The DOI matches its Crossref record; 182 of the 184 references it cites were found in a registry or an index; 29 of the 60 sources its claims cite were checked for support.
The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk
Open accessAbstract
Atherosclerotic cardiovascular disease (ASCVD) remains the leading cause of death worldwide. Low-density lipoprotein cholesterol (LDL-C) is a well-established mediator of atherosclerosis and a key target for intervention for the primary and secondary prevention of ASCVD. However, despite substantial reduction in LDL-C, patients continue to have recurrent ASCVD events. Hypertriglyceridemia may be an important contributor of this residual risk. Observational and genetic epidemiological data strongly support a causal role of triglycerides (TGs) and the cholesterol content within triglyceride-rich lipoproteins (TGRLs) and/or remnant cholesterol (RC) in the development of ASCVD.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
29 of 60 cited sources checked · 14 supported · 0 flagged · accuracy not yet measured
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“However, the association was attenuated after adjustment for HDL-C”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Epidemiologic Studies of TGs and Risk of CVD
What the sources say
- Partly supportedcites [72] Di Angelantonio, 2009, Major lipids, apolipoproteins, and risk of vascular disease, JAMA sourceExperimental — accuracy not yet measured
The Results (Triglyceride; page not provided) report that the triglyceride–CHD association weakened after adjustment for both HDL-C and non-HDL-C. The passage does not establish that adjustment for HDL-C alone produced the attenuation described in the claim. (LLM, conf=0.86)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“They found that the strength of an SNP's effect on TG levels correlated strongly with the magnitude of effect on CAD, after adjustment for the SNP's effects on LDL-C and HDL-C”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Genetic Studies of TGs and CVD
What the sources say
- Supportedcites [116] Do, 2013, Common variants associated with plasma triglycerides and risk for coronary artery disease, Nat Genet source
The Abstract states that the strength of a SNP’s effect on triglycerides correlates with its effect on CAD risk even after accounting for its effects on LDL-C and/or HDL-C. It also reports a strong association across 185 SNPs after adjustment for both LDL-C and HDL-C (P = 1×10−9). (LLM, conf=0.95)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“a well-known limitation of Mendelian randomization analyses is that they are susceptible to genetic pleiotropy”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Genetic Studies of TGs and CVD
What the sources say
- Supportedcites [110] Musunuru, 2016, Surprises from genetic analyses of lipid risk factors for atherosclerosis, Circ Res source
In “The Mendelian randomization study design,” the paper identifies pleiotropy as a possible shortcoming: a DNA variant may affect disease risk through mechanisms other than the biomarker being tested, undermining the causal inference. This directly supports the cited limitation. (LLM, conf=0.94)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Two large randomized controlled trials (RCTs) evaluating the efficacy of extended-release niacin vs placebo on background statin therapy in individuals with established ASCVD did not demonstrate a reduction in vascular events”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Epidemiologic Studies of TGs and Risk of CVD
What the sources say
- Partly supportedcites [18] Boden, 2011, Niacin in patients with low HDL cholesterol levels receiving intensive statin therapy, N Engl J Med sourceExperimental — accuracy not yet measured
The Study Design and Study Population sections describe a randomized, placebo-controlled trial of 3,414 patients, and the Discussion reports no significant reduction in cardiovascular events with extended-release niacin added to intensive statin therapy. This paper establishes the result for one trial, not two: its Discussion says the other large niacin trial, HPS2-THRIVE, was still in follow-up. (LLM, conf=0.88)
- Could not verifycites [19] Crosby, 2014, Loss-of-function mutations in APOC3, triglycerides, and coronary disease, N Engl J Med sourceExperimental — accuracy not yet measured
The Discovery Cohorts and APOC3 loss-of-function results sections describe genetic associations with coronary heart disease, not niacin treatment trials. Searches for extended-release niacin, placebo, background statin therapy, and vascular events found no passage in our copy addressing the two claimed randomized trials. (LLM, conf=0.78)
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Volanesorsen (previously known as ISIS-APOC-III RX ) is a second-generation ASO developed to inhibit apoCIII”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Emerging TG-Lowering Therapies
What the sources say
- Partly supportedcites [170] Gaudet, 2015, Antisense inhibition of apolipoprotein C-III in patients with hypertriglyceridemia, N Engl J Med sourceExperimental — accuracy not yet measured
The RESULTS passage describes ISIS 304801 as a second-generation antisense oligonucleotide designed to reduce APOC3 mRNA, supporting the drug class and intended target. Our copy does not identify ISIS 304801 as volanesorsen or ISIS-APOC-III RX, so it does not establish the name equivalence in the citing sentence. (LLM, conf=0.84)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- 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 of variants associated with TGs are commonly affected by the pleiotropic effects of single-nucleotide polymorphisms (SNPs) on multiple metabolic pathways affecting plasma lipids, including HDL-C and LDL-C”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Genetic Studies of TGs and CVD
What the sources say
- Supportedcites [110] Musunuru, 2016, Surprises from genetic analyses of lipid risk factors for atherosclerosis, Circ Res source
In “Plasma triglyceride-rich lipoproteins as causal,” the paper says Mendelian randomization studies using triglyceride-associated SNPs are difficult to interpret because most such SNPs have pleiotropic relationships with lipids. It specifies that 87 of 94 triglyceride-associated lead SNPs were also associated with LDL-C and/or HDL-C. (LLM, conf=0.94)
- Not checked — no full text of the sourcecites [115] Ference, 2018, Causal effect of lipids and lipoproteins on atherosclerosis: lessons from genomic studies, Cardiol Clin source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“was nonsignificant after adjustment for non-HDL-C”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Epidemiologic Studies of TGs and Risk of CVD
What the sources say
- Partly supportedcites [72] Di Angelantonio, 2009, Major lipids, apolipoproteins, and risk of vascular disease, JAMA sourceExperimental — accuracy not yet measured
The Results > Triglyceride section reports a null association between triglycerides and coronary heart disease after adjustment: HR 0.99 (95% CI, 0.94–1.05). However, that result followed adjustment for both HDL-C and non-HDL-C; the passage does not establish that adjustment for non-HDL-C alone made the association nonsignificant. (LLM, conf=0.86)
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“TGs were not associated with stroke after adjustment for lipids”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Epidemiologic Studies of TGs and Risk of CVD
What the sources say
- Supportedcites [72] Di Angelantonio, 2009, Major lipids, apolipoproteins, and risk of vascular disease, JAMA source
The Methods (Statistical Analyses; page not provided) say hazard ratios were progressively adjusted for lipid measures. The Results (Triglyceride; page not provided) report adjusted triglyceride hazard ratios close to 1 for ischemic, hemorrhagic, and unclassified stroke, with confidence intervals spanning 1. This supports the claim as a finding of no statistically significant association after adjustment. (LLM, conf=0.92)
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“This finding supported the notion that plasma TG levels are an independent causal risk factor for CAD”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Genetic Studies of TGs and CVD
What the sources say
- Partly supportedcites [116] Do, 2013, Common variants associated with plasma triglycerides and risk for coronary artery disease, Nat Genet sourceExperimental — accuracy not yet measured
The Abstract (page unavailable) reports that genetic effects on triglycerides correlate with CAD risk after accounting for effects on LDL-C and HDL-C, supporting the cited finding. But it concludes that triglyceride-rich lipoproteins may causally influence CAD, not that plasma triglyceride levels themselves are an independent causal risk factor. (LLM, conf=0.86)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In the Action to Control Cardiovascular Risk in Diabetes (ACCORD) study, addition of fenofibrate to statin therapy did not result in significant beneficial effects on CVD risk”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > TG-Lowering Therapies
What the sources say
- Supportedcites [146] Ginsberg, 2010, Effects of combination lipid therapy in type 2 diabetes mellitus, N Engl J Med source
The Results > Clinical Outcomes section reports no statistically significant reduction in the primary cardiovascular outcome when fenofibrate was added to simvastatin (hazard ratio 0.92; P = 0.32). No page number is provided in our copy. (LLM, conf=0.94)
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
- The quote only partly states this claim. 4
- It may state two separate claims as one. 37
- Probably not a substantial claim. 16
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“fasting and nonfasting TG levels were associated with increased risk of coronary heart disease”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Epidemiologic Studies of TGs and Risk of CVD
What the sources say
- Partly supportedcites [72] Di Angelantonio, 2009, Major lipids, apolipoproteins, and risk of vascular disease, JAMA sourceExperimental — accuracy not yet measured
The Results > Triglyceride section reports an increased CHD risk with triglycerides after adjustment for nonlipid risk factors (HR 1.37), supporting the overall association. It does not report separate fasting and nonfasting estimates for that adjustment alone; the fasting-status estimates it does report are essentially null after further adjustment for HDL-C and non-HDL-C. (LLM, conf=0.84)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesThe quote only partly states this claim.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Mendelian randomization is essentially an RCT that has been performed by nature, because there is a random allocation of alleles to offspring at the time of conception that is unaffected by reverse causation and independent of environmental and genetic confounders”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Epidemiologic Studies of TGs and Risk of CVD
What the sources say
- Partly supportedcites [110] Musunuru, 2016, Surprises from genetic analyses of lipid risk factors for atherosclerosis, Circ Res 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.
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
“The TG lowering is linear with a dose-dependent effect such that greater absolute reduction is seen in individuals with higher baseline TG levels”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Omega-3 fatty acids
What the sources say
- Supportedcites [148] Mozaffarian, 2011, Omega-3 fatty acids and cardiovascular disease: effects on risk factors, molecular pathways, and clinical events, J Am Coll Cardiol source
The Cardiovascular Risk Factors section states that triglyceride lowering is linearly dose-dependent and that absolute reductions are greater at higher baseline levels, while noting variable individual responses. Figure 4 also reports a larger reduction per gram of EPA+DHA in trials with higher starting triglycerides. Page numbers were not supplied in the copy. (LLM, conf=0.95)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“This phenomenon occurs when the gene variant under study affects more than one pathway; thus, the observed association between the variant and disease risk may not be due to the biomarker of interest”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Genetic Studies of TGs and CVD
What the sources say
- Supportedcites [110] Musunuru, 2016, Surprises from genetic analyses of lipid risk factors for atherosclerosis, Circ Res source
The section “The Mendelian randomization study design” explicitly defines pleiotropy as a DNA variant affecting multiple mechanisms and says that its association with disease risk may therefore not be due to the biomarker in question. (LLM, conf=0.95)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably 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
“LOF mutations in LPL are also associated with increased plasma TG levels and risk of ASCVD”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Genetic Studies of TGs and CVD
What the sources say
- Partly supportedcites [128] Wittrup, 1999, Lipoprotein lipase mutations, plasma lipids and lipoproteins, and risk of ischemic heart disease. A meta-analysis, Circulation sourceExperimental — accuracy not yet measured
The Plasma Triglycerides and Postheparin Plasma Lipoprotein Lipase Activity sections report that three LPL substitutions associated with reduced enzyme activity also increased triglycerides. The Risk of Ischemic Heart Disease and Discussion sections report increased risk for Gly188Glu carriers, but say any increase for Asp9Asn and Asn291Ser carriers was borderline at most. The claim overgeneralizes the cardiovascular-risk association across loss-of-function mutations. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites [129] Nordestgaard, 1997, Heterozygous lipoprotein lipase deficiency: frequency in the general population, effect on plasma lipid levels, and risk of ischemic heart disease, Circulation source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Partly supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“It inhibits adipose tissue lipolysis, which reduces the flux of FFAs to the liver and, therefore, leads to reduced hepatic VLDL synthesis”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Niacin
What the sources say
- Could not verifycites [167] Qin, 2011, Missense mutation in APOC3 within the C-terminal lipid binding domain of human ApoC-III results in impaired assembly and secretion of triacylglycerol-rich very low density lipoproteins: evidence that ApoC-III plays a major role in the formation of lipid precursors within the microsomal lumen, J Biol Chem sourceExperimental — accuracy not yet measured
The Discussion describes excess fatty acid influx and apoC-III’s role in hepatic VLDL assembly, but does not connect either to niacin or inhibition of adipose-tissue lipolysis. Searches for niacin, nicotinic acid, and adipose lipolysis found no passage addressing the claimed mechanism; page numbers were unavailable in our copy. (LLM, conf=0.73)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Could not verify
None of the sources cited for this claim have been checked yet.
In the paper
“However, despite reductions in LDL-C levels with statins and newer lipid-lowering agents, substantial residual risk persists, with the majority of predicted first and recurrent ASCVD events not being averted”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“TGRL remnants have been linked to impaired coronary vasomotor function, decreased brachial artery flow-mediated dilatation, and increased carotid intima media thickness”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > TGRLs and Atherosclerosis
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“In pregnancy, plasma TG levels can increase two-to fourfold during the third trimester owing to physiologic hormonal changes and are generally not clinically important”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Population Distribution and Causes of Hypertriglyceridemia
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Interestingly, Mendelian randomization suggests a causal association of elevated nonfasting RC with low-grade inflammation and ischemic heart disease (IHD), whereas elevated LDL-C associates with IHD but not inflammation”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > TGRL and Inflammation
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“These postprandial changes in TGs depend on baseline TG levels, fat load in the meal, and time since the last meal”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Fasting vs nonfasting measurement
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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
“However, the TGs are catabolized by macrophages and therefore do not accumulate in atherosclerotic plaque.”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Measurement of TGs and RC
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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
“Although lifestyle modification remains the cornerstone for management of hypertriglyceridemia, many novel drugs are in development and have shown impressive efficacy in lowering TG levels.”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Abstract
Strength:boosted· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✗ Based: failsProbably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Early epidemiologic studies demonstrated that fasting TG levels independently associated with cardiovascular disease (CVD) and correlated well with nonfasting TG levels”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Fasting vs nonfasting measurement
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Other secondary causes of hypertriglyceridemia include pregnancy, hypothyroidism, chronic kidney disease, poorly controlled diabetes and/or metabolic syndrome, and medications”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Population Distribution and Causes of Hypertriglyceridemia
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. 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
“These include inhibition of hepatic lipase activity and inhibition of hepatic TGRL remnant clearance”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > TG Metabolism
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt 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
“Collectively, these processes lead to enhanced platelet aggregation and clot formation”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > TGRL and Inflammation
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Hypertriglyceridemia is frequently associated with concomitant lipoprotein alterations such as decreased high-density lipoprotein (HDL) cholesterol (HDL-C) levels and elevated levels of non-HDL-C; small, dense and total LDL particles; intermediate-density lipoprotein (IDL); and total apolipoprotein CIII (apoCIII), all of which are associated with increased ASCVD risk”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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
“Low-density lipoprotein cholesterol (LDL-C) is a well-established mediator of atherosclerosis and a key target for intervention for the primary and secondary prevention of ASCVD.”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✗ Based: failsProbably not a substantial claim. The paper may give no reason why it holds. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Accordingly, several current recommendations support the use of a random, nonfasting lipid profile in clinical practice for CV risk prediction”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Fasting vs nonfasting measurement
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
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
“At these levels, chylomicrons are usually the main carriers of TG in plasma.”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Population Distribution and Causes of Hypertriglyceridemia
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
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
“Moderately elevated TG concentrations are commonly due to suboptimal lifestyle habits, including diets enriched in simple carbohydrates and/or saturated fats, excess alcohol consumption, obesity, and sedentary behavior.”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Population Distribution and Causes of Hypertriglyceridemia
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
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
“Thyroid hormone is an important regulator of LPL activity and elevated TG levels in hypothyroidism are due to decreased LPL activity”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Population Distribution and Causes of Hypertriglyceridemia
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Circulating plasma apoB-containing lipoproteins penetrate the endothelial cell lining of the artery wall in susceptible regions and enter the intimal space, where they may be trapped by interaction with subendothelial proteoglycans”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Measurement of TGs and RC
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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
“TGRLs can readily penetrate the arterial wall and are susceptible to retention by connective tissue matrix through interaction of the positively charged residues (arginine and lysine) on apoB with the negatively charged sulfate groups of subendothelial proteoglycans, similar to LDL.”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > TGRLs and Atherosclerosis
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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
“Endothelial dysfunction often precedes the development of atherosclerosis.”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > TGRLs and Atherosclerosis
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✗ Based: failsProbably not a substantial claim. The paper’s conclusions may not depend on it. 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
“Incomplete lipidation of apoB by MTP leads to its proteasomal degradation with subsequent decrease in VLDL production.”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > TG Metabolism
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
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
“Hypertriglyceridemia is a well-known cause of acute pancreatitis.”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Population Distribution and Causes of Hypertriglyceridemia
Strength:boosted· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
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
“Increase in estrogen levels during the third trimester stimulates hepatic VLDL secretion and reduces the clearance of TGs by lipoprotein lipases (LPLs) in the liver and adipose tissues resulting in elevated TG levels”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Population Distribution and Causes of Hypertriglyceridemia
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
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
“Hypertriglyceridemia occurs because of increased TG production, altered processing and catabolism of TGRLs, or reduced clearance.”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Population Distribution and Causes of Hypertriglyceridemia
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“It is important to note that although apoCIII is a potent inhibitor of LPL activation, recent studies have shown that it has a pleiotropic role in the regulation of TGRL metabolism independent of LPL pathways.”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > TG Metabolism
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt 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
“This suggests that the cholesterol content in TGRLs (e.g., RC), rather than the TGs, may be more important in atherogenesis, because it accumulates in atherosclerotic plaque and is in the causal pathway of atherosclerosis.”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Measurement of TGs and RC
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“More commonly, the genetic basis for moderate to severe hypertriglyceridemia is polygenic, which can synergize with environmental factors to profoundly alter TG/VLDL production and clearance”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > ESSENTIAL POINTS
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“This notion is of particular interest because the burgeoning epidemics of obesity, metabolic syndrome, and diabetes are associated with a dramatic increase in the prevalence of hypertriglyceridemia and its potential intersection with ASCVD”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
“Furthermore, impairment of endothelium-dependent vasodilation and increased oxidative stress may also play a role in promoting endothelial dysfunction”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > TGRLs and Atherosclerosis
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt 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
“The long-term clinical consequences of hepatic steatosis due to pharmacologic apoB or MTP inhibition in humans remain unclear”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > TG Metabolism
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
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
“The constitutive production and regulation of hepatic apoB plays a key role in VLDL synthesis and secretion, and safeguards against hepatic steatosis.”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > TG Metabolism
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt 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
“Furthermore, in the insulin-resistant state, increased adipocyte lipolysis results in increased FFA flux to the liver, which also fuels the lipidation of apoB leading to increased VLDL production and de novo hepatic lipogenesis”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > ESSENTIAL POINTS
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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 time, these direct assays to measure RC have limited clinical applicability because they do not measure all RC in the plasma and are labor intensive and costly.”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Measurement of TGs and RC
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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
“Within macrophages, cholesterol cannot be metabolized; thus it accumulates, leading to engorged, dysfunctional foam cells.”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Measurement of TGs and RC
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes? Based: unclearIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“In addition, equivocal clinical trial results of TG-lowering therapies have raised the question as to whether TGs represent a surrogate for other causal mechanisms at play for atherosclerotic disease”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
In the paper
“nonfasting calculated RC was associated with a stepwise increase in risk of IHD, MI, and all-cause mortality”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Epidemiologic Studies of TGs and Risk of CVD
What the sources say
- Not checked — no full text of the sourcecites [112] Varbo, 2015, Extreme nonfasting remnant cholesterol vs extreme LDL cholesterol as contributors to cardiovascular disease and all-cause mortality in 90000 individuals from the general population, Clin Chem source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesThe quote only partly states this claim.
