Key result
Treated HIV infection was not associated with faster progression of carotid intima media thickness compared to HIV-negative individuals (0.006 vs 0.004 mm/year; P=0.25).
Why the study?
Most people living with HIV reside in sub-Saharan Africa, but prospective data on the contributions of HIV infection to atherosclerosis in this region are minimal.
Does treated HIV infection increase the progression of carotid atherosclerosis in adults >40 years of age in rural Uganda?
Cohort (n=309)
Does treated HIV infection increase the progression of carotid atherosclerosis in adults >40 years of age in rural Uganda?
Absolute Event Rate: 0.006% vs 0.004%
p-value: p=0.25
Treated HIV infection was not associated with faster progression of subclinical carotid atherosclerosis in rural Uganda, challenging the assumption that treated HIV is a universal risk factor for atherosclerosis progression.
Supports similar carotid atherosclerosis progression in treated HIV; leaves open effects on clinical cardiovascular events.
Background Although ≈70% of the world's population of people living with HIV reside in sub‐Saharan Africa, there are minimal prospective data on the contributions of HIV infection to atherosclerosis in the region. Methods and Results We conducted a prospective observational cohort study of people living with HIV on antiretroviral therapy >40 years of age in rural Uganda, along with population‐based comparators not infected with HIV. We collected data on cardiovascular disease risk factors and carotid ultrasound measurements annually. We fitted linear mixed effects models, adjusted for cardiovascular disease risk factors, to estimate the association between HIV serostatus and progression of carotid intima media thickness (cIMT). We enrolled 155 people living with HIV and 154 individuals not infected with HIV and collected cIMT images at 1045 visits during a median of 4 annual visits per participant (interquartile range 3–4, range 1–5). Age (median 50.9 years) and sex (49% female) were similar by HIV serostatus. At enrollment, there was no difference in mean cIMT by HIV serostatus (0.665 versus 0.680 mm, P =0.15). In multivariable models, increasing age, blood pressure, and non–high‐density lipoprotein cholesterol were associated with greater cIMT ( P <0.05), however change in cIMT per year was also no different by HIV serostatus (0.004 mm/year for HIV negative [95% CI, 0.001–0.007 mm], 0.006 mm/year for people living with HIV [95% CI, 0.003–0.008 mm], HIV×time interaction P =0.25). Conclusions In rural Uganda, treated HIV infection was not associated with faster cIMT progression. These results do not support classification of treated HIV infection as a risk factor for subclinical atherosclerosis progression in rural sub‐Saharan Africa. Registration URL: https://www.ClinicalTrials.gov ; Unique identifier: NCT02445079.
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Siedner et al. (2021) conducted a cohort in HIV infection and carotid atherosclerosis (n=309). Treated HIV infection vs. HIV-negative comparators was evaluated on change in carotid intima media thickness (cIMT) per year (p=0.25). Treated HIV infection was not associated with faster progression of carotid intima media thickness compared to HIV-negative individuals (0.006 vs 0.004 mm/year; P=0.25).
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