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Patent Foramen Ovale

Patent foramen ovale (PFO) is that remnant of the fetal circulation — between the right and left atrium of the heart — characterized by persistent communication into adulthood. PFO is a common condition, with an incidence of ~27% in normal human hearts at autopsy (Hagen 17-20). It is found more frequently in young patients (younger than 55 years) with cryptogenic ischemic stroke (54%), than those with stroke of identifiable cause (21%) (Lechat 1148-1152).

The mechanism of this association is difficult to prove, but the presence of a PFO is speculated to facilitate right-to-left shunt of venous blood, carrying thromboemboli into the systemic circulation, thereby leading to "paradoxical" embolism. As an estimated 60,000-110,000 ischemic strokes per year are thought to coincide with a PFO, there has been significant interest in closure of PFO to prevent stroke recurrence. The availability of percutaneous transcatheter devices to close PFO has magnified this interest. PFO and right-to-left shunt has also been implicated in orthodeoxia-platypnea syndrome, decompression-induced neurologic dysfunction, migraine headaches, and cerebral fat-embolism syndrome (Wilmshurst 65-75). This review will focus on the evaluation and management of the PFO-associated ischemic stroke.

Embryological Development of PFO:
The foramen ovale forms during early cardiac development in the fetus as a one-way valve in the interatrial septum, resulting from incomplete closure of the septum primum and septum secundum. Oxygenated blood enters the right atrium from the inferior vena cava (IVC), where flow is directed preferentially across the PFO by the right valve of the sinus venosis, allowing oxygenated blood to enter systemic circulation. At birth, however, changes in intracardiac pressures close the flap in the septum. Typically, the apposition of the septum primum and secundum lead to fibrosis – sealing off the defect.
In a significant proportion of the population, however, the defect remains open, thereby termed and identified as a "patent foramen ovale".

Clinical Presentation of PFO:
Patent foramen ovale has no specific physical findings to indicate its presence. Its presence is manifest only when sought after based on a suggestive clinical scenario. In some individuals, right-to-left shunt across a PFO is readily seen with contrast echocardiography at rest, while in others, shunt is demonstrable with provocative maneuvers such as cough or Valsalva that lead to a transient elevation of the right atrial pressure. Other conditions may increase right-to-left shunt, such as positive end-expiratory pressure (i.e., mechanical ventilation or brass-instrument playing) or pulmonary hypertension (i.e., pulmonary embolism, fat embolism, or pneumonectomy) (Forteza 457).

PFO and Cryptogenic Stroke:
The association of PFO with cryptogenic stroke remains controversial (Tong 804-805). Reports of a strong association first surfaced in the 1980's, when echocardiographic methods for PFO detection became widely available and researchers grappled with the question of etiology for cryptogenic stroke, especially in young patients without significant risk factors for stroke. Although the presumed mechanism of ischemia in many of these patients is right-to-left shunt across the PFO of thromboemboli, this is difficult to demonstrate. Thromboemboli are rarely seen in actual transit across the PFO, and suggestive clinical evidence such as deep venous thrombosis, Valsalva maneuver at the onset of stroke, or hypercoagulable state is present only in some, but not all, patients with PFO and cryptogenic stroke.

Consequently, atrial anomalies associated with PFO have been considered as possible mediators of increased stroke risk with PFO. The atrial septal aneursym (ASA), a protrusion of the interatrial septum, although uncommon in the general population (2%), is found in ~19-58% of cryptogenic stroke patients with PFO (Lechat 1151).



Works Cited

Forteza, Alejandro, et al. "Endovascular Closure of a Patent Foramen Ovale in the Fat Embolism Syndrome: Changes in the Embolic Patterns as Detected by Transcranial Doppler". Arch Neurol. 59 (2002): 455-459.
Hagen, Philip, et al. "Incidence and Size of Patent Foramen Ovale During the First 10 Decades of Life: an Autopsy Study of 965 Normal Hearts". Mayo Clin Proc. 59 (1984): 17-20.
Lechat, Philippe, et al. "Prevalence of Patent Foramen Ovale in Patients with Stroke". N Engl J Med. 318 (1988): 1148-1152.
Tong, David and Kyra Becker. "Patent Foramen Ovale and Recurrent Stroke: Closure Is the Best Option: No". Stroke. 35 (2004): 804-805.
Wilmshurst Peter and Phillip Bryson. "Relationship Between the Clinical Features of Neurological Decompression Illness and its Causes". Clin Sci (Lond). 99 (2000): 65-75.

Posted by: Sancha Haysbert

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