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Rate and Predictors of Carotid Intima Media Thickness Progression in ARV-Naïve HIV-Infected and Uninfected Adults: A 48-Week Prospective Matched Cohort
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Reported by Jules Levin
CROI 2012 March 5-8 Seattle WA
Corrilynn O Hileman,1,3 Teresa L Carman,2,3 Chris T Longenecker,2,3 Danielle E Labbato,2 Norma J Storer,2 Cynthia A White2 and Grace A McComsey2,3 1MetroHealth Medical Center, 2University Hospitals Case Medical Center, 3Case Western Reserve University, Cleveland, Ohio, USA
Background: IMT progresses faster in HIV+ subjects on antiretroviral therapy (ART) than in HIV- subjects. In ART naïve subjects, the rate of IMT progression and the role of inflammation are unknown.
Methods: 48-wk prospective cohort study to compare changes in IMT and inflammation markers in ART-naïve HIV+ adults and age, sex and race-matched healthy controls. Diabetes and cardiovascular disease (CVD) were exclusionary. ANCOVA was used to adjust means. Correlation coefficients and multivariable linear regression were used to explore relationships between baseline and change in IMT and inflammation markers.
Results: 85 HIV+ and 45 HIV- were included. Groups were similar except HIV+ had more African Americans (58 vs 27%; p<0.01), smokers (52 vs 16%; p<0.01) and lower HDL-C (median (IQR) 43 (37-51) vs 48 (43-58) mg/dl; p<0.01). Median age was 40 (32-46) yrs. 74% were men. Median BMI was 28 (25-31) kg/m2. In HIV+ median CD4 count was 535 (469-691) cells/mm3, HIV-1 RNA was 6916 (1550-18400) cps/ml and HIV duration was 3.3 (1.3-7.6) yrs. Baseline common carotid artery (CCA) and bulb IMT were not different between HIV+ and HIV- (0.64 (0.6-0.69) vs 0.64 (0.56-0.69) mm; p=0.28; and 0.7 (0.62-0.78) vs 0.72 (0.62-0.82) mm; p=0.71, respectively). Changes in IMT to 48 wks at both sites were not different within- or between HIV+ and HIV- (-0.0071 (-0.0267-0.0233) vs 0.0113 (-0.0117-0.0306) mm; p=0.19 for between-group CCA IMT change; and 0.0017 (-0.0367-0.06167) vs 0.01 (-0.0383-0.0625) mm; p=0.54 for bulb change). After adjustment for CVD risk factors, change in CCA IMT was greater in HIV- (-0.0046 vs 0.0177 mm; p=0.01). IL-6, sTNFR-II, sVCAM-1 and sICAM-1 were higher in HIV+ vs. HIV- at both time points and D-Dimer was higher at wk 48 (p<0.01 for all). sTNFR-I and -II and VCAM-1 increased over 48 wks in HIV+ (p<0.01 for all). Changes in sTNFR-II and D-Dimer were significant between-groups (p<0.01 and p=0.03). Independent predictors of greater change in CCA IMT were higher BMI (p=0.05) and family history of MI (p<0.01). Independent predictors of greater change in bulb IMT were higher sTNFR-I (p=0.03) and higher diastolic BP (p<0.01).
Conclusions: IMT progression rate was not greater in HIV+ ART-naïve subjects compared to matched healthy controls. In addition to traditional CVD risk factors, higher levels of sTNFR-I predicted larger bulb IMT changes. Longer follow-up of this cohort is ongoing and will further clarify the risk of IMT progression in untreated subjects.
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