General · EdgepediaSeptember 17, 20267 min read

Ventricular septal defect

A ventricular septal defect (VSD) is a hole in the wall (septum) between the left and right ventricles, the two lower chambers of the heart. Rather than circulating to the rest of the body, blood from the left ventricle can cross into the right ventricle and mingle with the blood there; a large defect can force the heart and lungs to pump with extra effort, and fluid can accumulate in the lungs.¹ VSD is one of the most common congenital heart defects, present at birth, and in most children its cause is not known.²

Key fact	Detail
Definition	A hole in the interventricular septum allowing blood to shunt between the ventricles¹
Frequency	The most prevalent congenital cardiac anomaly in children and the second most common heart defect in adults, after bicuspid aortic valves³; about 20% of all congenital heart defects⁴
Most common type	Perimembranous VSD, about 80% of cases⁴
Shunt direction	Left to right in the usual case, determined by defect size and pulmonary vascular resistance⁵
Natural course	Many defects close spontaneously; small defects often need no treatment²
First repair	Pulmonary artery banding (Muller and Damann, UCLA, 1951); first direct closure by C. Walton Lillehei in March 1954 using cross-circulation⁶
Acquired form	Septal rupture after myocardial infarction occurs in about 0.2% of patients and carries about 90% mortality with supportive care alone⁷

Anatomy and types

The heart's four chambers are separated by a wall of tissue called the septum, and the ventricles are its two lower chambers.² VSDs are classified by their position in the septum. Perimembranous defects, located near the tricuspid and aortic valves, account for approximately 80% of VSDs.⁴ Other types include muscular defects in the lower muscular portion of the septum, and outlet (supracristal) defects near the pulmonary valve.⁸ A VSD may also occur as one component of complex defects: a large ventricular septal defect is one of the four defects of tetralogy of Fallot, the most common complex congenital heart disorder.¹

Pathophysiology

Shunt size and direction. The physiologic consequences of a hole between the ventricles depend on its size and on the relative resistances of the pulmonary and systemic vascular beds. A small defect is hemodynamically restrictive, limiting the size of the left-to-right shunt; a defect that is not restrictive is associated with significant flow to the lungs and pulmonary hypertension.⁵ Without pulmonary hypertension or obstruction to the right ventricle, the shunt runs left to right, producing pulmonary artery, left atrial, and left ventricular volume overload.⁹ When pulmonary vascular resistance exceeds systemic resistance, the shunt reverses to right to left regardless of defect size.⁷

Timing of symptoms. Pulmonary vascular resistance falls sharply after birth as the lungs expand and the alveoli are exposed to oxygen, a potent pulmonary vasodilator. When the defect is large, pulmonary blood flow keeps rising as the smooth muscle within the intrapulmonary arteries undergoes regression; infants born at term then become symptomatic between four and six weeks of age, whereas those born prematurely show symptoms within the first two weeks of life or even sooner.⁵ A small VSD may cause no symptoms at all; the only sign may be a heart murmur, an extra sound heard with a stethoscope. A large VSD can cause rapid or labored breathing, and infants may have trouble feeding and fail to gain weight as expected.²

Complications

Persistent large defects can lead to pulmonary arterial hypertension, Eisenmenger syndrome (in which high pulmonary vascular resistance allows the right ventricle to decompress through the defect), ventricular dysfunction, and increased risk of arrhythmias.³^•⁵ Over time, unrepaired defects can also produce acquired complications including double-chambered right ventricle, aortic valve prolapse with insufficiency, and subaortic stenosis, particularly in older children.⁶ People with a small VSD that remains open have a small risk of endocarditis, an infection of the heart's inner lining or valves, and the aortic valve may develop a leak that should be monitored.²

