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Cited by 3,549Lipoproteins and Cardiovascular HealthDiabetes, Cardiovascular Risks, and LipoproteinsBlood Pressure and Hypertension Studies

The DOI matches its Crossref record; 236 of the 237 references it cites were found in a registry or an index; 5 of the 254 sources its claims cite were checked for support.

ESC/EAS Guidelines for the management of dyslipidaemias

Open access
Reiner, Željko, Catapano, Alberico L., De Backer, Guy, Graham, Ian, Taskinen, Marja-Riitta, Wiklund, Olov, Agewall, Stefan, Alegria, Eduardo, Chapman, M. John, Durrington, Paul, Erdine, Serap, Halcox, Julian, Hobbs, Richard, Kjekshus, John, Filardi, Pasquale Perrone, Riccardi, Gabriele, Storey, Robert F., Wood, David, Bax, Jeroen, Vahanian, Alec, Auricchio, Angelo, Baumgartner, Helmut, Ceconi, Claudio, Dean, Veronica, Deaton, Christi, Fagard, Robert, Filippatos, Gerasimos, Funck-Brentano, Christian, Hasdai, David, Hobbs, Richard, Hoes, Arno, Kearney, Peter, Knuuti, Juhani, Kolh, Philippe, McDonagh, Theresa, Moulin, Cyril, Poldermans, Don, Popescu, Bogdan A., Reiner, Željko, Sechtem, Udo, Sirnes, Per Anton, Tendera, Michal, Torbicki, Adam, Vardas, Panos, Widimsky, Petr, Windecker, Stephan, Reviewers:, Document, Funck-Brentano, Christian, Poldermans, Don, Berkenboom, Guy, De Graaf, Jacqueline, Descamps, Olivier, Gotcheva, Nina, Griffith, Kathryn, Guida, Guido Francesco, Gulec, Sadi, Henkin, Yaakov, Huber, Kurt, Kesaniemi, Y. Antero, Lekakis, John, Manolis, Athanasios J., Marques-Vidal, Pedro, Masana, Luis, McMurray, John, Mendes, Miguel, Pagava, Zurab, Pedersen, Terje, Prescott, Eva, Rato, Quitéria, Rosano, Giuseppe, Sans, Susana, Stalenhoef, Anton, Tokgozoglu, Lale, Viigimaa, Margus, Wittekoek, M. E., Zamorano, Jose Luis·2011·European Heart Journal
DOI 10.1093/eurheartj/ehr158
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Abstract

Cardiovascular disease (CVD) due to atherosclerosis of the arterial vessel wall and to thrombosis is the foremost cause of premature mortality and of disability-adjusted life years (DALYs) in Europe, and is also increasingly common in developing countries.1 In the European Union, the economic cost of CVD represents annually E192 billion1 in direct and indirect healthcare costs. The main clinical entities are coronary artery disease (CAD), ischaemic stroke, and peripheral arterial disease (PAD). The causes of these CVDs are multifactorial. Some of these factors relate to lifestyles, such as tobacco smoking, lack of physical activity, and dietary habits, and are thus modifiable. Other risk factors are also modifiable, such as elevated blood pressure, type 2 diabetes, and dyslipidaemias, or non-modifiable, such as age and male gender. These guidelines deal with the management of dyslipidaemias as an essential and integral part of CVD prevention. Prevention and treatment of dyslipidaemias should always be considered within the broader framework of CVD prevention, which is addressed in guidelines of the Joint European Societies’ Task forces on CVD prevention in clinical practice.2 – 5 The latest version of these guidelines was published in 20075; an update will become available in 2012. These Joint ESC/European Atherosclerosis Society (EAS) guidelines on the management of dyslipidaemias are complementary to the guidelines on CVD prevention in clinical practice and address not only physicians [e.g. general practitioners (GPs) and cardiologists] interested in CVD prevention, but also specialists from lipid clinics or metabolic units who are dealing with dyslipidaemias that are more difficult to classify and treat.

Overview

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Crossref · 10.1093/eurheartj/ehr158

Cites

236 of 237 references verified1 citation errors · 0 not checkable

Statistics

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Verification

Claims the paper makes

203 Not checked yet · 82 No basis given · 26 Own interpretation · 3 Partly supported · 2 Own method · 1 Supported · 1 Supported so far · accuracy not yet measured

Verify all 249 references — free account
  • It may state two separate claims as one. 117
  • Probably not a substantial claim. 33
135 of 135

  • The authors state this as an assumption.

    The Friedewald formula assumes a constant cholesterol-to-triglyceride ratio in VLDL.

    “A constant cholesterol/TG ratio in VLDL is assumed.”

