Ventricular Septal Defect (VSD)
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Ventricular Septal Defect, or VSD, is a common congenital heart condition where an abnormal opening exists between the heart’s two lower chambers (ventricles). It might be present at birth due to a developmental issue or appear later as a complication of a heart attack.
The Human Heart
The heart is divided into four distinct chambers, separated by tight walls called septa, and valves that guide bloodBlood is composed of red blood cells, white blood cells, platelets, and plasma. Red blood cells are responsible for transporting oxygen and carbon dioxide. White blood cells make up our immune defense system. Platelets contribute to blood flow in the right direction.
You can think of it like a house with several rooms and doors that allow movement from one to another.
How does the heart develop?
Early in development, the heart begins as a single tube that folds onto itself, forming one atrium and one ventricle.
Over time, a wall (septum) forms to divide the heart into left and right sides. The part that divides the ventricles is called the ventricular septum.
Division of the original single ventricle
This process starts at the lower part of the heart, forming a muscular wall called the muscular ventricular septum. An opening in this wall remains until about the 7th week of pregnancy.
At that point, another structure (the bulbus arteriosus) merges to complete the closure using a thin, fibrous layer known as the membranous septum.
How can a VSD exist at birth?
There are four main types of VSDs; the two most common are muscular and perimembranous.
Muscular VSDs come from incomplete closure of the muscular septum, while perimembranous VSDs result from failure of the bulbus arteriosus to fuse properly with the membranous section.
In any case, a hole remains between the ventricles, allowing abnormal bloodBlood is composed of red blood cells, white blood cells, platelets, and plasma. Red blood cells are responsible for transporting oxygen and carbon dioxide. White blood cells make up our immune defense system. Platelets contribute to blood flow.
What happens as a result?
Normally, bloodBlood is composed of red blood cells, white blood cells, platelets, and plasma. Red blood cells are responsible for transporting oxygen and carbon dioxide. White blood cells make up our immune defense system. Platelets contribute to blood travels from the right ventricle to the lungs to get oxygenated, then returns to the left atrium and ventricle before being pumped throughout the body.
With a VSD—especially a perimembranous one located near the top—the higher pressure in the left ventricle forces bloodBlood is composed of red blood cells, white blood cells, platelets, and plasma. Red blood cells are responsible for transporting oxygen and carbon dioxide. White blood cells make up our immune defense system. Platelets contribute to blood into the right ventricle or directly into the pulmonary artery. This extra bloodBlood is composed of red blood cells, white blood cells, platelets, and plasma. Red blood cells are responsible for transporting oxygen and carbon dioxide. White blood cells make up our immune defense system. Platelets contribute to blood volume stresses the lungs and increases workload on the left atrium and ventricle.
If a large VSD remains untreated, this persistent overload can lead to high-output heart failure and eventually raise pressure in the lung’s bloodBlood is composed of red blood cells, white blood cells, platelets, and plasma. Red blood cells are responsible for transporting oxygen and carbon dioxide. White blood cells make up our immune defense system. Platelets contribute to blood vessels—a condition known as pulmonary hypertension.
What symptoms appear?
Symptoms depend on the size of the VSD.
Most VSDs are small. They generally do not cause any symptoms but often produce a heart murmur that a doctor can hear during auscultation.
Large VSDs can lead to:
- In infants: poor growth, breathlessness during feeding or play, even at rest, and frequent sweating (though this symptom is less specific).
- In adults (if undiagnosed in childhood): fatigue during exertion, shortness of breath, bluish lips or fingertips (cyanosis), and swollen legs (edema).
How is a VSD detected?
A VSD might be suspected during a prenatal ultrasound, though fetal circulation differs from postnatal circulation, making diagnosis challenging. This test is typically recommended if a family member has had a symptomatic VSD.
After birth, a heart murmur heard a few days into life may suggest VSD, which is then confirmed by echocardiography.
When VSD is associated with other anomalies, a genetics consultation may be advised to investigate chromosomal or syndromic causes.
How do VSDs evolve?
Small VSDs often close on their own—around 75% heal within the first two years.
Many individuals live symptom-free even if the VSD remains small and open. Perimembranous VSDs, even when small, should be monitored to ensure they don’t affect the nearby aortic valveThe aortic valve is located between the left ventricule and the aorta. It is one of the four valves ot the heart. >>.
Larger VSDs rarely close spontaneously. Symptomatic ones typically require intervention within 3–6 months of life—or earlier, depending on severity. Asymptomatic but sizeable VSDs warrant close monitoring to detect complications early.
Intervention is needed when a VSD causes:- Aortic valveThe aortic valve is located between the left ventricule and the aorta. It is one of the four valves ot the heart. >> leakage
- Enlargement of the left heart chambers
- Heart valve infection
- In some specific cases, pulmonary hypertension
How are VSDs treated?
There are two main approaches to correcting a VSD.
- One is traditional open-heart surgery, which has been performed for many years and is known for its excellent outcomes. It involves closing the defect under cardiopulmonary bypass.
- The other is a more recent technique called percutaneous closure, where a device is inserted through a vein in the leg to seal the opening without the need for open-heart surgery. This method also offers good results but is not suitable for all types of VSDs.
The choice of treatment depends on the type and location of the defect, and a thorough evaluation by a cardiologist specialized in congenital heart conditions is essential to determine the best option in each case.
Vaccination
Vaccination is important for all children and adults with a ventricular septal defect (VSD). This includes routine childhood vaccines, as well as the pneumococcal vaccine and the annual flu shot.
For children under one year of age with heart failure, the respiratory syncytial virus (RSV) vaccine may also be recommended.
Dental care and antibiotics
Good dental hygiene is essential since VSD slightly increases the risk of infective endocarditis—an infection of the heart lining—linked to oral bacteria.
Since 2007, preventive antibiotics before dental treatment are only needed in specific situations: within six months after cardiac intervention or when a defect remains open and is in contact with implanted material. Recommendations may change, so consulting a cardiologist is best.
Refer to: Prevention of bacterial endocarditis
Physical activity
Individuals with small, asymptomatic VSDs can usually participate in all sports without restriction.
After successful repair, most can resume sports about three months post-procedure—always after consulting their primary care doctor.
For those with symptomatic VSDs, intense exercise should be avoided unless cleared by a cardiologist.
Prognosis
People with a small, asymptomatic ventricular septal defect (VSD) who receive regular medical follow-up generally enjoy an excellent quality of life with no long-term consequences.
When a VSD is surgically corrected without residual defects or impaired heart function, life expectancy is similar to that of the general population, and women in this situation can usually carry a pregnancy without difficulty.
Although long-term data on percutaneous interventions remain limited, current results are very promising.
However, a large untreated VSD can lead to heart failure and, over time, to severe pulmonary hypertension known as Eisenmenger syndrome. This is why regular follow-up with a cardiologist is essential to detect early signs and offer appropriate treatment.
Long-term follow-up
Follow-up care depends on the VSD type and its repair status. For small asymptomatic defects, monitoring frequency is determined by the cardiologist.
After a successful repair, follow-up may be reduced or even discontinued if closure is complete and cardiac function is normal.
Follow-up is particularly important for patients with a large, unrepaired VSD who have developed pulmonary hypertension. In the past decade, new medications have become available and now help improve management in these cases.






















