A hole in the heart goes by different names depending on where it sits and how it formed. The three most common terms are atrial septal defect (ASD), ventricular septal defect (VSD), and patent foramen ovale (PFO). Each involves an opening in the wall separating the heart’s chambers, but they differ in location, origin, and what they mean for your health. Some close on their own, some never cause trouble, and some need intervention.
The Three Main Types
Your heart has four chambers: two upper ones called atria and two lower ones called ventricles. A wall of tissue called a septum divides the left side from the right. When that wall has an opening that shouldn’t be there, the result is a septal defect. The specific name depends on which wall is affected and whether the opening is a leftover from fetal development or a true structural gap.
An atrial septal defect is a hole in the wall between the two upper chambers. It allows blood to flow from one atrium to the other, and because pressure is typically higher on the left side, blood usually shunts from left to right. Over time, this extra blood flow overloads the right side of the heart and the lungs. The most common subtype is the secundum ASD, which sits near the center of the atrial septum. Other subtypes include primum defects (near the bottom of the septum, close to the heart valves), sinus venosus defects (near where the large veins enter), and the rare coronary sinus type.
A ventricular septal defect is a hole in the wall between the two lower chambers. Because the ventricles generate much more pressure than the atria, the shunting through a VSD can be larger and more consequential. VSDs are the most common congenital heart defect found in newborns. They range from tiny pinholes that produce a loud heart murmur but little else, to large openings that cause heart failure in infancy. Anatomically, they can be perimembranous (near the membranous part of the septum, the most common location) or muscular (surrounded entirely by muscle tissue). A detailed surgical classification breaks perimembranous VSDs into seven subtypes based on how the defect extends relative to surrounding structures.1PubMed Central. Applied Anatomy of Perimembranous Ventricular Septal Defect for Transcatheter Device Closure
A patent foramen ovale is something different. Before birth, every heart has a small flap-like opening between the atria called the foramen ovale. This passage lets blood bypass the lungs, which aren’t yet in use. After birth, when a baby starts breathing and the lungs expand, pressure shifts cause the flap to press shut.2PubMed Central. Progressive anatomical closure of foramen ovale in normal neonatal mouse hearts In most people the flap eventually seals permanently. But in roughly one in four adults, it never fully fuses, leaving a PFO. A PFO is not a true defect in the same sense as an ASD: the tissue formed correctly, it just didn’t seal all the way. Most people with a PFO live their entire lives without knowing it exists.
How a PFO Differs from an ASD
People sometimes confuse PFOs and ASDs because both involve openings in the atrial septum. The distinction matters because they behave differently and carry different risks. An ASD is a structural gap where tissue is missing. Blood flows through it continuously, driven by the pressure difference between left and right atria. A PFO, by contrast, is a flap that can open temporarily under certain conditions, like straining, coughing, or bearing down. Under normal resting conditions, the flap stays closed and no blood crosses.
This difference in mechanism explains why ASDs tend to cause problems related to chronic volume overload of the right heart and lungs, while PFOs are more associated with rare but dramatic events like stroke. When a blood clot forms in a vein (say, in the leg) and travels toward the heart, it normally gets trapped in the lungs. But if the clot arrives at the right atrium during a moment when the PFO flap is open, it can cross to the left side and travel to the brain, causing what’s called a paradoxical embolism.
When a Hole Causes Symptoms
Small ASDs and most PFOs cause no symptoms at all and are often discovered incidentally during imaging for something else. Larger ASDs are a different story. The chronic left-to-right shunt forces extra blood into the right ventricle, which gradually stretches and enlarges. This leads to shortness of breath, fatigue, and reduced exercise capacity.3PubMed Central. Impact of Right Ventricular Dilatation in Patients with Atrial Septal Defect Some adults with undiagnosed ASDs develop abnormal heart rhythms, particularly atrial fibrillation, as their right atrium stretches over decades. In severe cases, the persistent overload can raise pressure in the lung arteries enough to cause pulmonary hypertension.
VSDs follow a similar logic scaled by size. A small VSD often produces nothing more than a murmur that a doctor hears with a stethoscope. A moderate or large VSD in an infant can cause poor weight gain, rapid breathing, sweating during feeds, and congestive heart failure. If a large VSD goes unrepaired for years, the constant high-pressure shunting damages the blood vessels in the lungs. Eventually the pulmonary vascular resistance rises to match or exceed systemic pressure, and the shunt reverses direction so that oxygen-poor blood flows from the right ventricle into the left, causing cyanosis (a bluish tint to the skin).4Progress in Pediatric Cardiology. Eisenmenger syndrome in ventricular septal defect patients This irreversible condition, known as Eisenmenger syndrome, is one of the most serious consequences of a neglected large VSD and makes surgical repair much riskier.
Do Some Holes Close on Their Own?
