Key result
HIV infection was not associated with the incidence of new subclinical atherosclerosis (adjusted IRR 1.21; 95% CI 0.62-2.35) or progression of coronary calcium score compared with HIV-negative persons.
Why the study?
Cross-sectional data showed conflicting results regarding whether subclinical coronary atherosclerosis prevalence is increased or similar in HIV-positive versus HIV-negative persons.
Does HIV infection increase the progression of subclinical coronary atherosclerosis compared to HIV-negative status?
Cohort (n=430)
Does HIV infection increase the progression of subclinical coronary atherosclerosis compared to HIV-negative status?
In a Swiss cohort, traditional cardiovascular risk factors (Framingham risk score), rather than HIV infection itself, were associated with the progression of subclinical coronary atherosclerosis.
Answers are grounded in this paper and cite their sources.
May support standard risk-factor management without HIV-specific imaging intensification; leaves open confirmation outside well-suppressed Swiss men.
Background People with HIV (HIV+) may have increased cardiovascular event rates compared with HIV-negative (HIV-) persons. Cross-sectional data from the United States and Switzerland, based on coronary artery calcium scan (CAC) and coronary computed tomography angiography (CCTA), suggest, respectively, increased and similar prevalence of subclinical atherosclerosis in HIV+ vs HIV- persons. Methods We repeated CAC/CCTA in 340 HIV+ and 90 HIV- study participants >2 years after baseline CAC/CCTA. We assessed the association of HIV infection, Framingham risk score (FRS), and HIV-related factors with the progression of subclinical atherosclerosis. Results HIV+ were younger than HIV- participants (median age, 52 vs 56 years; P < .01) but had similar median 10-year FRS (8.9% vs 9.0%; P = .82); 94% had suppressed HIV viral load. In univariable and multivariable analyses, FRS was associated with the incidence rate ratio (IRR) of new subclinical atherosclerosis at the follow-up CAC/CCTA, but HIV infection was not: any plaque (adjusted IRR for HIV+ vs HIV- participants, 1.21; 95% CI, 0.62–2.35), calcified plaque (adjusted IRR for HIV+ vs HIV- participants, 1.06; 95% CI, 0.56–2), noncalcified/mixed plaque (adjusted IRR for HIV+ vs HIV- participants, 1.24; 95% CI, 0.69–2.21), and high-risk plaque (adjusted IRR for HIV+ vs HIV- participants, 1.46; 95% CI, 0.66–3.20). Progression of CAC score between baseline and follow-up CAC/CCTA was similar in HIV+ (median annualized change [interquartile range {IQR}], 0.41 [0–10.19]) and HIV- participants (median annualized change [IQR], 2.38 [0–16.29]; P = .11), as was progression of coronary segment severity score (HIV+: median annualized change [IQR], 0 [0–0.47]; HIV-: median annualized change [IQR], 0 [0–0.52]; P = .10) and coronary segment involvement score (HIV+: median annualized change [IQR], 0 [0–0.45]; HIV-: median annualized change [IQR], 0 [0–0.41]; P = .25). Conclusions In this longitudinal CAC/CCTA study from Switzerland, Framingham risk score was associated with progression of subclinical atherosclerosis, but HIV infection was not.
No takes yet. Share an insight, caveat, or question.
Tarr et al. (2020) conducted a cohort in HIV infection and subclinical coronary atherosclerosis (n=430). HIV infection vs. HIV-negative persons was evaluated on Incidence of new subclinical atherosclerosis (any plaque) (adjusted IRR 1.21, 95% CI 0.62-2.35). HIV infection was not associated with the incidence of new subclinical atherosclerosis (adjusted IRR 1.21; 95% CI 0.62-2.35) or progression of coronary calcium score compared with HIV-negative persons.
Synapse has enriched 10 related papers. Consider them for comparative context: