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Original Research: Pulmonary Vascular Disease |

Breath Analysis in Pulmonary Arterial HypertensionBreath in Pulmonary Hypertension

Frank S. Cikach, Jr, BS; Adriano R. Tonelli, MD; Jarrod Barnes, PhD; Kelly Paschke, BA; Jennie Newman, LPN; David Grove, PhD; Luma Dababneh, MD; Sihe Wang, MD; Raed A. Dweik, MD, FCCP
Author and Funding Information

From the Pathobiology Department (Mr Cikach; Drs Barnes, Grove, Dababneh, and Dweik; and Ms Paschke), Lerner Research Institute; the Department of Pulmonary, Allergy and Critical Care Medicine (Drs Tonelli and Dweik and Ms Newman), Respiratory Institute; and the Department of Clinical Pathology (Dr Wang), Cleveland Clinic, Cleveland, OH.

Correspondence to: Raed A. Dweik, MD, FCCP, 9500 Euclid Ave A-90, Cleveland, OH 44195; e-mail: dweikr@ccf.org


Part of this article has been presented in abstract form at the American Thoracic Society Conference, May 22, 2013, Philadelphia, PA.

Funding/Support: This publication was made possible by the Third Frontier Program of the Ohio Department of Development [Grant BRCP 08-049]. Dr Tonelli is supported by Clinical and Translational Science Awards KL2 [Grant RR024990] from the National Center for Research Resources, a component of the NIH, and by the NIH Roadmap for Medical Research. Dr Dweik is supported by the National Institutes of Health [Grants HL081064, HL107147, and RR026231].

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2014;145(3):551-558. doi:10.1378/chest.13-1363
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Background:  Pulmonary arterial hypertension (PAH) is a progressive and devastating condition characterized by vascular cell proliferation and is associated with several metabolic derangements. We hypothesized that metabolic derangements in PAH can be detected by measuring metabolic by-products in exhaled breath.

Methods:  We collected breath and blood samples from patients with PAH at the time of right-sided heart catheterization (n = 31) and from healthy control subjects (n = 34). Breath was analyzed by selected ion flow tube-mass spectrometry in predetermined training and validation cohorts.

Results:  Patients with PAH were 51.5 ± 14 years old, and 27 were women (85%). Control subjects were 38 ± 13 years old, and 22 were women (65%). Discriminant analysis in the training set identified three ion peaks (H3O+29+, NO+56+, and O2+98+) and the variable age that correctly classified 88.9% of the individuals. In an independent validation cohort, 82.8% of the individuals were classified correctly. The concentrations of the volatile organic compounds 2-propanol, acetaldehyde, ammonia, ethanol, pentane, 1-decene, 1-octene, and 2-nonene were different in patients with PAH compared with control subjects. Exhaled ammonia was higher in patients with PAH (median [interquartile range]: 94.7 parts per billion (ppb) [70-129 ppb] vs 60.9 ppb [46-77 ppb], P < .001) and was associated with right atrial pressure (ρ = 0.57, P < .001), mean pulmonary artery pressure (ρ = 0.43, P = .015), cardiac index by thermodilution (ρ = −0.39, P = .03), pulmonary vascular resistance (ρ = 0.40, P = .04), mixed venous oxygen (ρ = −0.59, P < .001), and right ventricular dilation (ρ = 0.42, P = .03).

Conclusions:  Breathprint is different between patients with PAH and healthy control subjects. Several specific compounds, including ammonia, were elevated in the breath of patients with PAH. Exhaled ammonia levels correlated with severity of disease.

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