The heart is divided into four chambers by muscular walls, known as septa, which prevent the mixing of oxygenated and deoxygenated blood. A septal defect, often referred to as a “hole in the heart,” is a common congenital heart issue where a portion of the septum is incomplete, allowing blood to flow abnormally between chambers. The likelihood of this defect closing naturally depends on its size and location, particularly within the first few years of life. Understanding the natural history of these defects is important for families facing this diagnosis, as many small defects resolve without the need for medical intervention.
Classifying Septal Defects
Septal defects are primarily categorized based on which dividing wall of the heart is affected. A Ventricular Septal Defect (VSD) is a hole in the wall separating the two lower pumping chambers, the ventricles, and is the most frequently diagnosed congenital heart anomaly in children. An Atrial Septal Defect (ASD) is a hole in the wall between the two upper receiving chambers, the atria, and is also common.
The location within the septum greatly influences the chance of spontaneous closure. VSDs are further classified into four types, with the muscular VSD being the most likely to close on its own, as it is surrounded entirely by muscle tissue. Perimembranous VSDs, the most common type, occur near the heart valves but also have a moderate chance of closing spontaneously.
ASDs are most often of the ostium secundum type, located in the middle of the atrial septum, which may close spontaneously in childhood if small. Other types of ASDs, such as ostium primum or sinus venosus defects, occur closer to other structures in the heart and rarely close without intervention.
The Spontaneous Closure Timeline
The window for spontaneous closure is generally concentrated within the first few years of life, particularly for smaller VSDs. For many small VSDs, closure typically occurs within the first year, with most expected closures finalized by two or three years of age.
The mechanism behind this closure involves the heart’s dynamic growth and changing shape. As the heart muscle develops, the muscular tissue around the defect can hypertrophy, or thicken, effectively shrinking the size of the hole. In VSDs located in the membranous section, a natural pouch of tissue, called a membranous septal aneurysm, can form and grow to cover the opening.
Defect size acts as a primary determinant of closure likelihood and speed. Defects measuring four millimeters or less are significantly more likely to close than those that are larger. If a VSD has not shown substantial regression or closure by the age of three or four, the probability of it closing naturally decreases significantly.
For small ostium secundum ASDs, spontaneous closure is also possible, often occurring within the first year of life, but this is less frequent than with VSDs. A general rule of thumb used by cardiologists is that if a small ASD is present, it will typically close by school age if it is going to close at all. Regular monitoring through echocardiograms is a standard part of care to track the defect’s size and the heart’s overall function while awaiting potential closure.
When Closure Does Not Occur
When a septal defect remains open past the typical spontaneous closure window, continued medical monitoring is often necessary. An open defect that is not causing any strain on the heart or lungs may simply be observed with routine check-ups and imaging studies. This approach is common for small VSDs or ASDs that do not result in significant blood shunting between the heart chambers.
Intervention becomes necessary if the defect is large, or if it causes signs of heart strain, such as chamber enlargement or elevated pressures in the lung arteries, known as pulmonary hypertension. These symptoms indicate that the excess blood flow through the defect is beginning to affect the heart’s efficiency and the health of the lungs.
Two main types of procedures are used to close persistent septal defects. Transcatheter closure is a minimally invasive option often preferred for appropriate ASDs and some VSDs, where a specialized device is guided through blood vessels and positioned to plug the hole. This procedure avoids open-heart surgery and typically results in a faster recovery.
Open-heart surgery is reserved for larger, more complex defects, such as ostium primum ASDs or large VSDs, or when a transcatheter approach is not anatomically feasible. During this surgery, the defect is closed using a patch, and the heart tissue eventually grows over the foreign material, sealing the hole permanently. Both intervention methods have high success rates, leading to excellent long-term outcomes for most patients.