  • The paper relies on this without support.

    Atherosclerotic cardiovascular disease results from multiple risk factors acting together.

    “in most people, atherosclerotic CVD is the product of a number of risk factors.”

  • The paper relies on this without support.

    Apolipoprotein B is the main apolipoprotein of VLDL, IDL, and LDL.

    “Apo B is the major apolipoprotein of the atherogenic lipoprotein families VLDL, IDL, and LDL.”

  • The paper relies on this without support.

    Apolipoprotein B concentration estimates the number of VLDL, IDL, and LDL particles in plasma.

    “The concentration of apo B is a good estimate of the number of these particles in plasma.”

  • The paper relies on this without support.

    Apolipoprotein A1 is the main protein of HDL and estimates HDL concentration.

    “Apo A1 is the major protein of HDL and provides a good estimate of HDL concentration.”

  • The paper relies on this without support.

    Plasma apolipoprotein A1 below 120 mg/dL in men and below 140 mg/dL in women corresponds to low HDL-cholesterol.

    “Plasma apo A1 of ,120 mg/dL for men and ,140 mg/dL for women approximately correspond to what is considered as low for HDL-C.”

  • The paper relies on this without support.

    Different lipid ratios give similar information.

    “The different ratios give similar information.”

  • The paper relies on this without support.

    Plasma lipoprotein(a) level is largely genetically determined.

    “The plasma level of Lp(a) is to a major extent genetically determined.”

  • The paper relies on this without support.

    Several genes are associated with cardiovascular disease.

    “Several genes have been associated with CVD.”

  • The paper relies on this without support.

    Apolipoprotein E exists in three isoforms: E2, E3, and E4.

    “Apo E is present in three isoforms (apo E2, apo E3, and apo E4).”

  • The paper relies on this without support.

    Treatment targets for dyslipidaemia are primarily based on clinical trial results.

    “Treatment targets of dyslipidaemia are primarily based on results from clinical trials.”

  • The paper relies on this without support.

    In nearly all lipid-lowering trials, LDL-cholesterol was used as the indicator of response to therapy.

    “In nearly all lipid-lowering trials the LDL-C level has been used as an indicator of response to therapy.”

  • The paper relies on this without support.

    In most patients, an LDL-cholesterol target below 1.8 mmol/L or a 50% reduction is achievable with statin monotherapy.

    “In the majority of patients, this is achievable with statin monotherapy.”

  • The paper relies on this without support.

    Apolipoprotein B determination has less laboratory error than LDL-cholesterol determination, particularly in patients with hypertriglyceridaemia.

    “there now appears to be less laboratory error in the determination of apo B than of LDL-C, particularly in patients with HTG.”

  • The paper relies on this without support.

    Apolipoprotein B is not presently measured in all clinical laboratories.

    “However, apo B is not presently being measured in all clinical laboratories.”

  • The paper relies on this without support.

    No specific targets for HDL-cholesterol or triglycerides have been determined in clinical trials.

    “To date, no specific targets for HDL-C or TG levels have been determined in clinical trials”

  • The paper relies on this without support.

    Clinical trial evidence is lacking on whether intervening on HDL-cholesterol or triglycerides reduces cardiovascular risk further.

    “clinical trial evidence is lacking on the effectiveness of intervening on these variables to reduce CV risk further”

  • The paper relies on this without support.

    Advanced age, small body size, female sex, renal or hepatic dysfunction, perioperative periods, hypothyroidism, multisystem disease, and alcohol abuse raise the chance of statin side effects.

    “Factors such as advanced age, small body size, female gender, renal and hepatic dysfunction, perioperative periods, hypothyroidism, multisystem disease, and alcohol abuse increase the likelihood of side effects with statins.”

  • The paper relies on this without support.

    The most serious adverse effect of statins is myopathy, which can progress to rhabdomyolysis and then to renal failure and death.

    “The most serious adverse effect associated with statin therapy is myopathy, which may progress to rhabdomyolysis, and that, in turn, can lead to renal failure and death.”

  • The paper relies on this without support.

    An increase in creatine phosphokinase is the best, though not definitive, indicator of statin-induced myopathy.

    “An elevation of CK is the best indicator, although not unequivocal, of statin-induced Table 13 Examples of causes of secondary hypercholesterolaemia myopathy.”

  • The paper relies on this without support.

    In clinical trials, myopathy occurs in fewer than 1 per 1000 treated patients, and the excess risk versus placebo is less than 1 per 10 000 treated patients.

    “The incidence of myopathy is low (,1/1000 patients treated) and the excess risk in comparison with placebotreated patients has been ,1/10 000 patients treated in clinical trials.”

