How Long Can You Live With a Hole in Your Heart?

Many people live a full, normal lifespan with a hole in their heart, while others face serious complications that shorten life considerably. The answer depends almost entirely on which type of hole you have and how large it is. A small ventricular septal defect, for example, carries survival rates above 90% at age 50, while the same defect left untreated for decades can eventually trigger irreversible lung damage that cuts life short. The range of outcomes is enormous, and the single biggest variable is whether and when the hole gets fixed.

Not All Holes Are the Same

The heart has four chambers separated by walls of muscle and tissue. A “hole in the heart” means an opening in one of those walls that shouldn’t be there, or one that should have closed and didn’t. The three most common types produce very different stories about life expectancy.

A patent foramen ovale, or PFO, is the most common by far. Every fetus has an opening between the upper chambers that normally seals after birth. In roughly a quarter of the population, that flap never fully fuses. An autopsy study of 965 hearts found PFOs in about 27% of people across all ages, with the rate running as high as a third in younger adults and declining somewhat with age.1Mayo Clinic Proceedings. Incidence and Size of Patent Foramen Ovale During the First 10 Decades of Life: An Autopsy Study of 965 Normal Hearts Most people with a PFO never know they have one and never experience symptoms. It is typically not considered a disease.

An atrial septal defect (ASD) is a true structural gap between the heart’s two upper chambers. Unlike a PFO, which is a flap that can be pushed open under pressure, an ASD is a missing piece of tissue that allows blood to flow continuously from one side to the other. People with an ASD often feel fine through childhood and young adulthood, but as they age, the extra blood flowing through the lungs gradually stretches the right side of the heart. Rates of exercise intolerance, irregular heart rhythms, and elevated lung pressures all climb with time if the defect goes unrepaired.2PubMed Central. Secundum atrial septal defect in adults: a practical review and recent developments

A ventricular septal defect (VSD) is a hole between the two lower chambers, and it is the most common congenital heart defect detected at birth. Many small VSDs close on their own during infancy or childhood.3PubMed Central. A review of spontaneous closure of ventricular septal defect Those that persist vary widely in their impact depending on size.

Survival Numbers for Unrepaired Defects

The most detailed long-term survival data comes from a large nationwide study of people born with VSDs. Among patients whose defect was never surgically repaired, survival stood at 95% at age 40, 92% at age 50, 85% at age 60, 70% at age 70, and 44% at age 80.4PubMed Central. Survival of patients with congenital ventricular septal defect Those numbers cover the full spectrum from tiny holes to larger ones, so a person with a small, hemodynamically insignificant VSD will likely do better than that average suggests. Still, the data illustrate a key pattern: survival is near normal in early and middle adulthood, then drops off noticeably past 60.

For unrepaired ASDs, the picture is broadly similar in youth but tends to deteriorate more aggressively in middle age. A nationwide cohort study found that patients with an ASD who never had their defect closed had an adjusted mortality risk roughly 2.4 times higher than the general population.5PubMed Central. Long-term mortality in patients with atrial septal defect: a nationwide cohort-study The excess risk accumulates gradually, driven by decades of extra blood volume passing through the lungs and stretching the right heart.

PFOs, by contrast, do not meaningfully shorten life for the vast majority of people who have them. The main concern with a PFO is a small risk of stroke from a blood clot crossing through the opening and reaching the brain, but even that risk is low enough that most PFOs are left alone.

When a PFO Becomes a Problem

If you have a PFO and have never had a stroke or other unexplained clotting event, there is usually nothing to treat. The situation changes when someone has a stroke with no identifiable cause and a PFO is discovered during the workup. In that scenario, the question becomes whether closing the PFO will prevent another stroke.

Three major randomized trials compared PFO closure devices against medication alone for preventing recurrent strokes. All three failed to show a clear advantage for device closure in their primary analyses.6PubMed. Patent foramen ovale and cryptogenic stroke: the hole story Later extended follow-up and pooled analyses from additional trials did tilt in favor of closure for carefully selected patients, particularly younger people without other vascular risk factors who had a larger shunt. But the evidence is not a slam dunk, and many people with a PFO and a prior stroke are managed with blood thinners alone. The point for life expectancy is that a PFO, even when it has caused a stroke, is not the kind of heart defect that broadly threatens survival.

Why Timing of Repair Matters So Much

For ASDs and larger VSDs, repair changes the trajectory. But the benefit of repair depends heavily on when it happens. In a study following ASD patients for up to 50 years, those who had their defect closed before age 30 showed no statistically significant increase in mortality compared to the general population.7PubMed Central. Cause-Specific Mortality of Patients With Atrial Septal Defect and Up to 50 Years of Follow-Up In other words, close the hole early enough and you can essentially erase the survival penalty.

