CAROTID ARTERY INTIMA-MEDIA THICKNESS IN HIV-INFECTED

AND UNINFECTED ADULTS: ACTG 5078

 

J. S. Currier, Kendall M, Henry, K, Torriani F, Basar M, Zackin R, and H.N Hodis for the ACTG 5078 Team.

 

Carotid Artery Intima-Media Thickness In Hiv-Infected

And Uninfected Adults: Actg 5078

 

J. S. Currier, Kendall M, Henry, K, Torriani F, Basar M, Zackin R, and H.N Hodis for the ACTG 5078 Team.

 

Background: The associationrelationship between HIV infection, protease inhibitor exposure, dyslipidemia, and subsequent risk of atherosclerosis remains undefined. A precise and reproducible measure of subclinical atherosclerosis, carotid intima-medial thickness (IMT), assessed with a non-invasive ultrasound  technique, significantly correlates with coronary artery atherosclerosis and clinical cardiovascular events. in the general population.  For this study, trained ultrasonographers at 6 sites sent standardized IMT images to a central reading site for measurement.
Methods: This study enrolled groups of   3 subjects (triads) who were matched on the following characteristics; age, sex, race/ethnicity, smoking status, blood pressure, and menopausal status.   Group I: HIV- infected subjects with continuous use of PI therapy for ³ 2 yrs; Group II: HIV- infected subjects without prior PI use; Group III: HIV uninfected subjects.   Subjects were excluded if they had known CAD, DM, a family history of CAD, uncontrolled HTN or BMI > 30. For this study, trained ultrasonographers at 6 sites sent standardized IMT images to a central reading site for measurement. Carotid IMT was compared within the HIV positive groups (I and II) and between the HIV positive and negative groups inn  a matched analysis.   The study had 80% power to detect a clinically relevant difference of 0.1mm in carotid IMT.

Longitudinal follow-up is ongoing;, baseline analysis is presented.
Results: We enrolled 134 subjects were enrolled in 45 triads; some triads were incomplete. The baseline characteristics by Group are shown below. The median time on PI among Group I was 192 weeks.

	Group 1 PI ³ 2yrs	Group 2 PI naïve	Group 3 HIV (-)
%maleMale %	91	89	89
Median age	42	41	42
Never smoked	57%	59%	59%
CD4 (median)	530	481	NA
TChol mg/dl (median)	219*	179	187
Direct LDL mg/dl	123*	108	115
Triglycerides mg/dl	192*	142	107
IMT (mm) median	0.693	0.711	0.687

*p < 0.05

 

The median difference in IMT between the matched pairs in Groups I  and II was +0.017 mm,,-- p = 0.22---.   The median difference of IMT between matched pairs incombined Groups II and III was + 0.009 mm, p = 0.89. The median difference of IMT between matched pairs incompared to  Groups II and III was + 0.0035 mm--, p = 0.43. In a preliminary multivariate analysis,  TChol, LDL, TG, age, and BMI, and current smoking were independent predictors of only ___ and ___ predicted  increased IMT.

Conclusions: In a matched analysis that controlled for well known risk factors for CHD, clinically relevant large ??? differences in baselineeline values for IMT were not demonstratected between subjecpatients with dyslipidemia and over two 2 years of PI exposure and dyslipidemia,, subjects who arecompared to  PI naïve, and HIV- uninfected controls. Longitudinal follow-up is ongoing to determine whether rates of progression of carotid IMT are influenced by PI exposure and chronic HIV infection.