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
Every source the paper cites for this claim was checked and supports it.
In the paper
“Small lipid-depleted LDL subfractions contain less cholesterol than larger ones.”
§ 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, “Small LDL Particles” (page not provided), describes small, dense LDL particles as depleted of cholesteryl esters. That supports the claim’s substance: these smaller LDL particles carry less cholesterol than larger ones. (LLM, conf=0.87)
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.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Elevated baseline and on-statin treatment Lp(a) concentration above the 80th percentile of the general population (50 mg/dL) is a strong genetic risk factor for cardiovascular disease independent of LDLC [23,24].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 2.3. Lipoprotein(a) particles
What the sources say
- Partly supportedcites [23] Nordestgaard, 2016, Lipoprotein(a) as a cause of cardiovascular disease: insights from epidemiology, genetics, and biology, J. Lipid Res. sourceExperimental — accuracy not yet measured
The Abstract identifies concentrations above 50 mg/dL as the highest-risk 20% and describes genetic evidence that elevated Lp(a) causes cardiovascular disease. The Familial Hypercholesterolemia section says this risk is irrespective of LDL-cholesterol concentration. The passages do not establish the claim specifically for Lp(a) measured during statin treatment. (LLM, conf=0.86)
- 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
boostedcorrelational- 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
“Findings from population studies showed that despite minor postprandial increases in TG and RemnantC, quantitative changes in other lipids, lipoproteins, and apolipoproteins appear to be negligible in response to the habitual meal intake for most individuals [2].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 4. When to use fasting and nonfasting blood samples?
What the sources say
- Supportedcites [2] Nordestgaard, 2016, 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.
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.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“This may erroneously exclude > 20% of patients for initiation or intensification of lipid-lowering therapy [45].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 5.3. Calculated LDLC
What the sources say
- Partly supportedcites [45] Martin, 2013, Friedewald-estimated versus directly measured low-density lipoprotein cholesterol and treatment implications, J. Am. Coll. Cardiol. sourceExperimental — accuracy not yet measured
The Results report that 23% of patients with Friedewald-estimated LDL-C below 70 mg/dl had directly measured LDL-C of at least 70 mg/dl. The Conclusions say this could lead to undertreatment, but the >20% figure applies to that subgroup, not all patients. The Study limitations also state that treatment implications were inferred from lipid profiles rather than observed treatment decisions. (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.
- Partly supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“Fasting is an option when nonfasting TG are ≥4.5 mmol/L, a concentration seen in ~3-5% of nonfasting individuals in the general population (Tables 23) [17]”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 4. When to use fasting and nonfasting blood samples?
What the sources say
- Could not verifycites [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 Measurement and Population Distribution section reports that 27% of adults in the Copenhagen population have triglycerides of 2–10 mmol/L, but gives no prevalence for nonfasting triglycerides ≥4.5 mmol/L. Figure 2 shows a distribution, yet the text available in our copy does not establish the claimed ~3–5% figure. I searched for the 4.5 mmol/L threshold and its associated percentage. (LLM, conf=0.72)
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.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Nonfasting lipid profiles are now endorsed by several guidelines including those in Europe, the UK, Canada, Brazil, and the US [4][5][6]35,38].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 4. When to use fasting and nonfasting blood samples?
What the sources say
- 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. source
Section 5.4.3 of the European ESC/EAS guidelines says non-fasting sampling can be used in most cases and that a number of guidelines recommend it. This supports the European-guideline part attributed to this source; the sentence's other regional guidelines have separate citations. (LLM, conf=0.91)
- 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
- Partly supportedcites [6] Grundy, 2018, AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA guideline on the management of blood cholesterol: a report of the American college of cardiology/American heart association Task force on clinical practice guidelines, J. Am. Coll. Cardiol. sourceExperimental — accuracy not yet measured
The guideline’s Primary Prevention section says screening can use fasting or nonfasting lipid measurements, supporting the US portion of the claim. Our copy does not establish endorsement by guidelines in the UK, Canada, or Brazil; it lists a European consensus statement in the references but does not substantiate the full international list. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites [35] Langsted, 2019, Nonfasting versus fasting lipid profile for cardiovascular risk prediction, Pathology source
- Not matchedcites [38] National Institute for Health and Care Excellence (NICE)
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
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.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Even in normotriglyceridemic samples and in samples with moderately elevated TG concentrations 2.0-4.5 mmol/L, dLDLC may not always agree with Friedewald cLDLC and translate to discrepant risk classifications as observed in fasting as well as nonfasting individuals [51].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 5.3. Calculated LDLC
What the sources say
- Partly supportedcites [51] Mora, 2009, Comparison of LDL cholesterol concentrations by Friedewald calculation and direct measurement in relation to cardiovascular events in 27,331 women, 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.
