Triglyceride-Rich Lipoproteins and Atherosclerotic Cardiovascular Disease: New Insights From Epidemiology, Genetics, and Biology
Abstract
Scientific interest in triglyceride-rich lipoproteins has fluctuated over the past many years, ranging from beliefs that these lipoproteins cause atherosclerotic cardiovascular disease (ASCVD) to being innocent bystanders. Correspondingly, clinical recommendations have fluctuated from a need to reduce levels to no advice on treatment. New insight in epidemiology now suggests that these lipoproteins, marked by high triglycerides, are strong and independent predictors of ASCVD and all-cause mortality, and that their cholesterol content or remnant cholesterol likewise are strong predictors of ASCVD. Of all adults, 27% have triglycerides >2 mmol/L (176 mg/dL), and 21% have remnant cholesterol >1 mmol/L (39 mg/dL). For individuals in the general population with nonfasting triglycerides of 6.6 mmol/L (580 mg/dL) compared with individuals with levels of 0.8 mmol/L (70 mg/dL), the risks were 5.1-fold for myocardial infarction, 3.2-fold for ischemic heart disease, 3.2-fold for ischemic stroke, and 2.2-fold for all-cause mortality. Also, genetic studies using the Mendelian randomization design, an approach that minimizes problems with confounding and reverse causation, now demonstrate that triglyceride-rich lipoproteins are causally associated with ASCVD and all-cause mortality. Finally, genetic evidence also demonstrates that high concentrations of triglyceride-rich lipoproteins are causally associated with low-grade inflammation. This suggests that an important part of inflammation in atherosclerosis and ASCVD is because of triglyceride-rich lipoprotein degradation and uptake into macrophage foam cells in the arterial intima. Taken together, new insights now strongly suggest that elevated triglyceride-rich lipoproteins represent causal risk factors for low-grade inflammation, ASCVD, and all-cause mortality.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Triglyceride-rich lipoproteins are thought to be at least as atherogenic as LDL cholesterol on a per-particle basis.
“triglyceride-rich lipoproteins are thought to be at least as atherogenic as LDL cholesterol on a perparticle basis. 19,21”
From Targeting <i>APOC3</i> with Olezarsen in Moderate Hypertriglyceridemia (2025) · cites this paper as [21]
The Biology section says medium-sized triglyceride-rich lipoproteins can enter the arterial intima and may be trapped there preferentially to LDL, supporting their atherogenic potential. It does not establish that they are at least as atherogenic as LDL on a per-particle basis; the same section notes that very large chylomicrons cannot enter the intima. (LLM, conf=0.84)
Experimental — accuracy not yet measuredTG reduction lowers several inflammatory markers associated with CV risk.
“Furthermore, TG reduction lowers several inflammatory markers associated with CV risk, and subgroup and post hoc analyses of outcome studies suggest possible reductions in major CV events with TG‐lowering therapy.3, 4, 5, 6, 7, 8, 9, 10, 11”
From Rationale and design of <scp>REDUCE‐IT</scp> : Reduction of Cardiovascular Events with Icosapent Ethyl–Intervention Trial (2017) · cites this paper as [3]
The Biology section reports a causal association between higher triglyceride-rich lipoproteins and low-grade inflammation, measured by C-reactive protein. It does not report reductions in several inflammatory markers following TG-lowering therapy; the Conclusion and Perspectives section says intervention-trial evidence for reduced inflammation is still needed. No page number is available in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredElevated levels of triglyceride-rich lipoproteins and remnant lipoproteins contribute directly to atherosclerosis by promoting endothelial dysfunction, inflammation, and foam cell formation.
“Elevated levels of TRLs and remnant lipoproteins contribute directly to atherosclerosis by promoting endothelial dysfunction, inflammation, and foam cell formation [8, 9].”
From Targeting Triglycerides in Cardiovascular Disease Prevention: Evidence, Mechanisms, and Emerging Therapies (2026) · cites this paper as [8]
The Biology section describes triglyceride-rich lipoproteins entering the arterial intima, likely generating local inflammation, and being taken up by macrophages to form foam cells. It cautions that evidence for the proposed intimal inflammation mechanism in humans is not strong. Our copy does not establish endothelial dysfunction as a mechanism; crossing the endothelial barrier is not the same claim. (LLM, conf=0.87)
Experimental — accuracy not yet measuredCholesterol-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.
“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].”
From Quantifying atherogenic lipoproteins for lipid-lowering strategies: Consensus-based recommendations from EAS and EFLM (2020) · cites this paper as [17]
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)
Experimental — accuracy not yet measuredTRL remnants range in diameter from approximately 30 to 80 nm, enabling passage across the endothelial barrier, unlike large chylomicrons whose size often exceeds 1000 nm.
“Unlike large chylomicrons, whose size often exceeds 1000 nm and restricts transendothelial passage, triglyceride-rich lipoprotein remnants, including chylomicron remnants, VLDL remnants, and IDL, range in diameter from approximately 30 to 80 nm, enabling passage across the endothelial barrier [16].”
From Targeting triglycerides for cardiovascular risk reduction (2026) · cites this paper as [16]
The Biology section (page unavailable) says large chylomicrons are too large to cross the endothelial barrier, while medium-sized triglyceride-rich lipoproteins can enter the arterial intima. The copy identifies VLDL, IDL, and chylomicron remnants as relevant lipoproteins, but does not give the claimed 30–80 nm remnant range or say chylomicrons often exceed 1000 nm. (LLM, conf=0.88)
Experimental — accuracy not yet measured
Atherogenicity of TRLs largely depends on the structural and functional properties of their remnant particles, which are smaller and enriched in cholesterol relative to parental TRLs.
“Atherogenicity of TRLs largely depends on the structural and functional properties of their remnant particles, which are smaller and enriched in cholesterol relative to their parental TRLs.”
From Targeting triglycerides for cardiovascular risk reduction (2026) · cites this paper as [16]
The Biology section links atherogenicity to particle size: very large chylomicrons cannot enter the arterial intima, whereas medium-sized triglyceride-rich lipoproteins can. The Copenhagen General Population Study section describes remnant cholesterol as a causal ASCVD risk factor. Our copy does not explicitly say that remnants are cholesterol-enriched relative to their parent particles or that TRL atherogenicity largely depends on those remnants’ structural and functional properties. (LLM, conf=0.83)
Experimental — accuracy not yet measuredIn familial chylomicronemia syndrome, standard lipid-lowering therapies such as fibrates and omega-3 fatty acids are largely ineffective, and statins often fail to achieve adequate triglyceride reduction.
“The absence of LPL activity renders standard lipid-lowering therapies—such as fibrates and omega-3 fatty acids—largely ineffective. Similarly, statins often fail to achieve adequate TG reduction in these patients.”
From The Efficacy and Safety of Plozasiran on Lipid Profile in Dyslipidemic Disorders: A Systematic Review and Meta-Analysis (2026) · cites this paper as [7]
The Biology section (page not provided) says chylomicronemia caused by lipoprotein lipase deficiency involves no triglyceride degradation in plasma, supporting the sentence’s premise. It does not say that fibrates or omega-3 fatty acids are ineffective in these patients, or that statins fail to reduce their triglycerides adequately. The Randomized Trials section discusses these drugs in other populations, not their efficacy in familial chylomicronemia. (LLM, conf=0.83)
Experimental — accuracy not yet measuredAll forms of dyslipidemia significantly increase the risk of atherosclerotic cardiovascular disease and all-cause mortality, primarily due to elevated LDL-C, triglycerides, triglyceride-rich lipoproteins, and their remnants.
“All forms of dyslipidemia significantly increase the risk of atherosclerotic cardiovascular disease (ASCVD) and all-cause mortality, primarily due to elevated LDL-C levels, triglycerides (TGs), triglyceride-rich lipoproteins (TRLs), and their remnants [7].”