  • The paper relies on this without support.

    Myopathy is most likely in people with complex medical problems, those taking multiple medications, and elderly individuals, especially women.

    “Myopathy is most likely to occur in persons with complex medical problems and/or who are taking multiple medications, or in elderly persons, especially women.”

  • The paper relies on this without support.

    Myalgia without creatine phosphokinase elevation occurs in 5–10% of patients in clinical practice.

    “Myalgia (without CK elevation) occurs in 5-10% of patients in clinical practice.”

  • The paper relies on this without support.

    Elevated hepatic transaminases occur in 0.5–2.0% of statin-treated patients and are dose dependent.

    “Elevated hepatic transaminases occur in 0.5 -2.0% of statin-treated patients and are dose dependent.”

  • The paper relies on this without support.

    Progression to liver failure is exceedingly rare.

    “Progression to liver failure is exceedingly rare.”

  • The paper relies on this without support.

    Transaminase elevation often reverses when the dose is reduced.

    “Reversal of transaminase elevation is frequently noted with reduction of dose;”

  • The paper relies on this without support.

    Several important drug interactions with statins can raise the risk of side effects.

    “A number of important drug interactions with statins have been described that may increase the risk of side effects.”

  • The paper relies on this without support.

    All currently available statins except pravastatin, rosuvastatin, and pitavastatin undergo major hepatic metabolism through cytochrome P450 enzymes.

    “All currently available statins, except pravastatin, rosuvastatin, and pitavastatin, undergo major hepatic metabolism via the CYPs.”

  • The paper relies on this without support.

    Bile acid sequestrants are not absorbed systemically and are not altered by digestive enzymes.

    “The bile acid sequestrants are not systemically absorbed or altered by digestive enzymes.”

  • The paper relies on this without support.

    Bile acid sequestrants also lower glucose levels in hyperglycaemic patients, though the mechanism is not fully clear.

    “These agents also reduce glucose levels in hyperglycaemic patients; however, the mechanism behind this reduction is not completely clear.”

  • The paper relies on this without support.

    At maximum doses—24 g cholestyramine, 20 g colestipol, or 4.5 g colestagel—LDL-C falls by 18–25%.

    “At the top dose of 24 g of cholestyramine, 20 g of colestipol, or 4.5 g of cholestagel, a reduction in LDL-C of 18-25% has been observed.”

  • The paper relies on this without support.

    Bile acid sequestrants have no major effect on HDL-C, but triglycerides may rise in some predisposed patients.

    “No major effect on HDL-C has been reported, while TG may increase in some predisposed patients.”

  • The paper relies on this without support.

    Gastrointestinal side effects—most often flatulence, constipation, dyspepsia, and nausea—are common with bile acid sequestrants even at low doses and limit their practical use.

    “Gastrointestinal adverse effects (most commonly flatulence, constipation, dyspepsia and nausea) are often present with these drugs even at low doses, which limit their practical use.”

  • The paper relies on this without support.

    Reduced absorption of fat-soluble vitamins has been reported with bile acid sequestrants.

    “Reduced absorption of fat-soluble vitamins has been reported.”

  • The paper relies on this without support.

    Bile acid sequestrants may raise triglycerides in some patients.

    “Furthermore, these drugs may increase TG in certain patients.”

  • The paper relies on this without support.

    Bile acid sequestrants have important interactions with many commonly prescribed drugs.

    “Bile acid sequestrants have important drug interactions with many commonly prescribed drugs and should therefore be administered either 4 h before or 1 h after other drugs.”

  • The paper relies on this without support.

    Colesevelam is a newer bile acid sequestrant that may be better tolerated than cholestyramine.

    “Colesevelam represents a newer formulation of the bile acid sequestrant, which may be better tolerated than cholestyramine.”

  • The paper relies on this without support.

    Colesevelam has fewer interactions with other drugs and can be taken with statins.

    “Colesevelam has fewer interactions with other drugs and can be taken together with statins.”

  • The paper relies on this without support.

    Ezetimibe is the first lipid-lowering drug that inhibits intestinal uptake of dietary and biliary cholesterol without affecting fat-soluble nutrient absorption.

    “Ezetimibe is the first lipid-lowering drug that inhibits intestinal uptake of dietary and biliary cholesterol without affecting the absorption of fat-soluble nutrients.”

  • The paper relies on this without support.

    In clinical studies, ezetimibe monotherapy lowers LDL-C by 15–22% in hypercholesterolaemic patients.

    “In clinical studies ezetimibe in monotherapy reduces LDL-C in hypercholesterolaemic patients by 15-22%.”

  • The paper relies on this without support.