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.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Like LDLC, non-HDLC is treatable with existing lipid-lowering agents and there is a direct, consistent relationship between the magnitude of non-HDLC lowering and cardiovascular risk reduction observed in meta-analyses and trials with statins and other lipid-lowering agents [56,57].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 7.1. Non-HDL cholesterol
What the sources say
- Supportedcites [56] Robinson, 2009, Meta-analysis of the relationship between non-high-density lipoprotein cholesterol reduction and coronary heart disease, J. Am. Coll. Cardiol. source
The Conclusions state a direct, consistent relationship between the magnitude of non-HDL-C lowering and cardiovascular risk reduction. The Discussion reports a similar relationship for statins and fibrates and an approximately 1:1 relationship for most lipid-modifying drugs used as monotherapy. (LLM, conf=0.93)
- Supportedcites [57] Silverman, 2016, Association between lowering LDL-C and cardiovascular risk reduction among different therapeutic interventions: a systematic review and meta-analysis, J. Am. Med. Assoc. source
The Results report that each 1-mmol/L reduction in non-HDL-C was associated with a relative risk of 0.80 for major vascular events, similar to the association for LDL-C. The paper’s meta-analysis includes statin and nonstatin interventions, and its non-HDL-C analysis found that the result for fibrates was no longer significantly different from the predicted relationship. The claim describes this overall association rather than asserting that every agent had an identical effect. (LLM, conf=0.86)
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
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“It should be noted that most clinical trials demonstrating the evidence base for clinical benefit of LDLC lowering have used Friedewald cLDLC; thus it cannot be excluded that dLDLC rather than cLDLC is the method that misclassifies risk [1].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 5.3. Calculated LDLC
What the sources say
- Partly supportedcites [1] Langlois, 2018, Clin. Chem. sourceExperimental — accuracy not yet measured
In “DISCORDANT cLDLC VS dLDLC” (p. 11), the paper says that most trials establishing the benefit of LDL-C lowering *with statin therapy* used the Friedewald equation. The citing claim omits the statin-therapy qualifier, extending the statement to LDL-C-lowering trials generally. (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
Every source the paper cites for this claim was checked and supports it.
In the paper
“For patients, laboratories, and clinicians alike, nonfasting lipid profiles represent an operational simplication without significant negative implications for prognostic, diagnostic, and therapeutic options for ASCVD prevention [36].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 4. When to use fasting and nonfasting blood samples?
What the sources say
- Supportedcites [36] Mora, 2019, Association of nonfasting vs fasting lipid levels with risk of major coronary events in the Anglo-Scandinavian cardiac outcomes trial-lipid lowering arm, JAMA Intern. Med. source
The Discussion reports that nonfasting testing has practical advantages and that fasting and nonfasting lipids were similarly associated with coronary and vascular events. It also reports 94.8% agreement in ASCVD risk classification, supporting comparable risk assessment and treatment decisions; the Abstract identifies screening for dyslipidemia as another use of lipid testing. The claim fairly summarizes these findings without asserting that the two approaches are identical. (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.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Non-HDLC provides a more comprehensive risk assessment than LDLC in certain individuals with hypertriglyceridemia because it adds Re-mnantC to LDLC and, therefore, takes into account the atherogenic potential of remnant lipoproteins [17].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 7.1. Non-HDL cholesterol
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 Copenhagen General Population Study section states that non-HDL cholesterol equals LDL plus remnant cholesterol and notes its use in cardiovascular risk prediction. The Abstract identifies remnant cholesterol as a strong predictor of ASCVD, supporting the claim that including it accounts for risk beyond LDL cholesterol alone. No page number is available in our copy. (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.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The novel Martin-Hopkins formula improves the accuracy of cLDLC at various conditions including very low LDLC < 1.8 mmol/L and in nonfasting samples [47,48].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 5.3. Calculated LDLC
What the sources say
- Supportedcites [47] Sathiyakumar, 2018, Fasting versus nonfasting and low-density lipoprotein cholesterol accuracy, Circulation source
The Accuracy in Clinical Categorization section reports that the novel method was more accurate than Friedewald estimation across LDL-C categories in both fasting and nonfasting samples. For estimated LDL-C below 70 mg/dL (approximately 1.8 mmol/L), its accuracy was 94% in fasting and 92% in nonfasting samples, versus 78% and 71% for Friedewald estimation. (LLM, conf=0.94)
- Partly supportedcites [48] Martin, 2018, Comparison of low-density lipoprotein cholesterol assessment by Martin/Hopkins estimation, Friedewald estimation, and preparative ultracentrifugation: insights from the FOURIER trial, JAMA Cardiol. sourceExperimental — accuracy not yet measured
The Results and Conclusions (pages not provided) show that Martin/Hopkins estimates were more accurate than Friedewald estimates in the studied patients with Friedewald LDL-C below 40 mg/dL—well below 1.8 mmol/L (about 70 mg/dL). The paper does not establish improved accuracy in nonfasting samples; nonfasting accuracy appears only in the title of a cited reference. Its findings are also limited to the studied low-LDL-C, PCSK9-inhibitor-treated setting rather than the full range below 1.8 mmol/L. (LLM, conf=0.86)
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
Every source the paper cites for this claim was checked and supports it.
In the paper
“The resulting underestimation of LDLC may translate to downward misclassification when using guideline-recommended 1.8 mmol/L or 1.4 mmol/L thresholds for patients at high and very high cardiovascular risk, respectively [4].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 5.3. Calculated LDLC
What the sources say
- 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. source
Section 5.4.2, “Lipid measurements” (page unavailable), says calculated LDL-C can underestimate LDL-C, particularly with elevated triglycerides. The guideline’s LDL-C treatment goals (page unavailable) are <1.8 mmol/L for high-risk patients and <1.4 mmol/L for very-high-risk patients. Downward classification against those goals is a reasonable conditional implication of underestimation. (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.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Most discordances in dyslipidemic samples are observed at lower concentration ranges of LDLC (< 1.8 mmol/L) and HDLC (< 1.0 mmol/L) [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
The Results (Trueness and Total Error) say that nearly all discordant results occurred in the diseased group and that, for most methods, they occurred mostly below HDL-C 1.0 mmol/L and LDL-C 2.5 mmol/L. The claimed LDL-C cutoff of 1.8 mmol/L is not the reported discordance range; the Discussion mentions 1.8 mmol/L as a treatment target instead. The Results also note an exception for the UMA methods. (LLM, conf=0.91)
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- 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
Every source the paper cites for this claim was checked and supports it.
