The heart is divided into four separate chambers. The lower chambers, or ventricles, are divided by a wall called the ventricular septum.

In the normal heart, the right and left ventricles are completely separated from each other by the ventricular septum.

It is normal for all infants to be born with a small hole between the two atria, which usually closes within the first few weeks of life. Normally, there is no hole between the two ventricles prior to birth, but some infants are born with a hole in the ventricular septum from incomplete or abnormal growth of the septum during fetal development.

Ventricular septal defects are among the most common congenital heart defects, occurring in about 2 to 4 of every 1,000 delivered babies each year, making up about 20 to 30 percent of congenital heart defects detected in newborns. VSDs are even more common in premature infants.

Ventricular septal defects are typically in two categories; peri-membranous or muscular.

Peri-membranous VSD in upper ventricular septum

Muscular VSD in lower ventricular septum

Peri-membranous VSDs are usually higher on the ventricle septum wall, closer to the valves and main vessels leading to and from the heart’s chambers. A peri-membranous defect is usually in the thinner, more flexible portion of the ventricular septum. Frequently, peri-membranous defects will also be aneurismal, meaning they have a thin, stretchy portion of tissue extending into the right ventricle. While many of these defect close during the first few months of life, larger defect s are more likely to remain open during early development.

Muscular VSDs are located lower in the venrtricular septum wall in the thicker, more muscular portion of the septum near the apex, or bottom of the heart’s ventricles. Smaller muscular defects are very likely to close over time and may only require observation in the first years of life, but larger defects require repair.

A VSD typically allows blood to pass from the left ventricle to the right ventricle.

The primary effect of smaller ventricular septal defects is an increased risk for sub-acute bacterial endocarditis (SBE). This is an infection of the heart caused by bacteria in the blood stream. SBE may occur after a dental or other medical procedure and can usually be prevented by taking antibiotics prior to the procedure.

Larger ventricular septal defects can allow blood to be pushed into the right ventricle, sending excessive blood flow to the lungs. Ordinarily, the pressure on the heart's left side is much higher than the pressure on the heart's right side. When there is a large defect, the blood takes the "path of least resistance" and goes back to the right ventricle instead of out to the body.

This results in extra work for the heart. If the heart is unable to meet this extra work load, symptoms of congestive heart failure can develop even in infants and small children. Symptoms include excessive sweating (a cold, clammy sweat often noted during feeding), poor feeding, slow weight gain, irritability or lethargy, and/or rapid breathing.

Treating Muscular Ventricular Defects

AGA Medical designed the AMPLATZER® Muscular VSD Occluder to allow closure of muscular ventricular defects using a minimally-invasive catheter procedure instead of surgery.