2016 ESC/EAS Guidelines for the Management of Dyslipidaemias

In the paper

“Many risk assessment systems are available and have been comprehensively reviewed, including different Framingham models, 41 Systemic Coronary Risk Estimation (SCORE), 42 ASSIGN (CV risk estimation model from the Scottish Intercollegiate Guidelines Network), 43 Q-Risk, 44 Prospective Cardiovascular Munster Study (PROCAM), 45 Reynolds, 46,47 CUORE, 48 the Pooled Cohort equations 49 and Globorisk. 5”

What the sources say

• Supported

  The citation is attached to “different Framingham models,” not to the entire subsequent list. In Assessment of Model Performance, the paper compares its new CVD risk model with an earlier Framingham risk score, supporting that attribution. (LLM, conf=0.92)

  cites [41] D'Agostino, 2008, General cardiovascular risk profile for use in primary care: the Framingham Heart Study, Circulation source
• Not checked yetcites [42] Conroy, 2003, Estimation of ten-year risk of fatal cardiovascular disease in Europe: the SCORE project, Eur Heart J source
• Supported

  Citation 43 is attached to ASSIGN, so this source need only identify that risk assessment system, not review every system in the list. The Methods describe the development and naming of the ASSIGN cardiovascular risk score using SIGN guidelines; the Discussion also identifies it as a new score. (LLM, conf=0.94)

  cites [43] Woodward, 2007, Adding social deprivation and family history to cardiovascular risk assessment: the ASSIGN score from the Scottish Heart Health Extended Cohort (SHHEC), Heart source
• Supported

  Citation 44 is attached to Q-Risk in the list, not to the statement that risk systems have been comprehensively reviewed. The paper’s Comparisons with the modified Framingham score section identifies QRISK1 and QRISK2 as cardiovascular risk equations, supporting that identification. (LLM, conf=0.92)

  cites [44] Hippisley-Cox, 2008, Predicting cardiovascular risk in England and Wales: prospective derivation and validation of QRISK2, BMJ source
• Not checked yetcites [45] Assmann, 2002, Simple scoring scheme for calculating the risk of acute coronary events based on the 10-year follow-up of the prospective cardiovascular Munster (PROCAM) study, Circulation source
• Supported

  The citation to this paper is attached to Reynolds in the list, identifying it as an example of a cardiovascular risk assessment system. The Methods (Analytic and Statistical Approach) explicitly identify Model B as the Reynolds Risk Score for men. The separate claim that the systems have been comprehensively reviewed is not attributed to this citation. (LLM, conf=0.93)

  cites [46] Ridker, 2008, C-reactive protein and parental history improve global cardiovascular risk prediction: the Reynolds Risk Score for men, Circulation source
• Not checked yetcites [47] Ridker, 2007, Development and validation of improved algorithms for the assessment of global cardiovascular risk in women: the Reynolds Risk Score, JAMA source
• Not checked yetcites [48] Ferrario, 2005, Prediction of coronary events in a low incidence population. Assessing accuracy of the CUORE Cohort Study prediction equation, Int J Epidemiol source
• Not checked yetcites [49] Goff, 2014, 2013 ACC/AHA guideline on the assessment of cardiovascular risk: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines, Circulation
• Supported

  Citation 5 follows “Globorisk” in a list where the other systems have their own citations, so it identifies the Globorisk risk assessment system rather than supporting a comprehensive review of every system listed. The Methods (Overview) describe this paper’s recalibratable risk prediction equation, and the Discussion compares it with other risk scores. (LLM, conf=0.94)

  cites [50] Hajifathalian, 2015, A novel risk score to predict cardiovascular disease risk in national populations (Globorisk): a pooled analysis of prospective cohorts and health examination surveys, Lancet Diabetes Endocrinol source

In the paper

“These trials are consistent in showing that the higher the initial LDL-C level, the greater the absolute reduction in risk, while the relative risk reduction remains constant at any given baseline LDL-C level.”

What the sources say

• ?Could not verify

  The Results section compares cardiovascular risk across achieved LDL-C levels, not initial LDL-C levels. Searches for baseline LDL-C and absolute and relative risk reduction found no passage in our copy establishing either a greater absolute risk reduction at higher initial LDL-C or a constant relative risk reduction. (LLM, conf=0.75)

  cites [61] Boekholdt, 2014, Very low levels of atherogenic lipoproteins and the risk for cardiovascular events: a meta-analysis of statin trials, J Am Coll Cardiol sourceExperimental — accuracy not yet measured
• ?Could not verify

  The Results report baseline LDL-C levels and overall treatment effects, while the subgroup analyses compare sex, age, and diabetes status—not baseline LDL-C. The Discussion’s statement about similar relative benefits across clinically defined groups does not establish that relative risk reduction is constant across LDL-C levels. No passage found establishes that higher initial LDL-C produces a greater absolute risk reduction. (LLM, conf=0.73)

  cites [62] Brugts, 2009, The benefits of statins in people without established cardiovascular disease but with cardiovascular risk factors: meta-analysis of randomised controlled trials, BMJ sourceExperimental — accuracy not yet measured
• Partly supported

  The Discussion (page unavailable) says the benefit of ezetimibe appeared similar in patients with lower and higher baseline LDL-C, supporting the claim of benefit across baseline levels. It only suggests that greater benefit might have occurred at higher baseline LDL-C; it does not establish a greater absolute risk reduction as baseline LDL-C rises or a constant relative risk reduction at every level. (LLM, conf=0.82)

  cites [63] Cannon, 2015, Ezetimibe added to statin therapy after acute coronary syndromes, N Engl J Med sourceExperimental — accuracy not yet measured
• Partly supported

  The Results report that the relative risk reduction per 1 mmol/L decrease in LDL-C did not depend on baseline LDL-C concentration. The Discussion likewise describes a similar proportional benefit across baseline concentrations. Neither passage establishes that a higher initial LDL-C level produces a greater absolute reduction in event risk; the paper instead links larger proportional benefits to larger achieved reductions in LDL-C. (LLM, conf=0.88)

  cites [64] Cholesterol Treatment Trialists' (CTT) Collaboration, 2010, Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26 randomised trials, Lancet sourceExperimental — accuracy not yet measured
• Not checked yetcites [65] Cholesterol Treatment Trialists' (CTT) Collaboration, 2015, Efficacy and safety of LDL-lowering therapy among men and women: meta-analysis of individual data from 174,000 participants in 27 randomised trials, Lancet source
• Partly supported