In the paper
“At very low LDLC concentration ranges < 1.8 mmol/L, in which VLDLC constitutes a relatively larger fraction of the blood cholesterol, VLDLC overestimation at high TG concentration > 2.3 mmol/L introduces a more significant error in the calculation of cLDLC [45].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 5.3. Calculated LDLC
What the sources say
- Supportedcites [45] Martin, 2013, Friedewald-estimated versus directly measured low-density lipoprotein cholesterol and treatment implications, J. Am. Coll. Cardiol. source
In “Impact of low LDL-C and high triglyceride levels on” (pp. 735–736), the paper reports larger discrepancies between Friedewald-estimated and directly measured LDL-C when estimated LDL-C is below 70 mg/dL (about 1.8 mmol/L) and triglycerides are 200–399 mg/dL (beginning at about 2.3 mmol/L). It says those discrepancies are compatible with errors in estimating VLDL-C as triglycerides/5; the introductory discussion explains why VLDL-C estimation matters more at lower LDL-C levels. (LLM, conf=0.88)
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“hypertriglyceridemic samples -TG > 2 mmol/L seen in ~25% of individuals in the general population (Tables 23) [17]”
§ 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
- 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 27% of adults have triglycerides above 2 mmol/L, which supports the claim’s approximate 25%. The Measurement and Population Distribution section identifies the underlying population as adults in the Copenhagen General Population Study. (LLM, conf=0.94)
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether 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
“The clinical effectiveness of LDLC-guided management of cardio- vascular risk is most strongly evidence-based [7,8].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > Table 7
What the sources say
- Partly 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. sourceExperimental — accuracy not yet measured
The Recommendations for treatment section (page unavailable) says that LDL-C reduction lowers atherosclerotic cardiovascular risk and uses baseline LDL-C and baseline risk to estimate treatment benefit. The randomized-trials section (page unavailable) describes compelling clinical evidence for LDL-C-lowering therapies. These passages support LDL-C-informed treatment, but do not establish the claim’s comparative assertion that it is the most strongly evidence-based approach to cardiovascular risk management. (LLM, conf=0.82)
- 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
The Discussion reports that greater LDL-cholesterol reductions with statin therapy reduce major vascular events and suggests making LDL reduction a goal for high-risk patients. It does not test LDL-C-guided management as a strategy or establish that its clinical effectiveness is the most strongly evidence-based approach to cardiovascular risk. (LLM, conf=0.86)
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
Every source the paper cites for this claim was checked and supports it.
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
- 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 Measurement Issues section (p. 9) explicitly states that fasting is not required for apo B measurement, directly supporting the quoted claim. (LLM, conf=0.94)
plain- Asserted: passes — The authors put it forward as true.
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- 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
“However, in ~20% of individuals in whom apoB is discordantly high with respect to population percentiles of LDLC, cardiovascular risk tracks with apoB, suggesting that replacing LDLC by apoB would identify more individuals with increased risk of ASCVD [74] -this implies an overall better clinical performance compared to LDLC in particular among this smaller subset of individuals with discordant ap”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 8.1. Clinical performance -risk estimation
What the sources say
- Partly supportedcites [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 reports that apoB was more strongly associated with CVD than LDL-C in a discordant subset comprising 18% of the main cohort, broadly supporting the approximate proportion and risk association. But the Methods define that subset by an absolute percentile difference, so it includes people whose apoB percentile was lower as well as higher than their LDL-C percentile; the paper does not establish the claim specifically for discordantly high apoB. The Discussion also reports no improvement in risk discrimination from adding apolipoproteins in that subset. (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
“Since each atherogenic particle contains one molecule of apoB, concentrations of apoB are therefore considered to be a direct measure of the total number of lipoproteins causing cardiovascular disease, that is, LDL, remnants, and Lp(a) [12].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 7.2. Apolipoprotein B
What the sources say
- 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 ‘apo B-CONTAINING LIPOPROTEINS AND CVD RISK’ section (p. 2) states that each atherogenic or potentially atherogenic particle contains one apo B molecule, making apo B a direct measure of their number. It explicitly includes LDL, VLDL, IDL, and Lp(a); VLDL and IDL account for the claim’s reference to remnants. (LLM, conf=0.94)
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
“These immunoassays obviate the need for lipoprotein subfractionation techniques such as nuclear magnetic resonance (NMR) spectroscopy or ion mobility to quantify LDLP and have been shown to be at least equivalent to LDLP in predicting cardiovascular risk [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
- Partly supportedcites [62] Mora, 2015, Circulation sourceExperimental — accuracy not yet measured
The paper explains that each VLDL, IDL and LDL particle contains one apoB molecule, so apoB measures total atherogenic lipoprotein concentration (introductory text indexed under Abstract > Conclusions; page unavailable). It distinguishes that measure from LDL particle number, which ion mobility determines directly. It does not say that apoB immunoassays quantify LDL-p specifically or obviate NMR or ion-mobility subfractionation. (LLM, conf=0.84)
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.
Every source the paper cites for this claim was checked and supports it.