Patients who had their defects closed via catheter-based procedures actually showed lower mortality than the control population in the same study, though that likely reflects some selection bias since catheter closure is typically offered to people with simpler anatomy and fewer complications.

Waiting longer still helps, but the benefit shrinks. A surgical study comparing outcomes by age at operation found that patients younger than 40 at the time of surgery had better functional improvement, a lower rate of persistent irregular heart rhythms, and more recovery of the right ventricle’s size than those operated on later.8PubMed Central. Surgical closure of atrial septal defects in adults: effect of age at operation on outcome Even after repair, the overall ASD population retains a modestly elevated mortality risk compared to people who never had a defect. The adjusted risk drops to about 1.4 times the general population after closure, down from 2.4 without it.5PubMed Central. Long-term mortality in patients with atrial septal defect: a nationwide cohort-study

The Arrhythmia Connection

Irregular heart rhythms are the most common lasting complication of living with a hole between the upper chambers, and they deserve their own discussion because they affect both quality of life and long-term risk even after repair. The constant extra blood flow through an ASD stretches the atria over time, altering the tissue’s electrical properties and making atrial fibrillation increasingly likely as the person ages.9PubMed Central. Atrial Septal Defect and Atrial Fibrillation: The Known and Unknown

In one study of adults undergoing surgical ASD closure, roughly one in five already had sustained atrial flutter or fibrillation before surgery. Of those, 60% continued to have the arrhythmia afterward. Patients older than 40 at the time of surgery were more likely to develop new irregular rhythms during follow-up than those who had surgery younger.10PubMed. Atrial arrhythmia after surgical closure of atrial septal defects in adults Closure does reduce the overall burden of arrhythmias compared with leaving the defect open, but the risk never fully returns to that of someone who never had an ASD.11PubMed Central. Pathophysiology and Management of Arrhythmias Associated with Atrial Septal Defect and Patent Foramen Ovale

This is one of the clearest illustrations of why early repair matters. Close the defect before the atria have been stretched for decades, and the electrical remodeling is minimized. Wait until your fifties or sixties, and the damage to the heart’s wiring is partly baked in.

Eisenmenger Syndrome and the Point of No Return

The most feared long-term consequence of an unrepaired hole is Eisenmenger syndrome, which develops when years of excess blood flow through the lungs permanently damages the pulmonary blood vessels. The lung arteries thicken and stiffen, resistance in the lungs rises, and eventually the shunt reverses direction so that oxygen-poor blood starts flowing into the body. The person turns blue, and at that point, closing the hole would be dangerous because the lungs can no longer handle normal blood flow.12European Cardiology. Pulmonary Arterial Hypertension in Adults with Congenital Heart Disease

A study of 109 adults with Eisenmenger syndrome found a median survival of 53 years, meaning half lived past that age but half did not. There was enormous individual variation. The strongest predictors of earlier death included more severe symptoms, abnormal heart rhythms, and more complex underlying anatomy.13The American Journal of Cardiology. Determinants of survival and length of survival in adults with Eisenmenger syndrome More recent reviews confirm that Eisenmenger syndrome remains a complex, multi-organ condition associated with premature death despite advances in targeted drug therapies.14PubMed. Eisenmenger Syndrome: JACC State-of-the-Art Review

Survival from the time of diagnosis was roughly 73% at three years and 50% at six years in one comparative study, though it’s worth noting that patients with Eisenmenger syndrome actually fared somewhat better than patients whose shunts had been closed after severe lung disease had already set in.15PubMed Central. Life span of patients with Eisenmenger syndrome is not superior to that of patients with other causes of pulmonary hypertension That counterintuitive finding reinforces an important clinical lesson: closing a hole too late, after the lungs are already severely damaged, can be worse than not closing it at all.

Exercise Capacity After Repair

A common worry for people living with a repaired or unrepaired defect is whether they can exercise normally. For those with unrepaired ASDs, exercise tolerance depends on how much blood is crossing the defect, how well the right ventricle is handling the extra load, lung pressures, and whether arrhythmias are present. For repaired ASDs, exercise capacity also hinges on how long the defect was open before closure and whether it was fixed by catheter or open surgery.16PubMed Central. Atrial septal defect and exercise capacity: value of cardio-pulmonary exercise test in assessment and follow-up

The good news is that for most people who have their ASD closed, exercise capacity is close to normal. Formal cardiopulmonary exercise testing is sometimes used to objectively measure how well the heart and lungs perform under stress, and it can help guide decisions about sports participation. Many people with repaired defects are cleared for competitive athletics.