    Adding ezetimibe to a statin gives an additional LDL-C reduction of 15–20%.

    “Combined therapy with ezetimibe and a statin provides an incremental reduction in LDL-C levels of 15 -20%.”

  • The paper relies on this without support.

    Ezetimibe is rapidly absorbed and extensively metabolized to the active ezetimibe glucuronide.

    “Ezetimibe is rapidly absorbed and extensively metabolized to the pharmacologically active ezetimibe glucuronide.”

  • The paper relies on this without support.

    Age, sex, and race have no clinically significant effect on ezetimibe pharmacokinetics, and no dose adjustment is needed for mild hepatic impairment or mild to severe renal insufficiency.

    “There are no clinically significant effects of age, sex, or race on ezetimibe pharmacokinetics, and no dosage adjustment is necessary in patients with mild hepatic impairment or mild to severe renal insufficiency.”

  • The paper relies on this without support.

    Ezetimibe can be co-administered with any dose of any statin.

    “Ezetimibe can be co-administered with any dose of any statin.”

  • The paper relies on this without support.

    No major side effects have been reported for ezetimibe; the most frequent are moderate liver enzyme elevations and muscle pain.

    “No major side effects have been reported; the most frequent side effects are moderate elevations of liver enzymes, and muscle pain.”

  • The paper relies on this without support.

    Adding a bile acid sequestrant to a statin lowers LDL-C by an additional 10–20% on average.

    “On average the addition of a bile acid sequestrant to a statin reduces LDL-C further by 10 -20%.”

  • The paper relies on this without support.

    Adding ezetimibe to a bile acid sequestrant (colesevelam, colestipol, or cholestyramine) further lowers LDL-C without extra adverse effects compared with the sequestrant alone.

    “Co-administration of ezetimibe and bile acid sequestrants (colesevelam, colestipol, or cholestyramine) resulted in an additional reduction of LDL-C levels without any additional adverse effects when compared with the stable bile acid sequestrant regimen alone.”

  • The paper relies on this without support.

    Adding ezetimibe to nicotinic acid further lowers LDL-C and does not affect the HDL-C increase caused by nicotinic acid.

    “Adding ezetimibe to nicotinic acid further reduces LDL-C and does not affect nicotinic acid-induced HDL-C increase.”

  • The paper relies on this without support.

    Triple therapy with a bile acid sequestrant, a statin, and either ezetimibe or nicotinic acid further lowers LDL-C.

    “Also triple therapy (bile acid sequestrant, statin, and ezetimibe or nicotinic acid) will further reduce LDL-C.”

  • The paper relies on this without support.

    Acute pancreatitis is one of the major clinical risks of markedly elevated triglycerides.

    “One of the major clinical risks of dramatically elevated TG is acute pancreatitis.”

  • The paper relies on this without support.

    The risk of pancreatitis becomes clinically significant when triglycerides exceed 10 mmol/L (880 mg/dL).

    “The risk of pancreatitis is clinically significant if TG exceed 10 mmol/L (more than 880 mg/dL) and actions to prevent acute pancreatitis are mandatory.”

  • The paper relies on this without support.

    Hypertriglyceridaemia causes 10% of all pancreatitis cases.

    “Notably HTG is the cause of 10% of all cases with pancreatitis,”

  • The paper relies on this without support.

    Pancreatitis can occur even when triglyceride levels are between 5 and 10 mmol/L (440–880 mg/dL).

    “and patients can develop pancreatitis even when their TG concentration is between 5 and 10 mmol/L ( 440 -880 mg/dL).”

  • The paper relies on this without support.

    In general, triglyceride levels fall sharply within 2–5 days.

    “In general a sharp decrease of TG values is seen within 2-5 days.”

  • The paper relies on this without support.

    The effect of lifestyle management on triglyceride levels is well documented.

    “The influence of lifestyle management on TG levels is well documented.”

  • The paper relies on this without support.

    Weight reduction plus regular moderate-intensity physical activity can lower triglycerides by 20–30%.

    “Weight reduction together with a regular physical activity programme of moderate intensity can reduce TG between 20 and 30%,”

  • The paper relies on this without support.

    Statins have significant effects on mortality and most cardiovascular outcome parameters.

    “As statins have significant effects on mortality as well as most CVD outcome parameters, these drugs are the first choice to reduce both total CVD risk and moderately elevated TG levels.”

  • The paper relies on this without support.

    More potent statins—atorvastatin, rosuvastatin, and pitavastatin—robustly lower triglycerides, especially at high doses and in patients with elevated triglycerides.

