2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: Executive Summary

Grundy, Scott M.; Stone, Neil J.; Bailey, Alison L.; Beam, Craig; Birtcher, Kim K.; Blumenthal, Roger S.; Braun, Lynne T.; Ferranti, Sarah D. de; Faiella-Tommasino, Joseph; Forman, Daniel E.; Goldberg, Ronald; Heidenreich, Paul A.; Mark, Daniel B.; Jones, Daniel W.; Lloyd‐Jones, Donald M.; Lopez-Pajares, Nuria; Ndumele, Chiadi E; Orringer, Carl E.; Peralta, Carmen A.; Saseen, Joseph J.; Smith, Sidney C.; Sperling, Laurence; Virani, Salim S.; Yeboah, Joseph

doi:10.1016/j.jacc.2018.11.002

Cited by 1,281 publications

(466 citation statements)

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“…New guidelines on cholesterol management were recently published in the United States. 57 In secondary prevention, high intensity or maximally tolerated statin therapy is recommended with the aim of reducing LDL-C by at least 50%. Target LDL-C is still 1.8 mmol/L, but more aggressive therapy with multiple drugs is recommended in patients at very high CVD risk (eg, history of multiple CVD events or multiple risk factors).…”

Section: Who and How To Treat With Lipid-modifying Drugsmentioning

confidence: 99%

“…In primary prevention, a target for LDL-C is not explicitly stated, but careful assessment of overall CVD risk is recommended. 57 In the context of primary prevention, it is essential to assess absolute CVD risk, either with one of the standard risk calculators 55 or manually by looking at the overall risk profile. Patients with a 5year CVD risk greater than 15% are certainly at high risk, but those at lower risk should still be considered for drug therapy when lipids are highly elevated or when multiple risk factors are present.…”

Section: Who and How To Treat With Lipid-modifying Drugsmentioning

confidence: 99%

“…Selection of patients in primary prevention for lipid therapy is sometimes challenging and guidelines suggest a potential role here for coronary artery calcium (CAC) scoring. 57,58 The CAC score has been shown to be predictive of CVD events. 59 The American guidelines, in brief, suggest that with a CAC score of 0, statins may be withheld if other major risk factors are absent; a CAC score from 1 to 99 favours statin therapy, especially in patients aged 55 years or over; a CAC score of 100 or over strongly favours statin therapy in any adult, if no contraindication exists.…”

Section: Who and How To Treat With Lipid-modifying Drugsmentioning

confidence: 99%

“…59 The American guidelines, in brief, suggest that with a CAC score of 0, statins may be withheld if other major risk factors are absent; a CAC score from 1 to 99 favours statin therapy, especially in patients aged 55 years or over; a CAC score of 100 or over strongly favours statin therapy in any adult, if no contraindication exists. 57 The pattern of recommendation in Australian guidelines is somewhat similar, but CAC assessment in not covered by Medicare reimbursement. 58 To summarise the general principles of lipid therapy, it is essential to exclude any contribution from subclinical hypothyroidism, nephrosis, diabetes or alcoholsensitivity, the latter in cases of marked hypertriglyceridaemia.…”

Section: Who and How To Treat With Lipid-modifying Drugsmentioning

confidence: 99%

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An updated review of lipid‐modifying therapy

Simons

2019

Medical Journal of Australia

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Summary Statin drugs reduce low‐density lipoprotein (LDL)‐cholesterol (LDL‐C) and cardiovascular risk. Ezetimibe may be used to supplement statin therapy, or used alone in cases of statin intolerance. Statin‐associated side effects do occur, especially muscle symptoms and new onset diabetes, but they do not detract from the benefits of statin therapy. Inhibitors of proprotein convertase subtilisin/kexin type 9 (PCSK9) reduce LDL‐C and cardiovascular risk. Evolocumab is subsidised in Australia for patients with familial hypercholesterolaemia when LDL‐C is not adequately controlled with maximum doses of statin or ezetimibe or when statin therapy is contraindicated. Fenofibrate reduces triglycerides and cardiovascular risk in patients with type 2 diabetes when triglycerides are elevated and high‐density lipoprotein (HDL) is low. A role for dietary omega‐3 fatty acids and esters in reducing cardiovascular risk remains controversial. All cases of secondary cardiovascular disease prevention merit intensive lipid therapy, unless a contraindication exists. Lipid therapy is justified in cases of primary prevention when absolute risk is high, especially when lipids are highly elevated or when multiple risk factors are present. Clinical management requires a focus on the predominant lipid disorder present, namely hypercholesterolaemia, hypertriglyceridaemia or combined hyperlipidaemia. There is an ongoing problem of poor long term persistence on lipid therapy, as well as reduced awareness by practitioners of poor risk factor control.

