How Does a Patent Foramen Ovale Cause a Stroke?

A Patent Foramen Ovale (PFO) is a common remnant of the heart’s fetal circulation. While often unnoticed, a PFO can be linked to serious health events, including stroke. A stroke occurs when blood flow to a part of the brain is blocked, interrupting the supply of oxygen and nutrients, which causes brain cells to die. For some individuals, a PFO provides a pathway connecting the venous circulation (blood returning to the heart) directly to the arterial circulation (blood supplying the brain). This connection creates a specific pathway for a stroke to occur, often in the absence of traditional risk factors.

The Patent Foramen Ovale Explained

The foramen ovale is an anatomical feature in a developing fetus that allows blood to bypass the non-functional lungs. This passage connects the heart’s two upper chambers: the right atrium and the left atrium. It permits oxygenated blood to move directly from the right side to the left side of the heart and into the systemic circulation.

When a baby takes its first breaths, the pressure dynamics change. Increased left atrial pressure forces a tissue flap (septum primum) against the septum secundum, causing the functional closure of the foramen ovale. The tissue layers typically fuse over months, creating the sealed fossa ovalis.

A PFO exists when this flap does not completely fuse, leaving a persistent opening between the atria. This variance is common, present in 25% to 34% of the adult population. Although most people with a PFO remain asymptomatic, the opening can sometimes allow a blood-borne particle to pass through, potentially leading to a stroke.

The Mechanism of Paradoxical Embolism

A PFO can lead to stroke through paradoxical embolism, where a venous-system particle enters the arterial system. Normally, a blood particle formed in a vein, such as a deep vein thrombosis (DVT), travels to the heart’s right side. Without a PFO, this particle would be pumped into the pulmonary arteries and filtered out by the lung capillaries.

With a PFO, the particle takes a shortcut through the interatrial opening. Instead of proceeding to the lungs, the venous particle passes directly from the right atrium through the PFO into the left atrium. This passage is often facilitated by a transient increase in right atrial pressure, which occurs during activities like coughing, sneezing, or straining.

Once in the left atrium, the particle bypasses the lungs and enters the systemic circulation. The left side of the heart pumps this particle out through the aorta and into the arteries supplying the body, including those leading to the brain.

When this venous particle lodges in a cerebral artery, it obstructs blood flow and causes an ischemic stroke. The event is paradoxical because a particle from the low-pressure venous system causes a blockage in the high-pressure arterial system. This mechanism is often the cause of stroke in young patients when no other clear etiology is found, a condition termed cryptogenic stroke.

Identifying PFO-Related Stroke

When a stroke occurs without an obvious cause, medical professionals investigate the possibility of a PFO. The primary diagnostic method for visualizing the PFO and abnormal blood flow is an echocardiogram with agitated saline contrast, commonly known as a “bubble study.” This test involves injecting a saline solution containing tiny microbubbles into a vein in the arm.

If a PFO is present, the microbubbles cross from the right side of the heart to the left side, visible on ultrasound imaging. The test is often performed with a Valsalva maneuver (patient straining down), which temporarily increases right atrial pressure and makes the right-to-left shunt more evident. While a transthoracic echocardiogram (TTE) can be used, a transesophageal echocardiogram (TEE) offers superior image quality and greater sensitivity for detection.

The bubble study can also utilize a transcranial Doppler (TCD) ultrasound, which monitors the middle cerebral artery. If microbubbles pass through the PFO and reach the cerebral circulation, the TCD detects them as high-intensity transient signals. These imaging studies confirm the PFO’s presence and determine the shunt size, helping estimate the likelihood of it causing the stroke.

Treatment and Risk Management

After a PFO is identified following a cryptogenic stroke, treatment focuses on preventing recurrence. One primary approach is medical management, involving medications to reduce particle formation or thin the blood. This includes antiplatelet drugs, such as aspirin, or anticoagulant medications, depending on the patient’s risk factors and coexisting conditions.

The alternate strategy is PFO closure, a minimally invasive, catheter-based procedure. A small device, often shaped like a disc, is guided through a vein to the heart and deployed to seal the opening between the atria. Clinical guidelines recommend device closure plus antiplatelet therapy over medical therapy alone for select patients, especially those under 60 years old with high-risk PFO features.

The decision between medical management and device closure is individualized, based on the patient’s age, PFO size, and other risk factors. PFO closure is more effective than antiplatelet therapy alone in reducing recurrent stroke risk for younger patients. However, for older patients or those with complicating health issues, antiplatelet therapy may remain the recommended course of action.