From The Efficacy and Safety of Plozasiran on Lipid Profile in Dyslipidemic Disorders: A Systematic Review and Meta-Analysis (2026) · cites this paper as [7]
The Abstract reports that triglyceride-rich lipoproteins predict ASCVD and all-cause mortality, and that remnant cholesterol predicts ASCVD. But the paper does not support the claim about *all* forms of dyslipidemia: its Abstract says low HDL cholesterol is unlikely to cause ASCVD, and its Biology section describes severe hypertriglyceridemia without increased atherosclerosis. It also distinguishes LDL-related cholesterol from triglycerides in its discussion of all-cause mortality. (LLM, conf=0.88)
Experimental — accuracy not yet measuredTriglyceride elevation is an independent risk factor for cardiovascular events.
“Clinical and epidemiological studies have demonstrated that triglyceride (TG) elevation is an independent risk factor for increased cardiovascular (CV) events”
From Rationale and design of <scp>REDUCE‐IT</scp> : Reduction of Cardiovascular Events with Icosapent Ethyl–Intervention Trial (2017) · cites this paper as [3]
Residual cardiovascular risk persists despite statin therapy.
“despite potent therapies for lowering low‐density lipoprotein cholesterol (LDL‐C), substantial residual risk remains.1, 2, 3”
From Rationale and design of <scp>REDUCE‐IT</scp> : Reduction of Cardiovascular Events with Icosapent Ethyl–Intervention Trial (2017) · cites this paper as [3]
Mendelian randomization studies support a causal role for triglycerides in the pathogenesis of cardiovascular disease.
“More recently, elegant Mendelian randomization studies have supported a causal role for TG in the pathogenesis of cardiovascular disease (CVD), showing that elevated TG are not merely a risk marker, but rather a risk factor and thus potentially modifiable.3”
From Rationale and design of <scp>REDUCE‐IT</scp> : Reduction of Cardiovascular Events with Icosapent Ethyl–Intervention Trial (2017) · cites this paper as [3]
Subgroup and post hoc analyses of outcome studies suggest possible reductions in major CV events with TG-lowering therapy.
“Furthermore, TG reduction lowers several inflammatory markers associated with CV risk, and subgroup and post hoc analyses of outcome studies suggest possible reductions in major CV events with TG‐lowering therapy.3, 4, 5, 6, 7, 8, 9, 10, 11”
From Rationale and design of <scp>REDUCE‐IT</scp> : Reduction of Cardiovascular Events with Icosapent Ethyl–Intervention Trial (2017) · cites this paper as [3]
Epidemiological, biological, and genetic studies have provided robust evidence of a strong association between elevated TG levels and higher rates of CV events.
“Epidemiological, biological, and genetic studies have provided robust evidence of a strong association between elevated TG levels and higher rates of CV events.1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11”
From Rationale and design of <scp>REDUCE‐IT</scp> : Reduction of Cardiovascular Events with Icosapent Ethyl–Intervention Trial (2017) · cites this paper as [3]
Randomized data from large outcome studies across broad populations regarding pharmacological TG lowering and effect on CV outcomes have been mixed.
“However, randomized data from large outcome studies across broad populations regarding pharmacological TG lowering and effect on CV outcomes have been mixed (Table 4).1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24”
From Rationale and design of <scp>REDUCE‐IT</scp> : Reduction of Cardiovascular Events with Icosapent Ethyl–Intervention Trial (2017) · cites this paper as [3]
Remnant lipoproteins are causal contributors to atherogenesis.
“Genetic studies and epidemiologic data increasingly implicate remnant lipoproteins as causal contributors to atherogenesis, providing a strong mechanistic and clinical rationale for targeted intervention [8–12].”
From Targeting Triglycerides in Cardiovascular Disease Prevention: Evidence, Mechanisms, and Emerging Therapies (2026) · cites this paper as [8]
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.
“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].”
From Quantifying atherogenic lipoproteins for lipid-lowering strategies: Consensus-based recommendations from EAS and EFLM (2020) · cites this paper as [17]
Hypertriglyceridemic samples with TG >2 mmol/L are seen in ~25% of individuals in the general population.
“hypertriglyceridemic samples -TG > 2 mmol/L seen in ~25% of individuals in the general population (Tables 23) [17]”
From Quantifying atherogenic lipoproteins for lipid-lowering strategies: Consensus-based recommendations from EAS and EFLM (2020) · cites this paper as [17]
Non-HDLC provides a more comprehensive risk assessment than LDLC in certain individuals with hypertriglyceridemia because it adds RemnantC to LDLC and, therefore, takes into account the atherogenic potential of remnant lipoproteins.
“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].”
From Quantifying atherogenic lipoproteins for lipid-lowering strategies: Consensus-based recommendations from EAS and EFLM (2020) · cites this paper as [17]
A TG concentration above 10 mmol/L in nonfasting blood samples is only seen in ~0.1% of individuals in the general population.
“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].”
From Quantifying atherogenic lipoproteins for lipid-lowering strategies: Consensus-based recommendations from EAS and EFLM (2020) · cites this paper as [17]
Triglyceride-rich lipoproteins are atherogenic and causally associated with cardiovascular disease.
“As triglyceride-rich lipoproteins are atherogenic and causally associated with cardiovascular disease,44,45”
The findings of high apoE levels and high cardiovascular mortality may be mediated by triglyceride-rich lipoproteins via remnant cholesterol content.
“our findings of high apoE levels and high cardiovascular mortality may be mediated by triglyceride-rich lipoproteins via remnant cholesterol content”
A concentration of nonfasting TG ≥4.5 mmol/L is seen in ~3-5% of nonfasting individuals in the general population.
“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]”
From Quantifying atherogenic lipoproteins for lipid-lowering strategies: Consensus-based recommendations from EAS and EFLM (2020) · cites this paper as [17]
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)
Experimental — accuracy not yet measuredCurrently available therapies are not effective enough to reach guideline-recommended therapeutic goals in acquired severe hypertriglyceridemia.
“Moreover, currently available therapies haven’t been effective enough to reach guideline-recommended therapeutic goals in acquired severe hypertriglyceridemia [5, 7, 8].”
From The Efficacy and Safety of Plozasiran on Lipid Profile in Dyslipidemic Disorders: A Systematic Review and Meta-Analysis (2026) · cites this paper as [7]
The Abstract (page unavailable) says guidelines recommend lowering severely elevated triglycerides to reduce pancreatitis risk. It does not say whether available therapies achieve those goals, and searches for acquired severe hypertriglyceridemia and treatment targets found no passage addressing their effectiveness. (LLM, conf=0.74)
Experimental — accuracy not yet measuredRecent advances in human genetics, epidemiologic, preclinical, and clinical trial results provide strong support for a causal association between triglycerides, triglyceride-rich lipoproteins, and triglyceride-rich lipoprotein remnants and increased risk of myocardial infarction, ischaemic stroke, and aortic valve stenosis.
“Recent advances in human genetics, together with a large body of epidemiologic, preclinical, and clinical trial results, provide strong support for a causal association between triglycerides (TG), TG-rich lipoproteins (TRL), and TRL remnants, and increased risk of myocardial infarction, ischaemic stroke, and aortic valve stenosis.”
Over the past three decades, epidemiologic and genetic evidence supports that elevated plasma levels of triglycerides, triglyceride-rich lipoproteins, and triglyceride-rich lipoprotein remnants are causally related to increased risk of atherosclerotic cardiovascular disease-related events, including myocardial infarction, stroke, and aortic valve stenosis, and all-cause mortality.
“Over the past three decades, epidemiologic and genetic evidence has accumulated to support the concept that elevated levels of plasma TG, TRL, and TRL remnants are causally related to an increased risk of ASCVD-related events—myocardial infarction (MI), stroke, and aortic valve stenosis—and all-cause mortality.1,2,17,19,20,24–28”
The increase in absolute risk is greatest for myocardial infarction, approximately four-fold at triglyceride levels above 5 mmol/L versus below 1 mmol/L, and less for ischaemic stroke and aortic stenosis.
“The increase in absolute risk is greatest for MI (approximately four-fold at TG levels >5 mmol/L or >440 mg/dL vs. <1 mmol/L or <88 mg/dL), and less for ischaemic stroke and aortic stenosis (Figure 3).11,17,27,28”
Hepatic clearance of VLDL remnants is mediated by either apoB100 or apoE through receptor-dependent and receptor-independent pathways; 25-75% of these particles are removed directly rather than converted to LDL.
