Ventricular septal defect (VSD)

Ventricular septal defect (VSD) is a heart defect in which the septum between the ventricles is not completely closed. The so-called ‘hole in the heart’ is the most common congenital heart defect. However, a VSD can also occur as a result of a heart attack or after heart surgery.
Depending on the localisation, a distinction is made between defects in the muscular, perimembranous, outlet or inlet area of the ventricular septum. Through the connection between the two ventricles, some of the oxygen-rich blood flows from the left ventricle into the right ventricle, where it mixes with the deoxygenated blood (left-to-right shunt). This causes a larger volume of blood to enter the pulmonary circulation, which increases the pressure in the pulmonary vessels and results in pulmonary hypertension. The right ventricle is exposed to an increased pressure load due to the increase in blood pressure in the pulmonary vessels. The left ventricle has an increased volume load due to the increased amount of blood that returns to the left ventricle via the pulmonary vessels. The extent of this pressure and volume load depends on the size and number of defects present (pressure-separating or non-pressure-separating VSD).

The symptoms depend on the size of the VSD and the extent of the shunt volume. The most common symptoms in infants are difficulty drinking, failure to thrive, rapid and laboured breathing (tachydyspnoea) or an increased tendency to become infected. In children and adults, VSD can be characterised by increased tiredness and fatigue as well as reduced resilience (breaks during play or physical exertion). Palpitations or a bluish discolouration of the skin (cyanosis) may also occur.

The symptoms of a ventricular septal defect can be temporarily reduced by initiating drug treatment. Depending on the size and number of VSDs, surgical or cardiac catheter-based procedures are available for definitive treatment.

Possible complications in the long term

The child's prognosis for the underlying heart defect is good in the short and long term. After an adaptation phase, the patient is considered to have a healthy heart. Immediately postoperatively, residual defects (<3 mm diameter) are often detectable, which are generally no longer haemodynamically relevant.

Recommendation for follow-up treatment

We recommend continuing endocarditis prophylaxis with the known indications for six months after surgical or catheter-interventional closure of the VSD.