A patent foramen ovale (PFO) causes stroke by allowing a blood clot to cross from the right side of the heart to the left, where it can travel to the brain. About 25% of all adults have a PFO, a small flap-like opening between the heart’s two upper chambers that persisted from fetal development. Most people never know it’s there, but in certain circumstances, this opening becomes a doorway for clots that would normally be filtered out by the lungs.
What a PFO Is and Why It Exists
Before birth, a baby’s lungs aren’t yet working. Blood needs to bypass them entirely, so the fetal heart has a small passage between the right and left atria called the foramen ovale. After birth, when the lungs inflate and start processing oxygen, pressure changes in the heart naturally push two overlapping flaps of tissue together, sealing this opening shut. In most people, those flaps fuse permanently within the first few years of life.
In roughly one in four adults, the flaps never fully seal. They sit against each other like a door without a latch. Under normal conditions, pressure on the left side of the heart is slightly higher than on the right, which keeps the flap pressed closed. No blood crosses, and the PFO causes no problems. The trouble starts when something temporarily reverses that pressure balance.
How a Clot Crosses to the Brain
The process that leads to stroke through a PFO is called paradoxical embolism. It’s “paradoxical” because venous blood clots, which form in the veins of the legs or pelvis, normally travel to the lungs, not the brain. The lungs act as a filter, trapping small clots before they can reach the arterial side of circulation. A PFO short-circuits that filter.
Here’s the sequence. A clot forms somewhere in the venous system, often in the deep veins of the legs. It breaks free and travels through the veins to the right side of the heart. At that moment, if pressure in the right atrium rises above the left, even briefly, the unsealed flap of the PFO opens. The clot passes through the opening into the left atrium, enters the left ventricle, and gets pumped out into the body’s arterial circulation. If it reaches a blood vessel in the brain, it blocks blood flow and causes a stroke.
The critical factor is that temporary pressure reversal. It doesn’t take much. Any action that increases pressure in the chest cavity can do it: straining during a bowel movement, heavy lifting, coughing, sneezing, or even bearing down during childbirth. These are all forms of what’s called a Valsalva maneuver, where you exhale forcefully against a closed airway. Research published in the Journal of the American College of Cardiology found that the shunt doesn’t actually occur during the straining itself. It happens in the seconds right after you release the strain, when blood rushes back into the right side of the heart and briefly overwhelms the left-sided pressure. A more forceful strain produces a larger opening.
Why PFO Strokes Are Often “Cryptogenic”
When doctors evaluate a stroke, they look for common causes: atrial fibrillation, blocked carotid arteries, small-vessel disease in the brain. In about 25% to 30% of strokes, no clear cause is found. These are called cryptogenic strokes, and PFOs are disproportionately common in this group. Roughly 50% of patients aged 60 or younger with a cryptogenic stroke have a PFO, double the rate in the general population.
That gap is strong circumstantial evidence, but finding a PFO after a stroke doesn’t automatically mean the PFO caused it. Since a quarter of all adults have one, it could be coincidental. Doctors use a clinical scoring tool called the RoPE score (Risk of Paradoxical Embolism) to estimate how likely it is that a given stroke was actually PFO-related. The score ranges from 0 to 10 and awards points for being younger, having no history of high blood pressure, diabetes, or prior strokes, being a nonsmoker, and having a specific pattern of brain damage on imaging called a cortical infarct. A younger, otherwise healthy patient who has a stroke with no other explanation and a high RoPE score is much more likely to have had a PFO-related event than an older patient with multiple vascular risk factors.
Anatomical Features That Raise Risk
Not all PFOs carry equal risk. The size of the opening matters, as does the presence of a related condition called an atrial septal aneurysm, where the wall of tissue between the atria bulges back and forth with each heartbeat. A study in the AHA journal Stroke found that patients who had both a PFO and an atrial septal aneurysm had 33 times the odds of cryptogenic stroke compared to patients with neither condition. When the aneurysm bulged more than 10 millimeters, stroke odds were about eight times higher than in those with a smaller aneurysm. The bulging wall may act like a bellows, intermittently pulling the PFO flap open and creating more opportunities for clots to cross.
How a PFO Is Detected
The standard test is a “bubble study.” A technician injects a small amount of saline mixed with tiny air bubbles into a vein in your arm while performing an ultrasound of the heart. Normally, the bubbles travel to the right side of the heart and get trapped in the lungs. If bubbles appear on the left side of the heart within a few heartbeats, it means they crossed through an opening like a PFO. You’ll be asked to bear down (a Valsalva maneuver) during the test to temporarily reverse the pressure gradient and provoke the shunt.
This can be done with a standard echocardiogram through the chest wall, or with a transesophageal echocardiogram, where a small ultrasound probe is guided down the esophagus to sit right behind the heart. The transesophageal approach provides much better images and has a sensitivity of about 89% and specificity of 91% for detecting right-to-left shunts. It’s the preferred test when PFO-related stroke is suspected.
Closure vs. Medication
For patients whose stroke is likely PFO-related, the two main options are closing the PFO with a device or managing it with medication alone. The REDUCE trial found that patients who had their PFO closed experienced clinical strokes at a rate of 1.3%, compared to 6.8% in those treated with medication only. That’s roughly an 80% relative reduction in stroke recurrence.
PFO closure is a catheter-based procedure, not open-heart surgery. A small device resembling a double umbrella is threaded through a vein in the leg, guided to the heart, and deployed across the opening. Over time, tissue grows over the device and permanently seals the flap. The procedure typically takes about an hour and most patients go home the same day or the next morning.
One notable trade-off is the risk of developing atrial fibrillation after the procedure. Systematic reviews have reported this occurs in 2% to 12% of patients, though a smaller study using implantable heart monitors detected it in 26% of patients, suggesting mild or brief episodes may go undetected in larger trials. Most post-closure atrial fibrillation is temporary and resolves within weeks, but it’s a real consideration since atrial fibrillation itself is a stroke risk factor.
For patients who don’t undergo closure, or who aren’t good candidates for it, medication is the alternative. A meta-analysis published in Neurology found that blood thinners (anticoagulants) reduced the risk of recurrent stroke by about 41% compared to antiplatelet drugs like aspirin in patients with PFO. This benefit was most clearly demonstrated with warfarin, a vitamin K antagonist. Whether newer oral anticoagulants offer the same advantage in this specific population is still being worked out, since most of the supporting data comes from warfarin-era studies.