“Hepatic clearance of VLDL remnants is mediated by either apoB100 or apoE through receptor-dependent and receptor-independent pathways;7,17,71,73 25–75% of these particles are removed directly rather than converted to LDL.”
Plasma triglyceride levels range from 0.33 to 120 mmol/L, reflecting variability in the rates of secretion and clearance of triglyceride and apoB in VLDL and chylomicrons.
“Plasma TG levels range from 0.33 to 120 mmol/L (30 to 10 000 mg/dL)13,17 (Figure 6), reflecting variability in the rates of secretion and clearance of TG and apoB in VLDL and chylomicrons.61,77”
The proteomes of TRL and remnant particles contain a single copy of either apoB48 or apoB100, together with other smaller apolipoproteins (CIII, CII, CI, AIV, AV, E, and traces of AI and II) and ANGPTL-3, -4, and -8.
“The proteomes of TRL and remnant particles contain a single copy of either apoB48 or apoB100, together with other, smaller apolipoproteins (CIII, CII, CI, AIV, AV, E, and traces of AI and II) and ANGPTL-3, -4, and -8.”
There is no evidence that TG directly exert atherogenic effects.
“While there is no evidence that TG directly exert atherogenic effects,17”
Any proatherogenic effects of TRL and remnants will be synergistic to those of other apoB-containing lipoproteins, particularly LDL and lipoprotein(a).
“any proatherogenic effects of TRL and remnants will be synergistic to those of other apoB-containing lipoproteins, particularly LDL and lipoprotein(a).17,25,93,104,206”
ApoE-mediated macrophage uptake of VLDL and remnants promotes an inflammatory (M1) phenotype, enhances inflammation, increases phagocytosis and foam cell formation, exerts defective efferocytotic activity, and favours fibrous cap thinning due to activation of metalloprotease expression.
“ApoE-mediated macrophage uptake of VLDL and remnants promotes an inflammatory (M1) phenotype,2,17,139 enhances inflammation, increases phagocytosis and foam cell formation, exerts defective efferocytotic activity, and favours fibrous cap thinning due to activation of metalloprotease expression140”
Particles below ∼70 nm diameter (excluding most newly secreted, non-lipolysed chylomicrons and very large VLDL) traverse the endothelium by active transcytosis and are retained in the subendothelial layer of the artery wall, contributing to lesion initiation and progression mainly by cholesterol deposition, inflammation, and prothrombotic effects.
“Particles below ∼70 nm diameter (which excludes most newly secreted, non-lipolysed chylomicrons and very large VLDL) traverse the endothelium by active transcytosis93 and are retained in the subendothelial layer of the artery wall, contributing to lesion initiation and progression mainly by mechanisms involving cholesterol deposition, inflammation, and prothrombotic effects”
Assays that specifically measure the cholesterol content of remnant particles have revealed significant associations with ASCVD.
“Assays that specifically measure the cholesterol content of remnant particles have revealed significant associations with ASCVD.17,86”
In patients with stable angina who were receiving lipid-lowering treatment, the risk for cardiovascular events after treatment using a drug-eluting stent increases by 1.14 times with every 10 U/L elevation in MDA-LDL levels.
“In patients with stable angina who were receiving lipid-lowering treatment, the risk for cardiovascular events after treatment using a drug-eluting stent has been shown to increase by 1.14 times with every 10 U/L elevation in MDALDL levels237).”
From Japan Atherosclerosis Society (JAS) guidelines for prevention of atherosclerotic cardiovascular diseases 2017 (2018) · cites this paper as [237]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Cites
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 · see citing works
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 · see citing works
European Guidelines on cardiovascular disease prevention in clinical practice (version 2012)
Authors/Task Force Members:, Perk, J., De Backer, G., Gohlke, H., Graham, I., Reiner, Ž., Verschuren, M., Albus, C., Benlian, P., Boysen, G., et al. (2012) · European Heart Journal · doi:10.1093/eurheartj/ehs092 · Cited by 8,490 · see citing works
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 · see citing works
Cholesterol Treatment Trialists' (CTT) Collaboration (2010) · The Lancet · doi:10.1016/s0140-6736(10)61350-5 · Cited by 6,550 · see citing works
Davey Smith, G., & Ebrahim, S. (2003) · International Journal of Epidemiology · doi:10.1093/ije/dyg070 · Cited by 5,882 · see citing works
Mendelian randomization: genetic anchors for causal inference in epidemiological studies
Davey Smith, G., & Hemani, G. (2014) · Human Molecular Genetics · doi:10.1093/hmg/ddu328 · Cited by 4,677 · see citing works
Mendelian randomization: Using genes as instruments for making causal inferences in epidemiology
Lawlor, D. A., Harbord, R. M., Sterne, J. A. C., Timpson, N., & Davey Smith, G. (2008) · Statistics in Medicine · doi:10.1002/sim.3034 · Cited by 4,618 · see citing works
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 · see citing works
European guidelines on cardiovascular disease prevention in clinical practice: executive summary
Graham, I., Atar, D., Borch‐Johnsen, K., Boysen, G., Burell, G. K., Cífková, R., Dallongeville, J., Backer, G. D., Ebrahim, S. B. J., Gjelsvik, B., et al. (2007) · European Heart Journal · doi:10.1093/eurheartj/ehm316 · Cited by 3,840 · see citing works
ESC/EAS Guidelines for the management of dyslipidaemias
Reiner, Ž., Catapano, A. L., De Backer, G., Graham, I., Taskinen, M.-R., Wiklund, O., Agewall, S., Alegria, E., Chapman, M. J., Durrington, P., et al. (2011) · European Heart Journal · doi:10.1093/eurheartj/ehr158 · Cited by 3,549 · see citing works
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 · see citing works
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 · see citing works
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 · see citing works
Effects of Combination Lipid Therapy in Type 2 Diabetes Mellitus
(2010) · New England Journal of Medicine · doi:10.1056/nejmoa1001282 · Cited by 2,837 · cited 1× · see citing works
“studies, and even when fibrate was used as add-on to statin treatment.(81) Although these effect sizes caused by triglyceridelowering are indeed larger than the corresponding reduction of 22% in ASCVD events and 10% in all-cause mortality per 1-mmol/L (39 mg/dL) reduction in LDL cholesterol in statin trials,(21) the s…”
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 · see citing works
Goodman, D. S. (1988) · Archives of Internal Medicine · doi:10.1001/archinte.1988.00380010040006 · Cited by 2,292 · see citing works
De Backer, G. (2003) · European Heart Journal · doi:10.1016/s0195-668x(03)00347-6 · Cited by 2,251 · see citing works
Nordestgaard, B. G., Benn, M., Schnohr, P., & Tybjærg-Hansen, A. (2007) · JAMA · doi:10.1001/jama.298.3.299 · Cited by 2,058 · see citing works
Self-citationEffects 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 · see citing works
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 · see citing works
Hokanson, J. E., & Austin, M. A. (1996) · Journal of Cardiovascular Risk · doi:10.1097/00043798-199604000-00014 · Cited by 1,706 · see citing works
Atherogenesis: a postprandial phenomenon.
