Journal
EUROPEAN HEART JOURNAL
Volume 32, Issue 11, Pages 1345-1361Publisher
OXFORD UNIV PRESS
DOI: 10.1093/eurheartj/ehr112
Keywords
High-density lipoprotein cholesterol; Triglycerides; Triglyceride-rich lipoproteins; Remnants; Cholesterol; Atherogenic dyslipidaemia; Cardiovascular disease; Atherosclerosis; Guidelines
Categories
Funding
- Merck
- Kowa
- Roche
- AstraZeneca
- Abbott
- Bayer
- Boehringer Ingelheim
- Bristol-Myers Squibb
- Daiichi-Sankyo
- Glaxo-Welcome
- Karo Bio
- Lilly
- Menarini
- Novartis
- Pfizer
- Sanofi-Aventis
- Takeda
- Novo Nordisk Fonden [NNF11OC1014864] Funding Source: researchfish
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Even at low-density lipoprotein cholesterol (LDL-C) goal, patients with cardiometabolic abnormalities remain at high risk of cardiovascular events. This paper aims (i) to critically appraise evidence for elevated levels of triglyceride-rich lipoproteins (TRLs) and low levels of high-density lipoprotein cholesterol (HDL-C) as cardiovascular risk factors, and (ii) to advise on therapeutic strategies for management. Current evidence supports a causal association between elevated TRL and their remnants, low HDL-C, and cardiovascular risk. This interpretation is based on mechanistic and genetic studies for TRL and remnants, together with the epidemiological data suggestive of the association for circulating triglycerides and cardiovascular disease. For HDL, epidemiological, mechanistic, and clinical intervention data are consistent with the view that low HDL-C contributes to elevated cardiovascular risk; genetic evidence is unclear however, potentially reflecting the complexity of HDL metabolism. The Panel believes that therapeutic targeting of elevated triglycerides (>= 1.7 mmol/L or 150 mg/dL), a marker of TRL and their remnants, and/or low HDL-C (< 1.0 mmol/L or 40 mg/dL) may provide further benefit. The first step should be lifestyle interventions together with consideration of compliance with pharmacotherapy and secondary causes of dyslipidaemia. If inadequately corrected, adding niacin or a fibrate, or intensifying LDL-C lowering therapy may be considered. Treatment decisions regarding statin combination therapy should take into account relevant safety concerns, i. e. the risk of elevation of blood glucose, uric acid or liver enzymes with niacin, and myopathy, increased serum creatinine and cholelithiasis with fibrates. These recommendations will facilitate reduction in the substantial cardiovascular risk that persists in patients with cardiometabolic abnormalities at LDL-C goal.
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