Acquired ventricular septal defect

A VSD can also be acquired. In about 0.2% of patients after myocardial infarction, rupture of the ventricular septum produces a significant left-to-right shunt with physiologic consequences identical to those of a congenital VSD. Over the first 10 to 14 days after the infarct, shunting may increase as surrounding tissue continues to necrose and enlarges the defect; supportive care alone results in about 90% mortality. Iatrogenic VSDs may also occur after aortic valve replacement, septal ablations, and the Konno procedure.⁷

Treatment

Observation. Many children with a VSD do not need surgery or other treatment. Small VSDs often close on their own, and no medication or other treatment can make a VSD get smaller or close faster.² A 25-year study of 790 untreated patients concluded that asymptomatic patients with small or moderate defects should be left to develop naturally without surgical interruption.¹⁰

Surgery. The first surgical treatment was banding of the main pulmonary artery, carried out by Muller and Damann at UCLA in 1951 to reduce distal pulmonary artery pressure and the left-to-right shunt. VSD closure was first performed by C. Walton Lillehei at the University of Minnesota in March 1954, using cross-circulation in which an adult served as the biological pump oxygenator for the patient; 8 of his first 12 patients survived. John Kirklin at the Mayo Clinic described the first closures using a mechanical pump oxygenator and cardiopulmonary bypass in 1955.⁶ Today, to close a large VSD a surgeon usually places a patch of surgical fabric or pericardium over the hole, and the heart's lining tissue grows over the patch, making it a permanent part of the heart. Pulmonary artery banding is still used as a temporary procedure for a very ill baby, or one with several VSDs or complex heart anatomy, before complete repair.² Surgical closure can be performed with low operative mortality of 1 to 2% and good long-term results.¹¹

Catheter-based closure. Transcatheter closure was introduced by Lock and colleagues in 1988 and has become an alternative, particularly for residual VSDs, defects poorly accessible for surgical closure, and muscular VSDs located centrally in the septum.⁴^•¹¹ A meta-analysis of 4381 pediatric patients comparing perventricular device closure with conventional surgical repair found no significant difference in minor or severe complications, but more residual shunts with device closure (RR 9.07, 95% CI 4.77 to 17.24) and more aortic regurgitation with surgery (RR 1.59, 95% CI 1.05 to 2.39).¹² A separate meta-analysis of 3580 pediatric patients found transcatheter closure associated with a lower risk of major complications (OR 0.51), less need for blood transfusion (OR 0.02), and shorter hospital stay, with similar success rates and residual shunts.¹³

Adults with a VSD

Because many children with large VSDs have surgery, large VSDs are uncommon in adults. Adults with a small VSD usually have no symptoms; a small unrepaired VSD slightly increases the risk of endocarditis. People whose VSD was repaired early in life are unlikely to have significant long-term problems, and those with normal heart function and normal pulmonary artery pressure usually have a normal life expectancy.² The 2025 ACC/AHA/HRS/ISACHD/SCAI guideline advises evaluating unrepaired VSD patients for pulmonary arterial hypertension to inform treatment and repair choices, and cautions against closing the defect in adults whose severe pulmonary artery hypertension involves systolic pulmonary artery pressure exceeding two-thirds of systemic, pulmonary vascular resistance above two-thirds of systemic, and a net right-to-left shunt.¹⁴^•⁸ For uncomplicated restrictive VSDs without complications or left ventricular overload, infrequent cardiology follow-up every 3 to 5 years is reasonable; Stage B patients with a hemodynamically insignificant shunt, normal chamber size, and no pulmonary hypertension can be seen every 36 to 60 months.¹⁴

References

Topic: Encyclopedia › Life and health › Human health and medicine › Diseases and injuries › Cardiovascular and blood conditions › Heart conditions › Congenital and genetic heart conditions › Septal, shunt, and simple obstructive lesions › Ventricular septal defects

Initially written Sep 17, 2026 · Reviewed: Sep 30, 2026; Oct 21, 2026 · Edited: Sep 30, 2026; Oct 21, 2026 · Last review: Oct 21, 2026

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