Zilversmit, D. B. (1979) · Circulation · doi:10.1161/01.cir.60.3.473 · Cited by 1,701 · see citing works
Effects of extended-release niacin with laropiprant in high-risk patients
The HPS2-THRIVE Collaborative Group (2014) · New England Journal of Medicine · doi:10.1056/nejmoa1300955 · Cited by 1,668 · see citing works
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 · see citing works
Triglycerides and cardiovascular disease
Nordestgaard, B. G., & Varbo, A. (2014) · The Lancet · doi:10.1016/s0140-6736(14)61177-6 · Cited by 1,419 · see citing works
Self-citationSarwar, 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 · see citing works
Genetically Elevated Lipoprotein(a) and Increased Risk of Myocardial Infarction
Kamstrup, P. R. (2009) · JAMA · doi:10.1001/jama.2009.801 · Cited by 1,357 · cited 2× · see citing works
“Importantly, when the effect size for the causal estimate is much larger than the observational for the same increase in a lipoprotein, then this represents additional strong evidence for a causal life-long exposure, exactly as observed for high lipoprotein(a) levels and increased risk of MI.(65) For nonfasting remnan…”
InfluentialWood, D., Backer, G. D., Færgeman, O., Graham, I. D., Mancia, G., & Pyörälà, K. (1998) · Atherosclerosis · doi:10.1016/s0021-9150(98)90209-x · Cited by 1,251 · see citing works
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 · see citing works
Self-citationMendelian randomization: prospects, potentials, and limitations
Smith, G. D. (2004) · International Journal of Epidemiology · doi:10.1093/ije/dyh132 · Cited by 1,222 · see citing works
Prevention of coronary heart disease in clinical practice
Pyörälà, K., Backer, G. D., Graham, I. M., Poole-Wilson, P. A., & Wood, D. A. (1994) · European Heart Journal · doi:10.1093/oxfordjournals.eurheartj.a060388 · Cited by 1,161 · see citing works
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 · see citing works
Self-citationLoss-of-Function Mutations in <i>APOC3,</i> 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 · see citing works
Lipid Alterations and Decline in the Incidence of Coronary Heart Disease in the Helsinki Heart Study
Manninen, V. (1988) · JAMA · doi:10.1001/jama.1988.03410050061031 · Cited by 954 · see citing works
Loss-of-Function Mutations in <i>APOC3</i> 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 · see citing works
Self-citationEvaluation 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 · see citing works
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 · see citing works
The discovery and development of HMG-CoA reductase inhibitors.
Endo, A. (1992) · Journal of Lipid Research · doi:10.1016/s0022-2275(20)41379-3 · Cited by 847 · see citing works
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 · see citing works
European guidelines on cardiovascular disease prevention in clinical practice: Executive summary
Graham, I. M. (2007) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2007.08.024 · Cited by 715 · see citing works
Varbo, A., Benn, M., Tybjærg-Hansen, A., & Nordestgaard, B. G. (2013) · Circulation · doi:10.1161/circulationaha.113.003008 · Cited by 692 · see citing works
Self-citationPollin, 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 · see citing works
Carlson, L. A., & Rosenhamer, G. (1988) · Acta Medica Scandinavica · doi:10.1111/j.0954-6820.1988.tb15891.x · Cited by 685 · see citing works
The LDL–receptor–related protein, LRP, is an apolipoprotein E-binding protein
Beisiegel†, U., Weber, W. T., Ihrke, G., Herz, J., & Stanley, K. K. (1989) · Nature · doi:10.1038/341162a0 · Cited by 680 · see citing works
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 · see citing works
Self-citationMiller, 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 · see citing works
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 · see citing works
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 548 · see citing works
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 · see citing works
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 · see citing works
Self-citationLipids, apolipoproteins, and their ratios in relation to cardiovascular events with statin treatment
Kastelein, J. J. P., van der Steeg, W. A., Holme, I., Gaffney, M., Cater, N. B., Barter, P., Deedwania, P., Olsson, A. G., Boekholdt, S. M., Demicco, D. A., et al. (2008) · Circulation · doi:10.1161/circulationaha.107.713438 · Cited by 478 · see citing works
Wittrup, H. H., Tybjærg-Hansen, A., & Nordestgaard, B. G. (1999) · Circulation · doi:10.1161/01.cir.99.22.2901 · Cited by 344 · see citing works
Self-citationNordestgaard, B. G., Wootton, R., & Lewis, B. (1995) · Arteriosclerosis, Thrombosis, and Vascular Biology · doi:10.1161/01.atv.15.4.534 · Cited by 334 · see citing works
Self-citationPyörälä, K., DeBacker, G., Graham, I. D., Poole-Wilson, P. A., & Wood, D. A. (1994) · Atherosclerosis · doi:10.1016/0021-9150(94)90200-3 · Cited by 327 · see citing works
Timpson, N. J., Nordestgaard, B. G., Harbord, R. M., Zacho, J., Frayling, T. M., Tybjærg-Hansen, A., & Davey Smith, G. (2011) · International Journal of Obesity · doi:10.1038/ijo.2010.137 · Cited by 310 · see citing works
Self-citationHaase, C. L., Tybjærg-Hansen, A., Ali Qayyum, A., Schou, J., Nordestgaard, B. G., & Frikke-Schmidt, R. (2012) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2011-1846 · Cited by 282 · see citing works
Self-citationNordestgaard, B. G., Palmer, T., Benn, M., Zacho, J., Tybjærg‐Hansen, A., Smith, G. D., & Timpson, N. J. (2012) · PLoS Medicine · doi:10.1371/journal.pmed.1001212 · Cited by 280 · see citing works
Self-citationSevere hypertriglyceridemia and pancreatitis: presentation and management
Ewald, N., Hardt, P. D., & Kloer, H.-U. (2009) · Current Opinion in Lipidology · doi:10.1097/mol.0b013e3283319a1d · Cited by 273 · see citing works
Schwartz, G. G., Abt, M., Bao, W., DeMicco, D., Kallend, D., Miller, M., Mundl, H., & Olsson, A. G. (2015) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2015.03.544 · Cited by 272 · see citing works
Agerholm-Larsen, B., Nordestgaard, B. G., Steffensen, R., Jensen, G., & Tybjærg‐Hansen, A. (2000) · Circulation · doi:10.1161/01.cir.101.16.1907 · Cited by 267 · see citing works
Self-citationZilversmit, D. B. (1995) · Clinical Chemistry · doi:10.1093/clinchem/41.1.153 · Cited by 262 · see citing works
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 · see citing works
Varbo, A., Benn, M., & Nordestgaard, B. G. (2014) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2013.11.008 · Cited by 251 · see citing works
Self-citationTHE EFFECT OF ALLOXAN DIABETES ON EXPERIMENTAL CHOLESTEROL ATHEROSCLEROSIS IN THE RABBIT
Duff, G. L., & McMillan, G. C. (1949) · The Journal of Experimental Medicine · doi:10.1084/jem.89.6.611 · Cited by 248 · see citing works
Macrophage lipoprotein lipase promotes foam cell formation and atherosclerosis in vivo
Babaev, V. R., Fazio, S., Gleaves, L. A., Carter, K. J., Semenkovich, C. F., & Linton, M. F. (1999) · Journal of Clinical Investigation · doi:10.1172/jci6117 · Cited by 241 · see citing works
STUDY GROUP, E. A. S. (1987) · European Heart Journal · doi:10.1093/oxfordjournals.eurheartj.a062165 · Cited by 231 · see citing works
Langsted, A., Freiberg, J., Tybjærg‐Hansen, A., Schnohr, P., Jensen, G. B., & Nordestgaard, B. G. (2010) · Journal of Internal Medicine · doi:10.1111/j.1365-2796.2010.02333.x · Cited by 230 · see citing works
Self-citation(2001) · Medical Entomology and Zoology · Cited by 227 · see citing works
Triglycerides and Heart Disease
Goldberg, I. J., Eckel, R. H., & McPherson, R. (2011) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.111.226100 · Cited by 219 · see citing works
The recognition and management of hyperlipidaemia in adults: A policy statement of the European
STUDY GROUP, E. A. S. (1988) · European Heart Journal · doi:10.1093/oxfordjournals.eurheartj.a062547 · Cited by 213 · see citing works
Mendelian randomization studies in coronary artery disease
Jansen, H., Samani, N. J., & Schunkert, H. (2014) · European Heart Journal · doi:10.1093/eurheartj/ehu208 · Cited by 210 · see citing works
Varbo, A., Freiberg, J. J., & Nordestgaard, B. G. (2015) · Clinical Chemistry · doi:10.1373/clinchem.2014.234146 · Cited by 209 · see citing works
Self-citationShaikh, M., Wootton, R., Nordestgaard, B. G., Baskerville, P., Lumley, J. S., La Ville, A. E., Quiney, J., & Lewis, B. (1991) · Arteriosclerosis and Thrombosis: A Journal of Vascular Biology · doi:10.1161/01.atv.11.3.569 · Cited by 206 · see citing works
Self-citationO’Brien, K. D., Gordon, D., Deeb, S. S., Ferguson, M. S., & Chait, A. (1992) · Journal of Clinical Investigation · doi:10.1172/jci115747 · Cited by 203 · see citing works
Arterial retention of apolipoprotein B48- and B100-containing lipoproteins in atherogenesis
Proctor, S. D., Vine, D. F., & Mamo, J. C. L. (2002) · Current Opinion in Lipidology · doi:10.1097/00041433-200210000-00001 · Cited by 200 · see citing works
Ylä‐Herttuala, S., Lipton, B. A., Rosenfeld, M. E., Goldberg, I. J., Steinberg, D. H., & Witztum, J. L. (1991) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.88.22.10143 · Cited by 196 · see citing works
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 188 · see citing works
Stender, S., & Zilversmit, D. B. (1981) · Arteriosclerosis An Official Journal of the American Heart Association Inc · doi:10.1161/01.atv.1.1.38 · Cited by 183 · see citing works
Postprandial hypertriglyceridemia as a coronary risk factor
Borén, J., Matikainen, N., Adiels, M., & Taskinen, M.-R. (2014) · Clinica Chimica Acta · doi:10.1016/j.cca.2014.01.015 · Cited by 182 · see citing works
Takahashi, S., Sakai, J., Fujino, T., Hattori, H., Zenimaru, Y., Suzuki, J., Miyamori, I., & Yamamoto, T. T. (2004) · Journal of Atherosclerosis and Thrombosis · doi:10.5551/jat.11.200 · Cited by 177 · see citing works
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 · see citing works
Self-citationVarbo, A., Benn, M., Smith, G. D., Timpson, N. J., Tybjærg‐Hansen, A., & Nordestgaard, B. G. (2014) · Circulation Research · doi:10.1161/circresaha.116.304846 · Cited by 171 · see citing works
Self-citationNordestgaard, B. G., Tybjaerg-Hansen, A., & Lewis, B. (1992) · Arteriosclerosis and Thrombosis: A Journal of Vascular Biology · doi:10.1161/01.atv.12.1.6 · Cited by 159 · see citing works
Self-citationGenetic Inhibition of CETP, Ischemic Vascular Disease and Mortality, and Possible Adverse Effects
Johannsen, T. H., Frikke-Schmidt, R., Schou, J., Nordestgaard, B. G., & Tybjærg-Hansen, A. (2012) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2012.07.045 · Cited by 156 · see citing works
Self-citationLarge 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 · see citing works
Self-citationFaergeman, 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 · see citing works
Backer, G. D., Ambrosio, G., Borch‐Johnsen, K., Brotons, C., Cífková, R., Dallongeville, J., Ebrahim, S. B. J., Færgeman, O., Graham, I. D., Mancia, G., et al. (2003) · PubMed · doi:10.1097/01.hjr.0000087913.96265.e2 · Cited by 151 · see citing works
Babaev, V. R., Patel, M., Semenkovich, C. F., Fazio, S., & Linton, M. F. (2000) · Journal of Biological Chemistry · doi:10.1074/jbc.m002423200 · Cited by 150 · see citing works
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 · see citing works
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 · see citing works
Self-citationNordestgaard, 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 · see citing works
Self-citationAgerholm-Larsen, B., Tybjærg‐Hansen, A., Schnohr, P., Steffensen, R., & Nordestgaard, B. G. (2000) · Circulation · doi:10.1161/01.cir.102.18.2197 · Cited by 130 · see citing works
Self-citationAndersen, R. V., Wittrup, H. H., Tybjærg‐Hansen, A., Steffensen, R., Schnohr, P., & Nordestgaard, B. G. (2003) · Journal of the American College of Cardiology · doi:10.1016/s0735-1097(03)00407-8 · Cited by 127 · see citing works
Self-citationAtherosclerosis and arterial influx of lipoproteins
Nordestgaard, B. G., & Nielsen, L. B. (1994) · Current Opinion in Lipidology · doi:10.1097/00041433-199408000-00002 · Cited by 126 · see citing works
Self-citationGeorge Lyman Duff memorial lecture. Persistent problems in the pathogenesis of atherosclerosis.
McGill, H. C. (1984) · Arteriosclerosis An Official Journal of the American Heart Association Inc · doi:10.1161/01.atv.4.5.443 · Cited by 116 · see citing works
Nonfasting Hyperlipidemia and Cardiovascular Disease
Nordestgaard, B. G., Langsted, A., & Freiberg, J. (2009) · Current Drug Targets · doi:10.2174/138945009787846434 · Cited by 115 · see citing works
Self-citationWittrup, H. H., Tybjærg‐Hansen, A., Abildgaard, S., Steffensen, R., Schnohr, P., & Nordestgaard, B. G. (1997) · Journal of Clinical Investigation · doi:10.1172/jci119323 · Cited by 114 · see citing works
Self-citationA macrophage receptor for apolipoprotein B48: Cloning, expression, and atherosclerosis
Brown, M. L., Ramprasad, M. P., Umeda, P. K., Tanaka, A., Kobayashi, Y., Watanabe, T., Shimoyamada, H., Kuo, W.-L., Li, R., Song, R., et al. (2000) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.120184097 · Cited by 109 · see citing works
Direct Visualization of Lipid Deposition and Reverse Lipid Transport in a Perfused Artery
Rutledge, J., Mullick, A. E., Gardner, G., & Goldberg, I. J. (2000) · Circulation Research · doi:10.1161/01.res.86.7.768 · Cited by 91 · see citing works
Wilson, K. M., Fry, G. L., Chappell, D. A., Sigmund, C. D., & Medh, J. D. (2001) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/hq1101.097805 · Cited by 87 · see citing works
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 · see citing works
Nordestgaard, B. G., & Zilversmit, D. B. (1989) · Arteriosclerosis An Official Journal of the American Heart Association Inc · doi:10.1161/01.atv.9.2.176 · Cited by 84 · see citing works
Self-citationTybjærg‐Hansen, A., Nordestgaard, B. G., Gerdes, L. U., Færgeman, O., & Humphries, S. E. (1993) · Atherosclerosis · doi:10.1016/0021-9150(93)90202-6 · Cited by 80 · see citing works
Self-citationFrikke-Schmidt, R., Tybjærg-Hansen, A., Steffensen, R., Jensen, G., & Nordestgaard, B. G. (2000) · Journal of the American College of Cardiology · doi:10.1016/s0735-1097(00)00520-9 · Cited by 77 · see citing works
Self-citationBatt, K. V., Avella, M., Moore, E. H., Jackson, B., Suckling, K. E., & Botham, K. M. (2004) · Experimental Biology and Medicine · doi:10.1177/153537020422900611 · Cited by 75 · see citing works
The vascular endothelial barrier — selective retention of lipoproteins
Nordestgaard, B. G. (1996) · Current Opinion in Lipidology · doi:10.1097/00041433-199610000-00002 · Cited by 74 · see citing works
Self-citationMacrophage-derived lipoprotein lipase increases aortic atherosclerosis in cholesterol-fed Tg rabbits
Ichikawa, T., Liang, J., Kitajima, S., et al. (2004) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2004.10.044 · Cited by 70 · see citing works
Guardamagna, O., Abello, F., Saracco, P., et al. (2009) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2009.06.006 · Cited by 68 · see citing works
The Influence of Alloxan Diabetes on Cholesterol Atheromatosis in the Rabbit.
McGill, H. C., & Holman, R. L. (1949) · Experimental Biology and Medicine · doi:10.3181/00379727-72-17335 · Cited by 60 · see citing works
Charakida, M., Tousoulis, D., Skoumas, I., Pitsavos, C., Vasiliadou, C., Stefanadi, E., Antoniades, C. A., Latsios, G., Siasos, G., & Stefanadis, C. (2008) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2008.09.025 · Cited by 56 · see citing works
Lipids and the Endothelium: Bidirectional Interactions
Goldberg, I. J., & Bornfeldt, K. (2013) · Current Atherosclerosis Reports · doi:10.1007/s11883-013-0365-1 · Cited by 55 · see citing works
Würtz, P., Kangas, A. J., Soininen, P., Lehtimäki, T. J., Kähönen, M. A. P., Viikari, J. S. A., Raitakari, O. T., Järvelin, M., Smith, G. D., & Ala‐Korpela, M. (2013) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2013.07.085 · Cited by 53 · see citing works
Narverud, I., Ueland, T., Nenseter, M. S., et al. (2010) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2010.10.002 · Cited by 48 · see citing works
Nielsen, L. B., Stender, S., Jauhiainen, M., & Nordestgaard, B. G. (1996) · Journal of Clinical Investigation · doi:10.1172/jci118824 · Cited by 48 · see citing works
Self-citationDifferent efflux pathways for high and low density lipoproteins from porcine aortic intima.
Nordestgaard, B. G., Hjelms, E., Stender, S., & Kjeldsen, K. (1990) · Arteriosclerosis An Official Journal of the American Heart Association Inc · doi:10.1161/01.atv.10.3.477 · Cited by 48 · see citing works
Self-citationAPOC3, 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 · see citing works
Increased inflammatory markers in children with familial hypercholesterolaemia
Ueland, T., Vissers, M. N., Wiegman, A., Rodenburg, J., Hutten, B. A., Gullestad, L. L., Ose, L., Rifai, N., Ridker, P. M., Kastelein, J. J. P., et al. (2006) · European Journal of Clinical Investigation · doi:10.1111/j.1365-2362.2006.01613.x · Cited by 45 · see citing works
Real, J. T., Martínez‐Hervás, S., García-García, A.-B., Civera, M., Pallardó, F. V., Ascaso, J. F., Vinã, J. R., Chaves, F. J., & Carmena, R. (2009) · European Journal of Clinical Investigation · doi:10.1111/j.1365-2362.2009.02218.x · Cited by 42 · see citing works
Grundy, S. M., Gotto, A. M., & Bierman, E. L. (1984) · PubMed · Cited by 39 · see citing works
Skarlatos, S. I., Dichek, H. L., Fojo, S. S., et al. (1993) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem.76.3.8383147 · Cited by 33 · see citing works
Species differences of macrophage very low-density-lipoprotein (VLDL) receptor protein expression
Takahashi, S., Ito, T., Zenimaru, Y., Suzuki, J., Miyamori, I., Takahashi, M., Takahashi, M., Ishida, T., Ishida, T., Hirata, K., et al. (2011) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2011.03.069 · Cited by 28 · see citing works
Stender, S., & Hjelms, E. (1984) · Journal of Clinical Investigation · doi:10.1172/jci111606 · Cited by 27 · see citing works
Hovland, A., Aagnes, I., Brekke, O., et al. (2010) · Journal of clinical lipidology · doi:10.1016/j.jacl.2010.02.011 · Cited by 19 · see citing works
Panz, V. R., Immelman, A., Paiker, J. E., Pilcher, G. J., & Raal, F. J. (2012) · Metabolic Syndrome and Related Disorders · doi:10.1089/met.2012.0063 · Cited by 16 · see citing works
Ye, Z.-X., Cheng, H.-M., Chiou, K.-R., et al. (2008) · The American Journal of Cardiology · doi:10.1016/j.amjcard.2008.03.039 · Cited by 13 · see citing works
Pancreatitis in Hyperlipemic Mink ( Mustela vison )
Nordstoga, K., Sørby, R., Olivecrona, G., Smith, A. J., & Christophersen, B. O. (2011) · Veterinary Pathology · doi:10.1177/0300985811417248 · Cited by 13 · see citing works
Barbero (2014) · doi:10.1016/j · Cited by 1 · see citing works
(2018) · Digital Commons@Becker (Washington University School of Medicine) · doi:10.1371/journal
Flagged first, then by citations
Research works printed but not linked: 2
- [7]7. Wood D, De Backer G, Faergeman O, Graham I, Mancia G, Pyörälä K. Prevention of coronary heart disease in clinical practice: recommenda- tions of the Second Joint Task Force of European and other Societies on Coronary Prevention. Atherosclerosis. 1998;140:199-270.
- [19]19. Goldstein JL, Hobbs HH, Brown MS. Familial hypercholesterolemia. In: Scriver CR, Beaudet AL, Sly WS, Valle D, eds. The Metabolic & Molecular Bases of Inherited Disease. 8th ed. New York: McGraw-Hill; 2001:2863-2913.
Cited by
Sorted by citations
2020 International Society of Hypertension Global Hypertension Practice Guidelines
Unger, T., Borghi, C., Charchar, F., Khan, N. A., Poulter, N. R., Prabhakaran, D., Ramirez, A., Schlaich, M., Stergiou, G. S., Tomaszewski, M., et al. (2020) · Hypertension · doi:10.1161/hypertensionaha.120.15026 · Cited by 4,132 · see citing works
Libby, P., Buring, J. E., Badimon, L., Hansson, G. K., Deanfield, J., Bittencourt, M. S., Tokgözoğlu, L., & Lewis, E. F. (2019) · Nature Reviews Disease Primers · doi:10.1038/s41572-019-0106-z · Cited by 3,211 · see citing works
Borén, J., Chapman, M. J., Krauss, R. M., Packard, C. J., Bentzon, J. F., Binder, C. J., Daemen, M. J., Demer, L. L., Hegele, R. A., Nicholls, S. J., et al. (2020) · European Heart Journal · doi:10.1093/eurheartj/ehz962 · Cited by 1,601 · see citing works
Self-citation2020 International Society of Hypertension global hypertension practice guidelines
Unger, T., Borghi, C., Charchar, F., Khan, N. A., Poulter, N. R., Prabhakaran, D., Ramirez, A., Schlaich, M., Stergiou, G. S., Tomaszewski, M., et al. (2020) · Journal of Hypertension · doi:10.1097/hjh.0000000000002453 · Cited by 1,283 · see citing works
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 · see citing works
Self-citationThe Discovery and Development of Liraglutide and Semaglutide
Knudsen, L. B., & Lau, J. (2019) · Frontiers in Endocrinology · doi:10.3389/fendo.2019.00155 · Cited by 970 · see citing works
Kinoshita, M., Yokote, K., Arai, H., Iida, M., Ishigaki, Y., Ishibashi, S., Umemoto, S., Egusa, G., Ohmura, H., Okamura, T., et al. (2018) · Journal of Atherosclerosis and Thrombosis · doi:10.5551/jat.gl2017 · Cited by 813 · see citing works
Sandesara, P. B., Virani, S. S., Fazio, S., & Shapiro, M. D. (2019) · Endocrine Reviews · doi:10.1210/er.2018-00184 · Cited by 626 · see citing works
Nordestgaard, B. G., & Langsted, A. (2016) · Journal of Lipid Research · doi:10.1194/jlr.r071233 · Cited by 575 · see citing works
Self-citationJohannesen, C. D. L., Mortensen, M. B., Langsted, A., & Nordestgaard, B. G. (2021) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2021.01.027 · Cited by 359 · see citing works