In the paper
“The Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study with fenofibrate did not demonstrate a reduction in the rate of the composite primary outcome (CHD death and nonfatal MI) compared with placebo but was associated with a reduction in total CV events”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > TG-Lowering Therapies
What the sources say
- Not checked — no full text of the sourcecites [137] Keech, 2005, Effects of long-term fenofibrate therapy on cardiovascular events in 9795 people with type 2 diabetes mellitus (the FIELD study): randomised controlled trial, Lancet source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“TG reduction is mediated by multiple mechanisms, including increased FA catabolism by peroxisomal b-oxidation, decreased hepatic lipogenesis, and increased clearance of plasma TGs”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Omega-3 fatty acids
What the sources say
- Not checked — no full text of the sourcecites [149] Jacobson, 2012, Effects of eicosapentaenoic acid and docosahexaenoic acid on low-density lipoprotein cholesterol and other lipids: a review, J Clin Lipidol source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“It is important to note that most of these observational epidemiologic studies were done in the prestatin era”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Epidemiologic Studies of TGs and Risk of CVD
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“a pooled analysis of the Incremental Decrease in End Points Through Aggressive Lipid Lowering (IDEAL) and Treating to New Targets (TNT) trials demonstrated that increased TG levels were associated with higher risk of CVD events in statin-treated patients, although the risk was attenuated after adjustment for HDL-C and apoB-to-apoA-I ratio”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Epidemiologic Studies of TGs and Risk of CVD
What the sources say
- Not checked — no full text of the sourcecites [109] Faergeman, 2009, Plasma triglycerides and cardiovascular events in the Treating to New Targets and Incremental Decrease in End-Points through Aggressive Lipid Lowering trials of statins in patients with coronary artery disease, Am J Cardiol source
Strength:boosted· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“#30%”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Emerging TG-Lowering Therapies
What the sources say
- Not checked — no full text of the sourcecites [15] Shapiro, 2016, From lipids to inflammation: new approaches to reducing atherosclerotic risk, Circ Res source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesThe quote only partly states this claim.
In the paper
“In clinical trials, intramuscular injection of alipogene tiparvovec was associated with reduction in the incidence of pancreatitis and was well tolerated”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Emerging TG-Lowering Therapies
What the sources say
- Not checked — no full text of the sourcecites [172] Gaudet, 2012, Gene therapy for lipoprotein lipase deficiency, Curr Opin Lipidol source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“#20% reduction in plasma TG levels with moderate to intense aerobic exercise”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Emerging TG-Lowering Therapies
What the sources say
- Not checked — no full text of the sourcecites [38] Watts, 2013, Demystifying the management of hypertriglyceridaemia, Nat Rev Cardiol source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesThe quote only partly states this claim.
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
“it is established that LDL is the primary causal factor in the development of atherosclerosis”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Emerging TG-Lowering Therapies
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✗ Based: failsProbably not a substantial claim. The paper may give no reason why it holds.
The paper relies on this without support.
Plasma triglyceride concentrations serve as a surrogate measure of triglyceride-rich lipoproteins and remnant cholesterol.
“Clinically, plasma TG concentrations serve as a surrogate measure of TGRLs and RC.”
The paper relies on this without support.
Residual confounding can limit the ability to draw causal inference from observational studies linking TGs and remnant cholesterol to ASCVD.
“However, the possibility of residual confounding limits the ability to draw causal inference from these observational studies”
The paper relies on this without support.
Elevated TG levels are closely linked to non-HDL-C with high intercorrelation between the variables.
“elevated TG levels are closely linked to non-HDL-C with high intercorrelation between the variables”
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Relatives are described as both wild-type and completely deficient
MinorThe imaging statement calls the relatives wild-type while also saying they had complete ANGPTL3 deficiency. The preceding statement attributes complete deficiency to loss-of-function mutations, so the relatives' genetic status is unclear.
“In three wild-type, first-degree relatives with complete ANGPTL deficiency, CT angiography showed no evidence of coronary atherosclerotic plaque ().”
“LOF mutations leading to complete deficiency of ANGPTL are associated with a familial combined hypolipidemia, characterized by extremely low circulating LDL-C, HDL-C, and TG levels (, ).”
Citations
Cites
Toprak, Ö., Kurt, H., Sarı, Y., Şarkış, C., Us, H., & Kırık, A. (2017) · Kidney & Blood Pressure Research · doi:10.1159/000468530 · Cited by 29,772
Grundy, S. M., Bilheimer, D. W., Chait, A., Clark, L. T., Denke, M. A., Havel, R. J., Hazzard, W. R., Hulley, S. B., Hunninghake, D. B., Kreisberg, R. A., et al. (1993) · JAMA · doi:10.1001/jama.269.23.3015 · Cited by 27,944
Expert Panel on Detection, E. (2001) · JAMA: The Journal of the American Medical Association · doi:10.1001/jama.285.19.2486 · Cited by 26,011
Stone, N. J., Robinson, J. G., Lichtenstein, A. H., Bairey Merz, C. N., Blum, C. B., Eckel, R. H., Goldberg, A. C., Gordon, D., Levy, D., Lloyd-Jones, D. M., et al. (2014) · Circulation · doi:10.1161/01.cir.0000437738.63853.7a · Cited by 7,081
Helsinki Heart Study: Primary-Prevention Trial with Gemfibrozil in Middle-Aged Men with Dyslipidemia
Frick, M. H., Elo, O., Haapa, K., Heinonen, O. P., Heinsalmi, P., Helo, P., Huttunen, J. K., Kaitaniemi, P., Koskinen, P., Manninen, V., et al. (1987) · New England Journal of Medicine · doi:10.1056/nejm198711123172001 · Cited by 3,881
Stone, N. J., Robinson, J. G., Lichtenstein, A. H., Bairey Merz, C. N., Blum, C. B., Eckel, R. H., Goldberg, A. C., Gordon, D., Levy, D., Lloyd-Jones, D. M., et al. (2014) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2013.11.002 · Cited by 3,845
Rubins, H. B., Robins, S. J., Collins, D., Fye, C. L., Anderson, J. W., Elam, M. B., Faas, F. H., Linares, E., Schaefer, E. J., Schectman, G., et al. (1999) · New England Journal of Medicine · doi:10.1056/nejm199908053410604 · Cited by 3,439
Cardiovascular Risk Reduction with Icosapent Ethyl for Hypertriglyceridemia
Bhatt, D. L., Steg, P. G., Miller, M., Brinton, E. A., Jacobson, T. A., Ketchum, S. B., Doyle, R. T., Juliano, R. A., Jiao, L., Granowitz, C., et al. (2019) · New England Journal of Medicine · doi:10.1056/nejmoa1812792 · Cited by 3,317
Sequence Variations in PCSK9, Low LDL, and Protection against Coronary Heart Disease
Cohen, J. C., Boerwinkle, E., Mosley, T. H., & Hobbs, H. H. (2006) · New England Journal of Medicine · doi:10.1056/nejmoa054013 · Cited by 3,181
2016 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) · European Heart Journal · doi:10.1093/eurheartj/ehw272 · Cited by 3,162
Effects of torcetrapib in patients at high risk for coronary events
Barter, P. J., Caulfield, M., Eriksson, M., Grundy, S. M., Kastelein, J. J. P., Komajda, M., Lopez-Sendon, J., Mosca, L., Tardif, J.-C., Waters, D. D., et al. (2007) · New England Journal of Medicine · doi:10.1056/nejmoa0706628 · Cited by 3,139
Niacin in Patients with Low HDL Cholesterol Levels Receiving Intensive Statin Therapy
The AIM-HIGH Investigators (2011) · New England Journal of Medicine · doi:10.1056/nejmoa1107579 · Cited by 2,911
Effects of Combination Lipid Therapy in Type 2 Diabetes Mellitus
