Patent foramen ovale (PFO), an embryonic remnant of the fetal circulation, is present in 20–25% of adults. Although recent observational studies and clinical trials have established the link between PFO-mediated right-to-left shunting with cryptogenic stroke and migraine with aura, the role of a PFO in exacerbating hypoxemic medical conditions (ie, sleep apnea, chronic obstructive pulmonary disease, pulmonary hypertension, platypnea–orthodeoxia, pulmonary arteriovenous malformation, high-altitude pulmonary edema, and exercise desaturation) remains less understood. PFO-mediated hypoxemia occurs when deoxygenated venous blood from the right atrium enters and mixes with oxygenated arterial blood in the left atrium. Patients with an intracardiac right-to-left shunt may have profound hypoxemia out of proportion to underlying primary lung disease, even in the presence of normal right-sided pressures. The presence of right-to-left cardiac shunting can exacerbate the degree of hypoxemia in patients with underlying pulmonary disorders. In a subset of these patients, percutaneous PFO closure may result in marked improvement in dyspnea and hypoxemia. This review discusses the association between PFO-mediated right-to-left shunting with medical conditions associated with hypoxemia and explores the role of percutaneous PFO closure in alleviating the hypoxemia.
From the *Division of Cardiovascular Medicine, Department of Medicine, University of Florida College of Medicine, Gainesville, FL
†Department of Medicine, Albert Einstein College of Medicine (Jacobi Program), New York, NY
‡Division of Pulmonary, Critical Care, and Sleep Medicine, University of Florida College of Medicine, Gainesville, FL
§Division of Cardiovascular Medicine, Virginia Commonwealth University, Richmond, VA
¶Division of Cardiovascular Medicine, University of Iowa Hospitals and Clinics, Iowa City, IA
‖Program in Interventional Cardiology, Division of Cardiology, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, CA
**Department of Cardiology, University Hospital of Bern, Bern, Switzerland.
Disclosures: Dr. Tobis has served as a consultant for St. Jude Medical and W.L. Gore, and as a proctor for Cardiac Dimensions. Dr. Meier has received speaker fees from Abbott. The other authors have no conflicts of interest to report.
Correspondence: Mohammad K. Mojadidi, MD, Division of Cardiology, Department of Medicine, University of Florida Health, Shands Hospital, 1600 SW Archer Road, P.O. Box 100288, Gainesville, FL 32610. E-mail: email@example.com.