Patent Foramen Ovale among Patients with Mild Chronic Obstructive Pulmonary Disease and Unexplained Hypoxia

• Published in: Echocardiography (Mount Kisco, N.Y.) N.Y.), 2010-07, Vol.27 (6), p.687-690
• Main Authors: Kilic, Harun, Balcı, Mustafa M., Aksoy, Murat N., Bilgin, Esra, Gülsoy, Kevser G., Yeter, Ekrem, Acikel, Sadik, Akdemir, Ramazan
• Format: Article
• Language: English
• Subjects: chronic obstructive pulmonary disease; Echocardiography; Female; Foramen Ovale, Patent - complications; Foramen Ovale, Patent - diagnosis; Foramen Ovale, Patent - physiopathology; Humans; hypoxia; Hypoxia - complications; Hypoxia - diagnosis; Hypoxia - physiopathology; Male; Middle Aged; Oxygen - blood; patent foramen ovale; Pulmonary Disease, Chronic Obstructive - complications; Pulmonary Disease, Chronic Obstructive - diagnosis; Pulmonary Disease, Chronic Obstructive - physiopathology
• ISSN: 0742-2822; 1540-8175
• DOI: 10.1111/j.1540-8175.2009.01105.x

Purpose: To evaluate whether patent foramen ovale (PFO) is a contributing factor to hypoxia in patients with chronic obstructive pulmonary disease (COPD). Methods: Twenty‐one patients over 40 years of age with mild COPD (Forced expiratory volume (FEV1)/Forced Vital Capacity (FVC): > 50%) who had hypoxia (PO2 < 80 mmHg, SaO2 < 95%) that could not be explained by COPD alone were included in this study. Arterial oxygen pressures (PO2) and arterial oxygen saturations (SaO2) were recorded from laboratory evaluations of arterial blood gases. Respiratory function tests were performed to analyze the degree of COPD. Standard and contrast echocardiography was used to calculate pulmonary artery pressure (PAP) levels and to determine patients with a PFO. Results: The mean age of the patients was 64 ± 12 years. Four patients (19%) had a PFO. The mean PO2, mean SaO2, and mean PAP levels were 57.4 ± 6.8 mmHg, 90 ± 3.2%, and 33.8 ± 5.4 mmHg, respectively, in patients without PFO. The mean PO2, mean SaO2, and mean PAP levels were 46.5 ± 13.7 mmHg, 79.3 ± 12.8%, and 42.5 ± 6.5 mmHg, respectively, in patients with PFO. There were no statistically significant differences noted between the two groups in the PO2 levels (P = 0.172) and SaO2 levels (P = 0.065). A comparison of the PAP levels revealed a statistically significant difference between the two groups, with values that were more elevated in the PFO group than in the non‐PFO group (P = 0.031). Conclusion: This study demonstrated that PFO is not a contributing factor to deep hypoxia in COPD patients with lower PO2 and SaO2 levels; however, higher PAP levels were detected in patients with a PFO. Further studies involving a larger number of patients are needed to be conclusive. (Echocardiography 2010;27:687‐690)