(2010) · New England Journal of Medicine · doi:10.1056/nejmoa1001282 · Cited by 2,837
Major lipids, apolipoproteins, and risk of vascular disease
The Emerging Risk Factors Collaboration* (2009) · JAMA · doi:10.1001/jama.2009.1619 · Cited by 2,731
Yokoyama, M., Origasa, H., Matsuzaki, M., Matsuzawa, Y., Saito, Y., Ishikawa, Y., Oikawa, S., Sasaki, J., Hishida, H., Itakura, H., et al. (2007) · The Lancet · doi:10.1016/s0140-6736(07)60527-3 · Cited by 2,516
Nordestgaard, B. G., Benn, M., Schnohr, P., & Tybjærg-Hansen, A. (2007) · JAMA · doi:10.1001/jama.298.3.299 · Cited by 2,058
Effects of dalcetrapib in patients with a recent acute coronary syndrome
Schwartz, G. G., Olsson, A. G., Abt, M., Ballantyne, C. M., Barter, P. J., Brumm, J., Chaitman, B. R., Holme, I. M., Kallend, D., Leiter, L. A., et al. (2012) · New England Journal of Medicine · doi:10.1056/nejmoa1206797 · Cited by 2,022
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
Omega-3 Fatty Acids and Cardiovascular Disease
Mozaffarian, D., & Wu, J. H. Y. (2011) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2011.06.063 · Cited by 1,771
Hokanson, J. E., & Austin, M. A. (1996) · Journal of Cardiovascular Risk · doi:10.1097/00043798-199604000-00014 · Cited by 1,706
Fasting compared with nonfasting triglycerides and risk of cardiovascular events in women
Bansal, S., Buring, J. E., Rifai, N., Mora, S., Sacks, F. M., & Ridker, P. M. (2007) · JAMA · doi:10.1001/jama.298.3.309 · Cited by 1,619
2016 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
Increasing Prevalence of the Metabolic Syndrome Among U.S. Adults
Ford, E. S., Giles, W. H., & Mokdad, A. H. (2004) · Diabetes Care · doi:10.2337/diacare.27.10.2444 · Cited by 1,488
Silverman, M. G., Ference, B. A., Im, K., Wiviott, S. D., Giugliano, R. P., Grundy, S. M., Braunwald, E., & Sabatine, M. S. (2016) · JAMA · doi:10.1001/jama.2016.13985 · Cited by 1,483
Triglycerides and cardiovascular disease
Nordestgaard, B. G., & Varbo, A. (2014) · The Lancet · doi:10.1016/s0140-6736(14)61177-6 · Cited by 1,419
Sarwar, N., Danesh, J., Eiriksdottir, G., Sigurdsson, G., Wareham, N., Bingham, S., Boekholdt, S. M., Khaw, K.-T., & Gudnason, V. (2007) · Circulation · doi:10.1161/circulationaha.106.637793 · Cited by 1,408
Manninen, V, Tenkanen, L., Koskinen, P., Huttunen, J. K., Mänttäri, M., Heinonen, O. P., & Frick, M. H. (1992) · Circulation · doi:10.1161/01.cir.85.1.37 · Cited by 1,329
Chapman, M. J., Ginsberg, H. N., Amarenco, P., Andreotti, F., Borén, J., Catapano, A. L., Descamps, O. S., Fisher, E., Kovanen, P. T., Kuivenhoven, J. A., et al. (2011) · European Heart Journal · doi:10.1093/eurheartj/ehr112 · Cited by 1,227
Anderson, T. J., Grégoire, J., Pearson, G. J., Barry, A. R., Couture, P., Dawes, M., Francis, G. A., Genest, J., Grover, S., Gupta, M., et al. (2016) · Canadian Journal of Cardiology · doi:10.1016/j.cjca.2016.07.510 · Cited by 1,173
Appel, L. J., Sacks, F. M., Carey, V. J., Obarzanek, E., Swain, J. F., Miller, E. R., Conlin, P. R., Erlinger, T. P., Rosner, B. A., Laranjo, N. M., et al. (2005) · JAMA · doi:10.1001/jama.294.19.2455 · Cited by 1,170
Nordestgaard, B. G. (2016) · Circulation Research · doi:10.1161/circresaha.115.306249 · Cited by 1,116
Remnant Cholesterol as a Causal Risk Factor for Ischemic Heart Disease
Varbo, A., Benn, M., Tybjærg-Hansen, A., Jørgensen, A. B., Frikke-Schmidt, R., & Nordestgaard, B. G. (2013) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2012.08.1026 · Cited by 1,115
Jellinger, P. S., Handelsman, Y., Rosenblit, P. D., Bloomgarden, Z. T., Fonseca, V. A., Garber, A. J., Grunberger, G., Guerin, C. K., Bell, D. S. H., Mechanick, J. I., et al. (2017) · Endocrine Practice · doi:10.4158/ep171764.appgl · Cited by 1,094
Self-citationLoss-of-Function Mutations in APOC3, Triglycerides, and Coronary Disease
The TG and HDL Working Group of the Exome Sequencing Project, N. H. (2014) · New England Journal of Medicine · doi:10.1056/nejmoa1307095 · Cited by 1,071
Effects of weight reduction on blood lipids and lipoproteins: a meta-analysis
Dattilo, A., & Kris-Etherton, P. (1992) · The American Journal of Clinical Nutrition · doi:10.1093/ajcn/56.2.320 · Cited by 1,055
Rizos, E. C., Ntzani, E. E., Bika, E., Kostapanos, M. S., & Elisaf, M. S. (2012) · JAMA · doi:10.1001/2012.jama.11374 · Cited by 960
Effects of fibrates on cardiovascular outcomes: a systematic review and meta-analysis
Jun, M., Foote, C., Lv, J., Neal, B., Patel, A., Nicholls, S. J., Grobbee, D. E., Cass, A., Chalmers, J., & Perkovic, V. (2010) · The Lancet · doi:10.1016/s0140-6736(10)60656-3 · Cited by 927
Loss-of-Function Mutations in APOC3 and Risk of Ischemic Vascular Disease
Jørgensen, A. B., Frikke-Schmidt, R., Nordestgaard, B. G., & Tybjærg-Hansen, A. (2014) · New England Journal of Medicine · doi:10.1056/nejmoa1308027 · Cited by 919
Relation of Gemfibrozil Treatment and Lipid Levels With Major Coronary Events
Robins, S. J., Collins, D. E., Wittes, J. T., Papademetriou, V., DEEDWANIA, P. C., Schaefer, E. J., McNamara, J. R., Kashyap, M. L., Hershman, J. M., WEXLER, L. F., et al. (2001) · JAMA · doi:10.1001/jama.285.12.1585 · Cited by 917
Ference, B. A., Yoo, W., Alesh, I., Mahajan, N., Mirowska, K. K., Mewada, A., Kahn, J., Afonso, L., Williams, K. A., & Flack, J. M. (2012) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2012.09.017 · Cited by 898
Evaluation and Treatment of Hypertriglyceridemia: An Endocrine Society Clinical Practice Guideline
Berglund, L., Brunzell, J. D., Goldberg, A. C., Goldberg, I. J., Sacks, F., Murad, M. H., & Stalenhoef, A. F. H. (2012) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2011-3213 · Cited by 887
Genetic and Pharmacologic Inactivation of ANGPTL3 and Cardiovascular Disease
Dewey, F. E., Gusarova, V., Dunbar, R. L., O’Dushlaine, C., Schurmann, C., Gottesman, O., McCarthy, S., Van Hout, C. V., Bruse, S., Dansky, H. M., et al. (2017) · New England Journal of Medicine · doi:10.1056/nejmoa1612790 · Cited by 885
Martin, S. S., Blaha, M. J., Elshazly, M. B., Toth, P. P., Kwiterovich, P. O., Blumenthal, R. S., & Jones, S. R. (2013) · JAMA · doi:10.1001/jama.2013.280532 · Cited by 883
Common variants associated with plasma triglycerides and risk for coronary artery disease
Do, R., Willer, C. J., Schmidt, E. M., Sengupta, S., Gao, C., Peloso, G. M., Gustafsson, S., Kanoni, S., Ganna, A., Chen, J., et al. (2013) · Nature Genetics · doi:10.1038/ng.2795 · Cited by 862
Nordestgaard, B. G., Langsted, A., Mora, S., Kolovou, G., Baum, H., Bruckert, E., Watts, G. F., Sypniewska, G., Wiklund, O., Borén, J., et al. (2016) · European Heart Journal · doi:10.1093/eurheartj/ehw152 · Cited by 847
Bucher, H. C., Hengstler, P., Schindler, C., & Meier, G. (2002) · The American Journal of Medicine · doi:10.1016/s0002-9343(01)01114-7 · Cited by 823
Evacetrapib and cardiovascular outcomes in high-risk vascular disease
Lincoff, A. M., Nicholls, S. J., Riesmeyer, J. S., Barter, P. J., Brewer, H. B., Fox, K. A. A., Gibson, C. M., Granger, C., Menon, V., Montalescot, G., et al. (2017) · New England Journal of Medicine · doi:10.1056/nejmoa1609581 · Cited by 801
Effect of a single high-fat meal on endothelial function in healthy subjects
Vogel, R. A., Corretti, M. C., & Plotnick, G. D. (1997) · The American Journal of Cardiology · doi:10.1016/s0002-9149(96)00760-6 · Cited by 798
National Lipid Association Recommendations for Patient-Centered Management of Dyslipidemia: Part 2
Jacobson, T. A., Maki, K. C., Orringer, C. E., Jones, P. H., Kris-Etherton, P., Sikand, G., La Forge, R., Daniels, S. R., Wilson, D. P., Morris, P. B., et al. (2015) · Journal of Clinical Lipidology · doi:10.1016/j.jacl.2015.09.002 · Cited by 784
Jacobson, T. A., Ito, M. K., Maki, K. C., Orringer, C. E., Bays, H. E., Jones, P. H., McKenney, J. M., Grundy, S. M., Gill, E. A., Wild, R. A., et al. (2015) · Journal of clinical lipidology · doi:10.1016/j.jacl.2015.02.003 · Cited by 781
Elevated circulating free fatty acid levels impair endothelium-dependent vasodilation
Steinberg, H. O., Tarshoby, M., Monestel, R., Hook, G., Cronin, J., Johnson, A., Bayazeed, B., & Baron, A. D. (1997) · Journal of Clinical Investigation · doi:10.1172/jci119636 · Cited by 761
High-Density Lipoprotein Subfractions - What the Clinicians Need to Know
Pirillo, A., Norata, G. D., & Catapano, A. L. (2013) · Cardiology · doi:10.1159/000346463 · Cited by 754
