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Cardiovascular disease (CVD) is a growing cause of morbidity and mortality in HIV-positive patients, in part because effective antiretroviral therapy (ART) is helping them to live longer. To assess the association between HIV infection and the risk for CVD, researchers compared ultrasound-measured carotid-artery intima–media thickness (IMT), a marker of preclinical atherosclerosis, in 433 HIV-positive patients (mean age, 49; 36% current smokers) from the FRAM study and 5749 HIV-negative controls (mean age, 61; 15% current smokers) from the FRAM and MESA studies. Measurements of both the common carotid artery and the internal carotid artery plus bulb region were examined. Neither HIV-positive patients nor controls had clinical CVD at the time of the ultrasound scans; 94% of the HIV-positive patients were taking ART.
Internal-carotid IMT was significantly greater in the HIV-positive group than in the control group, even after adjustment for demographic variables and traditional CVD risk factors (mean difference, 0.148 mm). For common-carotid IMT, the fully adjusted difference between HIV-positive patients and controls was also significant, although smaller in magnitude (mean difference, 0.033 mm). In both anatomical areas, HIV infection’s association with greater IMT was roughly similar to that of traditional CVD risk factors such as current smoking, diabetes, and elevated systolic blood pressure.
Grunfeld C et al. Preclinical atherosclerosis due to HIV infection: Carotid intima-medial thickness measurements from the FRAM study. AIDS 2009 May 18; [e-pub ahead of print].
Comment
In this cross-sectional study, carotid-artery intima–media thickness was significantly greater in ART-treated HIV-positive patients than in HIV-negative controls. The authors note that measuring both common-carotid and internal-carotid (plus bulb region) IMT yielded important findings that could not have been documented in studies using only carotid-artery IMT as a CVD risk marker in HIV-positive patients. The present study did not provide data on actual CVD outcomes or on key HIV-related markers, such as CD4-cell count and plasma viral load. The authors also did not identify any specific HIV-infection parameter or ART type that could explain the increased IMT thickness. Because 94% of the HIV-positive patients were taking ART, the risk contributions of HIV infection and ART use could not be distinguished from each other.