Atrial septal defects (ASDs) and ventricular septal defects (VSDs) are holes in the walls that separate the heart’s chambers. An ASD is a hole between the two upper chambers (atria), while a VSD is a hole between the two lower chambers (ventricles). Both are congenital heart defects, meaning they’re present at birth, and both allow blood to flow abnormally between the left and right sides of the heart. VSDs are among the most common congenital heart defects overall, while ASDs are the most frequently diagnosed in adults.
How the Heart Normally Works
Your heart has four chambers. The two upper chambers (atria) receive blood, and the two lower chambers (ventricles) pump it out. A muscular wall called the septum divides the left and right sides. This separation is critical: the right side pumps oxygen-poor blood to the lungs, while the left side pumps oxygen-rich blood to the rest of the body. When there’s a hole in the septum, blood crosses between the two sides, forcing the heart and lungs to handle more blood than they should.
Types of Atrial Septal Defects
ASDs are classified by where the hole sits in the wall between the upper chambers. There are four main types:
- Secundum defect: The most common type, located in the middle of the atrial septum. It occurs when the tissue that normally seals a natural opening in the fetal heart fails to close completely.
- Primum defect: The third most common ASD, found near the bottom of the septum close to the heart valves. It’s considered part of a broader category of defects involving the valves between the upper and lower chambers.
- Sinus venosus defect: Located near where the large veins (superior or inferior vena cava) enter the right atrium. The superior type is more common and is often accompanied by abnormal drainage of a pulmonary vein into the wrong chamber.
- Coronary sinus defect: The rarest type. The coronary sinus is a vein that drains blood from the heart muscle itself. A hole in the wall between this vein and the left atrium creates an indirect connection between the two upper chambers.
Types of Ventricular Septal Defects
VSDs are also classified by location, with four main types:
- Membranous (perimembranous): The most common type, located in the upper portion of the wall between the ventricles, near the heart valves.
- Muscular: Found in the lower, muscular part of the septum. This type sometimes involves more than one hole.
- Inlet: Sits just below the valves that control blood flow into the ventricles. Blood passing through these valves encounters the defect immediately upon entering the chambers.
- Outlet: Located just before the valves that control blood leaving the ventricles, near where blood exits toward the lungs and body.
What Happens Inside the Heart
In both ASDs and VSDs, the left side of the heart operates at higher pressure than the right. This pressure difference pushes oxygen-rich blood from the left side through the hole and into the right side, a pattern called a left-to-right shunt. The result is that the right side of the heart and the lungs receive more blood than normal.
Over time, the extra blood flow puts stress on the blood vessels in the lungs. The vessel walls thicken and stiffen in response to the constant high flow and pressure. This process, called pulmonary hypertension, can develop gradually over years. In the early stages, the elevated lung pressure is simply from too much blood flowing through. As the vessel walls remodel, the resistance becomes permanent, and the damage is no longer reversible.
Symptoms in Infants and Children
Small VSDs may produce no symptoms at all, and many close on their own during the first few years of life. Large VSDs, however, typically cause noticeable problems in infancy. Babies may breathe fast or heavily, sweat during feedings, tire out before finishing a bottle or nursing session, and struggle to gain weight. Some infants need a special high-calorie formula because they simply can’t take in enough nutrition during normal feedings.
ASDs tend to be quieter in childhood. Because the pressure difference between the atria is smaller than between the ventricles, the shunting is less dramatic. Many children with ASDs have no obvious symptoms, and the defect may go undetected for years or even decades.
Symptoms in Adults
Undiagnosed ASDs often become apparent in adulthood as the heart gradually struggles with the extra workload. Common symptoms include reduced exercise tolerance, fatigue, shortness of breath, and palpitations. A heart murmur (an extra sound caused by abnormal blood flow) is frequently the first clue, sometimes picked up during a routine physical exam. Adults with unrepaired ASDs also face a higher risk of abnormal heart rhythms, particularly atrial fibrillation, because the right atrium stretches over time from the extra blood volume.
