Human Immunodeficiency Virus as a Risk Factor for Cardiovascular Disease.
Antiretroviral Therapy
Cardiovascular Disease
Human Immunodeficiency Virus
Risk Factor
Journal
Cardiovascular toxicology
ISSN: 1559-0259
Titre abrégé: Cardiovasc Toxicol
Pays: United States
ID NLM: 101135818
Informations de publication
Date de publication:
20 Nov 2023
20 Nov 2023
Historique:
received:
10
06
2023
accepted:
10
11
2023
medline:
20
11
2023
pubmed:
20
11
2023
entrez:
20
11
2023
Statut:
aheadofprint
Résumé
The developments in HIV treatments have increased the life expectancy of people living with HIV (PLWH), a situation that makes cardiovascular disease (CVD) in that population as relevant as ever. PLWH are at increased risk of CVD, and our understanding of the underlying mechanisms is continually increasing. HIV infection is associated with elevated levels of multiple proinflammatory molecules, including IL-6, IL-1β, VCAM-1, ICAM-1, TNF-α, TGF-β, osteopontin, sCD14, hs-CRP, and D-dimer. Other currently examined mechanisms include CD4 + lymphocyte depletion, increased intestinal permeability, microbial translocation, and altered cholesterol metabolism. Antiretroviral therapy (ART) leads to decreases in the concentrations of the majority of proinflammatory molecules, although most remain higher than in the general population. Moreover, adverse effects of ART also play an important role in increased CVD risk, especially in the era of rapid advancement of new therapeutical options. Nevertheless, it is currently believed that HIV plays a more significant role in the development of metabolic syndromes than treatment-associated factors. PLWH being more prone to develop CVD is also due to the higher prevalence of smoking and chronic coinfections with viruses such as HCV and HBV. For these reasons, it is crucial to consider HIV a possible causal factor in CVD occurrence, especially among young patients or individuals without common CVD risk factors.
Identifiants
pubmed: 37982976
doi: 10.1007/s12012-023-09815-4
pii: 10.1007/s12012-023-09815-4
doi:
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
© 2023. The Author(s).
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