Triglyceride-rich lipoproteins and high-density lipoprotein cholesterol in patients at high risk of cardiovascular disease: evidence and guidance for management
Identifieur interne : 001C24 ( PascalFrancis/Corpus ); précédent : 001C23; suivant : 001C25Triglyceride-rich lipoproteins and high-density lipoprotein cholesterol in patients at high risk of cardiovascular disease: evidence and guidance for management
Auteurs : M. John Chapman ; Henry N. Ginsberg ; Pierre Amarenco ; Felicita Andreotti ; Jan Boren ; Alberico L. Catapano ; Olivier S. Descamps ; Edward Fisher ; Petri T. Kovanen ; Jan Albert Kuivenhoven ; Philippe Lesnik ; Luis Masana ; Borge G. Nordestgaard ; Kausik K. Ray ; Zeljko Reiner ; Marja-Riitta Taskinen ; Lale Tokgözoglu ; Anne Tybjaerg-Hansen ; Gerald F. WattsSource :
- European heart journal [ 0195-668X ] ; 2011.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
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 trigtycerides 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 (>1.7mmol/L or 150mg/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.
Notice en format standard (ISO 2709)
Pour connaître la documentation sur le format Inist Standard.
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Format Inist (serveur)
NO : | PASCAL 11-0287868 INIST |
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ET : | Triglyceride-rich lipoproteins and high-density lipoprotein cholesterol in patients at high risk of cardiovascular disease: evidence and guidance for management |
AU : | CHAPMAN (M. John); GINSBERG (Henry N.); AMARENCO (Pierre); ANDREOTTI (Felicita); BOREN (Jan); CATAPANO (Alberico L.); DESCAMPS (Olivier S.); FISHER (Edward); KOVANEN (Petri T.); ALBERT KUIVENHOVEN (Jan); LESNIK (Philippe); MASANA (Luis); NORDESTGAARD (Borge G.); RAY (Kausik K.); REINER (Zeljko); TASKINEN (Marja-Riitta); TOKGÖZOGLU (Lale); TYBJAERG-HANSEN (Anne); WATTS (Gerald F.) |
AF : | European Atherosclerosis Society, INSERM UMR-S939, Pitie-Salpetriere University Hospital/Paris 75651/France (1 aut., 11 aut.); Irving Institute for Clinical and Translational Research Columbia University, PH 10-305 630 West 168th Street/NewYork, NY 10032/Etats-Unis (2 aut.); Bichat University Hospital/Paris/France (3 aut.); Catholic University Medical School/Rome/Italie (4 aut.); University of Gothenburg/Suède (5 aut.); University of Milan/Italie (6 aut.); Hopital de Jolimont, Haine Saint-Paul/Belgique (7 aut.); New York University/New York/Etats-Unis (8 aut.); Wihuri Research Institute/Helsinki/Finlande (9 aut.); University of Amsterdam/Pays-Bas (10 aut.); Universitat Rovira & Virgili/Reus/Espagne (12 aut.); Heriev Hospital, Copenhagen University Hospital, University of Copenhagen/Danemark (13 aut.); St George's University of London/London/Royaume-Uni (14 aut.); University Hospital Center Zagreb/Croatie (15 aut.); Biomedicum/Helsinki/Finlande (16 aut.); Hacettepe University/Ankara/Turquie (17 aut.); Rigshospitalet, University of Copenhagen/Danemark (18 aut.); University of Western Australia/Perth/Australie (19 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | European heart journal; ISSN 0195-668X; Royaume-Uni; Da. 2011; Vol. 32; No. 11; Pp. 1345-1361; Bibl. 1/4 p. |
LA : | Anglais |
EA : | 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 trigtycerides 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 (>1.7mmol/L or 150mg/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. |
CC : | 002B12B01 |
FD : | Dyslipémie; Athérosclérose; Triglycéride; Lipoprotéine HDL; Cholestérol; Homme; Malade; Risque élevé; Pathologie de l'appareil circulatoire; Guidage; Conduite à tenir; Recommandation; Appareil circulatoire; Cardiologie; Lipide; Maladie cardiovasculaire |
FG : | Maladie métabolique; Pathologie des vaisseaux sanguins |
ED : | Dyslipemia; Atherosclerosis; Triglyceride; Lipoprotein HDL; Cholesterol; Human; Patient; High risk; Cardiovascular disease; Guidance; Clinical management; Recommendation; Circulatory system; Cardiology; Lipids; Cardiovascular disease |
EG : | Metabolic diseases; Vascular disease |
SD : | Dislipemia; Ateroesclerosis; Triglicérido; Lipoproteina HDL; Colesterol; Hombre; Enfermo; Riesgo alto; Aparato circulatorio patología; Guiado; Actitud médica; Recomendación; Aparato circulatorio; Cardiología; Lípido; Cardiovascular enfermedad |
LO : | INIST-18785.354000192171820060 |
ID : | 11-0287868 |
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Triglyceride-rich lipoproteins and high-density lipoprotein cholesterol in patients at high risk of cardiovascular disease: evidence and guidance for management</title>
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<author><name sortKey="Ray, Kausik K" sort="Ray, Kausik K" uniqKey="Ray K" first="Kausik K." last="Ray">Kausik K. Ray</name>
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<author><name sortKey="Watts, Gerald F" sort="Watts, Gerald F" uniqKey="Watts G" first="Gerald F." last="Watts">Gerald F. Watts</name>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Atherosclerosis</term>
<term>Cardiology</term>
<term>Cardiovascular disease</term>
<term>Cholesterol</term>
<term>Circulatory system</term>
<term>Clinical management</term>
<term>Dyslipemia</term>
<term>Guidance</term>