Exome Sequencing, ANGPTL3 Mutations, and Familial Combined Hypolipidemia
Musunuru, K., Pirruccello, J. P., Do, R., Peloso, G. M., Guiducci, C., Sougnez, C., Garimella, K. V., Fisher, S., Abreu, J., Barry, A. J., et al. (2010) · New England Journal of Medicine · doi:10.1056/nejmoa1002926 · Cited by 754
Mendelian randomization of blood lipids for coronary heart disease
Holmes, M. V., Asselbergs, F. W., Palmer, T. M., Drenos, F., Lanktree, M. B., Nelson, C. P., Dale, C. E., Padmanabhan, S., Finan, C., Swerdlow, D. I., et al. (2015) · European Heart Journal · doi:10.1093/eurheartj/eht571 · Cited by 748
Triglyceride-mediated pathways and coronary disease: collaborative analysis of 101 studies
(2010) · The Lancet · doi:10.1016/s0140-6736(10)60545-4 · Cited by 716
Varbo, A., Benn, M., Tybjærg-Hansen, A., & Nordestgaard, B. G. (2013) · Circulation · doi:10.1161/circulationaha.113.003008 · Cited by 692
Pollin, T. I., Damcott, C. M., Shen, H., Ott, S. H., Shelton, J., Horenstein, R. B., Post, W., McLenithan, J. C., Bielak, L. F., Peyser, P. A., et al. (2008) · Science · doi:10.1126/science.1161524 · Cited by 688
Triglyceride Concentration and Ischemic Heart Disease
Jeppesen, J., Hein, H. O., Suadicani, P., & Gyntelberg, F. (1998) · Circulation · doi:10.1161/01.cir.97.11.1029 · Cited by 678
Exome sequencing identifies rare LDLR and APOA5 alleles conferring risk for myocardial infarction
Do, R., Stitziel, N. O., Won, H.-H., Jørgensen, A. B., Duga, S., Angelica Merlini, P., Kiezun, A., Farrall, M., Goel, A., Zuk, O., et al. (2015) · Nature · doi:10.1038/nature13917 · Cited by 650
Hegele, R. A., Ginsberg, H. N., Chapman, M. J., Nordestgaard, B. G., Kuivenhoven, J. A., Averna, M., Borén, J., Bruckert, E., Catapano, A. L., Descamps, O. S., et al. (2014) · The Lancet Diabetes & Endocrinology · doi:10.1016/s2213-8587(13)70191-8 · Cited by 635
Siscovick, D. S., Barringer, T. A., Fretts, A. M., Wu, J. H. Y., Lichtenstein, A. H., Costello, R. B., Kris-Etherton, P. M., Jacobson, T. A., Engler, M. B., Alger, H. M., et al. (2017) · Circulation · doi:10.1161/cir.0000000000000482 · Cited by 629
Hypertriglyceridemia: its etiology, effects and treatment
Yuan, G., Al-Shali, K. Z., & Hegele, R. A. (2007) · Canadian Medical Association Journal · doi:10.1503/cmaj.060963 · Cited by 624
Miller, M., Cannon, C. P., Murphy, S. A., Qin, J., Ray, K. K., & Braunwald, E. (2008) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2007.10.038 · Cited by 610
Langsted, A., Freiberg, J. J., & Nordestgaard, B. G. (2008) · Circulation · doi:10.1161/circulationaha.108.804146 · Cited by 588
Physiological regulation of lipoprotein lipase
Kersten, S. (2014) · Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids · doi:10.1016/j.bbalip.2014.03.013 · Cited by 574
Cardiovascular and Metabolic Effects of ANGPTL3 Antisense Oligonucleotides
Graham, M. J., Lee, R. G., Brandt, T. A., Tai, L.-J., Fu, W., Peralta, R., Yu, R., Hurh, E., Paz, E., McEvoy, B. W., et al. (2017) · New England Journal of Medicine · doi:10.1056/nejmoa1701329 · Cited by 573
Scott, R., O'Brien, R., Fulcher, G., Pardy, C., d'Emden, M., Tse, D., Taskinen, M.-R., Ehnholm, C., Keech, A., & on behalf of the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) Study Investigators (2009) · Diabetes Care · doi:10.2337/dc08-1543 · Cited by 551
Lipid-Related Markers and Cardiovascular Disease Prediction
The Emerging Risk Factors Collaboration (2012) · JAMA · doi:10.1001/jama.2012.6571 · Cited by 547
Nonfasting triglycerides and risk of ischemic stroke in the general population
Freiberg, J. J. (2008) · JAMA · doi:10.1001/jama.2008.621 · Cited by 542
Antisense Inhibition of Apolipoprotein C-III in Patients with Hypertriglyceridemia
Gaudet, D., Alexander, V. J., Baker, B. F., Brisson, D., Tremblay, K., Singleton, W., Geary, R. S., Hughes, S. G., Viney, N. J., Graham, M. J., et al. (2015) · New England Journal of Medicine · doi:10.1056/nejmoa1400283 · Cited by 528
Lipids, lipoproteins, and metabolites and risk of myocardial infarction and stroke
Holmes, M. V., Millwood, I. Y., Kartsonaki, C., Hill, M. R., Bennett, D. A., Boxall, R., Guo, Y., Xu, X., Bian, Z., Hu, R., et al. (2018) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2017.12.006 · Cited by 508
Jørgensen, A. B., Frikke-Schmidt, R., West, A. S., Grande, P., Nordestgaard, B. G., & Tybjærg-Hansen, A. (2013) · European Heart Journal · doi:10.1093/eurheartj/ehs431 · Cited by 501
Inactivating Variants in ANGPTL4 and Risk of Coronary Artery Disease
Dewey, F. E., Gusarova, V., O’Dushlaine, C., Gottesman, O., Trejos, J., Hunt, C., Van Hout, C. V., Habegger, L., Buckler, D., Lai, K.-M. V., et al. (2016) · New England Journal of Medicine · doi:10.1056/nejmoa1510926 · Cited by 497
Targeting APOC3 in the familial chylomicronemia syndrome
Gaudet, D., Brisson, D., Tremblay, K., Alexander, V. J., Singleton, W., Hughes, S. G., Geary, R. S., Baker, B. F., Graham, M. J., Crooke, R. M., et al. (2014) · New England Journal of Medicine · doi:10.1056/nejmoa1400284 · Cited by 491
Issues in Hypertriglyceridemic Pancreatitis
Scherer, J., Singh, V. P., Pitchumoni, C. S., & Yadav, D. K. (2013) · Journal of Clinical Gastroenterology · doi:10.1097/01.mcg.0000436438.60145.5a · Cited by 482
ANGPTL3 deficiency and protection against coronary artery disease
Stitziel, N. O., Khera, A. V., Wang, X., Bierhals, A. J., Vourakis, A. C., Sperry, A. E., Natarajan, P., Klarin, D., Emdin, C. A., Zekavat, S. M., et al. (2017) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2017.02.030 · Cited by 467
Khera, A. V., Everett, B. M., Caulfield, M. P., Hantash, F. M., Wohlgemuth, J., Ridker, P. M., & Mora, S. (2014) · Circulation · doi:10.1161/circulationaha.113.004406 · Cited by 461
Sampson, U. K., Fazio, S., & Linton, M. F. (2012) · Current Atherosclerosis Reports · doi:10.1007/s11883-011-0219-7 · Cited by 439
Self-citationMartin, S. S., Blaha, M. J., Elshazly, M. B., Brinton, E. A., Toth, P. P., McEvoy, J. W., Joshi, P. H., Kulkarni, K. R., Mize, P. D., Kwiterovich, P. O., et al. (2013) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2013.01.079 · Cited by 428
Nakajima, K., SAITO, T., Tamura, A., Suzuki, M., Nakano, T., Adachi, M., Tanaka, A., Tada, N., Nakamura, H., Campos, E. M., et al. (1993) · Clinica Chimica Acta · doi:10.1016/0009-8981(93)90062-9 · Cited by 417
Small LDL, Atherogenic Dyslipidemia, and the Metabolic Syndrome
Grundy, S. M. (1997) · Circulation · doi:10.1161/01.cir.95.1.1 · Cited by 402
Hypertriglyceridaemia and risk of coronary artery disease
Reiner, Ž. (2017) · Nature Reviews Cardiology · doi:10.1038/nrcardio.2017.31 · Cited by 390
Comparison of statins in hypertriglyceridemia
Stein, E. A., Lane, M., & Laskarzewski, P. (1998) · The American Journal of Cardiology · doi:10.1016/s0002-9149(98)00041-1 · Cited by 386
Graham, M. J., Lee, R. G., Bell, T. A., Fu, W., Mullick, A. E., Alexander, V. J., Singleton, W., Viney, N., Geary, R., Su, J., et al. (2013) · Circulation Research · doi:10.1161/circresaha.111.300367 · Cited by 377
Kwak (2012) · doi:10.1001/archinternmed.2012.262 · Cited by 368
Wittrup, H. H., Tybjærg-Hansen, A., & Nordestgaard, B. G. (1999) · Circulation · doi:10.1161/01.cir.99.22.2901 · Cited by 344
GPIHBP1 Is Responsible for the Entry of Lipoprotein Lipase into Capillaries
Davies, B. S. J., Beigneux, A. P., Barnes, R. H., Tu, Y., Gin, P., Weinstein, M. M., Nobumori, C., Nyrén, R., Goldberg, I., Olivecrona, G., et al. (2010) · Cell Metabolism · doi:10.1016/j.cmet.2010.04.016 · Cited by 342
Borén, J., Olin, K., Lee, I., Chait, A., Wight, T. N., & Innerarity, T. L. (1998) · Journal of Clinical Investigation · doi:10.1172/jci2265 · Cited by 320
Relationship of Apolipoproteins A-1 and B, and Lipoprotein(a) to Cardiovascular Outcomes
Albers, J. J., Slee, A. E., O’Brien, K. D., Robinson, J. G., Kashyap, M. L., Kwiterovich, P. O., Xu, P., & Marcovina, S. M. (2013) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2013.06.051 · Cited by 317
Saito, Y., Yokoyama, M., Origasa, H., Matsuzaki, M., Matsuzawa, Y., Ishikawa, Y., Oikawa, S., Sasaki, J., Hishida, H., Itakura, H., et al. (2008) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2008.06.003 · Cited by 316
(1997) · PubMed · Cited by 302
Lipoprotein ApoC-II activation of lipoprotein lipase. Modulation by apolipoprotein A-IV.
