Background:  Untreated HIV infection may increase risk for cardiovascular disease (CVD). Assessment of large and small arterial elasticity provides information on functional and structural vascular changes, and changes in artery elasticity are associated with traditional CVD risk factors, early vascular disease and risk for clinical events. Assessment of large and small arterial elasticity in individuals with HIV infection has not been reported.

Methods:  HIV⁺ participants who had not used ART (n = 32) were compared to HIV^– (n = 30) controls with similar demographics and CVD risk profiles. Large and small arterial elasticity indices were derived from the radial artery diastolic pulse contour obtained with a hand-held non-invasive tonometer. Assessment of short-term reliability for 12 participants evaluated twice 1 to 4 months apart gave correlations of 0.84 for large arterial elasticity and 0.94 for small arterial elasticity. Differences in large and small arterial elasticity by HIV status and additional co-variates were examined with analysis of co-variance.

Results:  HIV infection was associated with lower levels of large arterial elasticity (–2.55 mL/mmHgx10; p = 0.02) and small arterial elasticity (–1.50 mL/mmHgx10; p = 0.02). Among all participants, higher Framingham 10-year CVD risk score (per 1%) was significantly associated with lower small arterial elasticity (–0.18, p = 0.01), but not large arterial elasticity (–0.19, p = 0.13). Fasting lipid levels were not associated with large and small arterial elasticity measures. After adjustment for age, gender, race/ethnicity, smoking status, injection drug use, hepatitis B or C infection and total cholesterol/HDL ratio, differences were reduced but remained lower for HIV-infected participants than in controls for small arterial elasticity (–1.30; p = 0.03), but was not significant for large arterial elasticity (–2.25; p = 0.08). In adjusted models, smoking status remained associated with large arterial elasticity (–2.07; p = 0.02) but not small arterial elasticity (–0.91; p = 0.13), and small arterial elasticity was lower for those with hepatitis B or C infection (–2.40; p = 0.004) and older age (–0.83 per 10 years older; p = 0.005). Among HIV-infected participants, CD4 count and HIV RNA level were not associated with large and small arterial elasticity.

Conclusions:  Untreated HIV infection is associated with differences in arterial elasticity that are clinically relevant for higher CVD risk. Impairment of the peripheral micro-vascular circulation (small arterial elasticity) with HIV infection was independent of traditional CVD risk factors. Assessment of arterial elasticity, via non-invasive diastolic radial pulse waveform analysis, is a useful method to assess early vascular disease among HIV-infected patients, its progression, and the influence of ART use.