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Even Totally Controlled HIV Linked to Atherosclerosis Risk
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15th Conference on Retroviruses and Opportunistic Infections
February 3-6, 2008
Boston
Mark Mascolini
A novel comparison of 387 people with HIV and 93 uninfected controls found evidence that HIV itself and antiretroviral therapy (ART) duration independently raise the risk of subclinical atherosclerosis [1]. But the impact of HIV alone on atherosclerosis risk appeared to be unrelated to viral replication rate or HIV disease progression because "elite controllers" not taking antiretrovirals had higher carotid intima media thickness (IMT) levels than uninfected controls.
The novel aspect of this case-control comparison by Priscilla Hsue (University of California, San Francisco) and colleagues is its inclusion of 28 so-called elite controllers--people whose HIV load stays below 75 copies even though they take no antiretrovirals. Hsue compared them with 87 untreated noncontrollers with a load above 75 copies, 180 people with a load below 75 copies thanks to antiretroviral therapy, 92 people with a load above 75 copies despite therapy, and 93 uninfected controls.
The researchers interviewed study participants and had them fill out questionnaires about sociodemographic factors, HIV disease history, and cardiovascular risk factors. A highly experienced technician blinded to study participant status measured carotid IMT at 12 sites.
Median age was 48 (interquartile range [IQR] 42 to 53) for the 387 people with HIV and 43 (IQR 38 to 49) for the 93 controls; 88% of HIV patients and 83% of controls were men. Thirty people with HIV (8%) and 1 without HIV (1%) had a history of coronary artery disease. Cardiovascular risk factor rates were slightly higher in the HIV group than in uninfected controls: ever smoked (66% versus 53%), diabetes (6% versus 2%), hypertension (27% versus 5%), and family history of coronary artery disease (20% versus 17%). Median values for high- and low-density lipoprotein (LDL) cholesterol, triglycerides, and glucose were equivalent between people with HIV and controls, while the HIV group had a higher median C-reactive protein level (2.0 versus 1.1 mg/L).
Median HIV duration measured 14 years and did not differ much among the four HIV groups. Elite controllers had the highest median nadir (lowest-ever) CD4 count (494 cells), followed by untreated noncontrollers (361 cells), antiretroviral responders (110 cells), and antiretroviral nonresponders (70 cells). Median antiretroviral duration stretched to 5.8 years in responders and 4.9 years in nonresponders. Most treated people took a protease inhibitor at least part of the time.
Compared with a median IMT of 0.73 mm in uninfected controls, all the HIV groups had significantly higher IMTs: 0.87 mm for elite controllers, 0.84 mm for untreated noncontrollers, 0.96 mm for treated responders, and 0.90 mm for treated nonresponders (P < 0.001 for all HIV groups versus controls). IMTs remained significantly higher in the HIV groups after statistical adjustment for traditional cardiovascular risk factors. After these adjustments, elite controllers had a 0.14-mm thicker median IMT than uninfected controls (P = 0.003).
Nine classic and HIV risk factors correlated with higher IMT in all four HIV groups--older age, wider waist, higher total and LDL cholesterol, prior coronary artery disease, hypertension, higher glucose, longer HIV duration, and longer antiretroviral therapy. In the 272 antiretroviral-treated people, longer antiretroviral therapy, longer PI duration, and longer nucleoside duration each independently correlated with higher IMT. Hsue also uncovered a strong correlation between fat loss and average IMT in antiretroviral-treated people and in all HIV groups (P < 0.001 for both correlations).
High IMTs in the elite controllers suggested to Hsue that something other than replication rate or advanced immunodeficiency must explain the antiretroviral-independent impact of HIV infection of IMT.
Reference
1. Hsue P, Hunt P, Martin J, et al. Role of ART, viral replication, and HIV infection in atherosclerosis. 15th Conference on Retroviruses and Opportunistic Infections. February 3-6, 2008. Boston. Abstract 951.
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