COPD is the most common non-infectious pulmonary disease among people living with HIV, independent of smoking. However, the cause for this enhanced susceptibility remains unclear, and the effects of HIV on pulmonary perfusion are unknown.
We used PET-CT in 46 smokers and non-smokers, 23 of whom had with documented HIV infection. Emphysema was assessed by CT and perfusion by nitrogen-13 (13NN) PET scans. After removal of image noise, vertical and axial gradients in perfusion were calculated. We tested for differences in the total spatial heterogeneity of perfusion (CV2Qtotal) and its components
(CV2Qtotal = CV2Qvgrad (vertical gradient) + CV2Qzgrad (axial gradient) + CV2Qr (residual heterogeneity)) among groups.
There were no significant differences in demographic parameters among groups, and all subjects had minimal radiographic evidence of emphysema. Compared to controls, non-smokers living with HIV had a significantly greater CV2 Qr/ CV2Qtotal (0.48 vs 0.36, p = 0.05) and reduced CV2Qvgrad/ CV2Qtotal (0.46 vs 0.65, p = 0.038). Smokers also had a reduced CV2Qvgrad/ CV2Qtotal, however, there was no significant difference in CV2Qvgrad/ CV2Qtotal between smokers living with and without HIV (0.39 vs 0.34, p = 0.58), despite a decreased vertical perfusion gradient (Qvgrad)
in smokers living with HIV.
In non-smokers living with well-controlled HIV and minimal radiographic emphysema, HIV infection contributes to pulmonary perfusion abnormalities similar to smokers. These data indicate the onset of subclinical pulmonary perfusion abnormalities that could herald the development of significant lung disease in these susceptible individuals.