TY - JOUR
T1 - Triglyceride-rich lipoproteins and high-density lipoprotein cholesterol in patients at high risk of cardiovascular disease
T2 - Evidence and guidance for management
AU - Chapman, M. John
AU - Ginsberg, Henry N.
AU - Amarenco, Pierre
AU - Andreotti, Felicita
AU - Borén, Jan
AU - Catapano, Alberico L.
AU - Descamps, Olivier S.
AU - Fisher, Edward
AU - Kovanen, Petri T.
AU - Kuivenhoven, Jan Albert
AU - Lesnik, Philippe
AU - Masana, Luis
AU - Nordestgaard, Børge G.
AU - Ray, Kausik K.
AU - Reiner, Zeljko
AU - Taskinen, Marja Riitta
AU - Tokgözoglu, Lale
AU - Tybjærg-Hansen, Anne
AU - Watts, Gerald F.
N1 - Funding Information:
This work including Consensus Panel meetings were supported by unrestricted educational grants to the EAS from Merck, Kowa, Roche, and AstraZeneca. This funding also supported the Open Access publication charges for this article. These companies were not present at the Consensus Panel meetings, had no role in the design or content of the Consensus Statement, and had no right to approve or disapprove of the final document.
PY - 2011/6
Y1 - 2011/6
N2 - 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.
AB - 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.
KW - Atherogenic dyslipidaemia
KW - Atherosclerosis
KW - Cardiovascular disease
KW - Cholesterol
KW - Guidelines
KW - High-density lipoprotein cholesterol
KW - Remnants
KW - Triglyceride-rich lipoproteins
KW - Triglycerides
UR - http://www.scopus.com/inward/record.url?scp=79958148945&partnerID=8YFLogxK
U2 - 10.1093/eurheartj/ehr112
DO - 10.1093/eurheartj/ehr112
M3 - Review article
C2 - 21531743
AN - SCOPUS:79958148945
SN - 0195-668X
VL - 32
SP - 1345
EP - 1361
JO - European Heart Journal
JF - European Heart Journal
IS - 11
ER -