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


Patients with HIV infection (n = 26) and controls (n = 20) did not have statistically significant differences with regard to demographics, medical history, body mass index, medication use (excluding antiretrovirals), blood pressure, fasting cholesterol and glucose, and Framingham risk score (Table 1). HIV-infected patients were more likely to report previous noninjecting illicit drug use, and had higher rates of clinical lipodystrophy and greater resting heart rates.

HIV-seropositive subjects had increased bilateral common carotid artery wall thickness as compared with controls, while no differences were observed in external vessel area, luminal area, wall area, normalized wall area or carotid distensibility index (Table 2).

The relationship between relevant clinical characteristics and carotid wall thickness in subjects with HIV infection is provided in Table 3. The presence of clinical lipodystrophy (specifically lipoaccumulation), an increased Framingham risk score, and greater duration of protease inhibitor therapy were each associated with increased carotid wall thickness.

There was a trend for increased time from HIV diagnosis to be associated with greater carotid wall thickness in linear regression (P = 0.08). In comparison to subjects with a shorter time from diagnosis, those with a time from HIV diagnosis of ≥ 10 years (≥ 25th percentile) were observed to have a significant increase in mean carotid artery wall thickness [+0.07 mm; 95% confidence interval (CI) 0.01–0.13 mm; P = 0.049], while no significant difference was observed in subjects with a time of ≥ 17 years (≥ 50th percentile) from HIV diagnosis (+0.02 mm; 95% CI −0.03–0.08; P = 0.40).

A longer duration of HAART was not associated with a difference in mean carotid artery wall thickness (P = 0.29), and no significant mean differences were observed in subjects with ≥ 6 years (≥ 25th percentile) of HAART (+0.10 mm; 95% CI −0.01–0.11; P = 0.10) or ≥ 14 years (≥ 50th percentile) of HAART (+0.01 mm; 95% CI −0.05–0.07; P = 0.78) in comparison to those with a shorter duration of HAART.

We further examined HIV-positive subjects stratified by treatment or no treatment with 'high-risk' antiretroviral agents. These 'high-risk' agents were those previously noted to be associated with an increased risk of myocardial infarction, and included: protease inhibitors, including amprenavir, fosamprenavir, indinavir and lopinavir, and nucleoside reverse transcriptase inhibitors, including abacavir and didanosine.[9,24–26] Any use of "high-risk" protease inhibitors was observed in 77% (20 of 26) of subjects, and was not associated with a significant difference in carotid artery mean wall thickness (+0.04 mm; 95% CI −0.03–0.10; P = 0.31). Prior use of "high-risk" nucleoside reverse transcriptase inhibitors was noted in 46% (12 of 26) of HIV-seropositive subjects, and was also not associated with a difference in mean wall thickness (+0.03 mm; 95% CI −0.03–0.09; P = 0.27).