Goldberg, I. J., Scheraldi, C. A., Yacoub, L. K., Saxena, U., & Bisgaier, C. L. (1990) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(19)39557-2 · Cited by 291
Schuchardt, J., Schneider, I., Meyer, H., Neubronner, J., von Schacky, C., & Hahn, A. (2011) · Lipids in Health and Disease · doi:10.1186/1476-511x-10-145 · Cited by 291
Shin, H. K., Kim, Y. K., Kim, K. Y., Lee, J. H., & Hong, K. W. (2004) · Circulation · doi:10.1161/01.cir.0000117403.64398.53 · Cited by 268
Genetic determinants of plasma triglycerides
Johansen, C. T., Kathiresan, S., & Hegele, R. A. (2010) · Journal of Lipid Research · doi:10.1194/jlr.r009720 · Cited by 264
Jacobson, T. A., Glickstein, S. B., Rowe, J. D., & Soni, P. N. (2012) · Journal of Clinical Lipidology · doi:10.1016/j.jacl.2011.10.018 · Cited by 263
Alexander, D. D., Miller, P. E., Elswyk, M. E. V., Kuratko, C. N., & Bylsma, L. C. (2017) · Mayo Clinic Proceedings · doi:10.1016/j.mayocp.2016.10.018 · Cited by 262
Genetics and causality of triglyceride-rich lipoproteins in atherosclerotic cardiovascular disease
Rosenson, R. S., Davidson, M. H., Hirsh, B. J., Kathiresan, S., & Gaudet, D. (2014) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2014.09.042 · Cited by 260
Boquist, S., Ruotolo, G., Tang, R., Björkegren, J., Bond, M. G., Fairé, U. D., Karpe, F., & Hamsten, A. (1999) · Circulation · doi:10.1161/01.cir.100.7.723 · Cited by 258
Anderson, R. A., Evans, M. L., Ellis, G. R., Graham, J., Morris, K., Jackson, S. K., Lewis, M. J., Rees, A., & Frenneaux, M. P. (2001) · Atherosclerosis · doi:10.1016/s0021-9150(00)00499-8 · Cited by 248
Rumawas, M. E., Meigs, J. B., Dwyer, J. T., McKeown, N. M., & Jacques, P. F. (2009) · The American Journal of Clinical Nutrition · doi:10.3945/ajcn.2009.27908 · Cited by 246
Combination lipid therapy in type 2 diabetes
(2010) · New England Journal of Medicine · doi:10.1056/nejmc1006407 · Cited by 245
Triglyceride-rich lipoproteins as a causal factor for cardiovascular disease
Toth, P. (2016) · Vascular Health and Risk Management · doi:10.2147/vhrm.s104369 · Cited by 237
Kastelein, J. J. P., Maki, K. C., Susekov, A., Ezhov, M., Nordestgaard, B. G., Machielse, B. N., Kling, D., & Davidson, M. H. (2014) · Journal of Clinical Lipidology · doi:10.1016/j.jacl.2013.10.003 · Cited by 233
Doi, H., Kugiyama, K., Oka, H., Sugiyama, S., Ogata, N., Koide, S.-I., Nakamura, S.-I., & Yasue, H. (2000) · Circulation · doi:10.1161/01.cir.102.6.670 · Cited by 227
Fibrates, Glitazones, and Peroxisome Proliferator–Activated Receptors
Lalloyer, F., & Staels, B. (2010) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.108.179689 · Cited by 226
Mutations in LMF1 cause combined lipase deficiency and severe hypertriglyceridemia.
Péterfy, M., Ben-Zeev, O., Mao, H. Z., Weissglas-Volkov, D., Aouizerat, B. E., Pullinger, C. R., Frost, P. H., Kane, J. P., Malloy, M. J., Reue, K., et al. (2007) · Nature Genetics · doi:10.1038/ng.2007.24 · Cited by 226
A Test in Context: Lipid Profile, Fasting Versus Nonfasting
Nordestgaard, B. G. (2017) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2017.08.006 · Cited by 223
Dubois, C., Beaumier-Gallon, G., Juhel, C., Armand, M., Portugal, H., Pauli, A.-M., Borel, P., Latge, C., & Lairon, D. (1998) · American Journal of Clinical Nutrition · doi:10.1093/ajcn/67.1.31 · Cited by 218
Jepsen, A.-M. K., Langsted, A., Varbo, A., Bang, L. E., Kamstrup, P. R., & Nordestgaard, B. G. (2016) · Clinical Chemistry · doi:10.1373/clinchem.2015.253757 · Cited by 218
From Lipids to Inflammation: New Approaches to Reducing Atherosclerotic Risk
Shapiro, M. D., & Fazio, S. (2016) · Circulation Research · doi:10.1161/circresaha.115.306471 · Cited by 217
Self-citationVarbo, A., Freiberg, J. J., & Nordestgaard, B. G. (2015) · Clinical Chemistry · doi:10.1373/clinchem.2014.234146 · Cited by 209
Ishibashi, S., Yamashita, S., Arai, H., Araki, E., Yokote, K., Suganami, H., Fruchart, J.-C., & Kodama, T. (2016) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2016.02.029 · Cited by 208
Regulation of lipoprotein lipase by Angptl4
Dijk, W., & Kersten, S. (2014) · Trends in Endocrinology and Metabolism · doi:10.1016/j.tem.2013.12.005 · Cited by 207
The regulation of ApoB metabolism by insulin
Haas, M. E., Attie, A., & Biddinger, S. B. (2013) · Trends in Endocrinology and Metabolism · doi:10.1016/j.tem.2013.04.001 · Cited by 202
Omega 3 Fatty Acids and Cardiovascular Outcomes: Systematic Review and Meta-Analysis
Kotwal, S., Jun, M., Sullivan, D., Perkovic, V., & Neal, B. (2012) · Circulation: Cardiovascular Quality and Outcomes · doi:10.1161/circoutcomes.112.966168 · Cited by 201
ANGPTL8 requires ANGPTL3 to inhibit lipoprotein lipase and plasma triglyceride clearance
Haller, J. F., Mintah, I. J., Shihanian, L. M., Stevis, P., Buckler, D., Alexa-Braun, C. A., Kleiner, S., Banfi, S., Cohen, J. C., Hobbs, H. H., et al. (2017) · Journal of Lipid Research · doi:10.1194/jlr.m075689 · Cited by 199
Unmet Need for Adjunctive Dyslipidemia Therapy in Hypertriglyceridemia Management
Ganda, O. P., Bhatt, D. L., Mason, R. P., Miller, M., & Boden, W. E. (2018) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2018.04.061 · Cited by 195
Hypertriglyceridemia: a too long unfairly neglected major cardiovascular risk factor
Tenenbaum, A., Klempfner, R., & Fisman, E. Z. (2014) · Cardiovascular Diabetology · doi:10.1186/s12933-014-0159-y · Cited by 193
Severe hypertriglyceridemia in pregnancy
Goldberg, A. S., & Hegele, R. A. (2012) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2012-1250 · Cited by 187
Dyslipidemia Associated with Chronic Kidney Disease
Tsimihodimos, V., Mitrogianni, Z., & Elisaf, M. (2011) · The Open Cardiovascular Medicine Journal · doi:10.2174/1874192401105010041 · Cited by 183
Relationship of Lipoproteins to Cardiovascular Events