In the paper
“Thus, even when cross-reactivity of immunoassays to apoB48 occurs in nonfasting measurements, apoB quantification is essentially an estimate of LDL particle number if TG and Lp(a) concentrations are low [1].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 7.2. Apolipoprotein B
What the sources say
- Supportedcites [1] Langlois, 2018, Clin. Chem. source
The APOLIPOPROTEIN B section (p. 14) says that at low triglyceride concentrations, apoB measurement is essentially an estimate of LDL particle number, while noting that most immunoassays detect both apoB100 and apoB48. The Special Report (p. 16) says postprandial apoB48 particles ordinarily make little difference to total apoB and identifies high Lp(a) as a potentially substantial contributor. (LLM, conf=0.91)
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
“this implies an overall better clinical performance compared to LDLC in particular among this smaller subset of individuals with discordant apoB.”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 8.1. Clinical performance -risk estimation
What the sources say
- Partly supportedcites [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 Results report that ApoB was more strongly associated with CVD than LDL-C in the discordant subgroup. But the Discussion says that, even in this subgroup, adding apolipoproteins did not improve risk-score discrimination. The stronger association therefore does not establish the claimed overall better clinical performance from replacing LDL-C with ApoB; the paper does not demonstrate that replacement benefit. (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.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Risk associations are similar in nonfasting study populations than in those who did fast [72,74].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 8.1. Clinical performance -risk estimation
What the sources say
- Supportedcites [72] Di Angelantonio, 2009, Emerging Risk Factors Collaboration. Major lipids, apolipoproteins, and risk of vascular disease, J. Am. Med. Assoc. source
The Comment section states that hazard ratios for vascular disease associated with lipid levels were at least as strong in participants who did not fast as in those who fasted. The Results section also reports similar CHD hazard ratios for HDL-C in the fasting and nonfasting groups. No page numbers are supplied in our copy. (LLM, conf=0.94)
- Partly supportedcites [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 Methods (page unavailable) state that blood samples were collected without fasting, and the Results (page unavailable) report associations between lipid measures and cardiovascular risk in that cohort. The paper does not compare those associations with associations in a fasting population, so it does not establish that they are similar. (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.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Furthermore, Mendelian randomization studies demonstrated that the reduction in cardiovascular risk associated with genetic variation in clearance and processing of apoB-containing lipoproteins, including LDL particles as well as TG-rich VLDL particles and their remnants, was correlated with the change of concentration of these particles as measured by apoB rather than the cholesterol mass carried”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 8.2. Clinical effectiveness -risk reduction
What the sources say
- Partly supportedcites [79] Ference, 2017, Association of genetic variants related to CETP inhibitors and statins with lipoprotein levels and cardiovascular risk, J. Am. Med. Assoc. sourceExperimental — accuracy not yet measured
The Discussion reports that cardiovascular risk tracked changes in apoB-containing particle concentration more closely than changes in cholesterol mass, and the Key Points describe the corresponding cardiovascular-event association. The paper's stated comparison concerns LDL-C and apoB; our copy does not establish the claim specifically for genetic variation in the clearance and processing of TG-rich VLDL particles and their remnants. (LLM, conf=0.85)
- Supportedcites [80] Ference, 2019, Association of triglyceride-lowering LPL variants and LDL-C-lowering LDLR variants with risk of coronary heart disease, J. Am. Med. Assoc. source
The Discussion reports that LPL and LDLR variants were associated with similar reductions in coronary heart disease risk per unit lower ApoB, and that the triglyceride and LDL-C associations became null after adjustment for ApoB. It also interprets the findings as suggesting that risk depends on the concentration of ApoB-containing particles, including LDL and triglyceride-rich remnants, rather than the lipid mass they carry. (LLM, conf=0.90)
boostedcorrelational- 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
“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; a TG concentration above this limit in nonfasting blood samples is only seen in ~0.1% of individuals in the general population [17].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 7.2. Apolipoprotein B
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 Measurement and Population Distribution section states that only 0.1% of adults in the Copenhagen General Population Study had triglycerides above 10 mmol/L. Figure 2 identifies the distribution as measurements of nonfasting plasma triglycerides in the general population. (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
“Meta-analyses of lipid-lowering trials showed that statins and other therapies which clear apoB-containing lipoproteins by upregulating LDL receptor expression, such as PCSK9 inhibitors, reduce cardiovascular risk proportional to the decrease in apoB concentration observed in these trials [77,78].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 8.2. Clinical effectiveness -risk reduction
What the sources say
- Partly supportedcites [77] Thanassoulis, 2014, Relations of change in plasma levels of LDL-C, non-HDL-C and apoB with risk reduction from statin therapy: a meta-analysis of randomized trials, J. Am. Heart Assoc. 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.
- Supportedcites [78] Khan, 2019, Association of lowering apolipoprotein B with cardiovascular outcomes across various lipid-lowering therapies: systematic review and meta-analysis of trials, Eur. J. Prev. Cardiol. source
Split into 2 atoms — 2 confirmed, 0 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.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“These immunoassays obviate the need for lipoprotein subfractionation techniques such as nuclear magnetic resonance (NMR) spectroscopy or ion mobility to quantify LDLP and have been shown to be at least equivalent to LDLP in predicting cardiovascular risk [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
- Partly supportedcites [62] Mora, 2015, Circulation sourceExperimental — accuracy not yet measured
The Results (Baseline measures and incident CVD events; page unavailable) report similar associations with cardiovascular events for apoB and ion-mobility-measured LDL-p in the placebo group (hazard ratios per SD: 1.28 and 1.21). The paper does not establish that apoB immunoassays are equivalent predictors or make subfractionation unnecessary; the Results (Incremental prognostic value; page unavailable) instead report improved prediction when ion-mobility subfractions were added to a risk model. (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.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“If the primary target LDLC is at goal, but non-HDLC or apoB are still high, attainment of all three targets will require intensified lipidlowering therapy, lifestyle (re)inforcement, and/or additional TG-lowering drugs (e.g., fibrate or omega-3 fatty acids) [4].”
