In recent years, patients who have echocardiograms are often told they have a condition called patent foramen ovale, or PFO. The advice they receive after being given this diagnosis will vary wildly. Some doctors will want to treat them with blood thinners to prevent blood clots. Others will recommend an invasive procedure to install a special device to close the PFO. Still others will tell the patient that a PFO has no real significance at all, and that no therapy is required.
In this review I will describe what is known about PFO, and will try to place the current controversy regarding its treatment into perspective.
What is a PFO?
In the developing fetus, the foramen ovale is a hole that is normally present in the atrial septum (the thin structure that separates the right atrium from the left atrium), which allows blood to flow freely from the right atrium directly into the left atrium. This flow of blood from the right atrium to the left atrium allows the blood to bypass the developing lungs in the fetus, and is necessary for normal fetal development.
At birth, as soon as the baby begins to breathe, the pressure in the left atrium increases, causing a flap of tissue to impose itself over the foramen ovale, effectively closing it. At this point, blood no longer is able to flow from the right to the left atrium. In most individuals, this flap of tissue becomes “tacked down,” so the foramen ovale is completely sealed off. However, in about 25% of nornal adults, the tissue flap is not completely tacked down, and relies on the higher pressure in the left atrium to keep the foramen ovale closed.
In these cases, when the pressure in the right atrium becomes intermittently higher than in the left atrium (as can occur, for instance, with coughing), for those moments the foramen ovale is open, and blood can again flow from the right to the left atrium. These patients are said to have a patent foramen ovale, PFO.
PFO is diagnosed by echocardiography. There are different degrees of PFO. In a few cases the PFO is fairly obvious and would be noticed by almost any echocardiographer. More often, special maneuvers are necessary to identify a PFO, including trans-esophageal echocardiography, injecting contrast material into the bloodstream, and even applying positive pressure to the airway through a special breathing apparatus. The harder one tries to identify a PFO the more likely one is to see a PFO (and the higher the incidence of PFO in the studied population.)
In some patients, the flap of tissue that covers the foramen ovale can develop a balloon-like bulge, which is called an atrial septal aneurysm (ASA). In most patients who have an ASA, a PFO is also present, so these two conditions are generally associated with one another. The ASA and PFO are thus very similar, and it is probably not incorrect to think of an ASA as an exaggerated (and likely somewhat more significant) instance of a PFO.
Why Is PFO Significant?
The concern with a PFO is that, during those transient episodes when the right atrial pressure is higher than the left atrial pressure, blood can flow from the right atrium to the left atrium. If a blood clot happens to be traveling through the right atrium at that moment, it too can enter the left atrium. From the left atrium the clot can then flow through the left ventricle and onward to any part of the body - if it goes to the brain, it could cause an embolic stroke. Therefore, the chief concern regarding a PFO is that it might lead to an increased risk of stroke.
However, it is not clear that people with a PFO have an increased risk of stroke. Even on its face, PFO would seem to be a rare cause of stroke, since in order to have a stroke from a PFO many relatively unlikely events would have to take place all at the same time. The person with a PFO would have to cough (or do some other maneuver to increase right atrial pressure, such as hold a high C note, or strain at the stool), at the precise moment that a blood clot is traversing the right atrium. That blood clot would then have to “decide” to go through the now-open PFO instead of following the major flow of blood (out the pulmonary artery and into the lungs). Once on the left side of the heart, the clot would then have to “decide” to join the 20% of the blood flow from the left heart that goes to the brain.
So, yes, it is possible that a PFO could cause a stroke, and PFOs have undoubtedly done so. But the event is decidedly rare.
Some investigators have reported an increased incidence of PFO in patients with migraine headache, and have attributed migraines to PFOs. However, nobody has advanced a plausible theory, based on actual human physiology, as to how a PFO might cause migraines. The lack of such a theory has not prevented some doctors from recommending PFO closure devices in these patients.
Scuba divers who have PFO have a 2 to 5-fold increased risk of developing serious decompression sickness (“the bends”) when finishing a dive. It is thought that nitrogen bubbles forming in the veins during decompression can increase right atrial pressure, thus opening a PFO. These nitrogen bubbles can then pass across the atrial septum and into the arterial circulation, where they can cause damage, for instance, to the brain.
When Does A PFO Require Treatment?
There are two general types of treatment that could be offered to patients with PFO: anti-clotting medications, and a PFO closure device. Fortunately, the vast majority of people who have a PFO do not need either of these treatments.
Most experts now agree that if a PFO is found incidentally on an echocardiogram, and is not suspected of ever having caused a problem, no therapy is necessary.
In patients who have had a cryotogenic stroke (a stroke whose cause is unknown), the presence of a PFO at least suggests a possible cause, and many doctors recommend treatment.
If a stroke has occurred that might have been caused by a PFO, PFO closure devices have been recommended by some physicians. However, three randomized clinical trials have now failed to show that closing the PFO after a stroke reduces the risk of subsequent stroke in these patients, as compared to medical therapy alone. Most experts agree today that PFO closure should be done only rarely in these cases, if at all.
Recent evidence suggests that a transcranial Doppler study, in conjunction with a bubble study, can more accurately detect patients whose cryptogenic strokes have been caused by a PFO. Studies are being planned that will assess the usefulness of PFO closure in this subset of patients.
In any case, if a PFO is thought likely to have caused a stroke, most experts today would recommend treating with drugs that inibit blood clotting - either with platelet inhibitors like aspirin or clopidogrel, or with anticoagulants such as warfarin - and not using a PFO closure device.
Migraine headache is not a reason to treat a PFO. In addition to the lack of any reasonable theory as to why PFO should cause migraines, randomized clinical trials have failed to show that migraine headaches in patients with PFO improve if a PFO closure device is inserted. At this time, PFO closure should not be regarded as a treatment for migraine headaches.
Scuba divers with a PFO should consult with their doctors about the advisability of continuing the sport. Part of the advice they receive will be based on the size of their PFO, since larger PFOs have been associated more strongly with decompression sickness.
Hara H, Virmani R, Ladich E, et al. Patent foramen ovale: current pathology, pathophysiology, and clinical status. J Am Coll Cardiol 2005; 46:1768.
Wu LA, Malouf JF, Dearani JA, et al. Patent foramen ovale in cryptogenic stroke: current understanding and management options. Arch Intern Med 2004; 164:950.
Schwedt TJ, Demaerschalk BM, Dodick DW. Patent foramen ovale and migraine: a quantitative systematic review. Cephalalgia 2008; 28:531.
Bove AA. Risk of decompression sickness with patent foramen ovale. Undersea Hyperb Med 1998; 25:175.