  The Results report broadly similar proportional reductions in major vascular events per 1.0 mmol/L LDL-C reduction after stratification by baseline LDL-C. The Discussion says larger LDL-C reductions can yield larger absolute benefits, but our copy does not establish that a higher *initial LDL-C level itself* produces a greater absolute risk reduction. The paper also describes proportional reductions as broadly similar, rather than constant at every baseline level. (LLM, conf=0.86)

  cites [66] Cholesterol Treatment Trialists' (CTT) Collaborators, 2012, The effects of lowering LDL cholesterol with statin therapy in people at low risk of vascular disease: meta-analysis of individual data from 27 randomised trials, Lancet sourceExperimental — accuracy not yet measured
• Partly supported

  The Management of hypertriglyceridaemia > Statins section reports a 23% reduction in cardiovascular risk per mmol/L of LDL cholesterol lowered, irrespective of baseline LDL cholesterol concentration. This supports the claim about a consistent relative reduction, but the paper does not state that a higher initial LDL-C level produces a greater absolute reduction in risk. (LLM, conf=0.86)

  cites [67] Hegele, 2014, The polygenic nature of hypertriglyceridaemia: implications for definition, diagnosis, and management, Lancet Diabetes Endocrinol sourceExperimental — accuracy not yet measured
• ?Could not verify

  The Results report pooled relative risks and test whether changes in LDL-C predict outcomes; they do not compare absolute or relative risk reductions across initial LDL-C levels. The discussion likewise addresses LDL-C reduction, not the claimed pattern by baseline LDL-C. Searches for baseline LDL-C, absolute risk reduction, and constant relative risk reduction found no passage establishing that pattern. (LLM, conf=0.74)

  cites [68] Mills, 2008, Primary prevention of cardiovascular mortality and events with statin treatments: a network meta-analysis involving more than 65,000 patients, J Am Coll Cardiol sourceExperimental — accuracy not yet measured
• Not checked yetcites [69] Pedersen, 2005, High-dose atorvastatin vs usual-dose simvastatin for secondary prevention after myocardial infarction: the IDEAL study: a randomized controlled trial, JAMA source
• ?Could not verify

  The Results (Clinical Outcomes; page unavailable) report the effect of intensive versus standard blood-pressure control, and the Discussion (page unavailable) says those benefits were consistent across prespecified subgroups. Searches for initial LDL-C, baseline LDL-C, and the claimed absolute-versus-relative risk pattern found no passage addressing how risk reduction varies by LDL-C level. (LLM, conf=0.78)

  cites [70] SPRINT Research Group, 2015, A randomized trial of intensive versus standard blood-pressure control, N Engl J Med sourceExperimental — accuracy not yet measured

In the paper

“ApoCIII has been identified as a new potential therapeutic target that is currently being studied, but whether it has a role in clinical practice is unknown and its measurements on a routine basis are not encouraged. 108”

What the sources say

• Partly supported

  The Discussion reports that an apoC-III antisense drug had advanced to phase 2 trials and that future studies would evaluate its therapeutic potential, supporting its status as a target under study rather than an established treatment. The paper does not advise against routine apoC-III measurement, so that part of the cited sentence is unsupported. (LLM, conf=0.85)

  cites [108] Graham, 2013, Antisense oligonucleotide inhibition of apolipoprotein C-III reduces plasma triglycerides in rodents, nonhuman primates, and humans, Circ Res sourceExperimental — accuracy not yet measured

In the paper

“Non-HDL-C also includes the atherogenic TG-rich lipoproteins (VLDL, IDL and remnants), which is essential considering the recent information from genome-wide association studies (GWASs) and Mendelian randomization 76,86 - 89 supporting TGs and remnant particles as causative factors in atherogenesis.”

What the sources say

• Not checked yetcites [76] Jorgensen, 2013, Genetically elevated non-fasting triglycerides and calculated remnant cholesterol as causal risk factors for myocardial infarction, Eur Heart J source
• Not checked yetcites [86] Varbo, 2013, Remnant cholesterol as a causal risk factor for ischemic heart disease, J Am Coll Cardiol source
• Partly supported

  The Discussion reports genetic evidence consistent with a causal role for triglyceride-mediated pathways in coronary heart disease and describes VLDL and remnant lipoproteins as potentially proatherogenic. It does not establish that remnant particles themselves cause atherogenesis or state that non-HDL-C includes VLDL, IDL and remnants. The Introduction discusses GWAS and Mendelian randomisation, but those methods do not fill these gaps. (LLM, conf=0.86)

  cites [87] Triglyceride Coronary Disease Genetics, Consortium and Emerging Risk Factors Collaboration, 2010, Triglyceride-mediated pathways and coronary disease: collaborative analysis of 101 studies, Lancet sourceExperimental — accuracy not yet measured
• Partly supported

  In the Abstract (page not provided), the authors use genetic variants to suggest that triglyceride-rich lipoproteins causally influence coronary artery disease risk and describe evidence that cholesterol-rich remnants are pro-atherogenic. They caution that plasma triglycerides may reflect several processes and that the direct links to atherosclerosis remain unclear, so the paper does not establish triglycerides themselves as causative factors. (LLM, conf=0.85)

  cites [88] Do, 2013, Common variants associated with plasma triglycerides and risk for coronary artery disease, Nat Genet sourceExperimental — accuracy not yet measured
• Partly supported

  The Discussion (page not provided) says the Mendelian randomization findings make a causal role for triglycerides in coronary heart disease likely. It does not establish that remnant particles specifically are causal; instead, it says the roles of triglyceride-containing lipoprotein subcomponents require further investigation. The paper also does not address the claim that non-HDL-C includes those particles. (LLM, conf=0.88)

  cites [89] Holmes, 2015, Mendelian randomization of blood lipids for coronary heart disease, Eur Heart J sourceExperimental — accuracy not yet measured

In the paper

“With increasing knowledge about common polymorphisms and lipoproteins, the importance of a polygenic background to familial hyperlipidaemias is emphasized. 67,122”

