Background: Previous research has demonstrated an increase in carotid intima–media thickness (cIMT) in HIV-infected individuals compared to controls. However, the reason for this increased level of subclinical vascular disease is unknown.
Objective: To identify HIV-related risk factors for increased cIMT.
Methods: We evaluated the relationship between HIV-related characteristics (including markers of HIV disease severity and use of antiretroviral therapy) and cIMT measurements in the internal/bulb and common carotid regions among 538 HIV-infected participants from the Study of Fat Redistribution and Metabolic Change in HIV Infection (FRAM). We used Bayesian model averaging to estimate the posterior probability of candidate HIV and non-HIV-related risk factors being true predictors of increased cIMT. Variables with a posterior probability of more than 50% were used to develop a selected regression model for each of the anatomic regions.
Results: For common cIMT, the Bayesian model selection process identified age, African-American race, and systolic and diastolic blood pressure with probability more than 95%, HDL cholesterol with probability 85% and Hispanic ethnicity with probability 51%. Among the HIV-related factors included in the analysis, only tenofovir use was selected (51% probability). In the selected model, duration of tenofovir use was associated with lower common cIMT (−0.0094 mm/year of use; 95% confidence interval: −0.0177 to −0.0010). For internal cIMT, no HIV-related risk factors were above the 50% posterior probability threshold.
Conclusion: We observed an inverse association between duration of tenofovir use and common carotid cIMT. Whether this association is causal or due to confounding by indication needs further investigation.
aUniversity of Florida, Gainesville, Florida, USA
bUniversity of California, USA
cDepartment of Veterans Affairs, San Francisco, California, USA
dDepartment of Biostatistics, University of Washington, Seattle, Washington, USA
eTufts Medical Center, Boston, Massachusetts, USA
fUniversity of California, Los Angeles, California, USA.
Received 29 March, 2010
Revised 9 June, 2010
Accepted 10 June, 2010
Correspondence to Dr Carl Grunfeld, MD, PhD, University of California, San Francisco, Veterans Affairs Medical Center, Metabolism Section 111F, 4150 Clement Street, San Francisco, CA 94121, USA. Tel: +1 415 750 2005; fax: +1 415 750 6927; e-mail: firstname.lastname@example.org