Last reviewed 12/2022

The prognosis is largely dependent on the size of the defect and the context in which the defect has occurred.

In general, the prognosis is good for patients with VSD (muscular and perimembranous)

  • in the first 2 years of life, approximately 80% of the defects close spontaneously. About 20% continue to have large volume shunt beyond infancy. These patients and patients who develop heart failure in infancy are best served with intervention. The development of pulmonary vascular disease is uncommon before the age of 2 years but the incidence increase significantly in patients who are above 2 years of age (1)
  • spontaneous closure is rare over 2 years old
    • after more than six years almost a third of all perimembranous and just over two thirds of all muscular defects close spontaneously
    • outlet ventricular septal defects (VSDs) have a low incidence of spontaneous closure, and inlet VSDs do not close.

Long-standing defects - about 60% of small defects close spontaneously compared to only 10% of large defects

  • in about 10% of large defects there is the development of right ventricular outflow obstruction and the condition becomes similar to that of tetralogy of Fallot. If the defect is not closed about 10% of patients with large defects may develop progressive pulmonary vascular disease during childhood. A small proportion of defects may be complicated by infective endocarditis or, if subarterial, aortic regurgitation.

Operative mortality and morbidity is largely dependent on the pulmonary vascular resistance and the pre-operative condition of the patient.

Post-infarct VSDs have high mortality with progressive haemodynamic deterioration leading to emergency surgery or death

  • septal perforation develops on the average 2-3 days after myocardial infarction
  • 86% of patients with acquired VSD or more will die within 2 months without surgical intervention
  • significant factors for hospital mortality included: preoperative and evolution of the clinical status, right ventricular function and type of repair. Mortality with only medical treatment is extremely high, over 90%; mortality after surgical repair varies between 19% and 60% in different studies (3)


  • there are various classifications of ventricular septal defects (VSDs)
    • perimembranous, also called infracristal VSDs, lie in the left ventricular outflow tract just below the aortic valve
      • account for approximaely 80% of all VSDs
      • have been subclassified as
        • perimembranous inlet
        • perimembranous outlet
        • perimembranous muscular
    • supracristal defects are also called conal, infundibular, subpulmonary, subarterial and outlet and comprise approximately 5-8% of isolated VSDs ( in Japan the figure is approximately 30%)
      • defect lies beneath the pulmonary valve
        • communicates with the right ventricular outflow tract above the supraventricular crest and is associated with aortic regurgitation due to prolapse of the right aortic cusp
    • muscular or trabecular VSDs are bounded entirely by muscular septum and are often multiple (also known as 'Swiss cheese septum' because of multiple defects)
    • other subclassifications depend on the location
      • account for 5-20% of all defects
        • posterior, also called canal-type, endocardial cushion-type, atrioventricular (AV) septum-type and inlet VSDs lie posterior to the septal leaflet of the tricuspid valve
          • not associated with defects in the AV valves and it accounts for 8-10% of VSDs.


  • Catheter Cardiovasc Interv. 2008 Jul 1;72(1):102-11.
  • Turner SW, Hunter S, Wyllie JP; The natural history of ventricular septal defects. Arch Dis Child. 1999 Nov;81(5):413-6
  • Coskun KO et al. Experiences with surgical treatment of ventricle septal defect as a post infarction complication.J Cardiothorac Surg. 2009;4:3.