Carotid Artery Thickness Is Associated With Chronic Use of Highly Active Antiretroviral Therapy in Patients Infected With Human Immunodeficiency Virus

A 3.0 Tesla Magnetic Resonance Imaging Study

TM LaBounty; WD Hardy; Z Fan; R Yumul; D Li; R Dharmakumar; A Hernandez Conte


HIV Medicine. 2016;17(7):516-523. 

In This Article

Abstract and Introduction


Objectives While patients with HIV infection have an elevated stroke risk, ultrasound studies of carotid artery wall thickness have reported variable results. We hypothesized that subjects with HIV infection on chronic highly active antiretroviral therapy (HAART) would have increased carotid artery wall thickness by magnetic resonance imaging (MRI).

Methods This cross-sectional study compared carotid artery wall thickness between 26 individuals infected with HIV on chronic HAART and 20 controls, without HIV infection but with similar cardiovascular risk factors, using 3.0-T noncontrast MRI. Inclusion criteria included male gender, age 35–55 years, and chronic HAART (≥ 3 years) among HIV-seropositive subjects; those with known cardiovascular disease or diabetes were excluded.

Results Between subjects with HIV infection and controls, there were no differences in mean (±SD) age (47.8 ± 5.0 vs. 47.8 ± 4.7 years, respectively; P = 0.19) or cardiovascular risk factors (P > 0.05 for each). Mean (±SD) wall thickness was increased in those with HIV infection vs. controls for the left (0.88 ± 0.08 vs. 0.83 ± 0.08 mm, respectively; P = 0.03) and right (0.90 ± 0.10 vs. 0.85 ± 0.07 mm, respectively; P = 0.046) common carotid arteries. Among individuals with HIV infection, variables associated with increased mean carotid artery wall thickness included lipoaccumulation [+0.09 mm; 95% confidence interval (CI) 0.03–0.14 mm; P = 0.003], Framingham risk score ≥ 5% (+0.07 mm; 95% CI 0.01–0.12; P = 0.02 mm), and increased duration of protease inhibitor therapy (+0.03 mm per 5 years; 95% CI 0.01–0.06 mm; P = 0.02).

Conclusions Individuals with HIV infection on chronic HAART had increased carotid artery wall thickness as compared to similar controls. In subjects with HIV infection, the presence of lipoaccumulation and longer duration of protease inhibitor therapy were associated with greater wall thickness.


HIV infection is a leading cause of morbidity and mortality, with over 1 million persons infected and 55 000 new cases annually in the USA alone.[1] Since the introduction of highly active antiretroviral therapy (HAART), HIV infection has become a chronic, treatable disease similar to hypertension and hyperlipidaemia, and life expectancy may approach that of uninfected persons in patients with durably suppressed virus.[2–5] As the population with HIV infection ages, an excess of strokes[6–8] and myocardial infarctions[9,10] has been observed. Comparisons of the carotid artery utilizing ultrasound between individuals with and without HIV infection have provided disparate results, with some studies finding an increase in carotid artery intimal medial thickness among HIV-infected patients as compared with controls,[11–15] and other studies observing no difference.[16,17] Existing studies have generally included untreated HIV-infected individuals, and it is not clear whether individuals with HIV infection on chronic, contemporary HAART have increased carotid wall thickness.

We hypothesized that individuals with HIV infection on chronic HAART would have increased carotid artery wall thickness. As carotid artery imaging by magnetic resonance imaging (MRI) may provide results similar to those of ultrasound with reduced inter-procedure variability,[18] we utilized 3.0-T MRI to compare carotid artery wall thickness between individuals with HIV infection on ≥ 3 years of HAART and similar controls. We further evaluated the relationship between selected clinical variables and carotid artery wall thickness among subjects with HIV infection.