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3-year Follow-up of Carotid Intima-media Thickness in HIV-infected and Uninfected Adults: ACTG 5078
Judith Currier*1, M Kendall2, K Henry3, F Torriani4, J Conley5, B Alston-Smith6, M Basar7, K Mickelberg8, Y Li9, H Howard9, and ACTG 5078 Study Team
1Univ of California CARE Ctr, Los Angeles, US; 2Harvard Sch of Publ Hlth, Boston, MA, US; 3Univ of Minnesota, Minneapolis, US; 4Univ of California, San Diego, US; 5Univ of Washington, Seattle, US; 6Div of AIDS, NIAID,, NIH, DHHS, Rockville, MD, US; 7Frontier Sci & Tech Res Fndn, Buffalo, NY, US; 8Univ of Pennsylvania, Philadelphia, US; and 9Univ of Southern California, Los Angeles, US
Background: Cross-sectional
studies reveal a high prevalence of atherosclerosis in patients on ART.
Uncontrolled studies suggest that the progression of atherosclerosis is
accelerated in HIV-infected adults. We followed individuals for 3 years using
carotid intima-media (IMT), a technique that
correlates with coronary artery atherosclerosis and clinical cardiovascular
events.
Methods: Groups
of 3 subjects (triads) who were matched on the following characteristics: age, sex, race/ethnicity, smoking status,
blood pressure status, and menopausal status were enrolled. Group I: HIV+ subjects with continuous use
of PI therapy for ³2
years; Group II: HIV+
subjects without prior protease inhibitor (PI) use; Group III: HIV.
Subjects were excluded if they had or had a family history of coronary artery disease,
diabetes mellitus, uncontrolled hypertension, or a body mass index >30. Ultrasonographers at 6 sites sent standardized IMT images
at weeks 0, 24, 48, 72, 96, and 144 to a central reading site for measurement.
Yearly change in carotid IMT was compared within the HIV-infected groups and
between the HIV+ and uninfected groups in a matched analysis. The
study had 80% power to detect a clinically relevant difference of 0.02 mm/y
change in carotid IMT.
Results: The study accrued
134 subjects in 45 triads. At baseline, more PI-treated subjects had
triglycerides >300 mg/dL (23%), total cholesterol
>200 mg/dL (64%) and met the National Cholesterol
Education Program definition of metabolic syndrome (32%) compared to the HIV
non-PI and HIV subjects. Within the PI group 34% received ritonavir. Median follow-up was 152 weeks. Median IMT
values (mm) and mean progression rates are shown in the table. Within-triad
matched analyses of the IMT yearly rates showed no statistically significant
differences between the PI-treated and PI-naïve groups (p = 0.19), between the PI-naive and HIV group (p = 0.78), or between the combined HIV
groups and the HIV controls (p
= 0.71).
|
Group
|
Baseline
|
Wk 24
|
Wk 48
|
Wk 72
|
Wk 96
|
Wk 144
|
IMT rate
mean (mm/yr)
|
|
PI
|
0.693
|
0.703
|
0.691
|
0.715
|
0.724
|
0.744
|
0.0102
|
|
PI-naïve
|
0.711
|
0.708
|
0.718
|
0.686
|
0.700
|
0.740
|
0.0047
|
|
HIV
|
0.690
|
0.685
|
0.694
|
0.714
|
0.720
|
0.726
|
0.0083
|
Conclusions: In this analysis, matching for known coronary heart disease
(CHD) risk factors, neither HIV infection nor PI exposure significantly affected
the rate of progression of carotid IMT over 3 years of follow-up. These
results suggest that “classic” CHD factors may play a more significant role
than ART in the increased incidence of cardiovascular events observed in HIV-infected
individuals.
|
