Diverse Cardiopulmonary Diseases are Associated with Distinct Xenon MRI Signatures.

Background: As an increasing munber of patients exhibit concomitant cardiac and pulmonary disease, limitations of standard diagnostic criteria are more frequently encountered. Here, we apply noninvasive Xe-129 magnetic resonance imaging (MRI) and spectroscopy to identify patterns of regional gas transfer impairment and haemodynamics that are uniquely associated with chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF), left heart failure (LHF) and pulmonary arterial hypertension (PAH). Methods: Healthy volunteers (n=23) and patients with COPD (n=8), IPF (n=12), LHF (n=6) and PAH (n=10) underwent Xe-129 gas transfer imaging and dynamic spectroscopy. For each patient, three-dimensional maps were generated to depict ventilation, barrier uptake (Xe-129 dissolved in interstitial tissue) and red blood cell (RBC) transfer (Xe-129 dissolved in RBCs). Dynamic Xe-129 spectroscopy was used to quantify cardiogenic oscillations in the RBC signal amplitude and frequency shift. Results: Compared with healthy volunteers, all patient groups exhibited decreased ventilation and RBC transfer (both p <= 0.01). Patients with COPD demonstrated more ventilation and barrier defects compared with all other groups (both p <= 0.02). In contrast, IPF patients demonstrated elevated barrier uptake compared with all other groups (p <= 0.007), and increased RBC amplitude and shift oscillations compared with healthy volunteers (p=0.007 and p <= 0.01, respectively). Patients with COPD and PAH both exhibited decreased RBC amplitude oscillations (p=0.02 and p=0.005, respectively) compared with healthy volunteers. LHF was distinguishable from PAH by enhanced RBC amplitude oscillations (p=0.01). Conclusion: COPD, IPF, LHF and PAH each exhibit unique Xe-129 MRI and dynamic spectroscopy signatures. These metrics may help with diagnostic challenges in cardiopulmonary disease and increase understanding of regional lung function and haemodynamics at the alveolar-capillary level.