Abstract
Lipid abnormalities are prevalent among persons living with HIV infection and contribute
to increasing the risk of cardiovascular events. Antiretroviral therapy (ART) is associated
with lipid abnormalities, most commonly hypertriglyceridemia, but also increases in
low-density lipoprotein cholesterol and total cholesterol. Different classes of ART,
and different drugs within classes, have differing effects on lipid levels, but in
general newer drugs have more favourable effects compared with older ones. Low-level
inflammation and chronic immune activation act on lipids through a variety of mechanisms
to make them more atherogenic. As a consequence, risk is higher than would be expected
for any given cholesterol level. Clinical outcome trials of cholesterol-lowering therapies
have not yet been completed in people living with HIV, so that treatment decisions
depend on extrapolation from studies in uninfected populations. Traditional risk assessment
tools underestimate cardiovascular risk in individuals with HIV. Statins are the mainstay
of lipid-lowering drug treatment; however, drug–drug interactions with ART must be
considered. Simvastatin and lovastatin are contraindicated in patients taking protease
inhibitors, and the dose of atorvastatin and rosuvastatin should be limited to 40
mg and 10 mg/d with some ART combinations. Switching from older forms of ART to lipid-friendly
newer ones is a useful strategy as long as virologic suppression is maintained, but
adding a statin lowers low-density lipoprotein cholesterol more effectively. Studies
indicate that lipid abnormalities are not treated as aggressively in individuals living
with HIV as they are in uninfected people, making this an opportunity to improve care.
Résumé
Les anomalies lipidiques sont répandues chez les personnes qui vivent avec le VIH
et contribuent à l’augmentation du risque d’événements cardiovasculaires. Le traitement
antirétroviral (TARV) est associé aux anomalies lipidiques, plus fréquemment à l’hypertriglycéridémie,
mais aussi à l’augmentation du cholestérol à lipoprotéines de basse densité et du
cholestérol total. Les différentes classes de TARV et les différents médicaments parmi
ces classes ont des effets distincts sur les taux de lipides, mais en général les
nouveaux médicaments ont des effets plus favorables que les anciens médicaments. L’inflammation
de faible degré et l’activation chronique du système immunitaire agissent sur les
lipides par divers mécanismes pour les rendre plus athérogènes. Par conséquent, le
risque est supérieur à ce que l’on s’attendrait pour tout taux de cholestérol donné.
Les études sur les résultats cliniques des traitements hypocholestérolémiants chez
les personnes atteintes du VIH n’étant pas encore achevées, les décisions en matière
de traitement dépendent donc de l’extrapolation des résultats des études auprès des
populations non infectées. Les outils traditionnels d’évaluation des risques sous-estiment
les risques cardiovasculaires chez les individus infectés par le VIH. Les statines
constituent le pilier du traitement par hypolipidémiants. Toutefois, les interactions
médicamenteuses avec le TARV doivent être considérées. La simvastatine et la lovastatine
sont contre-indiquées chez les patients qui prennent des inhibiteurs de protéase,
et la dose respective d’atorvastatine et de rosuvastatine devrait être limitée à 40
mg et à 10 mg/j avec certaines combinaisons de TARV. Le passage des anciens TARV vers
les nouveaux TARV dont les effets sur le profil lipidique sont favorables est une
stratégie utile pourvu que la suppression virologique soit maintenue, mais l’utilisation
supplémentaire d’une statine abaisse plus efficacement le cholestérol à lipoprotéines
de faible densité. Les études montrent que les anomalies des lipides ne sont pas traitées
aussi énergiquement chez les individus qui vivent avec le VIH qu’elles le sont chez
les personnes non infectées et offrent une occasion d’amélioration des soins.
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Article info
Publication history
Published online: November 14, 2018
Accepted:
November 6,
2018
Received:
August 23,
2018
Footnotes
See page 256 for disclosure information.
Identification
Copyright
© 2018 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.