2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk
Open accessAbstract
The ESC/EAS Guidelines represent the views of the ESC and EAS, and were produced after careful consideration of the scientific and medical knowledge, and the evidence available at the time of their publication.The ESC and EAS is not responsible in the event of any contradiction, discrepancy, and/or ambiguity between the ESC/EAS Guidelines and any other official recommendations or guidelines issued by the relevant public health authorities, in particular in relation to good use of healthcare or therapeutic strategies.Health professionals are encouraged to take the ESC/EAS Guidelines fully into account when exercising their clinical judgment, as well as in the determination and the implementation of preventive, diagnostic, or therapeutic medical strategies; however, the ESC/EAS Guidelines do not override, in any way whatsoever, the individual responsibility of health professionals to make appropriate and accurate decisions in consideration of each patient's health condition and in consultation with that patient and, where appropriate and/or necessary, the patient's caregiver.Nor do the ESC/EAS Guidelines exempt health professionals from taking into full and careful consideration the relevant official updated recommendations or guidelines issued by the competent public health authorities, in order to manage each patient's case in light of the scientifically accepted data pursuant to their respective ethical and professional obligations.It is also the health professional's responsibility to verify the applicable rules and regulations relating to drugs and medical devices at the time of prescription.
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Hypertriglyceridemia is frequently identified in clinical practice, yet effective therapies are lacking.
“Hypertriglyceridemia is frequently identified in clinical practice, yet effective therapies are lacking. 5,17,18”
From Targeting <i>APOC3</i> with Olezarsen in Moderate Hypertriglyceridemia (2025) · cites this paper as [17]
Section 9.4.2.2 reports a significant reduction in cardiovascular events with icosapent ethyl in high-risk patients with hypertriglyceridaemia. The guidelines also recommend statins and consider other drug treatments for specified patients, contrary to the unqualified claim that effective therapies are lacking. The cited passages do not establish how frequently hypertriglyceridaemia is identified in clinical practice. (LLM, conf=0.83)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredPhysical activity guidelines recommend ≥150 min/week moderate-intensity or ≥75 min/week vigorous-intensity activity.
“Regular aerobic and resistance exercise contributes to TG lowering, with physical activity guidelines recommending ≥ 150 min per week of moderate-intensity or ≥ 75 min of vigorous-intensity activity, though any amount of exercise is beneficial with a recommended weight loss goal of 5–10% in all individuals resulting in up to ~ 20–70% reduction in TG levels [66–69].”
From Targeting Triglycerides in Cardiovascular Disease Prevention: Evidence, Mechanisms, and Emerging Therapies (2026) · cites this paper as [69]
The Physical activity recommendation (page unavailable in our copy) specifies 3.5–7 hours of moderately vigorous activity per week or 30–60 minutes on most days, rather than the claimed 150-minute moderate or 75-minute vigorous alternatives. Section 7.4.1 likewise advises more than 30 minutes of moderate exercise per day for people with dyslipidaemia. (LLM, conf=0.84)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredFor secondary prevention in hypertriglyceridemia, second-line options such as statin add-on or statin-intolerant treatments are icosapent ethyl and fenofibrate.
“For secondary prevention in hypertriglyceridemia, second-line options such as statin add-on or statin-intolerant treatments are icosapent ethyl and fenofibrate.”
From Established and Emerging Lipid-Lowering Drugs for Primary and Secondary Cardiovascular Prevention (2023) · cites this paper as [19]
The drug-treatment recommendations for hypertriglyceridaemia consider icosapent ethyl with a statin for high-risk patients whose triglycerides remain elevated, and fenofibrate with a statin for certain patients who have reached their LDL-C goal. They do not present either drug as a statin-intolerance treatment; the statin-intolerance recommendations instead discuss ezetimibe and PCSK9 inhibitors. The claim also omits the conditions attached to the hypertriglyceridaemia recommendations. Page numbers were not available in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measuredESC guidelines refer to triglyceride levels >2.3 mmol/L (>200 mg/dL) for icosapent ethyl and/or fibrates, whilst AHA/ACC/multi-society guidelines refer to triglyceride levels >5.6 mmol/L (>500 mg/dL).
“ESC guidelines refer to triglyceride levels > 2.3 mmol/L (> 200 mg/dL) for icosapent ethyl and/or fibrates, whilst AHA/ACC/multi-society guidelines refer to triglyceride levels beyond > 5.6 mmol/L (> 500 mg/dL).”
From Established and Emerging Lipid-Lowering Drugs for Primary and Secondary Cardiovascular Prevention (2023) · cites this paper as [19]
The recommendations for drug treatment of hypertriglyceridaemia (page unavailable) use >2.3 mmol/L (>200 mg/dL) for considering fenofibrate or bezafibrate with statins. They give a different range—1.5–5.6 mmol/L (135–499 mg/dL)—for considering icosapent ethyl, so >2.3 mmol/L is not its stated threshold. The cited ESC/EAS guidelines do not substantiate the sentence’s comparison with AHA/ACC/multi-society guidelines. (LLM, conf=0.90)
Experimental — accuracy not yet measuredFor secondary prevention in hypercholesterinaemia, second-line options such as statin add-on or statin-intolerant treatments are ezetimibe, alirocumab and evolocumab.
“For secondary prevention in hypercholesterinaemia, second-line options such as statin add-on or statin-intolerant treatments are ezetimibe, alirocumab and evolocumab.”