    “More potent statins (atorvastatin, rosuvastatin, and pitavastatin) demonstrate a robust lowering of TG levels, especially at high doses and in patients with elevated TG.”

  • The paper relies on this without support.

    Fibrates are PPAR-α agonists that act through transcription factors regulating lipid and lipoprotein metabolism.

    “Fibrates are agonists of peroxisome proliferator-activated receptor-a (PPAR-a), acting via transcription factors regulating various steps in lipid and lipoprotein metabolism.”

  • The paper relies on this without support.

    Myopathy risk is higher in patients with chronic kidney disease and varies with the fibrate and statin used in combination.

    “The risk of myopathy is greater in patients with CKD, and it varies with different fibrates and statins used in combination.”

  • The paper relies on this without support.

    Gemfibrozil inhibits statin metabolism through glucuronidation, greatly increasing statin plasma concentrations.

    “Gemfibrozil inhibits the metabolism of statins via the glucuronidation pathway that leads to highly increased plasma concentrations of statins.”

  • The paper relies on this without support.

    Fibrates as a class have been reported to raise serum creatinine and homocysteine in short- and long-term studies, but the effect appears fibrate-specific.

    “As a class, fibrates have been reported to raise both serum creatinine and homocysteine in both short-term and long-term studies, but the effect seems to be fibrate specific.”

  • The paper relies on this without support.

    The homocysteine increase caused by fibrates has been considered relatively innocent for cardiovascular risk.

    “The increase in homocysteine by fibrates has been considered to be relatively innocent with respect to CVD risk.”

  • The paper relies on this without support.

    Nicotinic acid has been reported to reduce fatty acid influx to the liver and hepatic VLDL secretion, partly through effects on hormone-sensitive lipase in adipose tissue.

    “Nicotinic acid has been reported to decrease fatty acid influx to the liver and the secretion of VLDL by the liver; this effect appears to be mediated in part by the effects on hormone-sensitive lipase in the adipose tissue.”

  • The paper relies on this without support.

    In clinical practice, flushing is the most frequent and troublesome side effect of nicotinic acid and its derivatives, often preventing dose titration to maximal efficacy even with aspirin.

    “In clinical practice, skin reactions (flushing) are the most frequent and troublesome side effect of nicotinic acid and its derivatives, often preventing titration of the dose to maximal efficacy, even using aspirin as a modulator of flushing.”

  • The paper relies on this without support.

    Other side effects of nicotinic acid include hyperuricaemia, liver toxicity, and acanthosis nigricans.

    “Other side effects of nicotinic acid include hyperuricaemia, liver toxicity, and acanthosis nigricans.”

  • The paper relies on this without support.

    The mediator is prostaglandin D2 released from arachidonic acid.

    “The mediator is prostaglandin D2 released from arachidonic acid.”

  • The paper relies on this without support.

    A recent survey found that fewer than 15% of new users of extended-release nicotinic acid were still taking it after 1 year.

    “A recent survey revealed that ,15% of new users of ER nicotinic acid were still using the drug after 1 year.”

  • The paper relies on this without support.

    Liver enzyme elevation with extended-release nicotinic acid is less common (<1%) than with older nicotinic acid compounds.

    “Elevation of liver enzymes in users of ER nicotinic acid is less common (,1%) than with previous nicotinic acid compounds.”

  • The paper relies on this without support.

    Nicotinic acid may interfere with glycaemic control by raising blood glucose, which is a concern in diabetes.

    “The issue that nicotinic acid may interfere with glycaemic control by increasing blood glucose levels is of concern in treating people with diabetes.”

  • The paper relies on this without support.

    At pharmacological doses above 2 g/day, n-3 fatty acids affect serum lipids and lipoproteins, especially VLDL concentration.

    “n-3 fatty acids at pharmacological doses (.2 g/day) affect serum lipids and lipoproteins, in particular VLDL concentration.”

  • The paper relies on this without support.

    Fish oil lowers triglycerides by 30%, but its effects on other lipoproteins are trivial.

    “Fish oil reduces TG by 30%, but the effects on other lipoproteins are trivial in their magnitude.”

  • The paper relies on this without support.

    n-3 fatty acid administration appears safe and free of clinically significant interactions.

    “The administration of n-3 fatty acids appears to be safe and devoid of clinically significant interactions.”

  • The paper relies on this without support.

    The antithrombotic effects of n-3 fatty acids may increase bleeding tendency, especially when added to aspirin or clopidogrel.

    “However, the antithrombotic effects may increase the propensity to bleed, especially when given in addition to aspirin/clopidogrel.”

  • The paper relies on this without support.

    Patients taking nicotinic acid with a statin—mostly simvastatin or atorvastatin—report similar all-cause adverse event rates, and flushing incidence is similar with and without statin treatment.