§ 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
The guidelines’ secondary-goals section (page unavailable) says adjusting lipid-lowering therapy after reaching the LDL-C goal may be considered for patients at very high cardiovascular risk, subject to clinical judgment. The triglyceride-treatment recommendations (page unavailable) also discuss lifestyle measures and possible fibrate or omega-3 use, but under specific triglyceride and risk conditions. They do not say that elevated non-HDL-C or ApoB necessarily requires these measures to attain all three targets. (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.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Given the uncertainty of measurements and calculations of LDLC across different methods and laboratories, in hypertriglyceridemic patients the decision thresholds may not always be assumed to be universally applicable [1].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 10.1. Threshold values
What the sources say
- Supportedcites [1] Langlois, 2018, Clin. Chem. source
The ‘LDLC TEST ERRORS’ section (p. 12) says hypertriglyceridemia can confound LDL-C measurements and that between-method and between-laboratory errors matter; it recommends confirming values near therapeutic decision cutpoints. The ‘DIRECT LDLC AND HDLC ASSAYS’ section (p. 8) reports substantial method-dependent differences in hypertriglyceridemic samples, supporting the caution against assuming a threshold will apply identically across measurements. (LLM, conf=0.91)
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.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“For LDLC, the decision threshold for initiation of therapeutic intervention varies with the individual's risk score (Table 6) [4].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 10.1. Threshold values
What the sources say
- 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. source
Section 4.2.2 states that suggested LDL-C intervention strategies depend on both total cardiovascular risk and LDL-C level. Table 5 lays out different treatment recommendations across SCORE risk categories and untreated LDL-C levels, supporting the claim that the level at which intervention is considered varies with risk. (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.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“For example, patients with severe hypertriglyceridemia ≥10 mmol/L and chylomicronemia syndrome have high risk of acute pancreatitis but usually do not develop premature atherosclerosis, probably because chylomicrons and large VLDLs do not traverse the vascular endothelial barrier [33].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 10.3. Alert values
What the sources say
- Partly supportedcites [33] Hegele, 2014, European Atherosclerosis Society Consensus Panel. The polygenic nature of hypertriglyceridaemia: implications for definition, diagnosis, and management, Lancet Diabetes Endocrinol. sourceExperimental — accuracy not yet measured
The Monogenic hypertriglyceridaemia section (page not provided) says patients with monogenic disorders and triglycerides >10 mmol/L usually do not develop premature atherosclerosis, probably because chylomicrons cannot traverse the vascular endothelial barrier. The Introduction also identifies severe hypertriglyceridaemia as a risk factor for acute pancreatitis. The claim extends the atherosclerosis finding to patients with severe hypertriglyceridaemia and chylomicronemia syndrome generally; the source makes it specifically about monogenic disorders. (LLM, conf=0.86)
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.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“For example, patients with severe hypertriglyceridemia ≥10 mmol/L and chylomicronemia syndrome have high risk of acute pancreatitis but usually do not develop premature atherosclerosis, probably because chylomicrons and large VLDLs do not traverse the vascular endothelial barrier [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
The Introduction calls severe hypertriglyceridaemia a well-known risk factor for acute pancreatitis. The section on treatment for short-term and long-term risks identifies triglyceride concentrations above 10 mmol/L as requiring immediate reduction to minimise that risk; the monogenic hypertriglyceridaemia section describes patients with severe elevations and increased fasting chylomicrons. The paper uses >10 mmol/L rather than the claim’s ≥10 mmol/L. (LLM, conf=0.91)
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
Every source the paper cites for this claim was checked and supports it.
In the paper
“This is consistent with the notion that risk of ASCVD is more directly related to the number of apoB-containing particles (reflected by apoB measurement) than to the cholesterol content of lipoproteins [10].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 9.2. Apolipoprotein B
What the sources say
- Supportedcites [10] Mora, 2009, Advanced lipoprotein testing and subfractionation are not (yet) ready for routine clinical use, Circulation source
The Guideline Recommendations section describes the notion that cardiovascular risk may be more closely related to atherogenic particle number than to LDL cholesterol, and identifies apoB as a measure of particle concentration. Section 1.A adds that most, though not all, studies found apoB more closely associated with CVD risk than LDL cholesterol. The citing sentence presents this as a notion, consistent with the source's qualification. (LLM, conf=0.90)
plaincorrelational- Asserted: passes — The authors put it forward as true.
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Every source the paper cites for this claim was checked and supports it.
In the paper
“However, the compromised accuracy of dHDLC assays in samples with hypertriglyceridemia reduces the benefit in reporting non-HDLC in some individuals in whom an apoB or LDLP measurement may be clinically useful [1].”
§ 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
The Calculated Non-HDLC section (p. 13) says dHDLC measurement errors in hypertriglyceridemic samples affect non-HDLC calculations and calls for caution when using those values in treatment decisions. The consensus recommendation (p. 16) likewise says non-HDLC is compromised by dHDLC assay bias, while the Special Report (p. 20) says apoB or LDLP measurement can be more predictive for certain patients. (LLM, conf=0.90)
hedgeddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“The threshold for fasting TG at 1.7 mmol/L is 0.3 mmol/L lower than for nonfasting TG, corresponding to the mean maximal increase in TG following habitual food intake [2].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 10.1. Threshold values
What the sources say
- Supportedcites [2] Nordestgaard, 2016, Eur. Heart J. source
The Recommendations on laboratory reporting of abnormal non-fasting and fasting lipid profiles section states that the fasting triglyceride cut-point of 1.7 mmol/L is 0.3 mmol/L below the non-fasting cut-point and ties the difference to the mean maximal increase after habitual food intake. The Influence of food intake on the plasma lipid profile section also reports a mean maximal triglyceride increase of 0.3 mmol/L after habitual meals. (LLM, conf=0.95)
plaindirect- Asserted: passes — The authors put it forward as true.
