AEGiS-10CROI: Carotid Imtima-media Thickness in HIV-infected and Uninfected Adults: ACTG 5078.

10th Conference on Retroviruses and Opportunistic Infections

Boston, MA USA - February 10 -14, 2003

Carotid Imtima-media Thickness in HIV-infected and Uninfected Adults: ACTG 5078.

Conf Retroviruses Opportunistic Infect 2003 Feb 10-14;10th: abstract no. 131
J. Currier¹ , M. Kendall², K. Henry³, F. Torriani⁴, S. Storey⁵, C. Shikuma⁶, K. Mickelberg⁷, B. Alston⁸, M. Basar⁹, R. Zackin², H. Hodis¹⁰
¹Univ of California at Los Angeles; ²Harvard Sch of Public Hlth, Boston, MA; ³Univ of Minnesota, Minneapolis; ⁴Univ of California at San Diego; ⁵Univ of Washington, Seattle; ⁶Univ of Hawaii, Honolulu, HI; ⁷Univ of Pennsylvania, Philadelphia, PA; ⁸Natl Inst of Allergy and Infectious Diseases, NIH, Rockville, MD; ⁹Frontier Sci and Tech Res Fndn, Buffalo, NY; and ¹⁰Univ of Southern California at Los Angeles

BACKGROUND: The association between HIV infection, protease inhibitor exposure, dyslipidemia, and 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, correlates with coronary artery atherosclerosis and clinical cardiovascular events.

METHODS: This study enrolled groups of 3 subjects (triads) 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 in a matched analysis.The study had 80% power to detect a clinically relevant difference of 0.1mm in carotid IMT.

RESULTS: We enrolled 134 subjects 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 ≥2yrs	Group 2 PI naïve	Group 3 HIV (-)
Male %	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 in Groups I and III was +0.009 mm, p = 0.89. The median difference of IMT between matched pairs inGroups II and III was +0.0035 mm, p = 0.43. In a preliminary multivariate analysis, TChol, LDL, TG, age, BMI, and current smoking were independent predictors of IMT.

CONCLUSIONS: In a matched analysis that controlled for known risk factors for CHD, clinically relevant differences in baseline IMT were not demonstrated between subjects with dyslipidemia and over 2 yrs of PI exposure, subjects who arePI 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 HIV infection.

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Copyright © 2003 - Foundation for Retrovirology and Human Health. Reproduction of this abstract (other than one copy for personal reference) must be cleared through the Foundation for Retrovirology and Human Health. Licensed (AIDSLINE) from National Library of Medicine.