What the sources say

• Supported

  The ‘Complex genetic basis for hypertriglyceridaemia’ section says that more than 95% of patients with hypertriglyceridaemia have a multigenic susceptibility component, and that some patients with familial hypercholesterolaemia have elevated LDL cholesterol due to common risk variants. The ‘Role of common variants’ section likewise links an increased burden of triglyceride-raising alleles to susceptibility. These passages support the cited point that a polygenic background matters in familial lipid disorders. (LLM, conf=0.88)

  cites [67] Hegele, 2014, The polygenic nature of hypertriglyceridaemia: implications for definition, diagnosis, and management, Lancet Diabetes Endocrinol source
• Supported

  The Introduction describes LDL-C-raising common variants as a likely polygenic cause in some patients with clinical familial hypercholesterolemia and no identified mutation. The Conclusion reports that hypercholesterolemia in 88% of mutation-negative patients is likely to have a polygenic basis. This supports the cited sentence's general point, though the paper specifically studies familial hypercholesterolemia. (LLM, conf=0.86)

  cites [122] Futema, 2015, Refinement of variant selection for the LDL cholesterol genetic risk score in the diagnosis of the polygenic form of clinical familial hypercholesterolemia and replication in samples from 6 countries, Clin Chem source

In the paper

“Although the CVD risk is increased if fasting TGs are . 1.7 mmol/ L (150 mg/dL), 87 the use of drugs to lower TGs may only be considered in high-risk subjects when TGs are . 2.3 mmol/L (200 mg/dL) and cannot be lowered by lifestyle measures.”

What the sources say

• Partly supported

  The Results report an association between higher triglyceride concentration and coronary heart disease risk, but do not establish a fasting threshold of 1.7 mmol/L; the association also attenuated after adjustment for other risk factors. Citation 87 is attached to that risk statement, not to the subsequent drug-treatment recommendation, which the paper does not provide. (LLM, conf=0.84)

  cites [87] Triglyceride Coronary Disease Genetics, Consortium and Emerging Risk Factors Collaboration, 2010, Triglyceride-mediated pathways and coronary disease: collaborative analysis of 101 studies, Lancet sourceExperimental — accuracy not yet measured

In the paper

“Functional foods containing phytosterols as well as plant sterolcontaining tablets additionally reduce LDL-C levels by up to 5-10% in patients taking a stable dose of a statin, and this combination is also well tolerated and safe.”

What the sources say

• Not checked yetcites [142] Gylling, 2014, Plant sterols and plant stanols in the management of dyslipidaemia and prevention of cardiovascular disease, Atherosclerosis source
• Partly supported

  The Results report that plant sterol/stanol-containing foods lowered LDL-C versus placebo, supporting the general cholesterol-lowering point. They do not establish an additional 5–10% reduction for foods or tablets in patients on a stable statin dose, or assess whether that combination is well tolerated and safe. The paper cites a statin-combination trial in its References, but that citation alone does not establish the claimed magnitude or safety. (LLM, conf=0.86)

  cites [255] Abumweis, 2008, Plant sterols/stanols as cholesterol lowering agents: a meta-analysis of randomized controlled trials sourceExperimental — accuracy not yet measured

In the paper

“The IMPROVE-IT study 63 included patients at least 50 years of age who had been hospitalized within the preceding 10 days for an ACS (24% women).”

What the sources say

• Supported

  The Patient Population section states that men and women aged at least 50 were eligible if hospitalized within the preceding 10 days for an acute coronary syndrome. The Patients section reports that 24% of participants were women. (LLM, conf=0.95)

  cites [63] Cannon, 2015, Ezetimibe added to statin therapy after acute coronary syndromes, N Engl J Med source

In the paper

“The CV mortality in patients with stage 3 and stage 4 CKD is two-fold and three-fold higher, respectively, when compared with patients with normal renal function. 391”

What the sources say

• Partly supported

  The Discussion (page unavailable) reports approximately two-fold higher mortality risk around eGFR 30–45 than at optimal eGFR, with variation across outcomes and models. The Results (page unavailable) report a 3.14-fold hazard at eGFR 15 for all-cause mortality and say cardiovascular findings were similar. These selected eGFR comparisons do not establish two-fold and three-fold cardiovascular mortality across all of CKD stages 3 and 4, respectively. (LLM, conf=0.85)

  cites [391] Chronic Kidney Disease Prognosis Consortium, 2010, Association of estimated glomerular filtration rate and albuminuria with all-cause and cardiovascular mortality in general population cohorts: a collaborative meta-analysis, Lancet sourceExperimental — accuracy not yet measured

In the paper

“Importantly, a sizable portion of patients on hypolipidaemic or antihypertensive drug treatment fail to take their treatment adequately or to reach their therapeutic goals, 28,29 with clinical and economic consequences. 30”

What the sources say

• Not checked yetcites [28] Banegas, 2011, Achievement of treatment goals for primary prevention of cardiovascular disease in clinical practice across Europe: the EURIKA study, Eur Heart J source
• Not checked yetcites [29] Kotseva, 2010, EUROASPIRE III. Management of cardiovascular risk factors in asymptomatic high-risk patients in general practice: cross-sectional survey in 12 European countries, Eur J Cardiovasc Prev Rehabil source
• Not checked yetcites [30] Cherry, 2009, The clinical and economic burden of nonadherence with antihypertensive and lipid-lowering therapy in hypertensive patients, Value Health source

In the paper

“The SCORE data indicate that the total CVD event risk is about three times higher than the risk of fatal CVD for men, so that a SCORE risk of 5% translates into a CVD risk of ≏ 15% of total (fatal + non-fatal) hard CVD endpoints; the multiplier is ≏ 4 in women and lower in older persons.”

In the paper

“Quantitatively, dietary trans fatty acids have a similar elevating effect on LDL-C to that of SFAs; however, while SFAs increase HDL-C levels, trans fats decrease them. 137”

What the sources say

• Not checked yetcites [137] Estruch, 2013, Primary prevention of cardiovascular disease with a Mediterranean diet, N Engl J Med source

In the paper

“If 1% of the dietary energy derived from SFAs is replaced by n-6 polyunsaturated fatty acids (PUFAs), LDL-C decreases by 0.051 mmol/L (2.0 mg/ dL); if replaced by monounsaturated fatty acids (MUFAs), the decrease would be 0.041 mmol/L (1.6 mg/dL); and if replaced by carbohydrate, it would be 0.032 mmol/L (1.2 mg/dL).”