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Section: Who and How To Treat With Lipid-modifying Drugsmentioning

confidence: 99%

Section: Who and How To Treat With Lipid-modifying Drugsmentioning

confidence: 99%

Section: Who and How To Treat With Lipid-modifying Drugsmentioning

confidence: 99%

Section: Who and How To Treat With Lipid-modifying Drugsmentioning

confidence: 99%

See 2 more Smart Citations

An updated review of lipid‐modifying therapy

Simons

2019

Medical Journal of Australia

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“…Many studies have shown that hypertriglyceridaemia plays an important role in the development of premature atherosclerosis. [1][2][3][4][5][6][7] Disturbances in triglyceride (TG) metabolism are characterised by postprandial accumulation of TG-rich lipoprotein remnants and have been observed in various populations with elevated cardiovascular (CV) risk. [8][9][10] In individuals without diabetes mellitus (DM), abnormal postprandial hypertriglyceridaemia can increase plasma glucagon levels, leading to insufficient insulin-and glucose-induced glucagon suppression.…”

Section: Introductionmentioning

confidence: 99%

The influence of gene polymorphisms on postprandial triglyceride response after oral fat tolerance test meal in patients with diabetes mellitus

et al. 2019

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Summary Aims We evaluated the influence of CETP (rs5882 and rs708272), APOE (rs7412, rs429358) and LPL (rs328) gene polymorphisms on triglyceride (TG) response to oral fat tolerance test (OFTT) meal in patients with well‐controlled type 2 diabetes mellitus (T2DM). Methods Fifty‐one men underwent OFTT and according to postprandial TG response patients were divided into two subgroups (positive [TG ≥ 220 mg/dL, 31 patients] and negative [TG < 220 mg/dL, 20 patients]). All patients were genotyped, and study variants were detected using polymerase chain reaction (PCR) and restricted fragment length polymorphism (RFLP) analysis. Results Patients with genotype SS of LPL gene compared with genotype SX had more frequently positive response to OFTT (P = .04) and lower high‐density lipoprotein cholesterol (HDL‐C) concentration (P = .03). Patients with positive response to OFTT and genotype SS of LPL gene compared with genotype SX had lower AUC (area under the curve)‐TG, 1744 (368) vs 1887 (807) mg/dL/h, respectively, P = .04. CETP and APOE gene polymorphisms had no influence on postprandial TG response to OFTT. Conclusions In patients with well‐controlled T2DM, LPL but not CETP and APOE gene polymorphisms influenced TG postprandial response. Particularly, S447 allele carriers of LPL gene presented more frequently positive postprandial TG response to OFTT compared with 447X allele carriers. No differences were found between allele carriers of patients with negative response to OFTT in any other studied gene polymorphism.

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Bempedoic Acid for Lowering LDL Cholesterol

Honigberg

Natarajan

2019

JAMA

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Since the report of the first expert panel of the National Cholesterol Education Program in 1988, effectively the first contemporary professional cholesterol guidelines in the United States, lowering of low-density lipoprotein cholesterol (LDL-C) levels has been a cornerstone of atherosclerotic cardiovascular disease (ASCVD) prevention. Consistent with classical and genetic epidemiologic studies implying a causal relationship between LDL-C and ASCVD, multiple randomized clinical trials have consistently observed proportional relationships between LDL-C lowering and ASCVD risk reduction from statins. More recently, these findings have extended to nonstatin LDL-C-lowering medicines, ezetimibe and proprotein convertase subtilisin/kexin type 9 (PCSK9)-inhibiting monoclonal antibodies. [1][2][3] Given encouraging results from clinical trials, nonstatin LDL-C-lowering medicines are now guideline-recommended when the degree of LDL-Clowering attained by maximally tolerated statins is deemed insufficient. 4 Statins are generally well tolerated, with minimal differences compared with placebo for adverse symptoms in randomized clinical trials. 5 However, muscle symptoms are reported in 5% to 20% of patients prescribed statins in clinical practice and may lead to poor adherence. 6 Blinded studies of crossover statin

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2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: Executive Summary

Cited by 1,281 publications

References 264 publications

An updated review of lipid‐modifying therapy

An updated review of lipid‐modifying therapy

The influence of gene polymorphisms on postprandial triglyceride response after oral fat tolerance test meal in patients with diabetes mellitus

Bempedoic Acid for Lowering LDL Cholesterol

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