A PFO, or patent foramen ovale, is a small opening between the two upper chambers of the heart that never fully closed after birth. Every baby is born with this opening, called the foramen ovale, which allows blood to bypass the lungs during fetal development. In most people, it seals shut within the first few months of life. In roughly 20 to 25% of adults, it stays open, making PFO one of the most common heart findings in the general population.
Most people with a PFO never know they have one, and it causes no symptoms on its own. But in certain situations, this tiny flap-like opening can allow blood clots or other substances to cross from one side of the heart to the other, potentially reaching the brain. That connection to stroke, along with links to migraines and diving risks, is why PFO gets medical attention.
Why the Foramen Ovale Exists
Before birth, a developing baby gets oxygen from the placenta, not from breathing. The foramen ovale is a tunnel between the heart’s right and left upper chambers (the atria) that lets oxygen-rich blood from the placenta flow directly to the body without passing through the lungs, which aren’t being used yet. Once a baby takes its first breaths and the lungs begin working, pressure changes in the heart push a small flap of tissue against the opening, and over the following weeks or months, it typically fuses shut permanently.
When that fusion doesn’t happen, the flap remains. It acts like a one-way door that stays mostly closed under normal conditions but can swing open when pressure in the chest changes, such as during straining, coughing, or heavy lifting. That intermittent opening is what defines a patent foramen ovale.
The Link Between PFO and Stroke
The most significant medical concern with a PFO is its role in what’s called a cryptogenic stroke, meaning a stroke with no identifiable cause. The mechanism is known as paradoxical embolism: a blood clot forms in a vein (often in the legs), travels through the bloodstream to the right side of the heart, and instead of heading to the lungs where it would normally be filtered out, it slips through the PFO into the left side of the heart. From there, the clot can travel directly to the brain and block blood flow, causing a stroke.
This pathway explains why PFO is found at much higher rates in younger stroke patients who have no other risk factors like high blood pressure, diabetes, or irregular heart rhythms. When doctors investigate a stroke and can’t find an obvious cause, a PFO is one of the first things they look for.
PFO and Migraines With Aura
People with a PFO are about three times more likely to experience migraines than people without one. The link is even stronger for migraines with aura, the type that comes with visual disturbances like flashing lights or blind spots. Among migraine sufferers, those who experience aura are 2.3 times more likely to have a PFO than those without aura. Research has also found a positive correlation between the amount of blood flow through a PFO and the frequency of visual aura episodes.
The suspected mechanisms involve two main pathways. First, tiny blood clots or micro-bubbles passing through the PFO may trigger a slow wave of electrical activity across the brain’s surface, which is the same phenomenon thought to cause aura in migraines generally. Animal studies have confirmed that micro-embolization can cause brief reductions in brain blood flow, setting off this wave. Second, certain chemicals in the blood, particularly serotonin, normally get broken down as blood passes through the lungs. When blood bypasses the lungs through a PFO, higher concentrations of serotonin and other vasoactive substances reach the brain directly, potentially triggering migraine attacks. The shearing force of blood passing through the PFO itself may also activate platelets, which release additional serotonin into the bloodstream.
Risks for Scuba Divers
Scuba diving creates a unique hazard for people with a PFO. During a dive, nitrogen dissolves into the blood under pressure. As a diver ascends, that nitrogen forms tiny bubbles that are normally filtered out by the lungs. With a PFO, those bubbles can cross directly into the arterial circulation and reach the brain or spinal cord, causing decompression sickness.
Divers with a PFO have 2.5 times the overall risk of decompression sickness compared to divers without one, and four times the risk of neurological decompression sickness specifically. The absolute numbers are still relatively low: roughly 4.7 cases per 10,000 dives for divers with a PFO. But among divers who develop spinal decompression injuries, 44% are found to have a large PFO, compared to about 14% in control groups. This is why some diving medicine specialists recommend PFO screening for divers who have experienced unexplained decompression sickness, and why divers with a known PFO are often advised to use more conservative dive profiles.
How a PFO Is Detected
A PFO rarely causes any physical symptoms on its own, so it’s almost always discovered during testing for something else, most commonly after an unexplained stroke. The standard screening test is a “bubble study,” a type of echocardiogram where saline mixed with tiny air bubbles is injected into a vein. If bubbles appear on the left side of the heart within a few heartbeats, it confirms that blood is crossing between the chambers. A transesophageal echocardiogram, where the ultrasound probe is guided down the throat to get closer to the heart, provides a more detailed view and can measure the size of the opening.
When Treatment Is Recommended
Having a PFO alone is not a reason for treatment. The vast majority of people with a PFO live their entire lives without complications. Treatment becomes a conversation when a PFO is linked to an actual event, most commonly a cryptogenic stroke.
For stroke prevention, the two main options are blood-thinning medications or a procedure to physically close the opening. A meta-analysis of major clinical trials found that closing the PFO cut the rate of recurrent stroke roughly in half compared to medication alone: 0.53 strokes per 100 patient-years with closure versus 1.1 per 100 patient-years with medication, over an average follow-up of 3.7 years.
What PFO Closure Looks Like
PFO closure is a catheter-based procedure, meaning it doesn’t require open-heart surgery. A thin tube is threaded through a vein in the groin up to the heart, and a small device (shaped like a double disc) is placed across the opening. The device acts as a scaffold, and over time, the body’s own tissue grows over it, permanently sealing the gap.
Recovery is fast. Most people go home the same day or after one night in the hospital. Normal physical activity resumes within about a week, and most people return to work and driving shortly after that. Blood-thinning medication is typically needed for several months after the procedure to prevent clots from forming on the device while tissue grows over it.
The decision between closure and long-term medication depends on factors like age, the size of the PFO, whether there’s an associated atrial septal aneurysm (extra floppiness of the tissue between the chambers), and the likelihood that the PFO actually caused the stroke rather than being an incidental finding. For younger patients with a clearly cryptogenic stroke and a moderate-to-large PFO, closure generally offers the strongest benefit.