<term>High risk</term>
<term>Human</term>
<term>Lipids</term>
<term>Lipoprotein HDL</term>
<term>Patient</term>
<term>Recommendation</term>
<term>Triglyceride</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Dyslipémie</term>
<term>Athérosclérose</term>
<term>Triglycéride</term>
<term>Lipoprotéine HDL</term>
<term>Cholestérol</term>
<term>Homme</term>
<term>Malade</term>
<term>Risque élevé</term>
<term>Pathologie de l'appareil circulatoire</term>
<term>Guidage</term>
<term>Conduite à tenir</term>
<term>Recommandation</term>
<term>Appareil circulatoire</term>
<term>Cardiologie</term>
<term>Lipide</term>
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<front><div type="abstract" xml:lang="en">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 trigtycerides 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 (>1.7mmol/L or 150mg/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.</div>
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<fA08 i1="01" i2="1" l="ENG"><s1>Triglyceride-rich lipoproteins and high-density lipoprotein cholesterol in patients at high risk of cardiovascular disease: evidence and guidance for management</s1>
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<fA14 i1="04"><s1>Catholic University Medical School</s1>
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<s3>BEL</s3>
<sZ>7 aut.</sZ>
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<sZ>8 aut.</sZ>
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<fA14 i1="09"><s1>Wihuri Research Institute</s1>
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<s3>FIN</s3>
<sZ>9 aut.</sZ>
</fA14>
<fA14 i1="10"><s1>University of Amsterdam</s1>
<s3>NLD</s3>
<sZ>10 aut.</sZ>
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<fA14 i1="11"><s1>Universitat Rovira & Virgili</s1>
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<s3>ESP</s3>
<sZ>12 aut.</sZ>
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<sZ>14 aut.</sZ>
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<sZ>16 aut.</sZ>
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<s5>10</s5>
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<server><NO>PASCAL 11-0287868 INIST</NO>
<ET>Triglyceride-rich lipoproteins and high-density lipoprotein cholesterol in patients at high risk of cardiovascular disease: evidence and guidance for management</ET>
<AU>CHAPMAN (M. John); GINSBERG (Henry N.); AMARENCO (Pierre); ANDREOTTI (Felicita); BOREN (Jan); CATAPANO (Alberico L.); DESCAMPS (Olivier S.); FISHER (Edward); KOVANEN (Petri T.); ALBERT KUIVENHOVEN (Jan); LESNIK (Philippe); MASANA (Luis); NORDESTGAARD (Borge G.); RAY (Kausik K.); REINER (Zeljko); TASKINEN (Marja-Riitta); TOKGÖZOGLU (Lale); TYBJAERG-HANSEN (Anne); WATTS (Gerald F.)</AU>
<AF>European Atherosclerosis Society, INSERM UMR-S939, Pitie-Salpetriere University Hospital/Paris 75651/France (1 aut., 11 aut.); Irving Institute for Clinical and Translational Research Columbia University, PH 10-305 630 West 168th Street/NewYork, NY 10032/Etats-Unis (2 aut.); Bichat University Hospital/Paris/France (3 aut.); Catholic University Medical School/Rome/Italie (4 aut.); University of Gothenburg/Suède (5 aut.); University of Milan/Italie (6 aut.); Hopital de Jolimont, Haine Saint-Paul/Belgique (7 aut.); New York University/New York/Etats-Unis (8 aut.); Wihuri Research Institute/Helsinki/Finlande (9 aut.); University of Amsterdam/Pays-Bas (10 aut.); Universitat Rovira & Virgili/Reus/Espagne (12 aut.); Heriev Hospital, Copenhagen University Hospital, University of Copenhagen/Danemark (13 aut.); St George's University of London/London/Royaume-Uni (14 aut.); University Hospital Center Zagreb/Croatie (15 aut.); Biomedicum/Helsinki/Finlande (16 aut.); Hacettepe University/Ankara/Turquie (17 aut.); Rigshospitalet, University of Copenhagen/Danemark (18 aut.); University of Western Australia/Perth/Australie (19 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>European heart journal; ISSN 0195-668X; Royaume-Uni; Da. 2011; Vol. 32; No. 11; Pp. 1345-1361; Bibl. 1/4 p.</SO>
<LA>Anglais</LA>
<EA>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 trigtycerides 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 (>1.7mmol/L or 150mg/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.</EA>
<CC>002B12B01</CC>
<FD>Dyslipémie; Athérosclérose; Triglycéride; Lipoprotéine HDL; Cholestérol; Homme; Malade; Risque élevé; Pathologie de l'appareil circulatoire; Guidage; Conduite à tenir; Recommandation; Appareil circulatoire; Cardiologie; Lipide; Maladie cardiovasculaire</FD>
<FG>Maladie métabolique; Pathologie des vaisseaux sanguins</FG>
<ED>Dyslipemia; Atherosclerosis; Triglyceride; Lipoprotein HDL; Cholesterol; Human; Patient; High risk; Cardiovascular disease; Guidance; Clinical management; Recommendation; Circulatory system; Cardiology; Lipids; Cardiovascular disease</ED>
<EG>Metabolic diseases; Vascular disease</EG>
<SD>Dislipemia; Ateroesclerosis; Triglicérido; Lipoproteina HDL; Colesterol; Hombre; Enfermo; Riesgo alto; Aparato circulatorio patología; Guiado; Actitud médica; Recomendación; Aparato circulatorio; Cardiología; Lípido; Cardiovascular enfermedad</SD>
<LO>INIST-18785.354000192171820060</LO>
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