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Intima Media Thickness Is Associated with Residual Plasma Viremia in Treated Patients with Controlled HIV Infection
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Reported by Jules Levin
CROI 2012 March 5-8 Seattle WA
Anders Boyd*1,2, J-L Meynard1, L Morand-Joubert1, F Boccara1, J-P Bastard3, A Samri4, Z Mallat5, J Capeau3, M Desvarieux2,6,7, P-M Girard1,2, and Collaboration in HIV, Inflammation and Cardiovascular Disease
1Hosp St Antoine, Univ Pierre and Marie Curie, Paris, France; 2INSERM UMR S707, Paris, France; 3Hosp Tenon, Univ Paris 6, INSERM U938, France; 4INSERM UMR S945, Univ Pierre and Marie Curie, Paris, France; 5INSERM U970, Paris, France; 6Columbia Univ, Mailman Sch of Publ Hlth, New York, NY, US; and 7Ecole de Hautes Etudes en Sante Publ, Paris, France
Background: In this study, we aimed to measure inflammatory/anti-inflammatory markers and intima media thickness (IMT) in patients virologically controlled (plasma viral load <40 copies/mL) using combined ART (cART) and the potential impact of residual plasma viremia.
Methods: Of the 49 patients studied in this cross-sectional study, all were never-smokers and non-diabetics, with at least 4 years of cART and controlled HIV replication (HIV RNA viral load <40 copies/mL 12 months previously). Residual plasma viremia was measured using an ultrasensitive assay with a limit of quantification of 1 copy/mL. Patients were categorized as having residual (1 to 40 copies/mL) or ultra-low (<1 copies/mL) levels of HIV replication. Common carotid artery IMT (ccaIMT) was measured and averaged across 4 sites. Using median regression models, pro- and anti-inflammatory markers were adjusted by age, prior hypertension, and duration of cART; with CIMT additionally adjusted for nadir CD4+ cell count, and compared across replication groups.
Results: Of the patients, 15 (31%) had residual and 34 (71%) had ultra-low viremia. No statistically significant differences were observed between replication groups with respect to median age (40.5 years, IQR 37.0 to 44.9), duration of HIV infection (11.1 years, IQR 7.6 to 16.2), or cART (9.6 years, IQR 6.8 to 10.9), CD4+ T cell (555/mm3, IQR 459 to 717) and nadir CD4+ T cell count (214/mm3, IQR 146 to 383). Median adjusted pro-inflammatory markers tended to be higher in patients with residual than ultra-low viremia (us-CRP, 3.11 vs 2.43 mg/L; IL-18, 213.8 vs 89.7 pg/mL; resistin, 6.48 vs 6.25 ng/mL; IL-6, 1.33 vs 0.79 pg/mL; D-dimer, 147.4 vs 139.3 ng/mL, respectively) as was insulinemia (7.3 vs 6.0 Mu/L), although no significant differences were observed. Likewise, patients with residual viremia exhibited higher adjusted median levels of anti-inflammatory markers than those with ultra-low viremia (HMW/total adiponectin ,1.06/3.61 vs 0.92/2.54 μg/mL; IL-27, 1325 vs 1111 pg/mL; IL-10, 0.94 vs 0.65 pg/mL, respectively), with only differences in IL-10 being significant (p = 0.03). Finally, adjusted median ccaIMT was significantly higher in patients with residual (0.713 mm, SE = 0.017) vs ultra-low viremia (0.673 mm, SE = 0.011; p = 0.04).
Conclusions: Residual viremia between 1 and 40 copies/mL, is associated with increased IMT among HIV+, never-smoking, and non-diabetic patients with extensive cART. Our findings suggest only slightly higher systemic inflammation during low-grade replication.
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