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Triglyceride-rich lipoproteins and high-density lipoprotein cholesterol in patients at high risk of cardiovascular disease: evidence and guidance for management.

Chapman MJ, Ginsberg HN, Amarenco P, Andreotti F, Borén J, Catapano AL, Descamps OS, Fisher E, Kovanen PT, Kuivenhoven JA, Lesnik P, Masana L, Nordestgaard BG, Ray KK, Reiner Z, Taskinen MR, Tokgözoglu L, Tybjærg-Hansen A, Watts GF, European Atherosclerosis Society Consensus Pan - Eur. Heart J. (2011)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: European Atherosclerosis Society, INSERM UMR-S939, Pitié-Salpetriere University Hospital, Paris 75651, France. john.chapman@upmc.fr

ABSTRACT
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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Proposed algorithm for the management of high-risk individuals with elevated triglycerides and/or low HDL cholesterol at LDL cholesterol goal. aLDL-C at goal as recommended by the most recent European guidelines (2007);4 <2.5 mmol/L in high-risk patients, decreasing to <2.0 mmol/L in very high risk patients. High-dose omega-3 fatty acids, fibrate, or niacin may be considered if the patient has very high TG (>5.0 mmol/L) to prevent pancreatitis. bIf the patient still has elevated TG (≥1.7 mmol/L, as recommended by the most recent European guidelines4) and/or low HDL-C (<1.0 mmol/L) despite intensive lifestyle intervention, and addressing compliance with pharmacotherapy and secondary causes of dyslipidaemia, additional lipid-modifying therapy may be considered. cBased on clinical outcome data and safety considerations for combination statin–fibrate therapy, fenofibrate is the preferred fibrate. This fibrate may have particular value in patients with T2DM and mild-to-moderate retinopathy. dGreater LDL-C lowering may be achieved by the addition of ezetimibe to a statin. Ezetimibe has a dose-sparing advantage in patients intolerant of higher dose statins, although outcome evidence to support its use is awaited. Note: To convert LDL-C or HDL-C from mmol/L to mg/dL multiply by 38.7; to convert TG from mmol/L to mg/dL multiply by 88.5. Abbreviations: TG, triglycerides; HDL-C, high-density-lipoprotein cholesterol; LDL-C, low-density-lipoprotein cholesterol.
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EHR112F6: Proposed algorithm for the management of high-risk individuals with elevated triglycerides and/or low HDL cholesterol at LDL cholesterol goal. aLDL-C at goal as recommended by the most recent European guidelines (2007);4 <2.5 mmol/L in high-risk patients, decreasing to <2.0 mmol/L in very high risk patients. High-dose omega-3 fatty acids, fibrate, or niacin may be considered if the patient has very high TG (>5.0 mmol/L) to prevent pancreatitis. bIf the patient still has elevated TG (≥1.7 mmol/L, as recommended by the most recent European guidelines4) and/or low HDL-C (<1.0 mmol/L) despite intensive lifestyle intervention, and addressing compliance with pharmacotherapy and secondary causes of dyslipidaemia, additional lipid-modifying therapy may be considered. cBased on clinical outcome data and safety considerations for combination statin–fibrate therapy, fenofibrate is the preferred fibrate. This fibrate may have particular value in patients with T2DM and mild-to-moderate retinopathy. dGreater LDL-C lowering may be achieved by the addition of ezetimibe to a statin. Ezetimibe has a dose-sparing advantage in patients intolerant of higher dose statins, although outcome evidence to support its use is awaited. Note: To convert LDL-C or HDL-C from mmol/L to mg/dL multiply by 38.7; to convert TG from mmol/L to mg/dL multiply by 88.5. Abbreviations: TG, triglycerides; HDL-C, high-density-lipoprotein cholesterol; LDL-C, low-density-lipoprotein cholesterol.

Mentions: In summary, statins firmly remain the first line treatment of choice for attainment of LDL-C goal in patients at high risk of CVD.4,5 After LDL-C goal attainment however, and if triglyceride levels remain elevated (≥1.7 mmol/L or 150 mg/dL, as defined by recent European guidelines4) and HDL-C low (<1.0 mmol/L or 40 mg/dL) despite intensive lifestyle intervention, then addition of a fibrate or niacin may be considered (Figure 6).Figure 6


Triglyceride-rich lipoproteins and high-density lipoprotein cholesterol in patients at high risk of cardiovascular disease: evidence and guidance for management.