From Established and Emerging Lipid-Lowering Drugs for Primary and Secondary Cardiovascular Prevention (2023) · cites this paper as [19]
Section 8.2.3 identifies ezetimibe as second-line therapy when the statin goal is unmet or a statin cannot be prescribed; section 8.4.2 names alirocumab and evolocumab as LDL-lowering options. But the secondary-prevention recommendation (section IIb C) reserves a PCSK9 inhibitor for very-high-risk patients who remain above goal despite maximally tolerated statin and ezetimibe, rather than presenting all three drugs as equivalent second-line options. (LLM, conf=0.85)
Experimental — accuracy not yet measured
For hypercholesterinaemia, ESC and AHA/ACC/multi-society guidelines recommend risk-stratified treatment with statins, ezetimibe and PCSK9 inhibitors.
“For hypercholesterinaemia (Fig. 2), the ESC and AHA/ACC/multi-society guidelines recommend a risk-stratified treatment with statins, ezetimibe and PCSK9 inhibitors.”
From Established and Emerging Lipid-Lowering Drugs for Primary and Secondary Cardiovascular Prevention (2023) · cites this paper as [19]
The ESC/EAS guideline’s treatment algorithm (Figure 4; page not supplied) stratifies LDL-C treatment by cardiovascular risk and shows a statin followed, when needed, by ezetimibe and a PCSK9 inhibitor. The cited paper is an ESC/EAS guideline; these passages do not establish what the separate AHA/ACC/multi-society guidelines recommend. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThe recommended LDL-C level for very high-risk patients has been lowered from <70 to <55 mg/mL.
“For example, the recommended LDL-C level for very high-risk patients has been lowered from < 70 to < 55 mg/mL.”
From Established and Emerging Lipid-Lowering Drugs for Primary and Secondary Cardiovascular Prevention (2023) · cites this paper as [19]
The LDL-C treatment-goals section recommends <55 mg/dL for very-high-risk patients. It does not establish that their previous goal was <70; it lists <70 mg/dL as the current goal for high-risk patients. The citing sentence also prints mg/mL, whereas the guideline uses mg/dL. (LLM, conf=0.88)
Experimental — accuracy not yet measuredLow-/medium-intensity statins reduce LDL-C by -30% to -50% and triglycerides by -20%, whilst high-intensity statins reduce LDL-C by more than -50% and triglycerides by up to -40%.
“Low-/medium-intensity statins reduce LDL-C by − 30% to − 50% and triglycerides by − 20%, whilst high-intensity statins reduce LDL-C by more than − 50% and triglycerides by up to − 40% [19, 31].”
From Established and Emerging Lipid-Lowering Drugs for Primary and Secondary Cardiovascular Prevention (2023) · cites this paper as [19]
Section 8.1.2.1 defines moderate-intensity statins as reducing LDL-C by 30–50% and high-intensity statins as reducing it by at least 50%; it does not put low-intensity statins in the 30–50% range. Section 8.1.2.2 says statins usually reduce triglycerides by 10–20% and that more potent statins lower them more robustly at high doses, but it does not give a reduction of up to 40%. Page numbers are unavailable in our copy. (LLM, conf=0.90)
Experimental — accuracy not yet measuredPCSK9 inhibitors are recommended by both guidelines for secondary cardiovascular prevention in very high-risk patients who do not reach their LDL-C goal with maximum tolerated statin therapy and ezetimibe.
“PCSK9 inhibitors are recommended by both guidelines for secondary cardiovascular prevention in very high-risk patients who do not reach their LDL-C goal with maximum tolerated statin therapy and ezetimibe.”
From Established and Emerging Lipid-Lowering Drugs for Primary and Secondary Cardiovascular Prevention (2023) · cites this paper as [19]
The recommendation in the “I B” passage matches the stated population, LDL-C goal, and treatment conditions. This ESC/EAS guideline does not establish the claim that a second guideline makes the same recommendation. (LLM, conf=0.84)
Experimental — accuracy not yet measuredESC and AHA/ACC/multi-society guidelines recommend fibrates for patients with dyslipidaemia with elevated triglycerides despite statin treatment.
“ESC and AHA/ACC/multi-society guidelines recommend fibrates for patients with dyslipidaemia with elevated triglycerides despite statin treatment.”
From Established and Emerging Lipid-Lowering Drugs for Primary and Secondary Cardiovascular Prevention (2023) · cites this paper as [19]
The recommendations table for drug treatment of hypertriglyceridaemia (indexed under §9.1.1; page unavailable) says fenofibrate or bezafibrate may be considered with statins for patients at their LDL-C goal whose triglycerides exceed 200 mg/dL. That is a conditional ESC/EAS recommendation, not a general recommendation for everyone with elevated triglycerides despite statin treatment; this source also does not establish what the AHA/ACC/multi-society guidelines recommend. (LLM, conf=0.88)
Experimental — accuracy not yet measuredFibrates reduce concentrations of triglycerides by approximately -50% and LDL-C by -20% whilst increasing HDL-C by up to +20% depending on the fibrate class.
“Fibrates reduce concentrations of triglycerides by approximately − 50% and LDL-C by − 20% whilst increasing HDL-C by up to + 20% depending on the fibrate class [19].”
From Established and Emerging Lipid-Lowering Drugs for Primary and Secondary Cardiovascular Prevention (2023) · cites this paper as [19]
Section 8.7.2 (page unavailable) gives the same approximate magnitudes and says effects vary among fibrates. However, it describes the TG reduction as reaching 50% and the LDL-C reduction as no more than about 20%, rather than presenting those as typical reductions; it also notes that LDL-C can rise when TG levels are high and that effects depend strongly on baseline lipids. (LLM, conf=0.86)
Experimental — accuracy not yet measuredTreatment with fibrates is associated with an increased risk of gastrointestinal pain, skin rashes, myopathy and liver enzyme elevation.