What the sources say

• Not checked yetcites [165] Mensink, 2003, Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials, Am J Clin Nutr source

In the paper

“'Partially hydrogenated fatty acids' of industrial origin represent the major source of trans fatty acids in the diet; the average consumption of trans fatty acids ranges from 0.2% to 6.5% of the total energy intake in different populations. 166”

What the sources say

• Not checked yetcites [166] Micha, 2014, Global, regional, and national consumption levels of dietary fats and oils in 1990 and 2010: a systematic analysis including 266 country-specific nutrition surveys, BMJ source

In the paper

“PUFAs of the n-3 series have no hypocholesterolaemic effect; conversely, when they are used at high dosages ( . 3 g/day), the effect on LDL-C levels is either neutral or a slight increase [particularly with docosahexaenoic acid (DHA)] with a concomitant decrease of TGs. 165”

What the sources say

• Not checked yetcites [165] Mensink, 2003, Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials, Am J Clin Nutr source

In the paper

“the dietary patterns that have been more extensively evaluated are the Dietary Approaches to Stop Hypertension (DASH) diet, particularly in relation to blood pressure control, and the Mediterranean diet; both have been proven to be effective in reducing CV risk factors and, possibly, to contribute to CVD prevention. 133”

What the sources say

• Not checked yetcites [133] Eckel, 2014, 2013 AHA/ACC guideline on lifestyle management to reduce cardiovascular risk: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines, Circulation source

In the paper

“Some interventions resulted in significant CVD prevention, whereas others did not.”

What the sources say

• Not checked yetcites [132] Dalen, 2014, Diets to prevent coronary heart disease 1957–2013: what have we learned, Am J Med source

In the paper

“Body weight reduction also influences TC and LDL-C, but the magnitude of the effect is rather small; in grossly obese subjects, a decrease in LDL-C concentration of ≏ 0.2 mmol/L (8 mg/dL) is observed for every 10 kg of weight loss; the reduction of LDL-C is greater if weight loss is achieved with a low fat diet. 147,148”

What the sources say

• Not checked yetcites [147] Dattilo, 1992, Effects of weight reduction on blood lipids and lipoproteins: a meta-analysis, Am J Clin Nutr source
• Not checked yetcites [148] Nordmann, 2006, Effects of low-carbohydrate vs low-fat diets on weight loss and cardiovascular risk factors: a meta-analysis of randomized controlled trials, Arch Intern Med source

In the paper

“Particular consideration was given to results from systematic reviews confirming the dose-dependent reduction in CVD with LDL-C lowering; the greater the LDL-C reduction, the greater the CV risk reduction. 65,66”

What the sources say

• Not checked yetcites [65] Cholesterol Treatment Trialists' (CTT) Collaboration, 2015, Efficacy and safety of LDL-lowering therapy among men and women: meta-analysis of individual data from 174,000 participants in 27 randomised trials, Lancet source
• Not checked yetcites [66] Cholesterol Treatment Trialists' (CTT) Collaborators, 2012, The effects of lowering LDL cholesterol with statin therapy in people at low risk of vascular disease: meta-analysis of individual data from 27 randomised trials, Lancet source

In the paper

“the elimination of health risk behaviours would make it possible to prevent at least 80% of CVD and even 40% of cancers”

What the sources say

• Not checked yetcites [3] Liu, 2012, Healthy lifestyle through young adulthood and the presence of low cardiovascular disease risk profile in middle age: the Coronary Artery Risk Development in (Young) Adults (CARDIA) study, Circulation source
• Not checked yetcites [4] Ezzati, 2004, Comparative quantification of health risks: global and regional burden of disease attributable to selected major risk factors

In the paper

“Cost-effectiveness depends on several factors, including baseline CV risk, cost of drugs or other interventions, reimbursement procedures, and uptake of preventive strategies.”

In the paper

“According to the WHO, policy and environmental changes could reduce CVD in all countries for , US$1 per person per year, while interventions at the individual level are considerably more expensive. 37”

What the sources say

• Not checked yetcites [37] Brown, 2011, Medication adherence: WHO cares?, Mayo Clin Proc source

In the paper

“A report from the National Institute for Health and Care Excellence (NICE) estimated that a UK national programme reducing population CV risk by 1% would prevent 25 000 CVD cases and generate savings of E 40 million per year. 38”

What the sources say

• Not checked yetcites [38] National Institute for Health and Care Excellence

In the paper

“Lowering blood cholesterol levels using statins 10,11,23-25 and improving blood pressure control are also cost effective. 26,27”

What the sources say

• Not checked yetcites [10] McConnachie, 2014, Long-term impact on healthcare resource utilization of statin treatment, and its cost effectiveness in the primary prevention of cardiovascular disease: a record linkage study, Eur Heart J source
• Not checked yetcites [11] Ward, 2007, A systematic review and economic evaluation of statins for the prevention of coronary events, Health Technol Assess source
• Not checked yetcites [23] Neyt, 2009, Cost-effectiveness of statins in the primary prevention of cardiovascular disease: a systematic review and economic analysis for Belgium, Acta Cardiol source
• Not checked yetcites [24] Peura, 2008, Cost-effectiveness of statins in the prevention of coronary heart disease events in middle-aged Finnish men, Curr Med Res Opin source
• Not checked yetcites [25] Ito, 2011, Statins for cardiovascular prevention according to different strategies: a cost analysis, Am J Cardiovasc Drugs source
• Not checked yetcites [26] Stevanovic, 2014, Economic evaluation of primary prevention of cardiovascular diseases in mild hypertension: a scenario analysis for the Netherlands, Clin Ther source
• Not checked yetcites [27] Wisloff, 2012, Choice of generic antihypertensive drugs for the primary prevention of cardiovascular disease—a cost-effectiveness analysis, BMC Cardiovasc Disord source

In the paper

“Most studies assessing the cost-effectiveness of prevention of CVD combine evidence from clinical research with simulation approaches, while data from randomized controlled trials (RCTs) are relatively scarce. 7,10,11”

What the sources say

• Not checked yetcites [7] Mistry, 2012 11, Cost-effectiveness of a European preventive cardiology programme in primary care: a Markov modelling approach, BMJ Open source
• Not checked yetcites [10] McConnachie, 2014, Long-term impact on healthcare resource utilization of statin treatment, and its cost effectiveness in the primary prevention of cardiovascular disease: a record linkage study, Eur Heart J source
• Not checked yetcites [11] Ward, 2007, A systematic review and economic evaluation of statins for the prevention of coronary events, Health Technol Assess source

In the paper

“Coronary artery disease (CAD) mortality rates could be halved by only modest risk factor reduction, 39”

What the sources say

• Not checked yetcites [39] Capewell, 2010, Cardiovascular risk factor trends and potential for reducing coronary heart disease mortality in the United States of America, Bull World Health Org source

In the paper

“Cost-effectiveness results strongly depend on parameters such as the target population's age, the overall population risk of CVD and the cost of interventions. Hence, results obtained in one country might not be valid in another.”

