The role of HIV as a risk modifier for coronary endothelial function in young adults.

Background: People living with HIV have an increased risk of cardiovascular disease (CVD). Although coronary endothelial function (CEF) is an early direct indicator of CVD, only a few studies have been able to interrogate CEF directly. Most studies have examined vascular endothelial function through indirect assessment of brachial flow‐mediated dilatation (FMD). However, peripheral arteries are significantly larger and manifest atherogenesis differently from the coronary arteries, and so produce conflicting results. Additionally, none of these studies focused on young adults who acquired HIV perinatally or in early childhood. Objective: The present study investigates CEF in a unique population of young adults with lifelong HIV using direct magnetic resonance imaging (MRI) of coronary FMD (corFMD) with an in‐house developed MRI‐integrated isometric handgrip exercise system with continuous feedback and monitoring mechanisms (fmIHE). Methods: Young adults who acquired HIV perinatally or in early childhood (n = 23) and group‐matched healthy participants (n = 12) completed corFMD‐MRI with fmIHE. CorFMD was measured as the coronary cross‐sectional area response to the fmIHE. Results: In univariable and multivariable regression analysis, HIV status was a significant risk modifier. CD8+ T‐cell count and smoking pack‐years and their interaction with HIV status were independently associated with impaired coronary artery response to fmIHE. In people living with HIV, corFMD was significantly inversely correlated with CD8+ T‐cells and smoking pack‐years. In a multivariable regression analysis adjusted for age and body mass index, CD8+ T‐cells and smoking and their interaction with HIV status remained significant independent predictors of coronary endothelial dysfunction. Discussion: In this unique population of young adults, HIV status was a significant risk modifier, and immune activation and smoking were associated with decreased CEF, directly measured from the coronary vascular response to fmIHE. Conclusions: Management of CVD risk factors such as smoking and developing strategies that target immune activation in people living with HIV are warranted. [ABSTRACT FROM AUTHOR]