Many VSDs do close spontaneously, especially in the first year of life. Muscular VSDs have a particularly high rate of self-resolution. One large study found that roughly 87% of muscular VSDs closed on their own within the first year, compared with about 47% of perimembranous VSDs.5PubMed. The Prevalence and Spontaneous Closure of Ventricular Septal Defects the First Year of Life Smaller defects are much more likely to close than larger ones.6PubMed Central. Prediction of spontaneous closure of ventricular septal defect and guidance for clinical follow‐up This is why many pediatric cardiologists take a watchful-waiting approach with small VSDs in newborns, monitoring with periodic echocardiograms rather than rushing to intervene.
ASDs, unfortunately, rarely close on their own after infancy. A very small secundum ASD detected in a newborn might seal within the first few years, but most that persist past early childhood stay open. PFOs are a separate case entirely: they’re already the result of the foramen ovale not closing, so the question of spontaneous closure doesn’t apply in the same way. If the flap hasn’t fused by adulthood, it generally won’t.
How These Holes Are Found
A heart murmur heard during a routine exam is often the first clue that something might be going on. Not all murmurs indicate a septal defect (many are harmless), but an unusual sound can prompt a closer look. The primary diagnostic tool is an echocardiogram, which uses ultrasound to create real-time images of the heart’s chambers and blood flow. A standard transthoracic echocardiogram performed from the outside of the chest can detect most ASDs and VSDs.
PFOs are trickier to find because the flap may stay shut during a standard scan. The most reliable method involves a “bubble study,” in which a small amount of agitated saline is injected into a vein while the heart is imaged. If tiny bubbles appear on the left side of the heart shortly after they’re seen on the right, it confirms that something is letting them cross. Combining a bubble study with either transthoracic echocardiography or transcranial Doppler ultrasound improves diagnostic accuracy.7PubMed Central. Detecting Patent Foramen Ovale after Cryptogenic Stroke – A Single Center Experience in Taiwan For a more detailed view, transesophageal echocardiography (where a small probe is passed into the esophagus, right behind the heart) provides excellent images and is especially useful for guiding interventional procedures.8PubMed Central. Quantitative Analysis of Pulmonary Right-to-Left Shunts and Patent Foramen Ovale via Agitated Saline Contrast Transesophageal Echocardiography
Treatment Options
Whether a hole in the heart needs treatment depends on its type, size, and what it’s doing to the body. Small VSDs that aren’t causing heart failure are often left alone, particularly in children, given the strong odds of spontaneous closure. Small ASDs that don’t enlarge the right heart may also be monitored without intervention. PFOs in people who have never had a stroke or other embolic event typically require no treatment at all.
When closure is needed, two broad approaches exist: catheter-based (transcatheter) procedures and open-heart surgery. Transcatheter closure has become the standard first-line option for many secundum ASDs and PFOs. A thin catheter is threaded through a vein in the groin up to the heart, and a small device is deployed across the defect to plug it. The device acts as a scaffold for the body’s own tissue to grow over and permanently seal the opening. For PFO closure, observational data report procedural success rates above 95%, though complications such as device-related blood clots, abnormal heart rhythms, or in rare cases erosion into nearby structures can occur in a small percentage of procedures.9PubMed Central. Closure of patent foramen ovale: technique, pitfalls, complications, and follow up
Surgical repair remains the standard for defects that aren’t suitable for catheter-based closure: large ASDs, primum or sinus venosus ASDs (which sit in locations devices can’t easily reach), and most large VSDs in infants. The operation involves opening the chest, placing the patient on a heart-lung bypass machine, and patching or stitching the hole closed. Despite how dramatic that sounds, surgical ASD repair is considered a very safe operation with low rates of complications.10PubMed Central. Surgical closure of atrial septal defects Modern techniques increasingly use smaller incisions and minimally invasive approaches to reduce recovery time. For erosion, the rare but serious complication of transcatheter ASD closure, risk factors include deficient tissue rims around the defect and larger device sizes.11PubMed. Relative Risk Factors for Cardiac Erosion Following Transcatheter Closure of Atrial Septal Defects: A Case-Control Study
PFO and Stroke
The link between PFO and stroke is one of the more interesting stories in cardiology. About half of patients who have a stroke with no identifiable cause (called a cryptogenic stroke) turn out to have a PFO.12PubMed. Cryptogenic Stroke and Patent Foramen Ovale This is a strikingly high proportion, given that PFOs are present in roughly a quarter of the general population. The implication is that in some of these patients, a blood clot crossed through the PFO to reach the brain.
For years, doctors debated whether closing these PFOs actually prevented future strokes or whether the association was just a coincidence. That debate has largely been settled. Randomized trials now provide strong evidence that PFO closure reduces recurrent stroke in carefully selected patients, particularly younger adults who have had a cryptogenic stroke and whose PFO has high-risk features like a large opening or an associated atrial septal aneurysm.13PubMed. Patent Foramen Ovale Management for Secondary Stroke Prevention: State-of-the-Art Appraisal of Current Evidence Patient selection remains critical, though. Closing every PFO found in every stroke patient would not make sense, because many strokes in people with PFOs are actually caused by something else entirely, like small-vessel disease or atrial fibrillation. The challenge lies in identifying which patients’ strokes were truly PFO-related.
