Virally suppressed HIV-infected adults aged 30-50 years did not have significantly increased carotid intima media thickness compared to HIV-uninfected controls (0.607mm vs 0.599mm, p=0.37).
Cross-Sectional (n=432)
No
Does virally suppressed HIV infection increase carotid intima media thickness, carotid plaque prevalence, or monocyte activation (sCD163) in adults in Botswana compared to uninfected controls?
Virally suppressed HIV infection in adults in Botswana is associated with increased monocyte activation and carotid plaque prevalence, but not increased carotid intima-media thickness, compared to uninfected controls.
Absolute Event Rate: 0.607% vs 0.599%
p-value: p=0.37
OBJECTIVES: Human immune deficiency virus (HIV) is associated with increased cardiovascular disease (CVD) risk, yet the relationship between HIV and carotid atherosclerosis / monocyte activation among virally suppressed HIV-infected patients in sub-Saharan Africa is not well understood. METHODS: We measured traditional CVD risk factors, bilateral distal common carotid intima media thickness (cIMT), presence of carotid plaque and plasma sCD163 levels among virally suppressed HIV-infected adults and HIV-uninfected controls, in a cross-sectional study in Gaborone, Botswana. The associations between HIV status, traditional CVD risk factors, sCD163 and outcome of cIMT were assessed in univariate and multivariate linear regression models. RESULTS: We enrolled 208 HIV-infected adults (55% Female, mean age 39 years) who had undetectable HIV-1 RNA on antiretroviral therapy and 224 HIV-uninfected controls (47% Female, mean age 37 years). There was no difference in cIMT between study groups, with mean cIMT 0.607mm and 0.599mm in HIV-infected and HIV-uninfected, respectively (p = 0.37). Plasma sCD163 was significantly higher in HIV-infected versus HIV-uninfected persons (1917ng/ml vs 1593ng/ml, p = 0.003), but was not associated with cIMT (p = 0.43 among all, p = 0.72 for HIV-infected only). In the final multivariate model, increased cIMT was associated with older age, being treated for hypertension, and higher non-HDL cholesterol among all (p<0.001, p = 0.03, p<0.001 respectively), and with older age and waist-hip ratio in HIV-infected participants (p = 0.02 & p = 0.02 respectively). Carotid plaque was present in a significantly higher proportion of HIV-infected adults (RR 2.15, 95% CI 1.22, 3.81). CONCLUSIONS: HIV-infected participants aged 30-50 years who have achieved viral suppression did not have increased cIMT when compared to HIV-uninfected controls in Botswana. However, well-controlled HIV was associated with excess monocyte activation. Future work should explore the impact of subclinical atherosclerosis on CVD events among HIV-infected and -uninfected adults in Botswana.
Mosepele et al. (2017) conducted a cross-sectional in HIV infection (n=432). HIV infection (virally suppressed) vs. HIV-uninfected controls was evaluated on Mean carotid intima media thickness (cIMT) in mm (p=0.37). Virally suppressed HIV-infected adults aged 30-50 years did not have significantly increased carotid intima media thickness compared to HIV-uninfected controls (0.607mm vs 0.599mm, p=0.37).