10th Conference on Retroviruses and Opportunistic Infections Boston, MA USA - February 10 -14, 2003

Conf Retroviruses Opportunistic Infect 2003 Feb 10-14;10th: abstract no. 139lb
P. Hsue¹ , J. Lo¹, A. Franklin², A.F. Bolger¹, S.G. Deeks¹, D.D. Waters^1
1UCSF, SFGH, San Francisco, CA and ²SFGH, San Francisco, CA

BACKGROUND: While antiretroviral therapy has reduced HIV-associated morbidity and mortality, preliminary evidence suggests that treated patients may be at increased risk for coronary artery disease. The relationships between cardiovascular risk factors, HIV disease, HIV treatment, and atherosclerosis have not been well defined. The purpose of this study was to identify predictors of carotid artery intima-media thickness (IMT), a marker of atherosclerosis, in patients with HIV infection and to follow IMT progression over 1 year.

METHODS: We measured lipid and lipoprotein levels, inflammatory markers, and carotid artery IMT by B-mode ultrasound in a cross-sectional study of HIV-infected adults. We also assessed CAD risk factors, HIV disease characteristics, fat distribution, and anthropometry. The primary endpoint was the mean maximal IMT of 12 preselected segments in the carotid arteries. Multivariable linear regression was used to identify independent predictors of baseline IMT and IMT progression after 1 year.

RESULTS: A total of 106 subjects were studied. The mean age was 45+8yrs; 88 were male. The duration of HIV infection was 11+5yrs, the median CD4 count was 354 cells/mm³, and the median pre-enrollment protease inhibitor (PI) treament duration was 4 yrs. The mean IMT was 0.90+0.27mm; this was higher than expected from a large population study of similarly aged individuals. Multivariable predictors of increased IMT at baseline were age (0.12mm per decade), LDL-C (0.02mm per 10mg/dL), hypertension (0.15mm), and nadir CD4 200 (0.16mm). Of note, C-reactive protein, lipodystrophy, and duration of HIV infection were not predictive of increased baseline IMT. IMT progression over 1 year was measured in a subset of 21 patients. The mean rate of progression was 0.1+0.1mm/yr, which is greatly accelerated compared to 0.01mm/yr from published reports of non-HIV infected populations. Age and duration of PI therapy were multivariable predictors of IMT progression.

CONCLUSIONS: Among HIV-infected patients, carotid IMT was independently associated with classic coronary risk factors (age, LDL-C, and hypertension) and nadir CD4 count 200. These data suggest that both immunodeficiency and traditional risk factors contribute to atherosclerosis in HIV-infected individuals. Progression of IMT in the subset with 1 year followup was accelerated by tenfold compared to non-HIV infected populations, and was associated with age and duration of PI use.

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