028
“…Society (EAS) and the European Federation of Clinical Chemistry and Laboratory Medicine (EFLM) stated that the use of NMR and LC-MS/MS should be standardized and validated due to the inadequacy of routine clinical chemistry practices for Apo-B quantification, LDL-P, and VLDL count and size [17].”
Baylan, F. A., Özcan, M., Ercan, Ş., Ciriz, A., Avcı, E., & Ercan, M. (2025) · Scandinavian Journal of Clinical and Laboratory Investigation · doi:10.1080/00365513.2025.2605638
“At TG 4.5 mmol/L, nonfasting and fasting lipid profiles may be used alike for Friedewald calculated LDL-C, when LDLC is not 1.8 mmol/L (70 mg/dL) [4,5].”
InfluentialPoorebrahimi, M., Mirjalili, S. R., Soltani, S., Marques-Vidal, P. M., Namayandeh, S. M., & Sarebanhassanabadi, M. (2026) · Advanced Biomedical Research · doi:10.4103/abr.abr_221_25
“[25,26] Potential collinearity between BMI and the TG/HDL‑”
How to properly interpret lipid profile results
Soška, V. (2025) · Vnitřní lékařství · doi:10.36290/vnl.2025.060
Feng, L., Zhang, Z., Wen, Z., Liu, Y., & Wang, Y. (2026) · Research Square · doi:10.21203/rs.3.rs-9123147/v1
Zhang, L., Zhang, S., Sun, Y., Wang, L., Fan, F., Zhang, Y., & Li, J. (2026) · Journal of Translational Internal Medicine · doi:10.1515/jtim-2026-0025
“Atorvastatin [1-3] Hypercholesterolemia Positive Omega-3 fatty acids EPA [4,5] Metabolic syndrome and/not on statin Positive Cholesterol absorption inhibitor Ezetimibe [6,7] Hypercholesterolemia Positive PCSK9 inhibitor Evolocumab (mAb) [8,9] Patients with ASCVD and on statin * Positive Alirocumab…”
Dosage of lipoproteins for risk management according to guidelines
Bonnin, C., Fourgeaud, C., Mahé, G., Ezzaki, K., Gras, M., Himpens, F. X., Jacquet, R., Khider, L., Mirault, T., Poggi, J. N., et al. (2026) · Vascular Diseases · doi:10.1016/j.vasdi.2026.05.001
Villemin, A., Zaepfel, S., Benlyamani, I., et al. (2026) · Clinical Chemistry and Laboratory Medicine (CCLM) · doi:10.1515/cclm-2026-0570
Identifying and resolving analytical outliers in lipoprotein(a) immunoassay testing
Jackson, A. N., Wyness, S. P., Rudolf, J. W., et al. (2026) · Practical Laboratory Medicine · doi:10.1016/j.plabm.2026.e00557
Metadata
- Authors
- Nordestgaard, B. G., Langlois, M. R., Langsted, A., Chapman, M. J., Aakre, K. M., Baum, H., Borén, J., Bruckert, E., Catapano, A., Cobbaert, C., Collinson, P., Descamps, O. S., Duff, C. J., von Eckardstein, A., Hammerer-Lercher, A., Kamstrup, P. R., Kolovou, G., Kronenberg, F., Mora, S., Pulkki, K., Remaley, A. T., Rifai, N., Ros, E., Stankovic, S., Stavljenic-Rukavina, A., Sypniewska, G., Watts, G. F., Wiklund, O., & Laitinen, P.
- Affiliations
- University of Copenhagen (DK)
- Ghent University (BE)
- Inserm (FR)
- Haukeland University Hospital (NO)
- Klinikum Ludwigsburg (DE)
- Sahlgrenska University Hospital (SE)
- University of Milan (IT)
- Leiden University Medical Center (NL)
- St George's, University of London (GB)
- Cliniques Universitaires Saint-Luc (BE)
- University Hospitals of North Midlands NHS Trust (GB)
- University Hospital Zurich (CH)
- Onassis Cardiac Surgery Center (GR)
- Innsbruck Medical University (AT)
- Brigham and Women's Hospital (US)
- University of Turku (FI)
- National Institutes of Health (US)
- Boston Children's Hospital (US)
- Instituto de Salud Carlos III (ES)
- Univerzitetski Klinički Centar Srbije (RS)
- The University of Western Australia (AU)
- Helsinki University Hospital (FI)
- Corresponding author
- Nordestgaard, Børge G.
- Langlois, Michel R.
- ORCID
- Nordestgaard, Børge G.
- Langsted, Anne
- Chapman, M. John
- Aakre, Kristin M.
- Baum, Hannsjörg
- Borén, Jan
- Catapano, Alberico
- Cobbaert, Christa
- Collinson, Paul
- Descamps, Olivier S.
- Duff, Christopher J.
- von Eckardstein, Arnold
- Kamstrup, Pia R.
- Kolovou, Genovefa
- Kronenberg, Florian
- Mora, Samia
- Pulkki, Kari
- Remaley, Alan T.
- Rifai, Nader
- Ros, Emilio
- Stankovic, Sanja
- Watts, Gerald F.
- Wiklund, Olov
- Laitinen, Päivi
- Venue
- Atherosclerosis
- Publisher
- Elsevier BV
- Published
- 2020-02
- Volume
- 294
- Pages
- 46-61
- ISSN
- 0021-9150 (ISSN-L)
- OpenAlex
- W2996456596
- Semantic Scholar
- 440b3e0b67ecf979049e435e66f4f3e2ecb15ca5
- Cited by
- 246
- References
- 107
- Citations by year
- 2026: 19 · 2025: 18 · 2024: 32 · 2023: 58 · 2022: 30 · 2021: 46 · 2020: 43
- FWCI
- 28.66
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Atherosclerosis (publishedVersion)
- PubMed (publishedVersion)
- Ghent University Academic Bibliography (Ghent University) (publishedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (publishedVersion)
- Zurich Open Repository and Archive (University of Zurich) (acceptedVersion, other-oa)
- Leiden Repository (Leiden University) (submittedVersion, cc-by)
- UWA Profiles and Research Repository (UWA) (submittedVersion, other-oa)
- Data Archiving and Networked Services (DANS) (submittedVersion, cc-by)
- HAL (submittedVersion)
- DIAL (Catholic University of Leuven) (submittedVersion, other-oa)
- Työväentutkimus Vuosikirja (submittedVersion, other-oa)
- St George's Online Research Archive (St George's University of London) (submittedVersion)
- Leiden Repository (Leiden University) (submittedVersion, cc-by-nc-nd)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion)
- Zurich Open Repository and Archive (University of Zurich)
- Funders
- Merck
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Health Professions › Medical Laboratory Technology › Clinical Laboratory Practices and Quality Control
- Keywords
- atherogenic lipoproteins, lipid-lowering therapy, LDL cholesterol, non-HDL cholesterol, HDL cholesterol, triglycerides, lipoprotein(a), apolipoprotein B, remnant cholesterol, atherosclerotic cardiovascular disease risk, hypertriglyceridemia, reference values, residual cardiovascular risk
- MeSH terms
- Hypolipidemic Agents, Humans, Hyperlipidemias, Lipoproteins, 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.
A language model drew the claims from the paper on 2026-10-11, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-11 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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