Guyton, J. R., Slee, A. E., Anderson, T., Fleg, J. L., Goldberg, R. B., Kashyap, M. L., Marcovina, S. M., Nash, S. D., O'Brien, K. D., Weintraub, W. S., et al. (2013) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2013.07.023 · Cited by 182
Gene therapy for lipoprotein lipase deficiency
Gaudet, D., Méthot, J., & Kastelein, J. (2012) · Current Opinion in Lipidology · doi:10.1097/mol.0b013e3283555a7e · Cited by 178
Joshi, P. H., Khokhar, A. A., Massaro, J. M., Lirette, S. T., Griswold, M. E., Martin, S. S., Blaha, M. J., Kulkarni, K. R., Correa, A., D'Agostino, R. B., et al. (2016) · Journal of the American Heart Association · doi:10.1161/jaha.115.002765 · Cited by 177
Larsson, M., Vorrsjö, E., Talmud, P. J., Lõokene, A., & Olivecrona, G. (2013) · Journal of Biological Chemistry · doi:10.1074/jbc.m113.495366 · Cited by 176
Alcohol and plasma triglycerides
Klop, B., do Rego, A. T., & Cabezas, M. C. (2013) · Current Opinion in Lipidology · doi:10.1097/mol.0b013e3283606845 · Cited by 176
Low nonfasting triglycerides and reduced all-cause mortality: a mendelian randomization study
Thomsen, M., Varbo, A., Tybjærg-Hansen, A., & Nordestgaard, B. G. (2014) · Clinical Chemistry · doi:10.1373/clinchem.2013.219881 · Cited by 171
Surprises from genetic analyses of lipid risk factors for atherosclerosis
Musunuru, K., & Kathiresan, S. (2016) · Circulation Research · doi:10.1161/circresaha.115.306398 · Cited by 159
Cholesterol Profile Measurement by Vertical Auto Profile Method
Kulkarni, K. R. (2006) · Clinics in Laboratory Medicine · doi:10.1016/j.cll.2006.07.004 · Cited by 158
Lipoprotein Lipase S447X: A Naturally Occurring Gain-of-Function Mutation
Rip, J., Nierman, M. C., Ross, C. J., Jukema, J. W., Hayden, M. R., Kastelein, J. J. P., Stroes, E. S. G., & Kuivenhoven, J. A. (2006) · Arteriosclerosis, Thrombosis, and Vascular Biology · doi:10.1161/01.atv.0000219283.10832.43 · Cited by 157
Large lipoproteins are excluded from the arterial wall in diabetic cholesterol-fed rabbits
Nordestgaard, B. G., & Zilversmit, D. B. (1988) · Journal of Lipid Research · doi:10.1016/s0022-2275(20)38428-5 · Cited by 156
Miller, Y. I., Choi, S.-H., Fang, L., & Tsimikas, S. (2010) · Sub-cellular biochemistry/Subcellular biochemistry · doi:10.1007/978-90-481-8622-8_8 · Cited by 155
Faergeman, O., Holme, I., Fayyad, R., Bhatia, S., Grundy, S. M., Kastelein, J. J. P., LaRosa, J. C., Larsen, M. L., Lindahl, C., Olsson, A. G., et al. (2009) · The American Journal of Cardiology · doi:10.1016/j.amjcard.2009.04.008 · Cited by 154
Hypothyroidism and dyslipidemia: Modern concepts and approaches
Pearce, E. N. (2004) · Current Cardiology Reports · doi:10.1007/s11886-004-0054-3 · Cited by 153
Cohen, J. D., Cziraky, M. J., Cai, Q., Wallace, A. E., Wasser, T., Crouse, J. R., & Jacobson, T. A. (2010) · The American Journal of Cardiology · doi:10.1016/j.amjcard.2010.05.030 · Cited by 151
Advances in lipid-lowering therapy through gene-silencing technologies
Nordestgaard, B. G., Nicholls, S. J., Langsted, A., Ray, K. K., & Tybjærg‐Hansen, A. (2018) · Nature Reviews Cardiology · doi:10.1038/nrcardio.2018.3 · Cited by 148
Plasma HDL cholesterol and risk of myocardial infarction: a mendelian randomisation study
Voight, B. F., Peloso, G. M., Orho-Melander, M., Frikke-Schmidt, R., Barbalic, M., Jensen, M. K., Hindy, G., Hólm, H., Ding, E. L., Johnson, T., et al. (2012) · The Lancet · doi:10.1016/s0140-6736(12)60312-2 · Cited by 148
Fibrates for primary prevention of cardiovascular disease events
Jakob, T., Nordmann, A. J., Schandelmaier, S., Ferreira-González, I., & Briel, M. (2016) · Cochrane Database of Systematic Reviews · doi:10.1002/14651858.cd009753.pub2 · Cited by 147
Nordestgaard, B. G., Abildgaard, S., Wittrup, H. H., Steffensen, R., Jensen, G., & Tybjærg-Hansen, A. (1997) · Circulation · doi:10.1161/01.cir.96.6.1737 · Cited by 146
Postprandial Hyperlipidemia and Remnant Lipoproteins
Masuda, D., & Yamashita, S. (2017) · Journal of Atherosclerosis and Thrombosis · doi:10.5551/jat.rv16003 · Cited by 145
Stensvold, I., Tverdal, A., Urdal, P., & Graff‐Iversen, S. (1993) · BMJ · doi:10.1136/bmj.307.6915.1318 · Cited by 142
Fibrates for secondary prevention of cardiovascular disease and stroke
Wang, D., Liu, B., Tao, W., Hao, Z., & Liu, M. (2015) · Cochrane Database of Systematic Reviews · doi:10.1002/14651858.cd009580.pub2 · Cited by 142
Nordestgaard, B. G., Stender, S., & Kjeldsen, K. (1988) · Arteriosclerosis: An Official Journal of the American Heart Association, Inc. · doi:10.1161/01.atv.8.4.421 · Cited by 137
Doran, B., Guo, Y., Xu, J., WEINTRAUB, H. S., Mora, S., Maron, D. J., & Bangalore, S. (2014) · Circulation · doi:10.1161/circulationaha.114.010001 · Cited by 135
Varbo, A., & Nordestgaard, B. G. (2017) · Current Opinion in Lipidology · doi:10.1097/mol.0000000000000429 · Cited by 135
GPIHBP1, an endothelial cell transporter for lipoprotein lipase
Young, S. G., Davies, B. S. J., Voss, C. V., Gin, P., Weinstein, M. M., Tontonoz, P., Reue, K., Bensadoun, A., Fong, L. G., & Beigneux, A. P. (2011) · Journal of Lipid Research · doi:10.1194/jlr.r018689 · Cited by 117
Demystifying the management of hypertriglyceridaemia
Watts, G. F., Ooi, E. M. M., & Chan, D. C. (2013) · Nature Reviews Cardiology · doi:10.1038/nrcardio.2013.140 · Cited by 115
Effects of VLDL and remnant particles on platelets.
Olufadi, R., & Byrne, C. D. (2006) · Pathophysiology of Haemostasis and Thrombosis · doi:10.1159/000093221 · Cited by 111
Effects of torcetrapib in patients at high risk for coronary events
Barter, P. J., Caulfield, M. J., & Eriksson, M. (2008) · Journal of Vascular Surgery · doi:10.1016/j.jvs.2008.02.014 · Cited by 111
Hua, S. (2013) · Frontiers in Pharmacology · doi:10.3389/fphar.2013.00127 · Cited by 107
Qin, W., Sundaram, M., Wang, Y., Zhou, H., Zhong, S., Chang, C.-C., Manhas, S., Yao, E. F., Parks, R. J., McFie, P. J., et al. (2011) · Journal of Biological Chemistry · doi:10.1074/jbc.m110.203679 · Cited by 107
Triglycerides on the rise: should we swap seats on the seesaw?
