HIV INFECTION IS AN INDEPENDENT RISK FACTOR OF ARTERIAL STIFFNESS

Abstract

Objective: The initiation of highly active antiretroviral therapy (HAART) in 1996 dramatically changed the outcome of HIV infection from a fatal disease to a manageable chronic illness. However, HIV infection and/or HAART are associated with accelerated atherosclerosis and increased risk of cardiovascular events. According to 2018 ESH/ESC Guidelines for the management of arterial hypertension, arterial stiffness estimated as carotid-femoral pulse wave velocity (cfPWV) >10m/s is indicative of hypertension-mediated organ damage and increases total cardiovascular risk. The aim of this study is to determine whether HIV infection directly affects arterial stiffness, a hypothesis that remains controversial according to literature. Design and method: We measured cfPWV and other markers of arterial stiffness like augmentation index (AIx) and central aortic blood pressure by applanation tonometry using the Sphygmocor (Atcor, Australia) device in 36 HIV-infected male individuals and 36 age-, body mass index-, pack year- and blood pressure-matched healthy male controls. All subjects were over 48 years of age and had no history of hypertension, diabetes mellitus, moderate or severe renal failure and known cardiovascular disease. Cardiovascular risk was estimated using Hellenic Heart Score, alcohol abuse and physical activity described as metabolic equivalents (METS) were recorded and blood tests were performed for complete blood cell count, fasting plasma glucose, lipid analysis (total, HDL, LDL cholesterol and triglycerides) and the calculation of eGFR using MDRD formula. Time of first positive HIV test and years of antiretroviral therapy were also recorded in HIV-infected group. Results: HIV-infected individuals had higher cfPWV than healthy controls (9.35 ± 1,46m/s vs 8.61 ± 1.18m/s, p = 0.02). AIx (21.6 ± 7,39 vs 18.46 ± 8,17, p = 0.092), central systolic aortic blood pressure (116.75 ± 11.6mmHg vs 116.14 ± 13,34mmHg, p = 0.836) and central diastolic aortic blood pressure (81.61 ± 6.8mmHg vs 79.78 ± 10.12mmHg, P = 0.371) were similar to both groups. In multivariate analysis, age (b = −0.432, p < 0.001) and duration of HIV infection (b = 0.262, p = 0.005) were the two independent determinants of cfPWV. Conclusions: Our study supports that HIV infection is independently associated with cfPWV and, therefore, may increase cardiovascular risk through aortic stiffening.