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AIDS. 2009 Jun 1;23(9):1059-67. doi: 10.1097/QAD.0b013e32832b514b.

Role of viral replication, antiretroviral therapy, and immunodeficiency in HIV-associated atherosclerosis.

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  • 1Division of Cardiology, San Francisco General Hospital, San Francisco, California 94110, USA. phsue@medsfgh.ucsf.edu

Abstract

OBJECTIVE:

HIV-seropositive patients are at higher risk for atherosclerosis than HIV-seronegative persons. This has been variably attributed to antiretroviral drug toxicity, immunodeficiency, and/or HIV-associated inflammation. To evaluate the contributions of these factors to HIV-associated atherosclerosis, we assessed carotid artery intima-media thickness in a diverse cohort of HIV-seronegative and seropositive adults, including a unique group of HIV-infected patients who were untreated, had undetectable viral loads, and had preserved CD4 T-cell counts (HIV controllers).

METHODS AND RESULTS:

Carotid intima-media thickness was measured in 494 participants, including 33 HIV controllers and 93 HIV-seronegative controls. HIV controllers had higher intima-media thickness than seronegative controls even after adjustment for traditional risk factors (P = 0.003). Intima-media thickness in controllers was similar to antiretroviral-untreated patients with detectable viremia. Across all participants, intima-media thickness was strongly associated with the presence of HIV disease rather than viral load or CD4 T-cell count. C-reactive protein was higher in HIV controllers than HIV-seronegative persons. Antiretroviral drug exposure was also associated with higher intima-media thickness.

CONCLUSIONS:

Increased atherosclerosis with HIV infection can occur in the absence of antiretroviral therapy, detectable viremia, or overt immunodeficiency. Chronic inflammation - which is higher in controllers than in HIV-uninfected persons - may account for early atherosclerosis in these patients.

PMID:
19390417
[PubMed - indexed for MEDLINE]
PMCID:
PMC2691772
Free PMC Article

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