Objectives: To compare the rate of change in intima–media thickness (IMT) of the carotid artery among uninfected subjects and HIV-infected subjects receiving or not receiving protease inhibitor (PI) regimens over a 144 week period.
Design: This prospective, matched cohort study enrolled 133 subjects into 45 triads (groups of three subjects matched by age, sex, race/ethnicity, smoking status, blood pressure, and menopause) from university based outpatient HIV clinics. Each triad consisted of one subject from each of the following groups: 1, HIV-infected subjects with continuous use of PI therapy for ≥ 2 years; 2, HIV-infected subjects without prior PI use; 3, HIV-uninfected subjects.
Methods: Standardized ultrasound images of carotid IMT were collected at weeks 0, 2, 24, 48, 72, 96, and 144. The main outcome was the yearly progression rate of carotid IMT (mm/year).
Results: The median yearly IMT progression rate in groups 1, 2, and 3 was 0.0096, 0.0058, and 0.0085 mm/year, respectively. There were no statistically significant differences in progression between groups 1 and 2, or between the combined HIV-positive groups and the HIV-negative control group. A multicovariate model examining predictors of progression in carotid IMT among all subjects contained low density lipoprotein cholesterol and homocysteine. Among HIV subjects, predictors included nadir CD4 cell count and ritonavir use.
Conclusions: HIV infection and PI use did not contribute substantially to the rate of carotid IMT progression in our matched study.
From the aCenter for Clinical AIDS Research and Education, David Geffen School of Medicine at the University of California, Los Angeles, California
bStatistical and Data Analysis Center, Harvard School of Public Health, Boston, Massachusetts
cHIV Program, Hennepin County Medical Center, University of Minnesota, Minneapolis, Minnesota
dDivision of AIDS, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland
eDivision of Infectious Diseases, Department of Medicine, University of California, San Diego, California
fDivision of Infectious Diseases, University of Pennsylvania, Philadelphia, Pennsylvania
gAtherosclerosis Research Unit, Division of Cardiovascular Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California.
Received 3 November, 2006
Revised 6 February, 2007
Accepted 10 February, 2007
Dr J. S. Currier, Center for Clinical AIDS Research and Education, Division of Infectious Diseases, Department of Medicine, David Geffen School of Medicine at the University of California, Los Angeles, California, USA. E-mail: email@example.com