Patent Foramen Ovale and Hypoxemia

Abstract

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.

Clinical features of right‐to‐left shunt in the different subgroups of migraine

“…Transient hypoxic episodes—which occur when deoxygenated venous blood enters and combines with oxygenated arterial blood via the RLS—may also explain the mechanism of association between migraine and RLS (Mojadidi et al, ; Tobis & Azarbal, ). Moreover, hypoxemia has also been shown to be a potential trigger of CSD (Hildick‐Smith & Williams, ).…”

“…Transient hypoxic episodes-which occur when deoxygenated venous blood enters and combines with oxygenated arterial blood via the RLS-may also explain the mechanism of association between migraine and RLS (Mojadidi et al, 2019; (Gupta, 2004;Wahl et al, 2010). In recent years, a meta-analysis of randomized clinical trials-including three trials consisting of 448 total patients (average follow-up of 10 months)-has shown that between the PFO closure and control groups, there was no significant difference among subjects who experienced a complete cessation of migraine attacks.…”

Migraine and Ischemic Stroke in Women. A Narrative Review

“…An independent risk factor for ischemic stroke, it is present in nearly half of all cryptogenic ischemic strokes in a young population 157 . Putative mechanisms by which PFO predispose to stroke risk include: (1) providing a channel from venous to arterial circulation for paradoxical emboli; (2) providing a nidus for in situ thrombus formation; (3) allowing vasoactive substances such as biogenic amines (eg, serotonin, which causes vasoconstriction and platelet aggregation) to bypass pulmonary filtration; and (4) shunting deoxygenated venous blood into the cerebral circulation, where it increases plasminogen activator inhibitor‐1 thereby decreasing fibrinolysis 158,159 . It has been theorized that large PFO size, presence of right‐to‐left shunt at rest, and presence of hypermobile atrial septum are markers of heightened risk of PFO‐related cryptogenic stroke, but studies have not confirmed this 160,161 …”

Patent Foramen Ovale: Pivotal Role of Transesophageal Echocardiography in the Indications for Closure, Assessment of Varying Anatomies and Post-procedure Follow-up

“…Most of the cases with PFO are patients with additional pulmonary diseases such as chronic lung disease and pneumonectomy. Closure in POS could be considered in cases of severe symptomatic hypoxia in the absence of pulmonary hypertension (Mojadidi et al 2019;Shah et al 2016). In divers, albeit the incidence of decompression sickness is rare, the presence of PFO could cause venous bubbles to go into the arterial circulation and lead to cerebral or myocardial infarction.…”