    “Patients taking concomitant statin therapy, mostly simvastatin or atorvastatin, with nicotinic acid report a similar incidence of all-cause adverse events, and the incidence of flushing is similar in patients with and without statin treatment.”

  • The paper relies on this without support.

    Adding n-3 fatty acids to pravastatin and fenofibrate further lowered triglycerides and homocysteine in patients with diabetic dyslipidaemia.

    “Adding n-3 fatty acids to pravastatin and fenofibrate in a triple combination further decreased TG concentrations and homocysteine as well in patients with diabetic dyslipidaemia.”

  • The paper relies on this without support.

    No significant interactions of any drug with n-3 fatty acids have been described.

    “No significant interactions of any drug with n-3 fatty acids have been described.”

  • The paper relies on this without support.

    Therapeutic lifestyle changes (weight reduction, exercise, smoking cessation, and moderate alcohol consumption) can increase HDL-C levels by up to 10%.

    “While HDL-C levels may be increased by up to 10% by implementing therapeutic lifestyle changes, including weight reduction, exercise, smoking cessation, and moderate alcohol consumption”

  • The paper relies on this without support.

    Fibrates lower TG levels by up to 50% and raise HDL-C by up to 10-15% in short-term studies.

    “As a class, fibrates differ in their potential to modulate the atherogenic lipid profile by concomitantly lowering TG levels (up to 50%) and by raising those of HDL-C (up to 10 -15% in short-term studies).”

  • The paper relies on this without support.

    CETP inhibition by small molecule inhibitors is the most efficacious pharmacological approach to elevating low HDL-C levels.

    “To date, the most efficacious pharmacological approach to elevation of low HDL-C levels has involved direct inhibition of cholesteryl ester transfer protein (CETP) by small molecule inhibitors”

  • The paper relies on this without support.

    The deleterious effects of torcetrapib arose primarily from off-target toxicity related to activation of the renin-angiotensin-aldosterone system (RAAS).

    “Retrospectively, it appears that the deleterious effects of torcetrapib arose primarily from off-target toxicity related to activation of the renin-angiotensin -aldosterone system (RAAS).”

  • The paper relies on this without support.

    HeFH affects 1 in 500 people of European descent.

    “Heterozygous familial hypercholesterolaemia (HeFH) affects 1 in 500 people of European descent.”

  • The paper relies on this without support.

    FCH is a common genetic dyslipidaemia (1:100) and a major cause of premature CAD.

    “FCH is a highly prevalent genetic dyslipidaemia (1:100) and an important cause of premature CAD.”

  • The paper relies on this without support.

    Elevated LDL-C is more dangerous when HTG coexists.

    “It emphasizes both the importance of considering family history in deciding how rigorously to treat dyslipidaemia, and that raised LDL-C levels are riskier when HTG is also present.”

  • The paper relies on this without support.

    Statins lower CV risk by the same relative amount in people with and without HTG.

    “Statin treatment has been shown to decrease CV risk by the same relative amount in people with HTG as in those without.”

  • The paper relies on this without support.

    Without treatment, most HeFH patients develop symptomatic coronary disease by age 60, and half of men and 15% of women die.

    “Untreated, the majority of affected men and women will have symptomatic coronary disease by 60 years and half of the men and 15% of the women will have died.”

  • The paper relies on this without support.

    Tendon xanthomata are virtually diagnostic of HeFH.

    “The presence of tendon xanthomata is, however, virtually diagnostic of HeFH.”

  • The paper relies on this without support.

    In HeFH, TC levels are elevated from birth.

    “High TC levels are present from birth in HeFH.”

  • The paper relies on this without support.

    HoFH is rare in Europeans (about 1 in 10^6 births) except with founder effects or consanguinity.

    “HoFH is rare in European populations ( 1 in 10 6 births) unless there is a founder gene effect or consanguinity”

  • The paper relies on this without support.

    Without treatment, HoFH usually causes death in adolescence or early adulthood from myocardial ischaemia or aortic stenosis.

    “Regardless of this, HoFH is always an extremely serious disease, which untreated leads to death typically in adolescence or early adulthood due to myocardial ischaemia or aortic stenosis.”

  • The paper relies on this without support.

    Familial dysbetalipoproteinaemia is uncommon and usually follows autosomal recessive inheritance with variable penetrance.

    “Familial dysbetalipoproteinaemia (syn.type III hyperlipoproteinaemia; remnant removal disease) is rare and is generally inherited as an autosomal recessive disorder with variable penetrance.”

  • The paper relies on this without support.