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The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Lp(a) above the 97.5th percentile (> 120 mg/dL depending on the assay) should be noted because of very high risk for myocardial infarction and aortic valve stenosis [2].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 10.3. Alert values
What the sources say
- Partly supportedcites [2] Nordestgaard, 2016, Eur. Heart J. sourceExperimental — accuracy not yet measured
The “Life-threatening plasma lipid concentrations—what to do?” section and Table 8 link elevated Lp(a) to very high risk of myocardial infarction and aortic valve stenosis and recommend flagging it. But they specify >150 mg/dL (99th percentile), not >120 mg/dL (97.5th percentile); the claimed threshold is not supported. (LLM, conf=0.90)
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Partly supported
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In the paper
“> 10 mmol/L (880 mg/dL): severe hypertriglyceridemia with high risk of acute pancreatitis”
§ 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 7 defines severe hypertriglyceridaemia as triglycerides >10 mmol/L (>880 mg/dL). The “Life-threatening plasma lipid concentrations—what to do?” section states that triglycerides above this threshold warrant special attention because of the risk of acute pancreatitis; Table 8 describes the risk as high. (LLM, conf=0.95)
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“probably because chylomicrons and large VLDLs do not traverse the vascular endothelial barrier [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
The ‘Triglycerides and risk of cardiovascular disease’ section says nascent chylomicrons and very large VLDL particles are too large to penetrate the arterial wall. The ‘Monogenic hypertriglyceridaemia’ section also describes size exclusion as limiting chylomicrons’ ability to traverse the vascular endothelial barrier. (LLM, conf=0.92)
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- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“> 120 mg/dL: very high risk for myocardial infarction and aortic valve stenosis”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > Financial support
What the sources say
- Partly supportedcites [2] Nordestgaard, 2016, Eur. Heart J. sourceExperimental — accuracy not yet measured
The section “Life-threatening plasma lipid concentrations—what to do?” links elevated lipoprotein(a) to very high risk of myocardial infarction and aortic valve stenosis. It gives the threshold as >150 mg/dL, not >120 mg/dL, so the cited paper does not support the claimed cut-point. (LLM, conf=0.88)
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- Partly supported
In the paper
“Most discrepancies -with marked biases between assays and the CDC Reference Methods -are observed in samples from patients with hypertriglyceridemia > 2 mmol/L, mixed dyslipidemia, or other conditions involving altered lipoprotein composition and remodeling, such as diabetes and chronic kidney disease [41].”
§ 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 [41] Contois, 2011, Reliability of low-density lipoprotein cholesterol, non-high density lipoprotein cholesterol, and apolipoprotein B measurement, J. Clin. Lipidol. source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“The equation is increasingly inaccurate at TG concentrations from 2.3 to 4.5 mmol/L [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.
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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 different manufacturers' direct methods do not measure the same LDL and HDL subfractions [40,41].”
§ 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
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Despite improved analytical precision due to automation, data indicate that results can vary significantly between dLDLC and dHDLC assays from different manufacturers [41].”
§ 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 [41] Contois, 2011, Reliability of low-density lipoprotein cholesterol, non-high density lipoprotein cholesterol, and apolipoprotein B measurement, J. Clin. Lipidol. source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Using decision thresholds for flagging will lead to many lipid profiles reported with flags, as with more than 50% of LDLC results (Fig. 2).”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 10.3. Alert values
What the sources say
- Not matchedcites Fig. 2
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Because of the widespread unhealthy lifestyle, in most populations the upper reference limits of TC, LDLC, and TG are very high and far above the thresholds of increased ASCVD risk (Tables 23, Fig. 2).”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 10.2. Reference limits
What the sources say
- Not matchedcites Tables 2-3, Fig. 2
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
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- Not matched
In the paper
“In statin-treated patients the Lp(a)-associated risk for ASCVD becomes an even better predictor for residual risk as soon as the LDL-associated risk is decreased by statin therapy [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.
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In the paper
“The traditional lipid profile of TC, TG, HDLC, and LDLC remains the primary approach for diagnosis and ASCVD risk classification [30].”
§ 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 [30] Langlois, 2018, Which lipids should be analyzed for diagnostic workup and follow-up of patients with hyperlipidemias?, Curr. Cardiol. Rep. source
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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In the paper
“It has to be recognized that a simple conversion of Lp(a) from mg/dL to nmol/L or vice versa has its limitations since probably most of the available immunoassays cannot measure Lp(a) in strict molar terms due to the size heterogeneity of apo(a) isoforms and the high probability that antibodies against apo (a) recognize a repetitive KIV-2 epitope of apo(a) [53].”
§ 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 [53] Tsimikas, 2018, Relationship of lipoprotein(a) molar concentrations and mass according to lipoprotein(a) thresholds and apolipoprotein(a) isoform size, J. Clin. Lipidol. source
hedged- Asserted: passes — The authors put it forward as true.
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In the paper
“LDLC assays that attempt to specifically measure cholesterol in LDL may, therefore, show discordant results compared to the reference method [41].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 5.1. Operational definition of LDL
What the sources say
- 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.
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In the paper
“The biases noted in dHDLC measurements affect the calculations of LDLC and non-HDLC, since HDLC is used in the calculations [43].”
§ 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 [43] Langlois, 2014, Clinical impact of direct HDLc and LDLc method bias in hypertriglyceridemia. A simulation study of the EAS-EFLM Collaborative Project Group, Atherosclerosis source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“However, it is not widely recognized that the LDLC fraction on beta-quantification also contains the cholesterol from IDL with density 1.006-1.019g/mL and Lp(a) with density 1.04-1.13g/mL.”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 5.1. Operational definition of LDL
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
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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In the paper
“Because the TG:cholesterol ratio in TG-rich lipoproteins progressively increases as hypertriglyceridemia becomes more severe, the equation overestimates VLDLC and therefore underestimates LDLC at high TG concentrations [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.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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In the paper
“Non-HDLC shows better correlation and concordance with cLDLC when using the Martin-Hopkins formula compared to the Friedewald equation in patients with atherogenic dyslipidemia [59].”