In the paper

“The reasons for retaining a system that estimates fatal as opposed to total fatal + non-fatal events are that non-fatal events are dependent on definition, developments in diagnostic tests and methods of ascertainment, all of which can vary, resulting in very variable multipliers to convert fatal to total events.”

In the paper

“This is problematic since risk is a continuum and there is no threshold at which, for example, a drug is automatically indicated.”

In the paper

“Risk age can be used in any population regardless of baseline risk or secular changes in mortality, and therefore avoids the need for recalibration.”

In the paper

“This graded approach is based on evidence from multiple meta-analyses and individual RCTs, which show a consistent and graded reduction in CVD risk in response to reductions in TC and LDL-C levels. 61-71”

What the sources say

• Not checked yetcites [61] Boekholdt, 2014, Very low levels of atherogenic lipoproteins and the risk for cardiovascular events: a meta-analysis of statin trials, J Am Coll Cardiol source
• Not checked yetcites [62] Brugts, 2009, The benefits of statins in people without established cardiovascular disease but with cardiovascular risk factors: meta-analysis of randomised controlled trials, BMJ source
• Not checked yetcites [63] Cannon, 2015, Ezetimibe added to statin therapy after acute coronary syndromes, N Engl J Med source
• Not checked yetcites [64] Cholesterol Treatment Trialists' (CTT) Collaboration, 2010, Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26 randomised trials, Lancet source
• Not checked yetcites [65] Cholesterol Treatment Trialists' (CTT) Collaboration, 2015, Efficacy and safety of LDL-lowering therapy among men and women: meta-analysis of individual data from 174,000 participants in 27 randomised trials, Lancet source
• Not checked yetcites [66] Cholesterol Treatment Trialists' (CTT) Collaborators, 2012, The effects of lowering LDL cholesterol with statin therapy in people at low risk of vascular disease: meta-analysis of individual data from 27 randomised trials, Lancet source
• Not checked yetcites [67] Hegele, 2014, The polygenic nature of hypertriglyceridaemia: implications for definition, diagnosis, and management, Lancet Diabetes Endocrinol source
• Not checked yetcites [68] Mills, 2008, Primary prevention of cardiovascular mortality and events with statin treatments: a network meta-analysis involving more than 65,000 patients, J Am Coll Cardiol source
• Not checked yetcites [69] Pedersen, 2005, High-dose atorvastatin vs usual-dose simvastatin for secondary prevention after myocardial infarction: the IDEAL study: a randomized controlled trial, JAMA source
• Not checked yetcites [70] SPRINT Research Group, 2015, A randomized trial of intensive versus standard blood-pressure control, N Engl J Med source

In the paper

“Overall, HDL-C has a modest but useful effect in refining risk estimation, 56 but this may not be universal, as its effect may not be seen in some low-risk populations, particularly with a relatively high mean HDL-C level. 57”

What the sources say

• Not checked yetcites [56] Cooney, 2009, How much does HDL cholesterol add to risk estimation? A report from the SCORE Investigators, Eur J Cardiovasc Prev Rehabil source
• Not checked yetcites [57] Mortensen, 2015, The high-density lipoprotein-adjusted SCORE model worsens SCORE-based risk classification in a contemporary population of 30,824 Europeans: the Copenhagen General Population Study, Eur Heart J source

In the paper

“Risk estimates have been produced as charts for high- and low-risk regions in Europe ( Figures 2 and 3 ).”

In the paper

“Some other systems estimate CAD risk only.”

In the paper

“Other risk estimation systems can also be recalibrated, but the process is easier for mortality than for total events.”

In the paper

“Calibrated country-specific versions exist for Belgium, Cyprus, Czech Republic, Germany, Greece, Poland, Slovakia, Spain, Switzerland and Sweden, and country-specific electronic versions for Bosnia and Herzegovina, Croatia, Estonia, France, Romania, Russian Federation and Turkey can be found at http://www.heartscore.org.”

In the paper

“Such charts are likely to represent current risk levels better.”

In the paper

“All International Classification of Diseases (ICD) codes that are related to deaths from vascular origin caused by atherosclerosis are included.”

In the paper

“The SCORE system estimates the 10-year cumulative risk of a first fatal atherosclerotic event, whether heart attack, stroke or other occlusive arterial disease, including sudden cardiac death.”

In the paper

“Recent work has shown that b -coefficients are not constant with ageing and that SCORE overestimates risk in older people. 54”

What the sources say

• Not checked yetcites [54] Cooney, 2016, Cardiovascular risk estimation in older persons: SCORE O.P, Eur J Prev Cardiol source

In the paper

“The European Guidelines on CVD prevention in clinical practice (version 2012) 6 recommend use of the SCORE system because it is based on large, representative European cohort datasets.”

What the sources say

• Not checked yetcites [6] Perk, 2012, European Guidelines on cardiovascular disease prevention in clinical practice (version 2012). The Fifth Joint Task Force of the European Society of Cardiology and Other Societies on Cardiovascular Disease Prevention in Clinical Practice (constituted by representatives of nine societies and by invited experts), Eur Heart J

In the paper

“Most guidelines use one of these risk estimation systems. 50-52”

What the sources say

• Not checked yetcites [50] Hajifathalian, 2015, A novel risk score to predict cardiovascular disease risk in national populations (Globorisk): a pooled analysis of prospective cohorts and health examination surveys, Lancet Diabetes Endocrinol source
• Not checked yetcites [51] Cooney, 2009, Value and limitations of existing scores for the assessment of cardiovascular risk: a review for clinicians, J Am Coll Cardiol source
• Not checked yetcites [52] Cooney, 2010, Cardiovascular risk-estimation systems in primary prevention: do they differ? Do they make a difference? Can we see the future?, Circulation source

In the paper

“Patients who have had a clinical event such as acute coronary syndrome (ACS) or a stroke are at very high risk of a further event and automatically qualify for risk factor evaluation and management ( Table 6 ).”

