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Circulation. 2004;109:1603-1608
Published online before print March 15, 2004, doi: 10.1161/01.CIR.0000124480.32233.8A
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(Circulation. 2004;109:1603-1608.)
© 2004 American Heart Association, Inc.


Clinical Investigation and Reports

Progression of Atherosclerosis as Assessed by Carotid Intima-Media Thickness in Patients With HIV Infection

Priscilla Y. Hsue, MD; Joan C. Lo, MD; Arlana Franklin, RDMS; Ann F. Bolger, MD; Jeffrey N. Martin, MD; Steven G. Deeks, MD; David D. Waters, MD

From the Divisions of Cardiology, Endocrinology, and Infectious Diseases, San Francisco General Hospital, and the Department of Medicine, University of California, San Francisco.

Correspondence to David D. Waters, MD, Room 5G1, Division of Cardiology, San Francisco General Hospital, 1001 Potrero Ave, San Francisco, CA 94110. E-mail dwaters{at}medsfgh.ucsf.edu

Received August 19, 2003; de novo received November 26, 2003; revision received January 7, 2004; accepted January 12, 2004.

Background— HIV-infected patients may be at increased risk for coronary events. The purpose of this study was to identify predictors of carotid intima-media thickness (IMT) in HIV patients at baseline and to measure IMT progression over 1 year.

Methods and Results— We measured blood lipids, inflammatory markers, and IMT in 148 HIV-infected adults (mean age, 45±8 years) and in 63 age- and sex-matched HIV-uninfected control subjects. The mean duration of HIV infection was 11 years, and the median duration of protease inhibitor treatment was 3.3 years. Mean baseline IMT was 0.91±0.33 mm in HIV patients and 0.74±0.17 mm in control subjects (P=0.0001). Multivariable predictors of baseline IMT in HIV patients were age (P<0.001), LDL cholesterol (P<0.001), cigarette pack-years (P=0.005), Latino race (P=0.062), and hypertension (P=0.074). When the control group was added to the analysis, HIV infection was an independent predictor of IMT (P=0.001). The rate of progression among the 121 HIV patients with a repeated IMT measurement at 1 year was 0.074±0.13 mm, compared with –0.006±0.05 mm in 27 control subjects (P=0.002). Age (P<0.001), Latino race (P=0.02), and nadir CD4 count <=200 (P=0.082) were multivariable predictors of IMT progression.

Conclusions— Carotid IMT is higher in HIV patients than in age-matched control subjects and progresses much more rapidly than previously reported rates in non-HIV cohorts. In HIV patients, carotid IMT is associated with classic coronary risk factors and with nadir CD4 count <=200, suggesting that immunodeficiency and traditional coronary risk factors may contribute to atherosclerosis.


Key Words: AIDS • atherosclerosis • carotid arteries • risk factors




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