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Insulin resistance predicts endothelial dysfunction and cardiovascular risk in HIV-infected persons on long-term
Kristin E Mondy1, Lisa de las Fuentes, Alan Waggoner
1Washington University School of Medicine, St Louis, MO, USA.
Insights
Cardiovascular disease markers were similar between HIV-infected and HIV-negative individuals. However, insulin resistance emerged as a key predictor of endothelial dysfunction and increased carotid intima-media thickness in the HIV cohort.
Area of Science:
- Cardiology
- Infectious Diseases
- Vascular Biology
Background:
- Cardiovascular disease (CVD) risk is elevated in individuals with HIV, potentially due to multifactorial causes.
- Noninvasive vascular tests may yield varied results, necessitating comprehensive assessment of CVD predictors.
Purpose of the Study:
- To evaluate metabolic and clinical predictors of endothelial function and carotid intima-media thickness in HIV-infected individuals.
- To compare these markers between HIV-infected subjects on stable antiretroviral therapy and HIV-negative controls.
Main Methods:
- Prospective, cross-sectional study matching 50 HIV-infected adults to 50 HIV-negative controls.
- Assessed flow-mediated vasodilation, carotid intima-media thickness, body composition, and metabolic markers (insulin, lipids, glucose tolerance).
Main Results:
- No significant differences in flow-mediated vasodilation or carotid intima-media thickness between HIV-infected and control groups.
- In HIV-infected subjects, insulin resistance predicted endothelial dysfunction and increased carotid intima-media thickness.
- Hypertension and body fat distribution also predicted increased carotid intima-media thickness.
Conclusions:
- Preclinical CVD markers were comparable between HIV-infected individuals on modern therapy and controls.
- Insulin resistance is a significant predictor of vascular dysfunction in the HIV population.
- Managing insulin resistance may be crucial for mitigating CVD risk in people with HIV.
Objective:
Cardiovascular disease risk among persons with HIV is likely multifactorial, thus testing a variety of available noninvasive vascular ultrasound and other surrogate tests may yield differing results. To address this issue, we assessed multiple metabolic and clinical predictors of endothelial function and carotid intima-media thickness in HIV-infected subjects and compared results with HIV-negative controls.
Design:
Prospective, cross-sectional study of 50 HIV-infected, healthy adults on stable highly active antiretroviral therapy matched to 50 HIV-negative controls by age, sex, race, and body mass index.
Methods:
Flow-mediated vasodilation of the brachial artery, carotid intima-media thickness, dual energy X-ray absorptiometry (HIV-infected subjects), and fasting insulin, lipids, and oral glucose tolerance tests were performed. Results were compared between HIV-infected and control groups.
Results:
Fifty percent of subjects were African-American with 34% women. Among HIV-infected, mean CD4 cell count was 547 cells/microl; 90% had HIV RNA less than 50 copies/ml. There were no significant differences between HIV-infected and control subjects with regard to brachial artery flow-mediated vasodilation or carotid intima-media thickness. In multivariate analyses of the HIV cohort, independent predictors of endothelial dysfunction (lower flow-mediated vasodilation) were increasing insulin resistance, greater alcohol consumption, and higher baseline brachial artery diameter (P < 0.05); predictors of increased carotid intima-media thickness were hypertension, higher trunk/limb fat ratio, and insulin resistance (P < 0.05).
Conclusion:
In this HIV cohort on modern highly active antiretroviral therapy with well controlled HIV, there were no significant differences with regard to preclinical markers of cardiovascular disease. Insulin resistance was a strong predictor of impaired brachial artery flow-mediated vasodilation and increased carotid intima-media thickness, and may be an important cardiovascular disease risk factor in the HIV population.
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