Self-citationVirani, S. S., Morris, P. B., Agarwala, A., Ballantyne, C. M., Birtcher, K. K., Kris-Etherton, P. M., Ladden-Stirling, A. B., Miller, M., Orringer, C. E., & Stone, N. J. (2021) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2021.06.011 · Cited by 341 · see citing works
Metabolism of triglyceride-rich lipoproteins in health and dyslipidaemia
Borén, J., Taskinen, M.-R., Björnson, E., & Packard, C. J. (2022) · Nature Reviews Cardiology · doi:10.1038/s41569-022-00676-y · Cited by 315 · see citing works
Gaudet, D., Karwatowska-Prokopczuk, E., Baum, S. J., Hurh, E., Kingsbury, J., Bartlett, V. J., Figueroa, A. L., Piscitelli, P., Singleton, W., Witztum, J. L., et al. (2020) · European Heart Journal · doi:10.1093/eurheartj/ehaa689 · Cited by 279 · see citing works
Nonfasting mild-to-moderate hypertriglyceridemia and risk of acute pancreatitis
Pedersen, S. B., Langsted, A., & Nordestgaard, B. G. (2016) · JAMA Internal Medicine · doi:10.1001/jamainternmed.2016.6875 · Cited by 270 · see citing works
Self-citationLanglois, M. R., Chapman, M. J., Cobbaert, C., Mora, S., Remaley, A. T., Ros, E., Watts, G. F., Borén, J., Baum, H., Bruckert, E., et al. (2018) · Clinical Chemistry · doi:10.1373/clinchem.2018.287037 · Cited by 260 · see citing works
Self-citation2026 ACC/AHA/AACVPR/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Dyslipidemia
Blumenthal, R. S., Morris, P. B., Gaudino, M., Johnson, H. M., Anderson, T. S., Bittner, V. A., Blankstein, R., Brewer, L. C., Cho, L., de Ferranti, S. D., et al. (2026) · JACC · doi:10.1016/j.jacc.2025.11.016 · Cited by 304 · see citing works
Causes and consequences of hypertriglyceridemia
Packard, C. J., Boren, J., & Taskinen, M.-R. (2020) · Frontiers in Endocrinology · doi:10.3389/fendo.2020.00252 · Cited by 239 · see citing works
Nordestgaard, B. G., Langlois, M. R., Langsted, A., Chapman, M. J., Aakre, K. M., Baum, H., Borén, J., Bruckert, E., Catapano, A., Cobbaert, C., et al. (2020) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2019.12.005 · Cited by 240 · see citing works
Self-citationA 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 · see citing works
Self-citationZodasiran, an RNAi Therapeutic Targeting ANGPTL3, for Mixed Hyperlipidemia
Rosenson, R. S., Gaudet, D., Hegele, R. A., Ballantyne, C. M., Nicholls, S. J., Lucas, K. J., San Martin, J., Zhou, R., Muhsin, M., Chang, T., et al. (2024) · New England Journal of Medicine · doi:10.1056/nejmoa2404147 · Cited by 213 · see citing works
Plozasiran, an RNA Interference Agent Targeting APOC3, for Mixed Hyperlipidemia
Ballantyne, C. M., Vasas, S., Azizad, M., Clifton, P., Rosenson, R. S., Chang, T., Melquist, S., Zhou, R., Mushin, M., Leeper, N. J., et al. (2024) · New England Journal of Medicine · doi:10.1056/nejmoa2404143 · Cited by 210 · see citing works
Association of rare and common variation in the lipoprotein lipase gene with coronary artery disease
Khera, A. V., Won, H.-H., Peloso, G. M., O’Dushlaine, C., Liu, D., Stitziel, N. O., Natarajan, P., Nomura, A., Emdin, C. A., Gupta, N., et al. (2017) · JAMA · doi:10.1001/jama.2017.0972 · Cited by 198 · see citing works
Olezarsen for Hypertriglyceridemia in Patients at High Cardiovascular Risk
Bergmark, B. A., Marston, N. A., Prohaska, T. A., Alexander, V. J., Zimerman, A., Moura, F. A., Murphy, S. A., Goodrich, E. L., Zhang, S., Gaudet, D., et al. (2024) · New England Journal of Medicine · doi:10.1056/nejmoa2402309 · Cited by 198 · see citing works
Ishibashi, S., Arai, H., Yokote, K., Araki, E., Suganami, H., & Yamashita, S. (2018) · Journal of Clinical Lipidology · doi:10.1016/j.jacl.2017.10.006 · Cited by 184 · see citing works
Bhatt, D. L., Steg, P. G., Brinton, E. A., Jacobson, T. A., Miller, M., Tardif, J., Ketchum, S. B., Doyle, R. T., Murphy, S. A., Soni, P. N., et al. (2017) · Clinical Cardiology · doi:10.1002/clc.22692 · Cited by 183 · see citing works
Björnson, E., Adiels, M., Taskinen, M.-R., Burgess, S., Rawshani, A., Borén, J., & Packard, C. J. (2023) · European Heart Journal · doi:10.1093/eurheartj/ehad337 · Cited by 183 · see citing works
Balling, M., Afzal, S., Varbo, A., Langsted, A., Davey Smith, G., & Nordestgaard, B. G. (2020) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2020.09.610 · Cited by 175 · see citing works
Self-citationRemnant cholesterol and risk of ischemic stroke in 112,512 individuals from the general population
Varbo, A., & Nordestgaard, B. G. (2019) · Annals of Neurology · doi:10.1002/ana.25432 · Cited by 145 · see citing works
Self-citationVarbo, A., & Nordestgaard, B. G. (2017) · Current Opinion in Lipidology · doi:10.1097/mol.0000000000000429 · Cited by 135 · see citing works
Self-citationVarbo, A., Freiberg, J. J., & Nordestgaard, B. G. (2018) · Clinical Chemistry · doi:10.1373/clinchem.2017.279463 · Cited by 133 · see citing works
Self-citationKaltoft, M., Langsted, A., & Nordestgaard, B. G. (2020) · European Heart Journal · doi:10.1093/eurheartj/ehaa172 · Cited by 122 · see citing works
Self-citationWriting Committee Members, Blumenthal, R. S., Morris, P. B., Gaudino, M., Johnson, H. M., Anderson, T. S., Bittner, V. A., Blankstein, R., Brewer, L. C., Cho, L., et al. (2026) · Circulation · doi:10.1161/cir.0000000000001423 · Cited by 122 · see citing works
Hansen, S. E. J., Madsen, C. M., Varbo, A., & Nordestgaard, B. G. (2019) · Clinical Chemistry · doi:10.1373/clinchem.2018.294926 · Cited by 121 · see citing works
Self-citationLawler, P. R., Kotrri, G., Koh, M., Goodman, S. G., Farkouh, M. E., Lee, D. S., Austin, P. C., Udell, J. A., & Ko, D. T. (2020) · European Heart Journal · doi:10.1093/eurheartj/ehz767 · Cited by 113 · see citing works
Zhao, Y., Zhuang, Z., Li, Y., Xiao, W., Song, Z., Huang, N., Wang, W., Dong, X., Jia, J., Clarke, R., et al. (2024) · Nature Communications · doi:10.1038/s41467-024-46686-x · Cited by 117 · see citing works
Burén, J., Ericsson, M., Damasceno, N., & Sjödin, A. (2021) · Nutrients · doi:10.3390/nu13030814 · Cited by 104 · see citing works
Orringer, C. E., Jacobson, T. A., & Maki, K. C. (2019) · Journal of Clinical Lipidology · doi:10.1016/j.jacl.2019.10.014 · Cited by 103 · see citing works
Nichols, G. A., Philip, S., Reynolds, K., Granowitz, C. B., & Fazio, S. (2018) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2018-00470 · Cited by 102 · see citing works
Remnant lipoproteins: are they equal to or more atherogenic than LDL?
