Patients with pulmonary arterial hypertension (PAH) have complex vascular lessions that include inflammatory cells. Investigation of surgical specimens from patients with PAH demonstrate evidence of oxidative stress reflected by upregulation of cellular antioxidant defenses. The levels of hydrogen peroxide (H2O2) in exhaled breath condensate (EBC) have been found to be elevated in a variety of inflammatory diseases of the lower respiratory tract including asthma, COPD, cystic fibrosis and ARDS. H2O2 levels correlate with airway inflammation, lung neutrophilic activation and oxidative stress. It was hypothesised that H2O2 levels could be used to non-invasively evaluate the state of airway inflammation and oxidative stress in PAH.
Subjects with PAH (n=17), healthy controls (n=30) and cystic fibrosis as positive controls (n=13) were recruited for sample collection. Subjects with PAH and the healthy controls were age matched. Smokers or subjects with an upper respiratory infection were excluded. EBC was collected using the Jaeger ECoScreen device for fifteen minutes wearing a nose clip. H2O2 was measured using a method described by Ruch based on reaction with homovanillic acid producing a highly fluorescent dimer. Demographics and clinical data were collected from the medical record.
Average volume of EBC was 2.5 ml after 15 minutes. Patients with PAH were found to have higher levels of H2O2 (1.093 nm/ml ± 1.165) compared to CF (0.733 nm/ml ± 0.723) and healthy controls (0.355 ± 0.244, p =0.0322). The levels were not correlated with the PA pressure obtained by 2D echo (r2=.028), sex or age of the subjects.
Levels of hydrogen peroxide in EBC were higher in patients with pulmonary hypertension compared to healthy controls. No correlation between sex, age or pulmonary artery pressure of PAH subjects were found.
EBC is an easily performed, non-invasive method for sampling lung contents. In PAH, levels of H2O2 and other markers of inflammation and oxidative stress may provide a target to monitor therapeutic responses that reflect the underlying cellular pathophysiology.
Eduardo Vasquez, None.