“Treatment with fibrates is associated with an increased risk of gastrointestinal pain, skin rashes, myopathy and liver enzyme elevation [19].”
From Established and Emerging Lipid-Lowering Drugs for Primary and Secondary Cardiovascular Prevention (2023) · cites this paper as [19]
Section 8.7.4, “Adverse effects and interactions,” reports skin rashes, myopathy, and liver enzyme elevations with fibrate therapy. It reports gastrointestinal disturbances in fewer than 5% of patients, but does not specifically identify gastrointestinal pain. (LLM, conf=0.84)
Experimental — accuracy not yet measuredBile acid sequestrants bind to intestinal cholesterol and inhibit its absorption in the small intestine, removing it from the enterohepatic cholesterol circulation.
“Bile acid sequestrants, such as cholestyramine, colesevelam and colestipol, bind to intestinal cholesterol and thereby inhibit its absorption in the small intestine, effectively removing it from the enterohepatic cholesterol circulation [19].”
From Established and Emerging Lipid-Lowering Drugs for Primary and Secondary Cardiovascular Prevention (2023) · cites this paper as [19]
Section 8.3.1 identifies cholestyramine, colestipol and colesevelam as bile acid sequestrants and says their action prevents cholesterol reabsorption. But it says the drugs bind bile acids—not intestinal cholesterol—and remove bile acids from enterohepatic circulation, not cholesterol. (LLM, conf=0.88)
Experimental — accuracy not yet measuredMipomersen is an antisense oligonucleotide administered via a weekly subcutaneous injection that inhibits the messenger ribonucleic acid (mRNA) of ApoB-100.
“Mipomersen is an antisense oligonucleotide that is administered via a weekly subcutaneous injection, inhibiting the messenger ribonucleic acid (mRNA) of ApoB-100 [19, 162].”
From Established and Emerging Lipid-Lowering Drugs for Primary and Secondary Cardiovascular Prevention (2023) · cites this paper as [19]
Section 8.6, “Mipomersen” (page not provided), describes mipomersen as an antisense oligonucleotide injected subcutaneously that binds ApoB-100 mRNA and triggers its degradation. It does not state that the injections are weekly. (LLM, conf=0.88)
Experimental — accuracy not yet measuredExisting pharmacologic therapies such as statins, prescription-strength n-3 fatty acids, fibrates, and ezetimibe have only modest effects on triglyceride levels, with typical reductions ranging from less than 10% up to approximately 30%.
“Existing pharmacologic therapies such as statins, prescription-strength n-3 fatty acids, fibrates, and ezetimibe have only modest effects on triglyceride levels, with typical reductions ranging from less than 10% up to approximately 30%. 17”
From Targeting <i>APOC3</i> with Olezarsen in Moderate Hypertriglyceridemia (2025) · cites this paper as [17]
Sections 8.2.2 and 8.1.2.2 report triglyceride reductions of 8% with ezetimibe and usually 10–20% with statins; section 7.5.6 reports about 30% with pharmacological doses of n-3 fatty acids. But the claimed upper range understates effects reported elsewhere in the guidelines: section 8.7.2 estimates reductions reaching 50% with fibrates, and section 8.8.2 reports up to 45% with EPA in people with high triglycerides. Page numbers are unavailable in our copy. (LLM, conf=0.90)
Experimental — accuracy not yet measuredEvery 38.5 mg/dL or 1 mmol/L reduction in LDL is associated with a reduction in the risk of cardiovascular events by 21-25%.
“Every 38.5 mg/dL or 1 mmol/L reduction in LDL is associated with a reduction in the risk of cardiovascular events by 21–25% [42].”
From The Effect of Exercise Training on Blood Lipids: A Systematic Review and Meta-analysis (2025) · cites this paper as [42]
Section 8.1.3.1 reports a 22% reduction in major vascular events per 1 mmol/L reduction in LDL-C, within the claimed range. However, Figure 3 gives a general estimate of 20% for cardiovascular events, and the cited passages do not establish the full 21–25% range. (LLM, conf=0.86)
Experimental — accuracy not yet measuredRegular aerobic and resistance exercise contributes to TG lowering.
“Regular aerobic and resistance exercise contributes to TG lowering, with physical activity guidelines recommending ≥ 150 min per week of moderate-intensity or ≥ 75 min of vigorous-intensity activity, though any amount of exercise is beneficial with a recommended weight loss goal of 5–10% in all individuals resulting in up to ~ 20–70% reduction in TG levels [66–69].”
From Targeting Triglycerides in Cardiovascular Disease Prevention: Evidence, Mechanisms, and Emerging Therapies (2026) · cites this paper as [69]
Section 7.2 states that regular physical exercise reduces plasma triglycerides, and section 9.4.2.2 specifically associates aerobic exercise with lower triglycerides (page numbers unavailable). The passages do not establish that resistance exercise lowers triglycerides. (LLM, conf=0.84)
Experimental — accuracy not yet measuredA weight loss goal of 5-10% in all individuals results in up to ~20-70% reduction in TG levels.
“Regular aerobic and resistance exercise contributes to TG lowering, with physical activity guidelines recommending ≥ 150 min per week of moderate-intensity or ≥ 75 min of vigorous-intensity activity, though any amount of exercise is beneficial with a recommended weight loss goal of 5–10% in all individuals resulting in up to ~ 20–70% reduction in TG levels [66–69].”
