- Lung diseases are more common among people with HIV than in the general population and are a leading cause of morbidity and mortality
- In this cross-sectional study, positron emission tomography was used to examine 45 subjects—smokers and nonsmokers, with and without HIV
- Nonsmokers with HIV infection had increased residual perfusion heterogeneity and a reduced vertical perfusion gradient, approaching the values seen in smokers
- Smokers showed severe reduction in the vertical gradient of perfusion and greater residual perfusion heterogeneity, regardless of HIV status
Among people with HIV, chronic obstructive pulmonary disease (COPD) and other lung diseases are more common than in the general population and are a leading cause of morbidity and mortality. This is true even for nonsmokers with HIV—nearly one in six has emphysematous changes in their lungs.
Researchers at Massachusetts General Hospital have determined that pulmonary vascular dysfunction in patients with HIV can be detected by positron emission tomography prior to lung tissue destruction.
Physician-Researchers Puja Kohli, MD, and Kathryn Hibbert, MD, of the Division of Pulmonary & Critical Care Medicine at Massachusetts General Hospital; Tilo Winkler, PhD, assistant in Biomedical Engineering of the Department of Anesthesia, Critical Care and Pain Medicine; and colleagues report their observations in The Journal of Nuclear Medicine.
The study volunteers were ages 18–65 and had normal pulmonary function or stage I or II COPD according to the Global Initiative for Obstructive Lung Disease criteria.
- 26 were nonsmokers (15 HIV−, 11 HIV+)
- 19 were smokers (7 HIV−, 12 HIV+)
For each participant, a dynamic nitrogen-13 PET scan was acquired, and perfusion and ventilation images were generated. The images were used to calculate total spatial heterogeneity of perfusion and its components (systematic gradients in the vertical and axial directions and the residual heterogeneity).
Nonsmokers with HIV had increased residual perfusion heterogeneity and a reduced vertical perfusion gradient, approaching the values seen in smokers. This suggests HIV infection itself can cause pulmonary vascular dysfunction and contribute to the development of COPD.
Smokers showed severe reduction in the vertical gradient of perfusion and greater residual perfusion heterogeneity, regardless of HIV status.
Half of this cohort had normal echocardiography results, so perfusion imaging seems capable of detecting quite early stages of pulmonary vascular dysfunction, prior to development of overt lung disease.
These findings suggest opportunities for earlier risk prediction and novel preventive strategies, screening metrics and therapeutic targets for patients with HIV.
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