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Published on: August 26, 2017
Brief Report: Vascular Dysfunction and Monocyte Activation Among Women With HIV
Mabel Toribio1, Magid Awadalla2, Madeline Cetlin1
1Metabolism Unit, Division of Endocrinology, Massachusetts General Hospital and Harvard Medical School, Boston, MA.
Insights
Women with HIV on antiretroviral therapy have increased aortic stiffness, a key indicator of cardiovascular disease risk. This stiffness is linked to immune activation markers like sCD163 and myocardial fibrosis, highlighting potential therapeutic targets.
Area of Science:
- Cardiovascular Science
- Immunology
- Infectious Diseases
Background:
- Women with HIV (WHIV) on antiretroviral therapy (ART) exhibit heightened systemic immune activation, increasing their risk for cardiovascular disease (CVD).
- Aortic stiffness, a predictor of CVD outcomes, is significantly influenced by immune activation.
- Understanding the link between immune activation and aortic stiffness in WHIV is crucial for CVD prevention strategies.
Purpose of the Study:
- To compare aortic stiffness between women with and without HIV on ART.
- To investigate the relationship between aortic stiffness and key indicators of systemic immune activation in WHIV.
- To identify predictors of aortic stiffness in this population.
Main Methods:
- Prospective recruitment of 20 WHIV on ART and 14 age- and BMI-matched women without HIV.
- Cardiovascular magnetic resonance imaging to assess aortic stiffness (aortic pulse wave velocity, aPWV).
- Metabolic and immune phenotyping, including measurement of sCD163 levels and myocardial fibrosis (extracellular volume).
Main Results:
- WHIV demonstrated significantly higher aPWV (8.6 m/s) compared to controls (6.5 m/s), indicating increased aortic stiffness.
- Aortic stiffness (aPWV) was positively correlated with sCD163 levels (a marker of monocyte activation) and myocardial fibrosis in both groups.
- HIV status and sCD163 levels independently predicted aPWV, even after controlling for traditional CVD risk factors.
Conclusions:
- Asymptomatic WHIV on ART exhibit increased aortic stiffness compared to matched controls.
- Heightened monocyte activation (sCD163) and myocardial fibrosis are associated with increased aortic stiffness in WHIV.
- Targeting immune activation pathways may be a viable strategy to reduce CVD risk in WHIV.
Objective:
Women with HIV (WHIV) on antiretroviral therapy (ART) face an increased risk of cardiovascular disease (CVD) in the context of heightened systemic immune activation. Aortic stiffness, a measure of vascular dysfunction and a robust predictor of CVD outcomes, is highly influenced by immune activation. We compared aortic stiffness among women with and without HIV and examined interrelationships between aortic stiffness and key indices of systemic immune activation.
Methods:
Twenty WHIV on ART and 14 women without HIV group-matched on age and body mass index (BMI) were prospectively recruited and underwent cardiovascular magnetic resonance imaging, as well as metabolic and immune phenotyping.
Results:
Age and BMI did not differ significantly across groups (age: 52 ± 4 vs. 53 ± 6 years; BMI: 32 ± 7 vs. 32 ± 7 kg/m). Aortic pulse wave velocity (aPWV) was higher among WHIV (8.6 ± 1.3 vs. 6.5 ± 1.3 m/s, P < 0.0001), reflecting increased aortic stiffness. Among the whole group and among WHIV, aPWV related to sCD163 levels (whole group: R = 0.65, P < 0.0001; WHIV: R = 0.73, P = 0.0003) and to myocardial fibrosis (extracellular volume; whole group: R = 0.54, P = 0.001; WHIV: R = 0.47, P = 0.04). Both HIV status and sCD163 levels independently predicted aPWV, controlling for age, BMI, cigarette smoking status, and systolic blood pressure (HIV status: β-estimate = 0.69, 95% CI [0.1 to 1.3], P = 0.02; sCD163: β-estimate = 0.002, 95% CI [0.0006 to 0.004], P = 0.01). Among WHIV, sCD163 levels independently predicted aPWV, controlling for duration of HIV, CD4 count, and HIV viral load (sCD163: β-estimate = 0.004, 95% CI [0.002 to 0.005], P = 0.0005).
Conclusions:
Asymptomatic WHIV on ART have increased aortic stiffness as compared to matched control subjects. Among WHIV, aPWV related to heightened monocyte activation (sCD163) and to downstream CVD pathology (myocardial fibrosis). CLINICALTRIALS.
Gov Registration:
NCT02874703.
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