From Targeting Triglycerides in Cardiovascular Disease Prevention: Evidence, Mechanisms, and Emerging Therapies (2026) · cites this paper as [69]
Section 7.2 (page unavailable) states that weight reduction decreases triglyceride levels, and section 9.4.2.2 describes pronounced effects on triglycerides in people with atherogenic dyslipidaemia. Neither passage specifies a 5–10% weight-loss goal, a 20–70% triglyceride reduction, or that the claim applies to all individuals. (LLM, conf=0.86)
Experimental — accuracy not yet measuredCurrent guidelines emphasize lifestyle interventions-weight loss, reduction of alcohol intake, increased physical activity, and dietary changes-as central pillars for TG (~30-70%) and ASCVD risk reduction.
“Current guidelines emphasize lifestyle interventions—such as weight loss, reduction of alcohol intake, increased physical activity and dietary changes as the central pillars for TG (~ 30–70%) and ASCVD risk reduction.”
From Targeting Triglycerides in Cardiovascular Disease Prevention: Evidence, Mechanisms, and Emerging Therapies (2026) · cites this paper as [69]
Sections 7.2 and 9.4.2.2 describe weight loss, exercise and dietary changes as ways to lower triglycerides, and section 7.2 notes that alcohol intake has a major impact on triglyceride levels. The guidelines also support a healthy lifestyle for ASCVD prevention, but the passages do not substantiate the claimed ~30–70% triglyceride reduction from these interventions. (LLM, conf=0.87)
Experimental — accuracy not yet measuredLowering LDLC to concentrations below a target of 1.8 mmol/L in patients at high cardiovascular risk or 1.4 mmol/L in patients at very high risk (or by ≥ 50% if these targets cannot be attained) is of critical importance.
“Lowering LDLC to concentrations below a target of 1.8 mmol/L in patients at high cardiovascular risk or 1.4 mmol/L in patients at very high risk (or by ≥ 50% if these targets cannot be attained) is of critical importance [4].”
From Quantifying atherogenic lipoproteins for lipid-lowering strategies: Consensus-based recommendations from EAS and EFLM (2020) · cites this paper as [4]
The treatment-goals passage recommends LDL-C below 1.8 mmol/L for high-risk patients and below 1.4 mmol/L for very-high-risk patients. It recommends a ≥50% reduction from baseline alongside each absolute goal, not only as an alternative if the goal cannot be attained. (LLM, conf=0.91)
Experimental — accuracy not yet measuredApoB may be preferred over non-HDLC, if available, in persons with mild-to-moderate hypertriglyceridemia (2-10 mmol/L), diabetes, obesity or metabolic syndrome, or very low LDLC < 1.8 mmol/L.
“ApoB is recommended for risk assessment and may be preferred over non-HDLC, if available, in persons with mild-to-moderate hypertriglyceridemia (2-10 mmol/L), diabetes, obesity or metabolic syndrome, or very low LDLC < 1.8 mmol/L [4].”
From Quantifying atherogenic lipoproteins for lipid-lowering strategies: Consensus-based recommendations from EAS and EFLM (2020) · cites this paper as [4]
The “Changes in recommendations” section recommends ApoB for risk assessment in people with high triglycerides, diabetes, obesity or metabolic syndrome, or very low LDL-C, and says it may be preferred over non-HDL-C in several of those groups. It does not give the claimed triglyceride range of 2–10 mmol/L or define very low LDL-C as <1.8 mmol/L; its preference-over-non-HDL-C statement also does not explicitly include metabolic syndrome. Page numbers are unavailable in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measuredGuidelines propose using non-HDLC or apoB as a secondary treatment target in the management of patients with mild-to-moderate hypertriglyceridemia (2-10 mmol/L), including patients with diabetes.
“Guidelines propose using non-HDLC or apoB as a secondary treatment target in the management of patients with mild-to-moderate hypertriglyceridemia (2-10 mmol/L), including patients with diabetes [4,5].”
From Quantifying atherogenic lipoproteins for lipid-lowering strategies: Consensus-based recommendations from EAS and EFLM (2020) · cites this paper as [4]
Section 9.4.2.2 calls non-HDL-C or ApoB a secondary objective of therapy and discusses atherogenic dyslipidaemia in people with type 2 diabetes. The secondary-goals passage likewise recommends risk-based non-HDL-C and ApoB targets. Neither passage ties those targets specifically to the claimed triglyceride range of 2–10 mmol/L, so that qualifier is not supported by our copy. (LLM, conf=0.84)
Experimental — accuracy not yet measuredIf the primary target LDLC is at goal, but non-HDLC or apoB are still high, attainment of all three targets will require intensified lipid-lowering therapy, lifestyle (re)inforcement, and/or additional TG-lowering drugs.
“If the primary target LDLC is at goal, but non-HDLC or apoB are still high, attainment of all three targets will require intensified lipidlowering therapy, lifestyle (re)inforcement, and/or additional TG-lowering drugs (e.g., fibrate or omega-3 fatty acids) [4].”
From Quantifying atherogenic lipoproteins for lipid-lowering strategies: Consensus-based recommendations from EAS and EFLM (2020) · cites this paper as [4]
The guidelines’ secondary-goals section (page unavailable) says adjusting lipid-lowering therapy after reaching the LDL-C goal may be considered for patients at very high cardiovascular risk, subject to clinical judgment. The triglyceride-treatment recommendations (page unavailable) also discuss lifestyle measures and possible fibrate or omega-3 use, but under specific triglyceride and risk conditions. They do not say that elevated non-HDL-C or ApoB necessarily requires these measures to attain all three targets. (LLM, conf=0.88)
Experimental — accuracy not yet measuredCurrent guidelines for management of SAMS mostly rely on expert opinions.
