Objective: We compared aortic stiffness between HIV-infected and HIV-uninfected individuals and examined the determinants of vascular aging during HIV infection.
Methods: Aortic stiffness using carotid-femoral pulse wave velocity (cf-PWV) was evaluated cross-sectionally between HIV-infected individuals and uninfected controls frequency-matched for age and sex, and longitudinally in a subgroup of HIV-infected individuals. Determinants of elevated cf-PWV levels were assessed using logistic regression. Changes in cf-PWV levels during follow-up (mixed-effect linear regression) and risk factors for achieving cf-PWV below (Group 1) or above the median (Group 2) at last follow-up visit were evaluated only in HIV-infected individuals.
Results: A total of 133 HIV-infected and 135 HIV-uninfected individuals (mean age: 47.7 ± 8.9 years, 91% men) were enrolled. Median cf-PWV at baseline was similar between HIV-infected individuals and controls [7.5 m/s (interquartile range = 6.7-8.4) vs. 7.5 m/s (interquartile range = 6.6-8.4), respectively; P = 0.64]. In multivariable analysis, only mean arterial pressure showed significant association with elevated cf-PWV in the overall population (P = 0.036). In HIV-infected individuals, elevated cf-PWV was associated with current smoking (P = 0.042), and nadir CD4 T-cell count less than 200 cells/μl (P = 0.048). Ninety-one HIV-infected individuals were followed for a mean 7.6 ± 2.0 years. cf-PWV progression was associated with age (P = 0.018), mean arterial pressure (P = 0.020), and nadir CD4 T-cell count (P = 0.005). Patients from Group 2 had higher baseline waist circumference, pulse pressure, and nadir CD4 T-cell count less than 200 cells/μl.
Conclusion: We observed no difference in aortic stiffness between HIV-infected and controls. Moreover, aortic stiffness aging was independently associated with past severe immunodeficiency, along with other traditional risk factors. Our results call for early antiretroviral initiation.
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