Residual cardiovascular risk of lipid origin. Components and pathophysiological aspects
Clin Investig Arterioscler. 2019 Mar-Apr;31(2):75-88.
doi: 10.1016/j.arteri.2018.06.007.
Epub 2018 Sep 24.
[Article in
English,
Spanish]
Affiliations
- 1 Fundación para la Investigación Sanitaria y Biomédica de la Comunidad Valenciana FISABIO, Servicio de Endocrinología y Nutrición, Hospital Universitario Dr. Peset Valencia; Departamento de Medicina, Universitat de València, Valencia, España. Electronic address: hernandez_antmij@gva.es.
- 2 Servicio de Endocrinología, Hospital Clínico Universitario; Departamento de Medicina, Universitat de València, Valencia, España.
- 3 Área Sanitaria de Delicias, Atención Primaria, Zaragoza, España.
- 4 Servicio de Medicina Interna, Hospital San Pedro, Logroño, España.
- 5 Centro de Salud de Bembibre, Bembibre (León), España.
- 6 Centro de Salud de Prosperidad, Atención Primaria, Madrid, España.
- 7 Unidad de Lípidos y Riesgo Vascular, Servicio de Endocrinología y Nutrición, Hospital del Mar, Universitat Autònoma de Barcelona, Barcelona, España.
- 8 Unidad de Lípidos, Servicio de Medicina Interna, Hospital Universitario de Bellvitge, Universitat de Barcelona, CIBERobn-ISCIII, Barcelona, España.
- 9 Unidad de Lípidos, Servicio de Medicina Interna, Hospital General Universitario Gregorio Marañón, Universidad Complutense, Madrid, España. Electronic address: jesus.millan@salud.madrid.org.
Abstract
There is no doubt about the relationship between LDL-c and cardiovascular risk, as well as about the benefits of statin treatment. Once the objective of LDL-c has been achieved, the evidences that demonstrate the persistence of a high cardiovascular risk, a concept called residual risk, are notable. The residual risk of lipid origin is based on atherogenic dyslipidemia, characterized by an increase in triglycerides and triglyceride-rich lipoproteins, a decrease in HDL-c and qualitative alterations in LDL particles. The most commonly used measures to identify this dyslipidemia are based on the determination of total cholesterol, triglycerides, HDL, non-HDL cholesterol and remaining cholesterol, as well as apolipoprotein B100 and lipoprotein (a) in certain cases. The treatment of atherogenic dyslipidemia is based on weight loss and physical exercise. Regarding pharmacological treatment, we have no evidence of cardiovascular benefit with drugs aimed at lowering triglycerides and HDL-c, fenofibrate seems to be effective in situations of atherogenic dyslipidemia.
Keywords:
Apolipoprotein B; Apolipoproteína B; Atherogenic dyslipidemia; Colesterol no HDL; Dislipidemia aterogénica; Estatinas; Fenofibrate; Fenofibrato; Non-HDL cholesterol; Residual risk; Riesgo residual; Statins.
Copyright © 2018 Sociedad Española de Arteriosclerosis. Publicado por Elsevier España, S.L.U. All rights reserved.
MeSH terms
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Atherosclerosis / complications*
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Atherosclerosis / therapy
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Cardiovascular Diseases / etiology*
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Cardiovascular Diseases / physiopathology
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Cardiovascular Diseases / prevention & control
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Cholesterol / blood
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Dyslipidemias / complications*
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Dyslipidemias / therapy
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Fenofibrate / administration & dosage
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Humans
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Hydroxymethylglutaryl-CoA Reductase Inhibitors / administration & dosage
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Hypolipidemic Agents / administration & dosage
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Lipids / blood
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Risk Factors
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Triglycerides / blood
Substances
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Hydroxymethylglutaryl-CoA Reductase Inhibitors
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Hypolipidemic Agents
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Lipids
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Triglycerides
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Cholesterol
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Fenofibrate