Three-dimensional transesophageal echocardiography has improved the ability to visualize PFOs in detail, even locating residual shunts after previous surgical repair, and guiding transcatheter closure with greater precision.14PubMed Central. Recurrent Ischemic Stroke Caused by a Residual PFO Shunt After Surgical Repair: Three-Dimensional Transesophageal Echocardiography-Guided Localization and Transcatheter Closure
Other PFO-Related Conditions
Stroke is the most studied PFO complication, but it isn’t the only one. PFOs have been linked to migraine with aura, decompression sickness in divers, and certain blood-oxygen problems.15PubMed. European position paper on the management of patients with patent foramen ovale. Part II – Decompression sickness, migraine, arterial deoxygenation syndromes and select high-risk clinical conditions
The migraine connection has generated enormous interest, partly because both conditions are so common. Some patients report that their migraines with aura disappeared after PFO closure, and observational studies have been intriguing. But the evidence is not as clear-cut as the stroke data, and PFO closure specifically for migraine treatment is not currently a standard recommendation.
The diving connection is more straightforward. During a scuba dive, nitrogen dissolves into the blood under pressure. During ascent, that nitrogen forms tiny bubbles. Normally these bubbles get filtered out in the lungs. But if you have a PFO that opens during the pressure changes of ascent, those bubbles can cross to the arterial side and cause decompression sickness, even on dives that stayed within safe limits. Case reports describe divers developing neurological symptoms and headaches related to this mechanism.16PubMed. Migraine With Neurological Features in a Scuba Diver With a Patent Foramen Ovale Some diving medicine specialists recommend PFO screening for divers who experience unexplained decompression illness.
What Causes These Defects
For ASDs and VSDs, the cause is usually a disruption in how the heart forms during early fetal development. The heart starts as a simple tube and undergoes an intricate folding and partitioning process over several weeks. If that process doesn’t complete perfectly, a hole can remain. In most cases, the exact trigger is unknown and likely involves a combination of genetic susceptibility and environmental factors during pregnancy.
Research has identified inherited mutations in genes that control heart development as an underlying cause of familial cases, particularly for secundum ASDs.17PubMed Central. Molecular genetics of congenital atrial septal defects These mutations affect genes encoding transcription factors and structural proteins involved in building the cardiac septum. Having a first-degree relative with a congenital heart defect does increase your risk, though most cases still appear sporadically with no clear family history.
Certain maternal factors during pregnancy are associated with higher risk: poorly controlled diabetes, heavy alcohol use, certain medications (particularly some anti-seizure drugs), and infections like rubella during the first trimester. Down syndrome and other chromosomal conditions are also associated with a higher incidence of septal defects, especially the atrioventricular canal type.
Pregnancy with a Heart Defect
Women with congenital heart defects are surviving into adulthood in far greater numbers than previous generations, which makes pregnancy planning an increasingly relevant topic. The good news is that many women with repaired simple defects (like a closed ASD or small VSD) tolerate pregnancy well. Research comparing outcomes between women with repaired versus unrepaired congenital heart disease found that pregnancy outcomes were substantially better in the repaired group. In one study, all maternal and neonatal deaths, as well as fetal growth restriction and intensive care admissions, occurred exclusively among women with unrepaired defects.18University Heart Journal. Pregnancy in adult with repaired or unrepaired congenital heart disease – a hospital based observational study
Pregnancy increases blood volume by roughly 30 to 50 percent, which intensifies the hemodynamic stress on the heart. For a woman with an unrepaired large ASD, this added volume amplifies the left-to-right shunt and can worsen right heart strain. For someone with Eisenmenger syndrome (the irreversible complication of a long-standing VSD), pregnancy carries serious and sometimes fatal risks. Pre-pregnancy counseling with a cardiologist experienced in congenital heart disease is strongly recommended for anyone with a known septal defect, whether repaired or not.
Living with an Incidental Finding
With cardiac imaging becoming more widely available, it’s increasingly common for adults to learn they have a small ASD or PFO that was never previously detected. This can be alarming, but in many cases it changes very little. A small secundum ASD that hasn’t caused right heart enlargement by midlife may simply need periodic monitoring. A PFO discovered incidentally in someone who has never had a stroke or unexplained embolic event usually requires no treatment beyond awareness.
What matters most is context. If you’ve had a cryptogenic stroke and imaging reveals a PFO, that finding takes on a different significance than a PFO found during a workup for something unrelated. Similarly, an ASD that is already causing the right ventricle to dilate deserves attention regardless of symptoms, because the heart remodeling may progress. The presence of a hole is the starting point of a conversation, not an automatic path to the operating room. A cardiologist can assess the size, shunt direction, and downstream effects to determine whether intervention, monitoring, or reassurance is the right approach.