Salinas, C. A. A., & Chapman, M. J. (2020) · Current Opinion in Lipidology · doi:10.1097/mol.0000000000000682 · Cited by 87 · see citing works
Doi, T., Langsted, A., & Nordestgaard, B. G. (2021) · European Heart Journal · doi:10.1093/eurheartj/ehab555 · Cited by 87 · see citing works
Self-citationVarbo, A., & Nordestgaard, B. G. (2018) · Arteriosclerosis, Thrombosis, and Vascular Biology · doi:10.1161/atvbaha.117.310269 · Cited by 83 · see citing works
Self-citationRasmussen, K. L., Tybjærg-Hansen, A., Nordestgaard, B. G., & Frikke-Schmidt, R. (2019) · European Heart Journal · doi:10.1093/eurheartj/ehz402 · Cited by 86 · see citing works
Self-citationHaider, K. S., Haider, A., Saad, F., Doros, G., Hanefeld, M., Dhindsa, S., Dandona, P., & Traish, A. (2020) · Diabetes, Obesity and Metabolism · doi:10.1111/dom.14122 · Cited by 82 · see citing works
Targeting <i>APOC3</i> with Olezarsen in Moderate Hypertriglyceridemia
Bergmark, B. A., Marston, N. A., Prohaska, T. A., Alexander, V. J., Zimerman, A., Moura, F. A., Kang, Y. M., Weinland, J., Murphy, S. A., Goodrich, E. L., et al. (2025) · New England Journal of Medicine · doi:10.1056/nejmoa2507227 · Cited by 78 · see citing works
Cardiovascular Impact of Nutritional Supplementation With Omega-3 Fatty Acids
Weinberg, R. L., Brook, R. D., Rubenfire, M., & Eagle, K. A. (2021) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2020.11.060 · Cited by 63 · see citing works
Kolovou, G. D., Watts, G. F., Mikhailidis, D. P., Pérez-Martínez, P., Mora, S., Bilianou, H., Panotopoulos, G., Katsiki, N., Ooi, T. C., Lopez-Miranda, J., et al. (2019) · Current Vascular Pharmacology · doi:10.2174/1570161117666190507110519 · Cited by 61 · see citing works
Self-citationCasula, M., Olmastroni, E., Gazzotti, M., Galimberti, F., Zambon, A., & Catapano, A. L. (2020) · Pharmacological Research · doi:10.1016/j.phrs.2020.105060 · Cited by 54 · see citing works
The burden of familial chylomicronemia syndrome: interim results from the IN-FOCUS study
Davidson, M., Stevenson, M., Hsieh, A., Ahmad, Z., Crowson, C., & Witztum, J. L. (2017) · Expert Review of Cardiovascular Therapy · doi:10.1080/14779072.2017.1311786 · Cited by 54 · see citing works
Madsen, C. M., Varbo, A., & Nordestgaard, B. G. (2018) · European Heart Journal · doi:10.1093/eurheartj/ehx659 · Cited by 47 · see citing works
Self-citationStroes, E. S. G., Susekov, A. V., de Bruin, T. W. A., Kvarnström, M., Yang, H., & Davidson, M. H. (2018) · Journal of Clinical Lipidology · doi:10.1016/j.jacl.2017.10.012 · Cited by 38 · see citing works
Apolipoprotein profiling as a personalized approach to the diagnosis and treatment of dyslipidaemia
Renee Ruhaak, L., van der Laarse, A., & Cobbaert, C. M. (2019) · Annals of Clinical Biochemistry: International Journal of Laboratory Medicine · doi:10.1177/0004563219827620 · Cited by 38 · see citing works
Lorenzatti, A. J., Monsalvo, M. L., López, J. A. G., Wang, H., & Rosenson, R. S. (2021) · Cardiovascular Diabetology · doi:10.1186/s12933-021-01287-6 · Cited by 34 · see citing works
Sea Change for Marine Omega-3s
O'Keefe, E. L., Harris, W. S., DiNicolantonio, J. J., Elagizi, A., Milani, R. V., Lavie, C. J., & O'Keefe, J. H. (2019) · Mayo Clinic Proceedings · doi:10.1016/j.mayocp.2019.04.027 · Cited by 28 · see citing works
Langlois, M. R., & Nordestgaard, B. G. (2018) · Current Cardiology Reports · doi:10.1007/s11886-018-1036-1 · Cited by 19 · see citing works
Self-citationExpanding the triglyceride range in clinical trials: therapeutic opportunities
Nordestgaard, A. T., Pradhan, A. D., Everett, B. M., MacFadyen, J. G., Bhatt, D. L., Visseren, F. L. J., Libby, P., Santos, R. D., Nissen, S. E., Nordestgaard, B. G., et al. (2025) · European Heart Journal · doi:10.1093/eurheartj/ehaf074 · Cited by 20 · see citing works
Self-citationKamrul-Hasan, A. B. M., Dutta, D., Nagendra, L., Mondal, S., Bhattacharya, S., & Kalra, S. (2024) · Endocrine Practice · doi:10.1016/j.eprac.2024.08.013 · Cited by 17 · see citing works
Dinu, M., Sofi, F., Lotti, S., Colombini, B., Mattioli, A. V., Catapano, A. L., Casula, M., Baragetti, A., Wong, N. D., Steg, P. G., et al. (2024) · European Journal of Preventive Cardiology · doi:10.1093/eurjpc/zwae184 · Cited by 17 · see citing works
Mahmoud, A., Abdelsayed, K., Mohamed, A. A., Najah, Q., Abdulkader, A., Ali, K., Tabassum, S., Abouzid, M. R., Abdelazeem, B., & Mills, J. D. (2025) · Lipids in Health and Disease · doi:10.1186/s12944-024-02389-2 · Cited by 17 · see citing works
Lessons from PROMINENT and prospects for pemafibrate
Fruchart, J.-C., Fruchart-Najib, J., Yamashita, S., Libby, P., Yokote, K., Kodama, T., Tomita, Y., Ridker, P. M., Hermans, M. P., & Zambon, A. (2024) · Cardiovascular Diabetology · doi:10.1186/s12933-024-02305-z · Cited by 16 · see citing works
Jia, Y.-P., Wang, J.-M., Lyu, J.-Q., Yang, H.-H., Miao, M.-Y., Wang, X., Wan, Z.-X., Zheng, Y., Qin, L.-Q., Li, F.-R., et al. (2024) · Journal of Lipid Research · doi:10.1016/j.jlr.2024.100653 · Cited by 10 · see citing works
Sahebkar, A., Simental-Mendía, L. E., Pirro, M., Montecucco, F., Carbone, F., Banach, M., Barreto, G. E., & Butler, A. E. (2018) · Annals of Medicine · doi:10.1080/07853890.2018.1495338 · Cited by 9 · see citing works
Sydhom, P., Al-Quraishi, B., Gohar, A., El-Shawaf, M., Shehata, N., Ataya, M., Sydhom, M., Awwad, N., Motawade, H., Naji, N., et al. (2026) · Cardiovascular Drugs and Therapy · doi:10.1007/s10557-025-07798-8 · Cited by 5 · see citing works
Alam, U., Mathai, S. V., Filtz, A., Kuno, T., Badimon, J. J., Sniderman, A. D., Virani, S. S., Toth, P. P., Shapiro, M. D., Lavie, C. J., et al. (2026) · Current Cardiology Reports · doi:10.1007/s11886-025-02337-1 · Cited by 4 · see citing works
Targeting triglycerides for cardiovascular risk reduction
Maiorca, C., Tramontano, D., Di Costanzo, A., & D’Erasmo, L. (2026) · Internal and Emergency Medicine · doi:10.1007/s11739-026-04383-1
- Authors
- Nordestgaard, B. G.
- Affiliations
- University of Copenhagen (DK)
- Corresponding author
- Nordestgaard, Børge G.
- Venue
- Circulation Research
- Published
- 2016-02-19
- Volume
- 118
- Issue
- 4
- Pages
- 547-563
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W2286999219
- Cited by
- 1,116
- References
- 131
- Citations by year
- 2026: 121 · 2025: 146 · 2024: 140 · 2023: 138 · 2022: 123 · 2021: 116 · 2020: 106 · 2019: 82 · 2018: 61 · 2017: 64 · 2016: 18
- FWCI
- 83.03
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Circulation Research (publishedVersion)
- PubMed (publishedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (publishedVersion)
- Topics
- Health Sciences › Medicine › Surgery › 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
- triglyceride-rich lipoproteins, atherosclerotic cardiovascular disease, remnant cholesterol, hypertriglyceridemia, all-cause mortality, cardiovascular risk prediction, Mendelian randomization, low-grade inflammation, foam cells, atherosclerosis, ischemic heart disease, ischemic stroke, myocardial infarction
- MeSH terms
- Animals, Hypolipidemic Agents, Humans, Lipoproteins, Cholesterol, HDL, Cholesterol, LDL, Phenotype, Primary Prevention, Prognosis, Risk Factors, Triglycerides, Hypertriglyceridemia, Biomarkers, Risk Assessment, Genetic Predisposition to Disease, 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.
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