Adults with small, unrepaired VSDs may have few or no symptoms. Larger VSDs that weren’t closed in childhood can lead to symptoms similar to those of ASDs, including breathlessness and reduced stamina, though this scenario is less common because significant VSDs are usually caught and treated earlier in life.
How Septal Defects Are Diagnosed
Echocardiography (ultrasound of the heart) is the primary tool for diagnosing both ASDs and VSDs. A standard transthoracic echocardiogram, performed by placing a probe on the chest, can often reveal the defect directly or show indirect signs like an enlarged right ventricle that’s handling more blood than it should. For ASDs in adults, a transesophageal echocardiogram (where a small probe is passed into the esophagus for a closer view of the heart) is usually needed to confirm the exact anatomy and determine whether the defect can be closed with a catheter-based device. The transesophageal approach provides higher-resolution images of the atrial septum, which can be difficult to see clearly through the chest wall in adults.
Treatment for ASDs
Not all ASDs need treatment. Small defects that don’t cause the right side of the heart to enlarge may simply be monitored over time. When closure is needed, the approach depends on the type and size of the defect.
Secundum ASDs are often closed using a catheter-based (transcatheter) procedure. A thin tube is threaded through a vein, typically in the groin, and a small closure device is guided to the heart and positioned across the hole. This avoids open-heart surgery entirely, and recovery is significantly faster. Defects larger than about 38 millimeters, or those missing enough surrounding tissue to anchor a device securely, are generally referred for surgical repair instead. The one rim where a missing edge poses a particular risk is the one near the inferior vena cava, the large vein entering from below, because the device can slip and dislodge.
Other ASD types (primum, sinus venosus, coronary sinus) almost always require surgical repair because their locations don’t allow a catheter device to anchor properly.
Treatment for VSDs
Small VSDs that cause no symptoms and no heart enlargement are typically monitored, especially in children, since many close spontaneously. When a VSD is large enough to cause a significant shunt and signs of heart strain, closure is recommended.
Surgical repair through open-heart surgery remains the standard for most VSDs, particularly perimembranous defects. It works for virtually all patients regardless of age or defect size. Catheter-based and hybrid approaches (where a surgeon places a closure device through a small chest incision without using a heart-lung machine) have emerged as less invasive alternatives with similar success rates, shorter hospital stays, and faster recovery. These options are especially appealing for children, teenagers, and patients who want to avoid a large surgical scar. However, some patients undergoing device closure need conversion to open surgery if complications arise, such as new valve leakage or incomplete sealing of the hole.
Eisenmenger Syndrome: The Most Serious Risk
The most dangerous long-term complication of an untreated septal defect is Eisenmenger syndrome. After years of excess blood flowing to the lungs, the pulmonary blood vessels become so damaged and narrowed that the pressure on the right side of the heart rises above the pressure on the left. When this happens, the shunt reverses direction: oxygen-poor blood now flows from the right side into the left and out to the body. This causes cyanosis (a bluish tint to the skin and lips from low oxygen levels).
Eisenmenger syndrome is irreversible. Once it develops, closing the defect is no longer an option because the right side of the heart needs the hole as a pressure relief valve. The most common defects that lead to this condition are VSDs, ASDs, and patent ductus arteriosus (an open connection between two major blood vessels near the heart). Treatment at this stage focuses on managing symptoms and reducing lung pressure with specialized medications. This is why early detection and timely closure of significant septal defects matters so much.
Long-Term Outlook After Closure
For the vast majority of patients, closing a septal defect leads to excellent outcomes. A large study tracking adults with ASDs found that defect closure was an independent predictor of long-term survival, even after accounting for age, pulmonary hypertension, and other health factors. Among patients who had already developed pulmonary hypertension, those who had their ASD closed had a 20-year survival rate of 65%, compared to 41% for those whose defects remained open. The survival benefit held true even for patients over 40 at the time of diagnosis, countering the idea that repair is only worthwhile when done young.
For VSDs repaired in childhood, the long-term prognosis is generally excellent, with most patients living normal, active lives. Those who had surgical repair may need periodic follow-up to monitor for residual leaks or rhythm disturbances, but serious late complications are uncommon when the defect is closed before significant lung damage occurs.