    CAD risk is very high in familial dysbetalipoproteinaemia.

    “The risk of CAD is very high, and accelerated atherosclerosis of the femoral and tibial arteries is also prevalent.”

  • The paper relies on this without support.

    Familial LPL deficiency is an uncommon cause of severe HTG.

    “Familial LPL deficiency is a rare cause of severe HTG which may cause severe disorders of the pancreas.”

  • The paper relies on this without support.

    The most common genetic hypolipidaemia is hypobetalipoproteinaemia.

    “The most common genetic hypolipidaemia is hypobetalipoproteinaemia which is dominantly inherited and often due to truncation of apo B.”

  • The paper relies on this without support.

    Very high levels of HDL-C in CETP deficiency are not associated with disease.

    “This is not associated with disease.”

  • The paper relies on this without support.

    Low-dose third-generation oral contraceptives do not seem to raise adverse coronary event risk.

    “Currently used third-generation low oestrogen-progestin dose oral contraceptives do not appear to increase adverse coronary events”

  • The paper relies on this without support.

    Older adults are less likely to be prescribed lipid-lowering drugs or to adhere to statins.

    “Elderly individuals are less likely to receive lipid-lowering medications or adhere to statin therapy.”

  • The paper relies on this without support.

    Chronic kidney disease is a coronary artery disease risk equivalent.

    “CKD is acknowledged as a CAD risk equivalent.”

  • The authors state this as an assumption.

    Most problems related to adherence to lifestyle changes are similar to those related to compliance with lipid-lowering drug therapy.

    “Most of the problems related to adherence to lifestyles are currently assumed to be similar to those related to compliance with lipid-lowering drug therapy.”

  • The paper relies on this without support.

    Health system issues play an important role in promoting adherence.

    “Issues related to health systems also play an important role in the promotion of adherence.”

  • The paper relies on this without support.

    In most low-income countries, medication supplies are limited and often must be purchased out-of-pocket.

    “In most low income countries, supplies of medications are limited and they often have to be bought out-of-pocket.”

  • The paper relies on this without support.

    Strategies that improve access to drugs, such as sustainable financing, affordable prices, and reliable supply systems, have an important influence on patient adherence.

    “Strategies for improving access to drugs such as sustainable financing, affordable prices, and reliable supply systems have an important influence on patient adherence.”

  • The paper relies on this without support.

    Determinants of adherence to hypolipidaemic therapy include drug tolerability, regimen complexity, drug costs, and treatment duration.

    “Some of the better recognized determinants of adherence to hypolipidaemic therapy are related to aspects of the drug treatment itself, and include drug tolerability, regimen complexity, drug costs, and treatment duration.”

  • The paper relies on this without support.

    Regimen complexity is a treatment-related factor identified as a possible cause of poor adherence.

    “The complexity of the regimen is, for instance, a treatmentrelated factor that has been identified as a possible cause of poor adherence.”

  • The paper relies on this without support.

    Frequency of dosing, number of concurrent medications, and changes in medications contribute to regimen complexity.

    “Frequency of dosing, number of concurrent medications, and changes in medications are some of the factors that contribute to the complexity of a regimen, and these have been investigated in many observational studies.”

  • The paper relies on this without support.

    Fewer daily doses, monotherapies, and fewer changes in medications are associated with better adherence.

    “Fewer daily doses of drugs, monotherapies, and fewer changes in medications have all been associated with better adherence.”

  • The paper relies on this without support.

    The listed adherence interventions have tended to be used alone.

    “While many interventions (e.g.education in self-management; pharmacy management programmes; nurse, pharmacist, and other non-medical health professional intervention protocols; counselling; behavioural interventions; follow-up; and reminders) have been shown to be effective in significantly improving adherence rates, 224 they have tended to be used alone.”

  • The paper relies on this without support.

    Several programmes have demonstrated good results using multilevel team approaches.

    “Several programmes have demonstrated good results using multilevel team approaches.”

  • The paper relies on this without support.

    Patients with dyslipidaemia have low rates of adherence.