In the paper

“In some reports non-HDL-C is superior, but in others, LDL-C and non-HDL-C are reported to give similar information. 83-85”

What the sources say

• Not checked yetcites [83] Emerging Risk Factors Collaboration, 2012, Thompson SG, Boekholdt SM, Sattar N, Packard C, Gudnason V, Danesh J. Lipid-related markers and cardiovascular disease prediction, JAMA
• Not checked yetcites [84] Boekholdt, 2012, Association of LDL cholesterol, non-HDL cholesterol, and apolipoprotein B levels with risk of cardiovascular events among patients treated with statins: a meta-analysis, JAMA source
• Not checked yetcites [85] Robinson, 2012, Meta-analysis of comparison of effectiveness of lowering apolipoprotein B versus low-density lipoprotein cholesterol and nonhigh-density lipoprotein cholesterol for cardiovascular risk reduction in randomized trials, Am J Cardiol source

In the paper

“Based on epidemiological data, levels of HDL-C associated with increased risk for men are , 1.0 mmol/L (40 mg/dL) and for women are , 1.2 mmol/L (48 mg/dL).”

In the paper

“It should also be considered that HTG might interfere with the direct HDL-C assays. 72”

What the sources say

• Not checked yetcites [72] Langlois, 2014, Clinical impact of direct HDLc and LDLc method bias in hypertriglyceridemia. A simulation study of the EAS-EFLM Collaborative Project Group, Atherosclerosis source

In the paper

“This raises the issue that most older people in high-risk countries who smoke would be candidates for lipid-lowering drug treatment even if they have satisfactory blood pressure levels.”

In the paper

“For risk estimation, non-fasting has a prediction strength similar to fasting, and non-fasting lipid levels can be used in screening and in general risk estimation. 73-76”

What the sources say

• Not checked yetcites [73] Kolovou, 2011, Assessment and clinical relevance of non-fasting and postprandial triglycerides: an expert panel statement, Curr Vasc Pharmacol source
• Not checked yetcites [74] Mihas, 2011, Diagnostic value of postprandial triglyceride testing in healthy subjects: a meta-analysis, Curr Vasc Pharmacol source
• Not checked yetcites [75] Nordestgaard, 2014, Triglycerides and cardiovascular disease, Lancet source
• Not checked yetcites [76] Jorgensen, 2013, Genetically elevated non-fasting triglycerides and calculated remnant cholesterol as causal risk factors for myocardial infarction, Eur Heart J source

In the paper

“It should be emphasized, however, that the risk may be underestimated in patients with diabetes, because in one study, patients with diabetes had up to 0.6 mmol/L lower LDL-C in non-fasting samples. 77”

What the sources say

• Not checked yetcites [77] Langsted, 2011, Nonfasting lipids, lipoproteins, and apolipoproteins in individuals with and without diabetes: 58 434 individuals from the Copenhagen General Population Study, Clin Chem source

In the paper

“Low HDL-C has been shown to be a strong and independent risk factor in several studies and is included in most of the risk estimation tools available, including HeartScore.”

In the paper

“Furthermore, loss of function mutations are associated with low TGs as well as with reduced risk for CVD. 106,107”

What the sources say

• Not checked yetcites [106] TG and HDL Working Group of the Exome Sequencing Project, National Heart, Lung, and Blood Institute, 2014, Loss-of-function mutations in APOC3, triglycerides, and coronary disease, N Engl J Med source
• Not checked yetcites [107] Jorgensen, 2014, Loss-of-function mutations in APOC3 and risk of ischemic vascular disease, N Engl J Med source

In the paper

“Non-HDL-C has recently been proposed by locally developed guidelines such as NICE using the QRISK2 risk calculator. 79,80”

What the sources say

• Not checked yetcites [79] Rabar, 2014, Lipid modification and cardiovascular risk assessment for the primary and secondary prevention of cardiovascular disease: summary of updated NICE guidance, BMJ source
• Not checked yetcites [80] JBS3, 2014, Joint British Societies' consensus recommendations for the prevention of cardiovascular disease (JBS3), Heart source

In the paper

“The direct methods for HDL-C and LDL-C analysis are currently widely used and are reliable in patients with normal lipid levels. 72”

What the sources say

• Not checked yetcites [72] Langlois, 2014, Clinical impact of direct HDLc and LDLc method bias in hypertriglyceridemia. A simulation study of the EAS-EFLM Collaborative Project Group, Atherosclerosis source

In the paper

“Recent studies suggest that HDL has a complex role in atherogenesis and that the presence of dysfunctional HDL may be more relevant to the development of atherosclerosis than the HDL-C level. 93-95”

What the sources say

• Not checked yetcites [93] Khera, 2011, Cholesterol efflux capacity, high-density lipoprotein function, and atherosclerosis, N Engl J Med source
• Not checked yetcites [94] Li, 2013, Paradoxical association of enhanced cholesterol efflux with increased incident cardiovascular risks, Arterioscler Thromb Vasc Biol source
• Not checked yetcites [95] Rohatgi, 2014, HDL cholesterol efflux capacity and incident cardiovascular events, N Engl J Med source

In the paper

“This is to some extent due to analytical variation, but is also due to environmental factors such as diet and physical activity, and a seasonal variation, with higher levels of TC and HDL-C during the winter. 78”

What the sources say

• Not checked yetcites [78] Marti-Soler, 2014, Seasonality of cardiovascular risk factors: an analysis including over 230 000 participants in 15 countries, Heart source

In the paper

“Some recent guidelines recommend non-HDL-C as a better risk indicator than LDL-C. 82”

What the sources say

• Not checked yetcites [82] National Institute for Health and Care Excellence, 2014, Lipid modification: cardiovascular risk assessment and the modification of blood lipids for the primary and secondary prevention of cardiovascular disease

In the paper

“The risk is regarded as significant when Lp(a) is above the 80th percentile (50 mg/dL). 109”

What the sources say

• Not checked yetcites [109] Nordestgaard, 2010, Lipoprotein(a) as a cardiovascular risk factor: current status, Eur Heart J source

In the paper

“Glucose and lipid metabolism are strongly related, and any perturbation of carbohydrate metabolism induced by a high carbohydrate diet will also lead to an increase in TG concentrations. 148,165”

What the sources say

• Not checked yetcites [148] Nordmann, 2006, Effects of low-carbohydrate vs low-fat diets on weight loss and cardiovascular risk factors: a meta-analysis of randomized controlled trials, Arch Intern Med source
• Not checked yetcites [165] Mensink, 2003, Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials, Am J Clin Nutr source

In the paper

“Determination of small dense LDL may be regarded as an emerging risk factor and may be used in the future, but it is not currently recommended for risk estimation. 119”

What the sources say

• Not checked yetcites [119] Mora, 2007, LDL particle subclasses, LDL particle size, and carotid atherosclerosis in the Multi-Ethnic Study of Atherosclerosis (MESA), Atherosclerosis source

In the paper

“This is due not only to methodological problems, particularly inadequate sample size or the short duration of many trials included in the systematic revision, but also to the difficulty of evaluating the impact of a single dietary factor independently of any other changes in the diet.”