Libby, P. (2015) · European Heart Journal · doi:10.1093/eurheartj/ehu500 · Cited by 85
Varbo, A., & Nordestgaard, B. G. (2018) · Arteriosclerosis, Thrombosis, and Vascular Biology · doi:10.1161/atvbaha.117.310269 · Cited by 83 · cited 2×
“Abbreviations: ACS, acute coronary syndrome; CCHS, Copenhagen City Heart Study; CGPS, Copenhagen City General Population; EPIC, European Prospective Investigation of Cancer; FOCS, Framingham Offspring Cohort Study; IDEAL, Incremental Decrease in End Points Through Aggressive Lipid Lowering; JHS, Jackson Heart Study; N…”
BackgroundLipoprotein Remnants and Endothelial Dysfunction in the Postprandial Phase
Maggi, F. M., Raselli, S., Grigore, L., Redaelli, L., Fantappiè, S., & Catapano, A. L. (2004) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2003-031977 · Cited by 74
Nakajima, K., Nagamine, T., Fujita, M., Ai, M., Tanaka, A., & Schaefer, E. J. (2014) · Advances in clinical chemistry · doi:10.1016/b978-0-12-800263-6.00003-3 · Cited by 72
Premature myocardial infarction is strongly associated with increased levels of remnant cholesterol
Goliasch, G., Wiesbauer, F., Blessberger, H., Demyanets, S., Wojta, J., Huber, K., Maurer, G., Schillinger, M., & Speidl, W. S. (2015) · Journal of clinical lipidology · doi:10.1016/j.jacl.2015.08.009 · Cited by 67
Folsom, A. R., Peacock, J. M., Demerath, E., & Boerwinkle, E. (2008) · Metabolism · doi:10.1016/j.metabol.2008.06.016 · Cited by 64
Angiopoietin-Like 3 (ANGPTL3) and Atherosclerosis: Lipid and Non-Lipid Related Effects
Lupo, M. G., & Ferri, N. (2018) · Journal of Cardiovascular Development and Disease · doi:10.3390/jcdd5030039 · Cited by 64
Microsomal transfer protein inhibition in humans
Cuchel, M., & Rader, D. J. (2013) · Current Opinion in Lipidology · doi:10.1097/mol.0b013e32836139df · Cited by 62
PPAR-α agonists are still on the rise: an update on clinical and experimental findings
Ferri, N., Corsini, A., Sirtori, C. R., & Ruscica, M. (2017) · Expert Opinion on Investigational Drugs · doi:10.1080/13543784.2017.1312339 · Cited by 59
Nonfasting for Routine Lipid Testing
Mora, S. (2016) · JAMA Internal Medicine · doi:10.1001/jamainternmed.2016.1979 · Cited by 58
Low density lipoprotein retention by aortic tissue☆Contribution of extracellular matrix
Srinivasan, S. R., Vijayagopal, P., Dalferes, E. R., Abbate, B., Radhakrishnamurthy, B., & Berenson, G. S. (1986) · Atherosclerosis · doi:10.1016/0021-9150(86)90094-8 · Cited by 57
Conlon, D., Thomas, T. A., Fedotova, T. V., Hernández‐Ono, A., Paolo, G. D., Chan, R., Ruggles, K. V., Gibeley, S. B., Liu, J., & Ginsberg, H. N. (2016) · Journal of Clinical Investigation · doi:10.1172/jci86028 · Cited by 54
Karalis, D. G. (2016) · Advances in Therapy · doi:10.1007/s12325-016-0462-y · Cited by 48
APOC3, Coronary Disease, and Complexities of Mendelian Randomization
Cohen, J. C., Stender, S., & Hobbs, H. H. (2014) · Cell Metabolism · doi:10.1016/j.cmet.2014.08.007 · Cited by 45
Positioning about the Flexibility of Fasting for Lipid Profiling
Scartezini, M., Ferreira, C. E. D. S., Izar, M. C. D. O., Bertoluci, M. C., Vencio, S. A. C., Campana, G. A., Sumita, N. M., Barcelos, L. F., Faludi, A. Á., Santos, R. D., et al. (2017) · Arquivos Brasileiros de Cardiologia · doi:10.5935/abc.20170039 · Cited by 43
Stavenow, L., & Kjellström, T. (1999) · Atherosclerosis · doi:10.1016/s0021-9150(99)00190-2 · Cited by 38
Bittencourt, M. S., Santos, R. D., Staniak, H. L., Sharovsky, R., Kondapally, R., Vallejo‐Vaz, A. J., Ray, K. K., Benseñor, I. M., & Lotufo, P. A. (2017) · The American Journal of Cardiology · doi:10.1016/j.amjcard.2017.01.033 · Cited by 38
Lee, R. G., Fu, W., Graham, M. J., Mullick, A. E., Sipe, D., Gattis, D., Bell, T. A., Booten, S. L., & Crooke, R. M. (2012) · Journal of Lipid Research · doi:10.1194/jlr.m029215 · Cited by 33
Nguyen, S. V., Nakamura, T., Uematsu, M., Fujioka, D., Watanabe, K., Watanabe, Y., Obata, J.-E., Nakamura, K., & Kugiyama, K. (2017) · Journal of Cardiology · doi:10.1016/j.jjcc.2016.04.011 · Cited by 33
Saito, Y., Yokoyama, M., Origasa, H., Matsuzaki, M., Matsuzawa, Y., Ishikawa, Y., Oikawa, S., Sasaki, J., Hishida, H., Itakura, H., et al. (2009) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2008.09.002 · Cited by 29
Causal Effect of Lipids and Lipoproteins on Atherosclerosis
Ference, B. A. (2018) · Cardiology Clinics · doi:10.1016/j.ccl.2017.12.001 · Cited by 28
Molecular and functional characterization of familial chylomicronemia syndrome
Teramoto, R., Tada, H., Kawashiri, M., et al. (2017) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2017.11.006 · Cited by 23
Lee, S. H., Lee, B., Won, H. K., Moon, J. H., Kim, K. J., Kang, E. S., Soo, B., & Lee, H. C. (2011) · Diabetes & Metabolism Journal · doi:10.4093/dmj.2011.35.4.404 · Cited by 19
Icosapent Ethyl for Treatment of Elevated Triglyceride Levels
Nelson, S. D., & Munger, M. A. (2013) · Annals of Pharmacotherapy · doi:10.1177/1060028013504079 · Cited by 14
Kastelein, J. J. P., Hallén, J., Vige, R., Fraser, D. A., Zhou, R., Hustvedt, S. O., Orloff, D. G., & Bays, H. E. (2016) · Cardiology · doi:10.1159/000445047 · Cited by 14
Brandt, T. A., Lee, R. G., DIGENIO, A. G., Graham, M. G., Crooke, R. M., Hughes, S. G., Singleton, W., Witztum, J. L., & Tsimikas, S. (2015) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2015.04.115 · Cited by 13
Ference, B. A., Yoo, W., Alesh, I. G., Mahajan, N., Mirowska, K. K., Mewada, A., Kahn, J., Afonso, L. A. P. M., Williams, K., & Flack, J. (2013) · Rational Pharmacotherapy in Cardiology · doi:10.20996/1819-6446-2013-9-1-90-98 · Cited by 13
Irawati, D., Mamo, J. C. L., Dhaliwal, S. S., Soares, M. J., Clark, K., & James, A. P. (2016) · Lipids in Health and Disease · doi:10.1186/s12944-016-0330-4 · Cited by 10
Flagged first, then by citations
2 of the 184 references couldn’t be matched to a known paper.
Research works printed but not linked: 1
- Chait, 2000, Endotext
Cited by
Sorted by citations
Ginsberg, H. N., Packard, C. J., Chapman, M. J., Borén, J., Aguilar-Salinas, C. A., Averna, M., Ference, B. A., Gaudet, D., Hegele, R. A., Kersten, S., et al. (2021) · European Heart Journal · doi:10.1093/eurheartj/ehab551 · Cited by 979
Remnant cholesterol predicts cardiovascular disease beyond LDL and ApoB: A primary prevention study
Quispe, R., Martin, S. S., Michos, E. D., Lamba, I., Blumenthal, R. S., Saeed, A., Lima, J., Puri, R., Nomura, S., Tsai, M., et al. (2021) · European Heart Journal · doi:10.1093/eurheartj/ehab432 · Cited by 441
Yin, K., Wang, Y., Zhao, H., Wang, D., Guo, M., Mu, M., Liu, Y., Nie, X., Li, B., Li, J., et al. (2021) · The Science of The Total Environment · doi:10.1016/j.scitotenv.2021.145758 · Cited by 447
Soppert, J., Lehrke, M., Marx, N., Jankowski, J., & Noels, H. (2020) · Advanced Drug Delivery Reviews · doi:10.1016/j.addr.2020.07.019 · Cited by 440
ATP-citrate lyase (ACLY) in lipid metabolism and atherosclerosis: An updated review
Feng, X., Zhang, L., Xu, S., & Shen, A.-Z. (2019) · Progress in Lipid Research · doi:10.1016/j.plipres.2019.101006 · Cited by 242
Metadata
- Authors
- Sandesara, P. B., Virani, S. S., Fazio, S., & Shapiro, M. D.
- Affiliations
- Emory University (US)
- Michael E. DeBakey VA Medical Center (US)
- Oregon Health & Science University (US)
- Corresponding author
- Shapiro, Michael D
- Venue
- Endocrine Reviews
- Publisher
- The Endocrine Society
- Published
- 2018-10-11
- Volume
- 40
- Issue
- 2
- Pages
- 537-557
- ISSN
- 0163-769X (ISSN-L)
- 1945-7189
- PMC
- PMC6416708
- OpenAlex
- W2896008418
- Cited by
- 608
- References
- 184
- Citations by year
- 2026: 92 · 2025: 103 · 2024: 122 · 2023: 117 · 2022: 62 · 2021: 61 · 2020: 30 · 2019: 18 · 2018: 2
- FWCI
- 5.28
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Endocrine Reviews (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- eCommons - AKU (Aga Khan University) (submittedVersion)
- Funders
- National Institutes of Health (5R01HL132985)
- U.S. Department of Veterans Affairs (09-028)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (K12HD043488)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Keywords
- triglycerides, remnant cholesterol, triglyceride-rich lipoproteins, atherosclerotic cardiovascular disease, hypertriglyceridemia, residual cardiovascular risk, VLDL, chylomicrons, LDL cholesterol
- MeSH terms
- Cholesterol, Humans, Lipoproteins, Triglycerides, Hypertriglyceridemia, Dyslipidemias, 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 ›
Are you an author, or do you see a problem with this page? Request a review