Chapman MJ, Ginsberg HN, Amarenco P, Andreotti F, Borén J, Catapano AL, Descamps OS, Fisher E, Kovanen PT, Kuivenhoven JA, Lesnik P, Masana L, Nordestgaard BG, Ray KK, Reiner Z, Taskinen MR, Tokgözoglu L, Tybjærg-Hansen A, Watts GF, European Atherosclerosis Society Consensus Pan - Eur. Heart J. (2011)

Proposed algorithm for the management of high-risk individuals with elevated triglycerides and/or low HDL cholesterol at LDL cholesterol goal. aLDL-C at goal as recommended by the most recent European guidelines (2007);4 <2.5 mmol/L in high-risk patients, decreasing to <2.0 mmol/L in very high risk patients. High-dose omega-3 fatty acids, fibrate, or niacin may be considered if the patient has very high TG (>5.0 mmol/L) to prevent pancreatitis. bIf the patient still has elevated TG (≥1.7 mmol/L, as recommended by the most recent European guidelines4) and/or low HDL-C (<1.0 mmol/L) despite intensive lifestyle intervention, and addressing compliance with pharmacotherapy and secondary causes of dyslipidaemia, additional lipid-modifying therapy may be considered. cBased on clinical outcome data and safety considerations for combination statin–fibrate therapy, fenofibrate is the preferred fibrate. This fibrate may have particular value in patients with T2DM and mild-to-moderate retinopathy. dGreater LDL-C lowering may be achieved by the addition of ezetimibe to a statin. Ezetimibe has a dose-sparing advantage in patients intolerant of higher dose statins, although outcome evidence to support its use is awaited. Note: To convert LDL-C or HDL-C from mmol/L to mg/dL multiply by 38.7; to convert TG from mmol/L to mg/dL multiply by 88.5. Abbreviations: TG, triglycerides; HDL-C, high-density-lipoprotein cholesterol; LDL-C, low-density-lipoprotein cholesterol.
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Related In: Results  -  Collection

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EHR112F6: Proposed algorithm for the management of high-risk individuals with elevated triglycerides and/or low HDL cholesterol at LDL cholesterol goal. aLDL-C at goal as recommended by the most recent European guidelines (2007);4 <2.5 mmol/L in high-risk patients, decreasing to <2.0 mmol/L in very high risk patients. High-dose omega-3 fatty acids, fibrate, or niacin may be considered if the patient has very high TG (>5.0 mmol/L) to prevent pancreatitis. bIf the patient still has elevated TG (≥1.7 mmol/L, as recommended by the most recent European guidelines4) and/or low HDL-C (<1.0 mmol/L) despite intensive lifestyle intervention, and addressing compliance with pharmacotherapy and secondary causes of dyslipidaemia, additional lipid-modifying therapy may be considered. cBased on clinical outcome data and safety considerations for combination statin–fibrate therapy, fenofibrate is the preferred fibrate. This fibrate may have particular value in patients with T2DM and mild-to-moderate retinopathy. dGreater LDL-C lowering may be achieved by the addition of ezetimibe to a statin. Ezetimibe has a dose-sparing advantage in patients intolerant of higher dose statins, although outcome evidence to support its use is awaited. Note: To convert LDL-C or HDL-C from mmol/L to mg/dL multiply by 38.7; to convert TG from mmol/L to mg/dL multiply by 88.5. Abbreviations: TG, triglycerides; HDL-C, high-density-lipoprotein cholesterol; LDL-C, low-density-lipoprotein cholesterol.
Mentions: In summary, statins firmly remain the first line treatment of choice for attainment of LDL-C goal in patients at high risk of CVD.4,5 After LDL-C goal attainment however, and if triglyceride levels remain elevated (≥1.7 mmol/L or 150 mg/dL, as defined by recent European guidelines4) and HDL-C low (<1.0 mmol/L or 40 mg/dL) despite intensive lifestyle intervention, then addition of a fibrate or niacin may be considered (Figure 6).Figure 6

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: European Atherosclerosis Society, INSERM UMR-S939, Pitié-Salpetriere University Hospital, Paris 75651, France. john.chapman@upmc.fr

ABSTRACT
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.

Show MeSH
Related in: MedlinePlus