“This variability is evident in the current guidelines, which mostly rely on expert opinions. [6,9].”
From Safety outcomes of statin vs non-statin lipid-lowering interventions in patients with prior statin-associated muscle symptoms: A systematic review and meta-analysis (2025) · cites this paper as [9]
Section 8.1.4.1 provides suggested management for statin-associated muscle symptoms, and the Monitoring section gives practical steps for patients with muscle symptoms. The guidelines define one evidence level as expert consensus, but our copy does not establish that SAMS guidance—or current SAMS guidelines generally—mostly relies on expert opinion; it also discusses trial evidence relevant to statin intolerance. No page numbers are available in the indexed passages. (LLM, conf=0.76)
Experimental — accuracy not yet measuredCurrent international guidelines (ESC/EAS and ACC/AHA 2018) endorse statins as the first-line pharmacologic intervention in patients with moderate hypertriglyceridemia (150-499 mg/dL), especially in high-risk or very-high-risk patients.
“Current international guidelines, including the ESC/EAS [67] and ACC/AHA 2018 recommendations [74], endorse statins as the first-line pharmacologic intervention in patients with moderate hypertriglyceridemia (150–499 mg/dL), especially in high-risk or very-high-risk patients.”
From Targeting triglycerides for cardiovascular risk reduction (2026) · cites this paper as [67]
The ESC/EAS recommendations for drug treatment of hypertriglyceridaemia (page not provided) recommend statins as the first drug of choice to reduce cardiovascular risk in high-risk patients with triglycerides above 200 mg/dL. They do not make that first-line recommendation across the full claimed range of 150–499 mg/dL; the separate ACC/AHA citation is not assessed here. (LLM, conf=0.88)
Experimental — accuracy not yet measuredapoB is a more accurate measure of the adequacy of lipid-lowering therapy than LDL-C or non-HDL-C.
“given that apoB is a more accurate measure of the adequacy of lipid-lowering therapy than LDL-C or non-HDL-C,1,3–13,27”
From Discordance among apoB, non-high-density lipoprotein cholesterol, and triglycerides: implications for cardiovascular prevention (2024) · cites this paper as [1]
Section 5.4.1 says ApoB measurement has superior analytical performance to measurement or calculation of LDL-C and non-HDL-C. But section 11 recommends LDL-C as the minimum measure for monitoring therapy and treats ApoB or non-HDL-C as secondary treatment targets; it does not establish that ApoB is generally a more accurate measure of whether lipid-lowering therapy is adequate. (LLM, conf=0.86)
Experimental — accuracy not yet measuredMultiple recommendations prioritize or restrict the measurement of apoB to subjects with elevated triglycerides based on the assumption that this is when cholesterol-depleted apoB particles would be present and that apoB would be more informative than LDL-C.
“Multiple recommendations prioritize or restrict the measurement of apoB to subjects with elevated triglycerides based on the assumption this is when cholesterol-depleted apoB particles would be present and that apoB would be more informative than LDL-C.1,21”
From Discordance among apoB, non-high-density lipoprotein cholesterol, and triglycerides: implications for cardiovascular prevention (2024) · cites this paper as [1]
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredIndividuals with loss-of-function mutations in APOC-III have significantly reduced triglycerides and remnant cholesterol, and a nearly 40% lower ASCVD risk.
“Individuals with loss-of-function mutations in APOC-III exhibit significantly reduced levels of triglycerides and remnant cholesterol, along with a nearly 40% reduction in ASCVD risk [32, 33].”
From The Efficacy and Safety of Plozasiran on Lipid Profile in Dyslipidemic Disorders: A Systematic Review and Meta-Analysis (2026) · cites this paper as [33]
Section 9.1.4 (page unavailable) says that ApoC-III loss-of-function mutations are associated with low triglyceride levels. The passages in our copy do not establish reduced remnant cholesterol or a nearly 40% reduction in ASCVD risk for mutation carriers. (LLM, conf=0.87)
Experimental — accuracy not yet measuredESC and AHA/ACC/multi-society guidelines have recently pursued more strict LDL-C reductions according to the principle 'the lower, the better'.
“First, ESC and AHA/ACC/multi-society guidelines have recently pursued more string LDL-C reductions according to the principle ‘the lower, the better’ [18–20]”
From Established and Emerging Lipid-Lowering Drugs for Primary and Secondary Cardiovascular Prevention (2023) · cites this paper as [19]
ESC guidelines state that PCSK9 inhibitors may be considered for primary cardiovascular prevention in very high-risk patients who do not achieve their LDL-C goal with maximum tolerated statin therapy and ezetimibe.
“ESC guidelines further state that PCSK9 inhibitors may be considered for primary cardiovascular prevention in very high-risk patients who do not achieve their LDL-C goal with maximum tolerated statin therapy and ezetimibe.”
From Established and Emerging Lipid-Lowering Drugs for Primary and Secondary Cardiovascular Prevention (2023) · cites this paper as [19]
Statins reduce the internal synthesis of cholesterol by competitive inhibition of HMG-CoA reductase.
“Statins reduce the internal synthesis of cholesterol by a competitive inhibition of the rate-limiting 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase [19].”
From Established and Emerging Lipid-Lowering Drugs for Primary and Secondary Cardiovascular Prevention (2023) · cites this paper as [19]
Icosapent ethyl and fibrate are second-line treatments that should/may be considered in combination with a statin for hypertriglyceridemia.
“Icosapent ethyl and fibrate are second-line treatments that should/may be considered in combination with a statin.”
From Established and Emerging Lipid-Lowering Drugs for Primary and Secondary Cardiovascular Prevention (2023) · cites this paper as [19]
For hypertriglyceridemia, both guidelines recommend risk-stratified treatment with statins, icosapent ethyl and/or fibrates.
“For hypertriglyceridemia (Fig. 3), both guidelines recommend a risk-stratified treatment with statins, icosapent ethyl and/or fibrates.”
From Established and Emerging Lipid-Lowering Drugs for Primary and Secondary Cardiovascular Prevention (2023) · cites this paper as [19]
Ezetimibe is recommended as second-line treatment in patients who do not attain their LDL-C goal on maximum tolerated statin therapy by both guidelines for primary and secondary prevention.
“Ezetimibe is recommended as the second-line treatment in patients who do not attain their LDL-C goal on maximum tolerated statin therapy by both guidelines for primary and secondary prevention.”
From Established and Emerging Lipid-Lowering Drugs for Primary and Secondary Cardiovascular Prevention (2023) · cites this paper as [19]
ESC guidelines specify that ezetimibe and/or PCSK9 inhibitors should be considered in patients with hypercholesterinaemia who are intolerant to statins.
“ESC guidelines further specify that ezetimibe and/or PSCK9 inhibitors should be considered in patients with hypercholesterinaemia who are intolerant to statins.”
From Established and Emerging Lipid-Lowering Drugs for Primary and Secondary Cardiovascular Prevention (2023) · cites this paper as [19]
ApoB-containing lipoproteins, including very low-density lipoproteins, triglyceride-rich remnant particles, and LDL, are central causal factors in the progression of atherosclerotic plaque.
“ApoB‐containing lipoproteins, including very low‐density lipoproteins, triglyceride‐rich remnant particles, and LDL, are central causal factors in the progression of atherosclerotic plaque. 2 , 3”
From Association Between Omega-3 Fatty Acid Intake and Dyslipidemia: A Continuous Dose-Response Meta-Analysis of Randomized Controlled Trials (2023) · cites this paper as [3]
The resulting underestimation of LDLC may translate to downward misclassification when using guideline-recommended 1.8 mmol/L or 1.4 mmol/L thresholds for patients at high and very high cardiovascular risk, respectively.
“The resulting underestimation of LDLC may translate to downward misclassification when using guideline-recommended 1.8 mmol/L or 1.4 mmol/L thresholds for patients at high and very high cardiovascular risk, respectively [4].”
From Quantifying atherogenic lipoproteins for lipid-lowering strategies: Consensus-based recommendations from EAS and EFLM (2020) · cites this paper as [4]
Nonfasting lipid profiles are now endorsed by several guidelines including those in Europe, the UK, Canada, Brazil, and the US.
“Nonfasting lipid profiles are now endorsed by several guidelines including those in Europe, the UK, Canada, Brazil, and the US [4][5][6]35,38].”
From Quantifying atherogenic lipoproteins for lipid-lowering strategies: Consensus-based recommendations from EAS and EFLM (2020) · cites this paper as [4]
For LDLC, the decision threshold for initiation of therapeutic intervention varies with the individual's risk score.
“For LDLC, the decision threshold for initiation of therapeutic intervention varies with the individual's risk score (Table 6) [4].”
From Quantifying atherogenic lipoproteins for lipid-lowering strategies: Consensus-based recommendations from EAS and EFLM (2020) · cites this paper as [4]
Non-fasting TG are on average only ~0.3 mmol/L (27 mg/dL) higher than fasting TG and have comparable prognostic value.
“non-fasting TG are on average only ~ 0.3 mmol/L (27 mg/dL) higher and have comparable prognostic value.”
From Targeting triglycerides for cardiovascular risk reduction (2026) · cites this paper as [67]
apoB can be measured more accurately, more precisely, and more selectively than LDL-C or non-HDL-C.
“Taken together with the evidence that apoB can be measured more accurately, more precisely, and more selectively than LDL-C or non-HDL-C,1,29–31”
From Discordance among apoB, non-high-density lipoprotein cholesterol, and triglycerides: implications for cardiovascular prevention (2024) · cites this paper as [1]
After REDUCE-IT, several national and international guidelines endorsed EPA in their therapeutic recommendations.
“After REDUCE-IT, several national and international guidelines endorsed EPA in their therapeutic recommendations [18,34].”
From Effect of omega-3 fatty acids on cardiovascular outcomes: A systematic review and meta-analysis (2021) · cites this paper as [34]
Legume seeds, such as chickpeas, are a rich source of resistant starch and have a low glycemic index.
“Legume seeds, such as chickpeas, are a rich source of resistant starch (RS) and have a low glycemic index (GI).”
From The Effect of Cooking and Cooling Chickpea Pasta on Resistant Starch Content, Glycemic Response, and Glycemic Index in Healthy Adults (2024) · cites this paper as [6]
Section 7.4.3 says legumes contain dietary fibre, and Table 9 lists chickpeas among legumes. Neither passage addresses resistant starch or glycemic index; searches for those terms with legumes and chickpeas found no supporting passage in our copy. Page numbers were not available. (LLM, conf=0.72)
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”
Elevated plasma triglyceride levels with accumulation of triglyceride-rich lipoproteins and remnant particles are related to residual cardiovascular risk among statin-treated patients, especially those with diabetes mellitus.
