Ventricular septal defect(VSD) is one the commonest congenital heart disease . Right from the days of Gasul , Abbot, and Keith we have analysed the natural history for nearly a century . VSD is an intriguing congenital heart disease where a child can develop a florid cardiac failure within weeks of birth in one end to a totally asymptomatic adult with a benign cardiac acoustics defect (Namely a systolic murmur in the left parasternal area.) But for this murmur , the patient would be labeled absolutely healthy.
In between these two spectra is the huge population of VSD that gets closed spontaneously. A rough estimate says 60 % of all small VSDs get closed by age 10 .
So ,what we are supposed to do once a child is diagnosed of VSD ?
Should we close or should we wait ?
The indication for closing a VSD is discussed elsewhere ( Read this link )
What are the factors that determine VSD closure ?
- The size
- The site
- Age of the child
- The Rim morphology
- Associated lesions*
- Hemodynamic stress
- Inherent tissue factors
- Infection **
* Associated defects like PDA, RVOT obstruction are strong deerrants against spontaneous closure
General rules of VSD closure
Size
VSDs <5mm have great chance of closing Large VSD > 1cm is rarely get closed .
Supracristal VSDs located sub arterially are immune to spontaneous closure however small the size is .
Location & Site
VSDs that are located exclusively within the membranous septum rarely close . VSDs which are located in the perimembranous area (With at least 50% circumference is fenced by muscular or trabecular septum has the greatest potential to close by natural forces.)
Isolated muscular VSD if large can not get closed . Inlet VSD has anatomical difficulty to get closed.
Rim Morphology
Small muscular VSDs have a potential to close , but it is believed differential cellular lining of VSD rims (Eg : A combination of muscle, membrane , is more likely to close .)
Process of tissue growth As the child grows the it is expected the heart will outgrow the lesion . This is thought to be the commonest mode of VSD closure. As the IVS mass increases as he child grows it brings he rims together . But logic would suggest unless some degree of neocardiac proliferation occur a VSD may never get closed completely .
Some times even large VSDs try to close with the help of the neighboring structures like septal tricuspid valve leaflet . Indeed this can be the dominate mode of closure in many. This can induce a tricuspid regurgitation .
**Role of infection
Paradoxically an episode of infective endocaditis in the edges of VSD accelerate the process of approximation of tissue plane and healing .
Relation with Pulmonary arterial hypertension (PAH)
Once PAH sets in the VSD never gets closed spontaneously , This may be due to all VSDs that result in PAH has to be significantly large
Can a VSD get larger progressively?
In physics and hydraulics a hole under hemodynamic stress is destined to progress In human biology this is thought to be rare .Post MI VSRs can behave in an unpredictable manner as he edges of the defect a often softened and prone for tissue plane dissection and extension .
Why some VSDs never close ?
It is clear , size and location matters the most , but there are other issues some of them may be unique tissue properties .
Why is it important to know the biology of VSD closure ?
In this era of interventional cardiology we are using mechanical devices to close VSDs and ASDs .It is fraught with many technical issues. If there is a biological glue or membrane that can be delivered by catheter to close small VSDs or ASDs .
So for no therapeutic approach to hasten the natural closure of these defects has been practiced .Further research is required to explore the cellular adhesiveness and help accelerate closure of these defects.
Dr.S.Venkatesan MD 