In the paper

“Several methods for determination of Lp(a) are available, but standardization between assays is needed. 112”

What the sources say

• Not checked yetcites [112] Marcovina, 2003, Report of the National Heart, Lung, and Blood Institute Workshop on Lipoprotein(a) and Cardiovascular Disease: recent advances and future directions, Clin Chem source

In the paper

“In both the 2011 EAS/ESC guidelines for the management of dyslipidaemias 125 and the American Heart Association/American College of Cardiology (AHA/ACC) guidelines on the treatment of blood cholesterol to reduce atherosclerotic CV risk in adults, 71 the importance of LDL-C lowering to prevent CVD is strongly emphasized.”

What the sources say

• Not checked yetcites [125] European Association for Cardiovascular Prevention & Rehabilitation, 2011, ESC/EAS Guidelines for the management of dyslipidaemias: the Task Force for the management of dyslipidaemias of the European Society of Cardiology (ESC) and the European Atherosclerosis Society (EAS), Eur Heart J source
• Not checked yetcites [71] Stone, 2014, 2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines, Circulation

In the paper

“In FH, a genetic diagnosis is important for family screening, to establish the diagnosis in patients with borderline LDL-C and to improve patient adherence to therapy. 121”

What the sources say

• Not checked yetcites [121] Nordestgaard, 2013, Familial hypercholesterolaemia is underdiagnosed and undertreated in the general population: guidance for clinicians to prevent coronary heart disease: consensus statement of the European Atherosclerosis Society, Eur Heart J source

In the paper

“Secondary targets have also been defined by inference for non-HDL-C and for apoB; they receive a moderate grading, as they have not been extensively studied in RCTs.”

In the paper

“A fat-modified diet that provides 25-40 g of total dietary fibre, including at least 7-13 g of soluble fibre, is well tolerated, effective and recommended for plasma lipid control; conversely, there is no justification for the recommendation of very low carbohydrate diets. 164”

What the sources say

• Not checked yetcites [164] Poli, 2008, Non-pharmacological control of plasma cholesterol levels, Nutr Metab Cardiovasc Dis source

In the paper

“In particular, the detrimental effects of a high carbohydrate diet on TGs occur mainly when refined carbohydrate-rich foods are consumed, while they are much less prominent if the diet is based largely on fibre-rich, low glycaemic index foods.”

What the sources say

• Not checked yetcites [173] Liu, 2001, Dietary glycemic load assessed by food-frequency questionnaire in relation to plasma high-density-lipoprotein cholesterol and fasting plasma triacylglycerols in postmenopausal women, Am J Clin Nutr source
• Not checked yetcites [174] De Natale, 2009, Effects of a plant-based high-carbohydrate/high-fiber diet versus high-monounsaturated fat/low-carbohydrate diet on postprandial lipids in type 2 diabetic patients, Diabetes Care source

In the paper

“This treatment seems to induce beneficial effects not only on the overall risk factor profile, but also on CV events. 181”

What the sources say

• Not checked yetcites [181] Puzziferri, 2014, Long-term follow-up after bariatric surgery: a systematic review, JAMA source

In the paper

“It has to be kept in mind that dietary components, other lifestyle factors and weight loss also contribute to reducing the overall CV risk through their influence on other risk factors, e.g. hypertension, subclinical inflammation or impaired insulin sensitivity.”

In the paper

“Measurements of waist circumference . 80 cm for women of any ethnicity and . 94 cm for men of European ancestry or . 90 cm for men of Asian origin indicate the presence of abdominal adiposity, even in people of normal weight ( Table 14 ). 180”

What the sources say

• Not checked yetcites [180] Alberti, 2009, Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity, Circulation source

In the paper

“Conversely, a low intake of fats and oils increases the risk of inadequate intakes of vitamin E and of essential fatty acids, and may contribute to unfavourable changes in HDL-C. 165”

What the sources say

• Not checked yetcites [165] Mensink, 2003, Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials, Am J Clin Nutr source

In the paper

“Overall, the available evidence on functional foods so far identified in this field is incomplete; the major gap is the absence of diet-based intervention trials of sufficient duration to be relevant for the natural history of dyslipidaemia and CVD.”

In the paper

“Modest weight reduction and regular physical exercise of moderate intensity are very effective in preventing type 2 diabetes and improving all the metabolic abnormalities and CV risk factors clustering with insulin resistance, which are often associated with abdominal adiposity.”

What the sources say

• Not checked yetcites [169] Huffman, 2012, Exercise effects on lipids in persons with varying dietary patterns-does diet matter if they exercise? Responses in Studies of a Targeted Risk Reduction Intervention through Defined Exercise I, Am Heart J source

In the paper

“These effects are dose dependent; with a habitual fructose consumption between 15 and 20% of the total energy intake, plasma TG increases as much as 30-40%.”

What the sources say

• Not checked yetcites [158] Stanhope, 2009, Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans, J Clin Invest source
• Not checked yetcites [175] Stanhope, 2015, A dose-response study of consuming high-fructose corn syrup-sweetened beverages on lipid/lipoprotein risk factors for cardiovascular disease in young adults, Am J Clin Nutr source

In the paper

“Weight reduction improves insulin sensitivity and decreases TG levels.”

What the sources say

• Not checked yetcites [150] Shaw, 2006, Exercise for overweight or obesity, Cochrane Database Syst Rev
• Not checked yetcites [169] Huffman, 2012, Exercise effects on lipids in persons with varying dietary patterns-does diet matter if they exercise? Responses in Studies of a Targeted Risk Reduction Intervention through Defined Exercise I, Am Heart J source
• Not checked yetcites [176] Kraus, 2002, Effects of the amount and intensity of exercise on plasma lipoproteins, N Engl J Med source

In the paper

“Different commercial preparations of RYR have different concentrations of monacolins, and lower TC and LDL-C to a variable extent, 145 but the long-term safety of the regular consumption of these products is not fully documented.”