“but also equally to residual cardiovascular risk among statin-treated patients, especially those with diabetes mellitus.2,20,36–38”
At fasting triglyceride levels above 1.7 mmol/L, there is consensus that atherosclerotic cardiovascular disease risk becomes clinically relevant.
“At fasting TG levels >1.7 mmol/L (>150 mg/dL), there is consensus that ASCVD risk becomes clinically relevant;4,20,38”
Elevated plasma triglyceride levels with accumulation of triglyceride-rich lipoproteins and remnant particles are related to subclinical atherosclerosis and vascular inflammation independently of LDL-C in statin-naïve, apparently healthy subjects.
“elevated plasma TG levels (with the accumulation of TRL and remnant particles) are related not only to subclinical atherosclerosis and vascular inflammation independently of LDL-C in statin-naïve, apparently healthy subjects”
Current clinical practice guidelines for dyslipidemia recommend initiating statins for serum TG levels >200 mg/dl only in patients at high cardiovascular risk.
“Current clinical practice guidelines for the treatment of dyslipidemia recommend initiation of statins for serum TG levels >200 mg/dl, but only in patients at high CV risk (12).”
From Triglycerides and residual atherosclerotic risk (2021) · cites this paper as [12]
ESC guidelines recommend treating hypertriglyceridemia as a primary prevention measure to reduce CV risk only in high-risk individuals with TG >200 mg/dl (Class I recommendation, Level of Evidence: B) or with TG between 135 and 499 mg/dl despite statin treatment (Class IIa recommendation, Level of Evidence: B).
“ESC guidelines recommend treating hypertriglyceridemia as a primary prevention measure to reduce CV risk only in high-risk individuals with TG >200 mg/dl (Class I recommendation, Level of Evidence: B) or with TG between 135 and 499 mg/dl despite statin treatment (Class IIa recommendation, Level of Evidence: B) (12).”
From Triglycerides and residual atherosclerotic risk (2021) · cites this paper as [12]
Several national and international guidelines have incorporated icosapent ethyl into their recommendations.
“In light of the strong results in REDUCE-IT, several national and international guidelines have incorporated icosapent ethyl into their recommendations.10–13”
From REDUCE-IT USA: Results From the 3146 Patients Randomized in the United States (2020) · cites this paper as [12]
The Mediterranean diet is a dietary pattern recommended for cardiovascular prevention and has been promoted by the European Society of Cardiology/European Atherosclerosis Society 2019 guidelines for the management of dyslipidemia in addition to other lifestyle changes.
“MD is a dietary pattern recommended for cardiovascular prevention and has been promoted by the European Society of Cardiology/European Atherosclerosis Society (ESC/EAS) 2019 guidelines for the management of dyslipidemia in addition to other lifestyle changes (Table 1) [103].”
From Mediterranean Diet and Obesity-related Disorders: What is the Evidence? (2022) · cites this paper as [103]
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Self-citationVariation in<i>PCSK9</i>and<i>HMGCR</i>and Risk of Cardiovascular Disease and Diabetes
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Self-citationTriglyceride-mediated pathways and coronary disease: collaborative analysis of 101 studies
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- Authors
- Mach, F., Baigent, C., Catapano, A. L., Koskinas, K. C., Casula, M., Badimon, L., Chapman, M. J., De Backer, G. G., Delgado, V., Ference, B. A., Graham, I. M., Halliday, A., Landmesser, U., Mihaylova, B., Pedersen, T. R., Riccardi, G., Richter, D. J., Sabatine, M. S., Taskinen, M.-R., Tokgozoglu, L., Wiklund, O., ESC Scientific Document Group, Mueller, C., Drexel, H., Aboyans, V., Corsini, A., Doehner, W., Farnier, M., Gigante, B., Kayikcioglu, M., Krstacic, G., Lambrinou, E., Lewis, B. S., Masip, J., Moulin, P., Petersen, S., Petronio, A. S., Piepoli, M. F., Pintó, X., Räber, L., Ray, K. K., Reiner, Ž., Riesen, W. F., Roffi, M., Schmid, J.-P., Shlyakhto, E., Simpson, I. A., Stroes, E., Sudano, I., Tselepis, A. D., Viigimaa, M., Vindis, C., Vonbank, A., Vrablik, M., Vrsalovic, M., Zamorano, J. L., Collet, J.-P., Koskinas, K. C., Casula, M., Badimon, L., John Chapman, M., De Backer, G. G., Delgado, V., Ference, B. A., Graham, I. M., Halliday, A., Landmesser, U., Mihaylova, B., Pedersen, T. R., Riccardi, G., Richter, D. J., Sabatine, M. S., Taskinen, M.-R., Tokgozoglu, L., Wiklund, O., Windecker, S., Aboyans, V., Baigent, C., Collet, J.-P., Dean, V., Delgado, V., Fitzsimons, D., Gale, C. P., Grobbee, D., Halvorsen, S., Hindricks, G., Iung, B., Jüni, P., Katus, H. A., Landmesser, U., Leclercq, C., Lettino, M., Lewis, B. S., Merkely, B., Mueller, C., Petersen, S., Petronio, A. S., Richter, D. J., Roffi, M., Shlyakhto, E., Simpson, I. A., Sousa-Uva, M., Touyz, R. M., Nibouche, D., Zelveian, P. H., Siostrzonek, P., Najafov, R., van de Borne, P., Pojskic, B., Postadzhiyan, A., Kypris, L., Špinar, J., Larsen, M. L., Eldin, H. S., Viigimaa, M., Strandberg, T. E., Ferrières, J., Agladze, R., Laufs, U., Rallidis, L., Bajnok, L., Gudjónsson, T., Maher, V., Henkin, Y., Gulizia, M. M., Mussagaliyeva, A., Bajraktari, G., Kerimkulova, A., Latkovskis, G., Hamoui, O., Slapikas, R., Visser, L., Dingli, P., Ivanov, V., Boskovic, A., Nazzi, M., Visseren, F., Mitevska, I., Retterstøl, K., Jankowski, P., Fontes-Carvalho, R., Gaita, D., Ezhov, M., Foscoli, M., Giga, V., Pella, D., Fras, Z., de Isla, L. P., Hagström, E., Lehmann, R., Abid, L., Ozdogan, O., Mitchenko, O., & Patel, R. S.
