Chronic HIV infection leads to premature atherosclerosis. Arterial stiffness is considered a subclinical marker of cardiovascular disease.
Pulse wave velocity (PWV) was determined in 254 individuals (174 HIV-infected patients and 80 healthy controls, 2:1 matched by age and gender) to compare the prevalence of arterial stiffness and to identify associated factors. PWV was determined using noninvasive automated device (Complior). Factors associated with impaired PWV were assessed among cardiovascular risk factors, HIV infection parameters, and laboratory data. Logistic regression analyses were performed to determine differences between groups and factors associated to arterial stiffness.
Overall, 81.4% of participants were male, median age was 46.54 [interquartile range (IQR): 41–52] years. Higher percentages of HIV-infected subjects showed dyslipemia (P = 0.012) and smoking habit (P = 0.002). The median time from HIV diagnosis was 13 (IQR: 6–18) years and the median time on antiretroviral therapy was 11 (IQR: 5–15) years. Nearly, all patients were virologically suppressed (89.7%) at the time of PWV. Arterial stiffness in the global population was 20.5%, 18.9% in HIV-infected group, and 23.8% in controls (P = 0.405). High diastolic blood pressure and high levels of triglycerides at time of PWV were associated with increased PWV (P = 0.009 and P = 0.023, respectively).
Virologically suppressed HIV-infected patients showed similar arterial elasticity to non–HIV-infected patients. HIV-related conditions were not associated with arterial stiffness, probably because of the good immunologic and virological status of this group. However, high diastolic pressure at the time of PWV and high levels of triglycerides were associated risk factors.
*Lluita contra la Sida Foundation, Department of Internal Medicine, Germans Trias i Pujol University Hospital, Autonomous University of Barcelona, Barcelona, Spain; and
†Department of Econometrics, Statistics and Spanish Economy, University of Barcelona, Barcelona, Spain.
Correspondence to: Patricia Echeverría, MD, Lluita contra la SIDA Foundation, Hospital Universitari Germans Trias i Pujol, Autonomous University of Barcelona, 08916 Badalona, Catalonia, Spain (e-mail: firstname.lastname@example.org).
Supported by the Spanish AIDS network “Red Temática Cooperativa de Investigación en SIDA” (RD06/0006) and the Gala contra la sida, Barcelona 2011. P.E. is a researcher from Fundació Lluita contra la SIDA, Universitary Hospital Germans Trias i Pujo, Barcelona, Spain.
Presented as a poster at the 6th IAS Conference on HIV Pathogenesis, Treatment and Prevention, July17–20, 2011, Rome, Italy.
The authors have no conflicts of interest to disclose.
All authors have contributed to write and approved the final submitted version of the manuscript.
Received June 03, 2013
Accepted August 12, 2013