What the sources say

• Not checked yetcites [145] Gordon, 2010, Marked variability of monacolin levels in commercial red yeast rice products: buyer beware, Arch Intern Med source

In the paper

“In many studies the reduction of TG levels due to weight reduction is between 20-30%; this effect is usually preserved as long as weight is not regained.”

What the sources say

• Not checked yetcites [150] Shaw, 2006, Exercise for overweight or obesity, Cochrane Database Syst Rev
• Not checked yetcites [169] Huffman, 2012, Exercise effects on lipids in persons with varying dietary patterns-does diet matter if they exercise? Responses in Studies of a Targeted Risk Reduction Intervention through Defined Exercise I, Am Heart J source
• Not checked yetcites [176] Kraus, 2002, Effects of the amount and intensity of exercise on plasma lipoproteins, N Engl J Med source

In the paper

“The daily consumption of 2 g of phytosterols can effectively lower TC and LDL-C by 7-10% in humans (with a certain degree of heterogeneity among individuals), while it has little or no effect on HDL-C and TG levels. 143”

What the sources say

• Not checked yetcites [143] Musa-Veloso, 2011, A comparison of the LDL-cholesterol lowering efficacy of plant stanols and plant sterols over a continuous dose range: results of a meta-analysis of randomized, placebo-controlled trials, Prostaglandins Leukot Essent Fatty Acids source

In the paper

“Smoking cessation may also contribute to HDL-C elevation, provided that weight gain is prevented; this is often observed soon after quitting smoking. 163”

What the sources say

• Not checked yetcites [163] Maeda, 2003, The effects of cessation from cigarette smoking on the lipid and lipoprotein profiles: a meta-analysis, Prev Med source

In the paper

“Smoking cessation has clear benefits on the overall CV risk, and specifically on HDL-C, but special attention should be paid in order to prevent weight gain in people who stop smoking. 163”

What the sources say

• Not checked yetcites [163] Maeda, 2003, The effects of cessation from cigarette smoking on the lipid and lipoprotein profiles: a meta-analysis, Prev Med source

In the paper

“SFAs increase HDL-C levels in parallel with LDL-C; in contrast, trans fats decrease them. 137”

What the sources say

• Not checked yetcites [137] Estruch, 2013, Primary prevention of cardiovascular disease with a Mediterranean diet, N Engl J Med source

In the paper

“As for berberine, a recent meta-analysis has evaluated its effects on plasma lipids in humans; six trials were available for this purpose: the berberine group contained 229 patients and the control group contained 222 patients. 190”

What the sources say

• Not checked yetcites [190] Lan, 2015, Meta-analysis of the effect and safety of berberine in the treatment of type 2 diabetes mellitus, hyperlipemia and hypertension, J Ethnopharmacol source

In the paper

“Patients with mild ALT elevation due to steatosis have been studied during statin treatment and there is no indication that statins cause any worsening of liver disease. 222-224”

What the sources say

• Not checked yetcites [222] Chalasani, 2004, Patients with elevated liver enzymes are not at higher risk for statin hepatotoxicity, Gastroenterology source
• Not checked yetcites [223] Vuppalanchi, 2005, Patients with elevated baseline liver enzymes do not have higher frequency of hepatotoxicity from lovastatin than those with normal baseline liver enzymes, Am J Med Sci source
• Not checked yetcites [224] Dongiovanni, 2015, Statin use and non-alcoholic steatohepatitis in at risk individuals, J Hepatol source

In the paper

“In rhabdomyolysis, creatine kinase (CK) levels are elevated at least 10 times, often up to 40 times the upper limit of normal. 211”

What the sources say

• Not checked yetcites [211] Stroes, 2015, Statin-associated muscle symptoms: impact on statin therapy—European Atherosclerosis Society Consensus Panel Statement on Assessment, Aetiology and Management, Eur Heart J source

In the paper

“Statins also reduce TGs by 30-50% and may increase HDL-C by 5-10%.”

In the paper

“Alfa-linolenic acid (a medium chain n-3 fatty acid present in chestnuts, some vegetables and some seed oils) is less effective on TG levels.”

What the sources say

• Not checked yetcites [156] Rivellese, 2003, Effects of dietary saturated, monounsaturated and n-3 fatty acids on fasting lipoproteins, LDL size and post-prandial lipid metabolism in healthy subjects, Atherosclerosis source
• Not checked yetcites [172] Jacobson, 2012, Effects of eicosapentaenoic acid and docosahexaenoic acid on low-density lipoprotein cholesterol and other lipids: a review, J Clin Lipidol source

In the paper

“Observational evidence supports the recommendation that the intake of fish (at least twice a week) and long chain n-3 fatty acids supplements at low dosage may reduce the risk of CV death and stroke in primary prevention, but have no major effects on plasma lipoprotein metabolism. 183”

What the sources say

• Not checked yetcites [183] Mozaffarian, 2013, Plasma phospholipid long-chain omega-3 fatty acids and total and cause-specific mortality in older adults: a cohort study, Ann Intern Med source

In the paper

“Current available evidence from meta-analyses suggests that the clinical benefit is largely independent of the type of statin but depends on the extent of LDL-C lowering, therefore the type of statin used should reflect the LDL-C goal in a given patient.”

In the paper

“The benefits were significant within the first year, but were greater in subsequent years.”

What the sources say

• Not checked yetcites [64] Cholesterol Treatment Trialists' (CTT) Collaboration, 2010, Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26 randomised trials, Lancet source

In the paper

“Mild elevation of ALT occurs in 0.5-2.0% of patients on statin treatment, more commonly with potent statins or high doses.”

In the paper

“The frequency of rhabdomyolysis has been estimated to represent 1-3 cases/100 p 000 patient-years. 212”

What the sources say

• Not checked yetcites [212] Law, 2006, Statin safety: a systematic review, Am J Cardiol source

In the paper

“New evidence is accumulating on the possible beneficial effects of these compounds, which are also present in olive oil, red wine, coffee, tea and cocoa, on subclinical inflammation and endothelial function, as well as their beneficial influence on plasma TGs at fasting and particularly in the postprandial period.”

In the paper

“Progression to liver failure is exceedingly rare, therefore routine monitoring of ALT during statin treatment is no longer recommended. 221”