§ 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 [59] Mehta, 2018, Performance of LDL-C calculated with Martin's formula compared to the Friedewald equation in familial combined hyperlipidemia, Atherosclerosis source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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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
“However, non-HDLC cannot substitute for RemnantC because it does not differentiate between Re-mnantC and LDLC and Lp(a)-cholesterol.”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 7.1. Non-HDL cholesterol
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“The IFCC has therefore initiated development of LC-MSMS as candidate definitive reference method for apoB [67].”
§ 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 [67] Delatour, 2018, Comparability of lipoprotein particle number concentrations across ES-DMA, NMR, LC-MS/MS, immunonephelometry, and VAP: in search of a candidate reference measurement procedure for apoB and non-HDL-P standardization, Clin. Chem. source
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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In the paper
“All guidelines concur that LDLC remains the primary target of lipid-lowering strategies to prevent ASCVD [4][5][6].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > Table 7
What the sources say
- Not matchedcites [4][5][6]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plain- Asserted: passes — The authors put it forward as true.
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- Not matched
In the paper
“Given the improvements of standardization initiated by the IFCC [69], measurements of apolipoproteins have the potential to meet analytical performance criteria including accuracy, harmonisation across laboratories, unambiguous definition of the measurand, and unequivocal test results in both normo-and dyslipidemic sera -important prerequisites for medical use of a test which can not be met with L”
§ 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 [69] Contois, 2018, Apolipoprotein B measurement: need for standardization, J. Clin. Lipidol. source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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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
hedgeddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Common calibration with the IFCC/WHO SP3 reference material has reduced between-laboratory variability of apoB measurements from > 19% to < 10%, although concerns about the variability among immunoassays and their comparability with apoB100 derived from NMR and other methods still exist [65][66][67].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 7.2. Apolipoprotein B
What the sources say
- Not matchedcites [65][66][67]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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- Not matched
In the paper
“Common calibration with the IFCC/WHO SP3 reference material has reduced between-laboratory variability of apoB measurements from > 19% to < 10%, although concerns about the variability among immunoassays and their comparability with apoB100 derived from NMR and other methods still exist [65][66][67].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 7.2. Apolipoprotein B
What the sources say
- Not matchedcites [65][66][67]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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- Not matched
In the paper
“However, the apoB test has not yet been completely validated for this clinical purpose according to key criteria defined by the EFLM Test Evaluation Working Group [70] clinical performance, clinical effectiveness, and cost-effectivenessbeyond analytical performance to become a medically useful test (Table 7).”
§ 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 [70] Horvath, 2014, From biomarkers to medical tests: the changing landscape of test evaluation, Clin. Chim. Acta source
plain- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“Data and meta-analyses of prospective population-based cohort studies [71][72][73][74] and statin trials [75,76] suggest that the clinical performance of apoB and non-HDLC, although superior to LDLC in some studies, is on average comparable to dLDLC, Friedewald cLDLC or Martin-Hopkins cLDLC to predict risk of fatal or nonfatal ASCVD on the population level.”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 8.1. Clinical performance -risk estimation
What the sources say
- Not matchedcites [71][72][73][74]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not checked — no full text of the sourcecites [75] Boekholdt, 2012, Association of LDL cholesterol, non-HDL cholesterol, and apolipoprotein B levels with risk of cardiovascular events among patients treated with statins: a meta-analysis, J. Am. Med. Assoc. source
- Not checked — no full text of the sourcecites [76] Robinson, 2012, Meta-analysis of comparison of effectiveness of lowering apolipoprotein B versus low-density lipoprotein cholesterol and non high-density lipoprotein cholesterol for cardiovascular risk reduction in randomized trials, Am. J. Cardiol. source
hedged- Asserted: passes — The authors put it forward as true.
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- Not matched
In the paper
“important prerequisites for medical use of a test which can not be met with LDLC and non-HDLC measurements or calculations.”
§ 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 [69] Contois, 2018, Apolipoprotein B measurement: need for standardization, J. Clin. Lipidol. 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.
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
“These findings suggest a potential role of apoB as therapeutic target.”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 8.2. Clinical effectiveness -risk reduction
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.
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
“ApoB measurement is superior to LDLC and non-HDLC measure- ments and calculations for the assessment of exposure to atherogenic lipoprotein particle numbers in the circulation.”
§ 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: passes — The paper gives a reason why it holds.
In the paper
“The International Federation of Clinical Chemistry (IFCC) and World Health Organization (WHO) developed the SP3 reference material, value-assigned using immunonephelometry as interim reference method for apoB [64].”
§ 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 [64] Marcovina, 1994, International federation of clinical Chemistry standardization project for measurements of apolipoproteins A-I and B. IV. Comparability of apolipoprotein B values by use of international reference material, Clin. Chem. 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.
In the paper
“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
What the sources say
- Not matchedcites Table 7
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
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.
- Not matched
In the paper
“LDLC does not provide incremental risk prediction of ASCVD relative to non-HDLC [81][82][83].”
§ 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.
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.
- 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
“This personalized reporting of optimal thresholds is difficult to implement in laboratory reports because usually the clinical conditions and risk factors of the individual patients are not known to the laboratory personnel.”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 10.1. Threshold values
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.
