Key result
Long-term combination antiretroviral therapy significantly increased the risk of cardiovascular structural lesions in HIV-infected patients compared to no treatment (OR 3.76).
Why the study?
The effects of long-term combination antiretroviral therapy on carotid artery lesions, cardiac structure, hemodynamics, and dyslipidemia in HIV-infected patients were not fully evaluated with adjustment for confounders.
Does long-term combination antiretroviral therapy impact carotid artery function, cardiac structure, and hemodynamics in HIV-infected patients?
Cross-Sectional (n=100)
No
Does long-term combination antiretroviral therapy impact carotid artery function, cardiac structure, and hemodynamics in HIV-infected patients?
Long-term cART is associated with increased risks of carotid atherosclerosis, cardiac remodeling, and hemodynamic abnormalities in HIV-infected patients, largely mediated by dyslipidemia.
To evaluate the effects of long-term combination antiretroviral therapy (cART) on carotid artery lesions, cardiac structure/hemodynamics, and dyslipidemia in HIV-infected patients via multimodal ultrasound, and explore independent risk factors for cardiovascular comorbidities, with adjustment for key confounding factors such as age and CD4 + T-cell count. A cross-sectional study included 100 HIV-infected patients, divided into a cART-treated group (58 cases, receiving standardized cART for ≥ 3 years) and an untreated group (42 cases, no antiretroviral therapy since diagnosis). Multimodal ultrasound was applied to measure carotid intima-media thickness (IMT), plaque characteristics, vascular hemodynamic parameters, and cardiac structural/functional indicators. Laboratory tests included lipid profiles, glucose metabolism indices, CD4 + T-cell count, and HIV viral load (VL). Univariate bivariate analysis and multivariate logistic regression analyses (adjusted for age and CD4 + T-cell count) were performed, with P < 0.05 considered statistically significant. Compared with the untreated group, the cART-treated group had higher carotid IMT (0.81 ± 0.03 vs. 0.71 ± 0.03 mm), carotid plaque incidence (37.9% vs. 14.3%), vascular resistance index (RI, 0.72 ± 0.04 vs. 0.65 ± 0.05), increased left ventricular end-diastolic diameter (LVEDD), interventricular septal thickness (IVST), and pulmonary artery systolic pressure (PASP), accompanied by decreased left ventricular ejection fraction (LVEF) and higher incidence of abnormal E/A ratio ( P < 0.05). The incidences of dyslipidemia (56.9% vs. 26.2%) and fatty liver (55.2% vs. 28.6%) were significantly higher in the treated group (all P < 0.01). Multivariate regression analysis showed that fatty liver, increased BMI, hyperglycemia, elevated LDL-C, older age, and decreased CD4 + T-cell count were independent risk factors for dyslipidemia. Subgroup analysis revealed that the tenofovir disoproxil fumarate (TDF) group had higher IMT and PASP than the tenofovir alafenamide (TAF) group ( P < 0.05). Long-term cART increases the risks of carotid atherosclerotic lesions, cardiac remodeling, and hemodynamic abnormalities in HIV-infected patients, with dyslipidemia as a potential mediating factor. TAF-based regimens may be safer for the cardiovascular system, and multimodal ultrasound enables non-invasive, comprehensive assessment to guide personalized clinical management.
No takes yet. Share an insight, caveat, or question.
Zhi et al. (2026) conducted a cross-sectional in HIV infection (n=100). Combination antiretroviral therapy (cART) vs. No antiretroviral therapy (untreated) was evaluated on Cardiovascular structural lesions (carotid plaque combined with cardiac structural abnormalities) (OR 3.76, 95% CI 1.45-9.75, p=0.006). Long-term combination antiretroviral therapy significantly increased the risk of cardiovascular structural lesions in HIV-infected patients compared to no treatment (OR 3.76).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: