Key result
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).
Why the study?
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?
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?
Absolute Event Rate: 0.607% vs 0.599%
p-value: p=0.37
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.
May reassure against elevated subclinical atherosclerosis in younger virally suppressed HIV; leaves open effects on events or other subgroups.
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.
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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).
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