In the paper
“Ideally, these reference intervals should be regularly updated because significant changes in population lipid concentrations occur mainly related to the substantial increase in unhealthy lifestyle and obesity and changes of analytical methods over time [95][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 matchedcites [95][96][97]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
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.
- Not matched
In the paper
“Reference intervals in children and adolescents are available from recent populationbased cohort studies and databases [92][93][94].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 10.2. Reference limits
What the sources say
- Not matchedcites [92][93][94]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
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.
- Not matched
In the paper
“Data from concordance/discordance analyses in large case-control and prospective cohort studies reveal that the addition of apoB to LDLC and even to non-HDLC has the potential to improve risk prediction by identifying more high-risk individuals [74,[84][85][86].”
§ Quantifying atherogenic lipoproteins for lipid-lowering strategies: consensus-based recommendations from EAS and EFLM > 9.2. Apolipoprotein B
What the sources say
- Not matchedcites [74,[84][85][86]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
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.
- Not matched
- 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
Mach, F., Baigent, C., Catapano, A. L., Koskinas, K. C., Casula, M., Badimon, L., Chapman, M. J., De Backer, G. G., Delgado, V., Ference, B. A., et al. (2020) · European Heart Journal · doi:10.1093/eurheartj/ehz455 · Cited by 8,961
Self-citationCholesterol Treatment Trialists' (CTT) Collaboration (2010) · The Lancet · doi:10.1016/s0140-6736(10)61350-5 · Cited by 6,550
Grundy, S. M., Stone, N. J., Bailey, A. L., Beam, C., Birtcher, K. K., Blumenthal, R. S., Braun, L. T., de Ferranti, S., Faiella-Tommasino, J., Forman, D. E., et al. (2019) · Circulation · doi:10.1161/cir.0000000000000625 · Cited by 6,185
Ference, B. A., Ginsberg, H. N., Graham, I., Ray, K. K., Packard, C. J., Bruckert, E., Hegele, R. A., Krauss, R. M., Raal, F. J., Schunkert, H., et al. (2017) · European Heart Journal · doi:10.1093/eurheartj/ehx144 · Cited by 3,962
Self-citationNordestgaard, B. G., Chapman, M. J., Humphries, S. E., Ginsberg, H. N., Masana, L., Descamps, O. S., Wiklund, O., Hegele, R. A., Raal, F. J., Defesche, J. C., et al. (2013) · European Heart Journal · doi:10.1093/eurheartj/eht273 · Cited by 2,761
Self-citationMajor lipids, apolipoproteins, and risk of vascular disease
The Emerging Risk Factors Collaboration* (2009) · JAMA · doi:10.1001/jama.2009.1619 · Cited by 2,731
Grundy, S. M., Stone, N. J., Bailey, A. L., Beam, C., Birtcher, K. K., Blumenthal, R. S., Braun, L. T., de Ferranti, S., Faiella-Tommasino, J., Forman, D. E., et al. (2019) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2018.11.003 · Cited by 2,691
Triglycerides and Cardiovascular Disease: A Scientific Statement From the American Heart Association
Miller, M., Stone, N. J., Ballantyne, C., Bittner, V., Criqui, M. H., Ginsberg, H. N., Goldberg, A. C., Howard, W. J., Jacobson, M. S., Kris-Etherton, P. M., et al. (2011) · Circulation · doi:10.1161/cir.0b013e3182160726 · Cited by 1,871
Lipoprotein(a) as a cardiovascular risk factor: current status
Nordestgaard, B. G., Chapman, M. J., Ray, K., Borén, J., Andreotti, F., Watts, G. F., Ginsberg, H., Amarenco, P., Catapano, A., Descamps, O. S., et al. (2010) · European Heart Journal · doi:10.1093/eurheartj/ehq386 · Cited by 1,807
Self-citation2016 ESC/EAS Guidelines for the Management of Dyslipidaemias
Catapano, A. L., Graham, I., De Backer, G., Wiklund, O., Chapman, M. J., Drexel, H., Hoes, A. W., Jennings, C. S., Landmesser, U., Pedersen, T. R., et al. (2016) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2016.08.018 · Cited by 1,582
Self-citation
Cited by
Sorted by citations
Pearson, G. J., Thanassoulis, G., Anderson, T. J., Barry, A. R., Couture, P., Dayan, N., Francis, G. A., Genest, J. J., Grégoire, J. C., Grover, S. A., et al. (2021) · Canadian Journal of Cardiology · doi:10.1016/j.cjca.2021.03.016 · Cited by 900
Reyes-Soffer, G., Ginsberg, H. N., Berglund, L., Duell, P. B., Heffron, S. P., Kamstrup, P. R., Lloyd-Jones, D. M., Marcovina, S. M., Yeang, C., Koschinsky, M. L., et al. (2022) · Arteriosclerosis, Thrombosis, and Vascular Biology · doi:10.1161/atv.0000000000000147 · Cited by 836
Self-citationA Modern Approach to Dyslipidemia
Berberich, A. J., & Hegele, R. A. (2021) · Endocrine Reviews · doi:10.1210/endrev/bnab037 · Cited by 529
Residual Cardiovascular Risk at Low LDL: Remnants, Lipoprotein(a), and Inflammation
Hoogeveen, R. C., & Ballantyne, C. M. (2020) · Clinical Chemistry · doi:10.1093/clinchem/hvaa252 · Cited by 322
Okamura, T., Tsukamoto, K., Arai, H., Fujioka, Y., Ishigaki, Y., Koba, S., Ohmura, H., Shoji, T., Yokote, K., Yoshida, H., et al. (2023) · Journal of Atherosclerosis and Thrombosis · doi:10.5551/jat.gl2022 · Cited by 345
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.
What counts as a claim ›How we measure confidence ›How we check this ›
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