    “Healthcare providers need to be made aware of the low rates of adherence of patients with dyslipidaemia.”
109 of 109

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2 of 2

Citations

Cites

Show all 236 references

Research works printed but not linked: 5

  1. Sniderman, Meta-analysis of LDL-C, non-HDL-C and apo B as markers of cardiovascular risk, Circulation
  2. The European Atherosclerosis Society Consensus Panel, 2011, Triglyceride-rich lipoprotein and high-density lipoprotein cholesterol in patients at high risk of cardiovascular disease: evidence and guidance for management, Eur Heart J
  3. Poulter, 1999, The impact of micronized fenofibrate on lipid subfractions and on reaching HDL-target levels in 7,098 patients with dyslipidaemia, Br J Cardiol, 6, 682
  4. DeMott, 2008, Clinical guidelines and evidence review for familial hypercholesterolaemia: the identification and management of adults and children with familial hypercholesterolaemia.
  5. World Health Organization, Human Genetics Programme, 1999, Familial hypercholesterolemia: Report of a second WHO consultation

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Metadata

Authors
Reiner, Ž., Catapano, A. L., De Backer, G., Graham, I., Taskinen, M.-R., Wiklund, O., Agewall, S., Alegria, E., Chapman, M. J., Durrington, P., Erdine, S., Halcox, J., Hobbs, R., Kjekshus, J., Filardi, P. P., Riccardi, G., Storey, R. F., Wood, D., Bax, J., Vahanian, A., Auricchio, A., Baumgartner, H., Ceconi, C., Dean, V., Deaton, C., Fagard, R., Filippatos, G., Funck-Brentano, C., Hasdai, D., Hobbs, R., Hoes, A., Kearney, P., Knuuti, J., Kolh, P., McDonagh, T., Moulin, C., Poldermans, D., Popescu, B. A., Reiner, Ž., Sechtem, U., Sirnes, P. A., Tendera, M., Torbicki, A., Vardas, P., Widimsky, P., Windecker, S., Reviewers:, D., Funck-Brentano, C., Poldermans, D., Berkenboom, G., De Graaf, J., Descamps, O., Gotcheva, N., Griffith, K., Guida, G. F., Gulec, S., Henkin, Y., Huber, K., Kesaniemi, Y. A., Lekakis, J., Manolis, A. J., Marques-Vidal, P., Masana, L., McMurray, J., Mendes, M., Pagava, Z., Pedersen, T., Prescott, E., Rato, Q., Rosano, G., Sans, S., Stalenhoef, A., Tokgozoglu, L., Viigimaa, M., Wittekoek, M. E., & Zamorano, J. L.
Affiliations
  • University of Milan (IT)
  • The disclosure forms of the authors and reviewers are available on the ESC website www.escardio.org/guidelines
ORCID
Venue
European Heart Journal
Publisher
Oxford University Press (OUP)
Published
2011-01-01
Volume
32
Issue
14
Pages
1769-1818
ISSN
  • 0195-668X (ISSN-L)
  • 1522-9645
DOI
10.1093/eurheartj/ehr158
OpenAlex
W1972661406
Cited by
3,549
References
236
Citations by year
2026: 31 · 2025: 69 · 2024: 71 · 2023: 88 · 2022: 108 · 2021: 128 · 2020: 167 · 2019: 165 · 2018: 212 · 2017: 312 · 2016: 490 · 2015: 504 · 2014: 492 · 2013: 383 · 2012: 271
FWCI
390.95
Type
journal article
Language
en
Open access
Locations
  • European Heart Journal (publishedVersion)
  • PubMed (publishedVersion)
  • Radboud Repository (Radboud University) (publishedVersion)
  • SERVAL (Université de Lausanne) (publishedVersion)
  • Bern Open Repository and Information System (University of Bern) (submittedVersion, other-oa)
  • Dépôt institutionnel de l'Université libre de Bruxelles (Université Libre de Bruxelles) (submittedVersion)
  • ORCA Online Research @Cardiff (Cardiff University) (submittedVersion)
  • IRIS (submittedVersion)
  • Open Repository and Bibliography (University of Liège) (submittedVersion, other-oa)
  • Radboud Repository (Radboud University) (submittedVersion)
Funders
  • European Atherosclerosis Society
  • European Society of Cardiology
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
Keywords
dyslipidemia, dyslipidemia management, cardiovascular disease prevention, atherosclerosis, cardiovascular risk factors, lipid-lowering therapy, coronary artery disease, ischemic stroke, peripheral arterial disease, cardiovascular risk assessment
MeSH terms
Adult, Hypolipidemic Agents, Energy Intake, Cardiovascular Diseases, Child, Diet, Dietary Fats, Female, Humans, Kidney Failure, Chronic, Life Style, Male, Patient Compliance, Primary Prevention, Risk Factors, Specimen Handling, Transplantation, Weight Loss, Exercise, Risk Assessment, Dietary Supplements, Early Diagnosis, Dyslipidemias, Lipid Metabolism, Secondary Prevention

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

A language model drew the claims from the paper on 2026-10-04, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).

A second model labelled each claim on 2026-10-04 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).

Cited sources are checked with a language model’s help (gpt-6-sol).

Statistics and arithmetic are recomputed, not judged.

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