Pregnancy With a Heart Defect

Pregnancy places extra demands on the cardiovascular system, so women with a known hole in the heart understandably want to know whether it’s safe. For ASDs without elevated lung pressures, pregnancy is generally tolerated well. The most common cardiac complication is arrhythmia, occurring in roughly 4 to 5% of pregnancies, and paradoxical embolism (a clot crossing through the defect) occurs in about 2 to 5%. There is also a somewhat higher rate of preeclampsia and of babies born smaller than expected.17PubMed Central. Pregnancy in adults with repaired/unrepaired atrial septal defect

For women with a PFO, the main concern is stroke during pregnancy, particularly in early pregnancy. A review of PFO-related strokes during pregnancy found that most occurred during the first and second trimesters, which differs from pregnancy-related strokes of other causes that tend to cluster around delivery and the postpartum period. Importantly, the vast majority of affected women had good neurological outcomes, and 93% went on to have uneventful deliveries of healthy babies.18PubMed Central. Patent foramen ovale (PFO), stroke and pregnancy When Eisenmenger syndrome is present, pregnancy carries severe risks and is strongly discouraged.

Infection Risk and Endocarditis

One underappreciated risk of living with a congenital heart defect is infective endocarditis, a bacterial infection of the heart’s inner lining or valves. Among ASD patients, the incidence of endocarditis is about ten times higher than in the general population, and the adjusted risk ratio was roughly 13.5 times higher in one large cohort study. Patients with both ASD and endocarditis also had higher long-term mortality than matched controls.19PubMed. Atrial septal defect patients have an elevated risk for infective endocarditis

That said, the absolute risk is still low. The incidence was about 0.11 per 1,000 person-years in the ASD group, meaning that in any given year, roughly one in 9,000 ASD patients developed endocarditis. And among congenital heart defects, ASDs actually carry one of the lower risks. A case-control study in children found that cyanotic heart defects and certain other complex lesions carried endocarditis risk several times higher than ASDs.20International Journal of Cardiology. Risk factors for infective endocarditis in children with congenital heart diseases – A nationwide population-based case control study Interestingly, that same study found that dental procedures did not increase endocarditis risk regardless of whether antibiotics were used, though invasive cardiac procedures and central venous catheters did.

Holes Discovered Late in Life

It is not unusual for a heart defect to be found for the first time in someone over 60 or even 70. Some people have lived their entire lives with a moderate ASD and never had symptoms severe enough to prompt a cardiac workup. With improved imaging technology, more elderly patients are being diagnosed incidentally.21PubMed Central. Surgical Repair of a Coronary Sinus Atrial Septal Defect in an Elderly Patient

For these patients, the decision about whether to close the defect is nuanced. The benefits of closure are smaller when the heart has adapted to the shunt over many decades, and the procedural risk is higher in older adults with other medical conditions. Some elderly patients are managed conservatively with monitoring and medications for symptoms like fluid retention or irregular rhythms, rather than undergoing repair. Others who are otherwise healthy and have significant shunts are still offered closure, even in their seventies, because it can relieve symptoms and slow further deterioration. Every case involves weighing the cumulative damage already done against the risks and likely gains of intervention at an advanced age.

How Heart-Lung Machines Changed Everything

For most of human history, a hole in the heart was simply a condition you lived and died with. The first successful open-heart repair using a machine to temporarily take over the work of the heart and lungs happened on May 6, 1953, when an 18-year-old woman with a large ASD underwent surgery by Dr. John Gibbon.22PubMed. John H. Gibbon, Jr. Part I. The development of the first successful heart-lung machine That single operation opened the door to repairing defects that had previously been untouchable. Within a few years, surgeons were successfully correcting a wide range of congenital heart malformations.23Journal of the American College of Cardiology. Origins and Evolution of Extracorporeal Circulation: JACC Historical Breakthroughs in Perspective

Today, many ASDs and some VSDs are closed without open surgery at all, using catheter-based devices threaded through a vein in the leg. These minimally invasive procedures have shorter recovery times and, in the ASD data mentioned earlier, have been associated with excellent long-term outcomes. The contrast with the era before repair was possible is stark: a condition that once quietly eroded life expectancy over decades can now be corrected in a single procedure, often with no visible scar, and the person can go on to live a functionally normal life.