People living with HIV had a higher prevalence of noncalcified coronary plaques compared with HIV-negative individuals.  Coronary artery calcification (CAC) prevalence, however, was similar between groups regardless of HIV status. These results were published in the Journal of the American Heart Association.

Because the current data on CAC in HIV is inconclusive, researchers performed a systematic review and meta-analysis of the literature on CAC and coronary plaque burden in people with HIV in order to compare with people without HIV and clarify the subclinical atherosclerosis burden.

A total of 119 articles were identified for review. Forty-three were reviewed, and 27 unique studies were identified for the meta-analysis. These studies included a total of 10,867 participants (HIV positive n=6699; HIV negative n=4168). Mean participant age ranged from 23 to 60 years (weighted average, 52 years), with a range of 48% to 100% men (weighted average, 86%); between 7% and 100% of the participants were Black (weighted average, 32%).

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Participants in the HIV-positive subgroup were younger and had a lower proportion of men participating (mean age, 49±5 vs 57±5 years; 79% vs 96%), with more Black participants (37% vs 24%).

A total of 15 studies allowed for direct within-study comparison of people living with and without HIV. This included 6357 participants (HIV positive, n=2189; HIV negative, n=4168) with a weighted average of 55 years. The subgroup of people living with HIV was younger, with a lower proportion of men but a similar proportion of Black participants.

In terms of clinical characteristics, 10±4% of participants had diabetes and 32±13% had hypertension. More participants in the HIV negative group had diabetes and hypertension. Mean systolic blood pressure was 123±5 mm Hg and 125±3 mm Hg for those living with and without HIV. More participants living with HIV were smokers (45±18% vs 20±14%) and mean Framingham Risk Score (FRS) was 6±3 vs 18±5.

Just over 90% (91±21%) of participants living with HIV were taking antiretroviral (ART) therapy; the mean ART duration was 6±5 years and CD4 count was 543±89 cells/µL.

Clinical characteristics were similar when analysis was restricted to the 15 studies with both HIV-positive and negative participants, although those living with HIV had a higher prevalence of smoking and a similar prevalence of diabetes and hypertension.

In the 12 studies with HIV negative controls, pooled estimate percentage of the presence of CAC was 45% (43%-47%) and 52% (50%-53%) for those living with and without HIV; the difference was not statistically significant after accounting for the difference in FRS.

Predicted CAC presence after adjusting to an FRS value of 8 was 44% and 36% for those with and without HIV, respectively. Results were comparable when pooled across all studies with available CAC information.

The combined estimate of the proportion of patients with CAC score >100—restricted to studies including HIV-negative controls—was 18% and 19% for those with and without HIV. Significant heterogeneity was noted across studies for the assessed outcomes.

The pooled CAC progression percentage in those with HIV was 13% in studies that defined CAC progression as the development of new CAC only; these percentages were 13% and 21% in studies that defined CAC progression as a significant change in CAC values only and in studies that used a combination of both definitions, respectively. Odds ratio (OR) of plaque progression in people with vs without HIV was 1.64 (95% CI, 0.91-2.34) for the 2 studies making direct comparisons.

Among studies reporting coronary plaque data, all but 1 included both HIV positive and negative participants. Pooled estimates for the percentage of participants with plaque on coronary CT angiogram was 64% vs 64% (95% CI, 61%-67% and 60%-67%, respectively) in HIV positive and negative groups. Significant heterogeneity was noted across studies.

Predicted prevalence for coronary plaque, adjusted to an FRS value of 9, was 53% for those living with HIV and 48% for those without. Pooled prevalence of participants with calcified plaque was 31% and 41% for those living with and without HIV, respectively. Conversely, the corresponding estimates for noncalcified plaque were 49% and 20% in each group.

Pooled ORs for the presence of plaque across 3 studies was 1.09 (95% CI, 1.00-1.17), with corresponding ORs for calcified and noncalcified plaque of 0.79 and 1.23 (95% CI, 0.65-0.92 and 1.09-1.38) respectively.

Evidence of significant heterogeneity was noted across studies for most assessed outcomes, excluding the OR estimate for noncalcified plaque. The proportion of Black participants was significantly inversely associated with CAC presence, but not with coronary plaque presence.

Evaluation with the Newcastle-Ottawa scoring system found that the majority of included studies were of at least moderate quality.

Study limitations include significant heterogeneity across the studies, the small sample sizes of each study, the limited data for CAC progression and the nature of plaques in those with HIV, and a lack of studies reporting data on statin usage.

“Participants with HIV had a similar likelihood for having CAC and total coronary plaque as HIV-negative individuals, with higher prevalence of noncalcified plaque and lower burden of calcified plaque, despite their younger age and lower overall burden of traditional cardiovascular risk factors,” the researchers concluded. “Together, these data suggest that [people with HIV] have a higher burden of noncalcified plaques and may developed subclinical atherosclerosis at a younger age.”


Soares C, Samara A, Yuyun MF, et al. Coronary artery calcification and plaque characteristics in people living with HIV: A systematic review and meta-analysis. J Am Heart Assoc. Published online September 29, 2021. doi:10.1161/JAHA.120.019291

This article originally appeared on The Cardiology Advisor