Canadian Journal of Cardiology

Mechanisms of Cardiovascular Disease in the Setting of HIV Infection

  • Priscilla Y. Hsue
    Corresponding author: Dr Priscilla Y. Hsue, Room 5G1 Cardiology, Zuckerberg San Francisco General Hospital, 1001 Potrero Avenue, San Francisco, California 94110, USA. Tel.: +1-415-206-8257; fax: +1-415-206-5447.
    University of California San Francisco (UCSF), Zuckerberg San Francisco General Hospital, San Francisco, California, USA
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Published:December 28, 2018DOI:


      Although the initial reports of increased cardiovascular (CV) disease in the setting of advanced AIDS were reported approximately 30 years ago, advances in antiretroviral therapy and immediate initiation of therapy on diagnosis have transformed what was once a deadly infectious disease into a chronic health condition. Accordingly, the types of CV diseases occurring in HIV have shifted from pericardial effusions and dilated cardiomyopathy to atherosclerosis and heart failure. The underlying pathophysiology of HIV-associated CV disease remains poorly understood, partly because of the rapidly evolving nature of HIV treatment and because clinical endpoints take many years to develop. The gut plays an important role in the early pathogenesis of HIV infection as HIV preferentially infects CD4+ T cells, 80% of which are located in gut mucosa. The loss of these T cells damages gut mucosa resulting in increased gut permeability and microbial translocation, which incites chronic inflammation and immune activation. Antiretroviral therapy does not cure HIV infection and immune abnormalities persist. These abnormalities correlate with mortality and CV events. The effects of antiretroviral therapy on CV risk are complex; treatment reduces inflammation and other markers of CV risk but induces lipid abnormalities, most commonly hypertriglyceridemia. On a molecular level, monocytes/macrophages, platelet reactivity, and immune cell activation, which play a role in the general population, may be heightened in the setting of HIV and contribute to HIV-associated atherosclerosis. Chronic inflammation represents an inviting therapeutic target in HIV, as it does in uninfected persons with atherosclerosis.


      Même si les premiers signes d’augmentation des maladies cardiovasculaires (CV) en présence du SIDA au stade avancé ont été rapportés il y a environ 30 ans, les progrès réalisés en matière de traitement antirétroviral et l’instauration immédiate du traitement au moment du diagnostic ont transformé ce qui était jadis une maladie infectieuse mortelle en problème de santé chronique. En conséquence, les types de maladies CV survenant en présence d’une infection par le VIH sont passés des épanchements péricardiques et de la cardiomyopathie dilatée à l’athérosclérose et à l’insuffisance cardiaque. La physiopathologie sous-jacente des maladies CV associées au VIH demeure mal comprise, en partie parce que le traitement du VIH a évolué rapidement et que l’élaboration des critères cliniques nécessite de nombreuses années. L’intestin joue un rôle important au début de la pathogenèse de l’infection par le VIH, car le virus infecte préférablement les lymphocytes T CD4+, dont 80 % se trouvent dans la muqueuse intestinale. La perte de ces lymphocytes T endommage la muqueuse intestinale, augmentant ainsi la perméabilité intestinale et permettant la translocation microbienne, ce qui favorise l’inflammation chronique et l’activation immunitaire. Le traitement antirétroviral ne guérit pas l’infection par le VIH, et les anomalies immunitaires persistent. Ces anomalies ont une corrélation avec la mortalité et les événements CV. Les effets du traitement antirétroviral sur le risque CV sont complexes; le traitement réduit l’inflammation et d’autres marqueurs du risque CV, mais induit des anomalies lipidiques, le plus souvent sous forme d’hypertriglycéridémie. Au niveau moléculaire, les monocytes/macrophages, la réactivité plaquettaire et l’activation des cellules immunitaires, qui jouent un rôle dans la population générale, peuvent être augmentés en présence du VIH et contribuer à l’athérosclérose associée au VIH. L’inflammation chronique représente une cible tentante dans le traitement du VIH, comme chez les personnes non infectées atteintes d’athérosclérose.
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