- Affiliations
- MultiMedica (IT)
- Centre d'Epidémiologie et de Recherche en santé des POPulations de Toulouse (FR)
- ORCID
- Catapano, Alberico L
- Drexel, Heinz
- Corsini, Alberto
- Doehner, Wolfram
- Farnier, Michel
- Gigante, Bruna
- Lambrinou, Ekaterini
- Moulin, Philippe
- Piepoli, Massimo Francesco
- Pintó, Xavier
- Räber, Lorenz
- Ray, Kausik K
- Schmid, Jean-Paul
- Stroes, Erik
- Tselepis, Alexandros D
- Vonbank, Alexander
- Zamorano, José Luis
- Windecker, Stephan
- Fitzsimons, Donna
- Gale, Chris P
- Grobbee, Diederick
- Halvorsen, Sigrun
- Hindricks, Gerhard
- Iung, Bernard
- Jüni, Peter
- Katus, Hugo A
- Leclercq, Christophe
- Lettino, Maddalena
- Touyz, Rhian M
- Zelveian, Parounak H
- Siostrzonek, Peter
- Najafov, Ruslan
- Postadzhiyan, Arman
- Špinar, Jindřich
- Strandberg, Timo E
- Ferrières, Jean
- Agladze, Rusudan
- Laufs, Ulrich
- Gulizia, Michele Massimo
- Mussagaliyeva, Aisulu
- Bajraktari, Gani
- Kerimkulova, Alina
- Hamoui, Omar
- Dingli, Philip
- Ivanov, Victoria
- Visseren, Frank
- Mitevska, Irena
- Retterstøl, Kjetil
- Jankowski, Piotr
- Giga, Vojislav
- Pella, Daniel
- Hagström, Emil
- Mitchenko, Olena
- Patel, Riyaz S
- Venue
- European Heart Journal
- Publisher
- Oxford University Press (OUP)
- Published
- 2019-08-31
- Volume
- 41
- Issue
- 1
- Pages
- 111-188
- ISSN
- 0195-668X (ISSN-L)
- 1522-9645
- OpenAlex
- W3183857127
- Semantic Scholar
- e18e442c082b3336721cfbe3c013de2f21e22eed
- Cited by
- 8,961
- References
- 233
- Citations by year
- 2026: 902 · 2025: 1408 · 2024: 1402 · 2023: 1442 · 2022: 1358 · 2021: 1386 · 2020: 940 · 2019: 109 · 2018: 3 · 2017: 1 · 2016: 1
- FWCI
- 905.48
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model (vor)
- Locations
- European Heart Journal (publishedVersion)
- PubMed (publishedVersion)
- Pure Amsterdam UMC (publishedVersion, cc-by)
- Archive ouverte UNIGE (University of Geneva) (publishedVersion, other-oa)
- Data Archiving and Networked Services (DANS) (submittedVersion, other-oa)
- HAL (submittedVersion)
- Archivio Istituzionale della Ricerca (Universita Degli Studi Di Milano) (submittedVersion, other-oa)
- Ghent University Academic Bibliography (Ghent University) (submittedVersion)
- Ktisis at Cyprus University of Technology (Cyprus University of Technology) (submittedVersion, cc-by-nc-nd)
- Research Portal (Queen's University Belfast) (submittedVersion, other-oa)
- Queen Mary Research Online (Queen Mary University of London) (submittedVersion)
- Leiden Repository (Leiden University) (submittedVersion, cc-by)
- Archive ouverte UNIGE (University of Geneva) (submittedVersion, cc-by)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion)
- Funders
- Brigham and Women's Hospital
- Helsingin Yliopisto
- Queen Mary University of London
- Deutsches Zentrum für Herz-Kreislaufforschung
- Università degli Studi di Milano
- Inselspital, Universitätsspital Bern
- National Institute for Health and Care Research (CL-2011-11-003)
- British Heart Foundation (CH/1996001/9454, FS/14/76/30933)
- University of Oxford
- Institut National de la Santé et de la Recherche Médicale
- Universiteit Leiden
- Universiteit Gent
- Leids Universitair Medisch Centrum
- Hacettepe Üniversitesi
- Göteborgs Universitet
- Berlin Institute of Health
- Sorbonne Université
- Medical Research Council (MC_UU_00017/4)
- Barts and The London School of Medicine and Dentistry
- Sahlgrenska Akademin
- NIHR Oxford Biomedical Research Centre
- Faculty of Medicine and Health, University of Sydney
- Topics
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
- Keywords
- dyslipidemia, lipid-lowering therapy, cardiovascular risk reduction, dyslipidemia management, cardiovascular disease prevention, lipid-modifying drugs, ESC/EAS guidelines
- MeSH terms
- Heart Disease Risk Factors, Cardiovascular Diseases, Humans, Lipids, Risk Factors, Triglycerides, Dyslipidemias
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