michael s
(Michael S)
#1
45 When and how should a ventricular septal
defect be closed in adults?
Seamus Cullen
Indications for surgical closure of a ventricular septal defect in
childhood include congestive cardiac failure, pulmonary hyper-
tension, severe aortic insufficiency and prior bacterial endo-
carditis. It is unlikely that a significant ventricular septal defect
will be missed in childhood and therefore ventricular septal
defects seen in adulthood tend to be small and isolated. In a small
number of patients with Eisenmenger syndrome, i.e. ventricular
septal defect with established pulmonary vascular disease, no
intervention is possible.
The natural history of small congenital ventricular septal
defects was thought to be favourable but longer follow up has
demonstrated that 25% of adults with small ventricular septal
defects may suffer from complications over longer periods of time.
The complications documented were: infective endocarditis,
aortic regurgitation, arrhythmias and myocardial dysfunction.
Whilst closure of a ventricular septal defect protects against
infective endocarditis, there are no data to suggest a protective
effect against the development of late arrhythmias, sudden death
or ventricular dysfunction.
The risk of bacterial endocarditis in patients with a ventricular
septal defect is low (14.5 per 10,000 patient years). Prior or
recurrent endocarditis on a ventricular septal defect would be
deemed an indication for surgical closure even though the risks of
endocarditis are low.
Whilst the majority of congenital ventricular septal defects are
in the perimembranous or trabecular septum, a small percentage
are found in the doubly committed subarterial position. This
small sub group may be complicated by aortic valve cusp
prolapse into the defect with development of subsequent aortic
regurgitation which may be progressive and severe. The detection
of aortic regurgitation in such a defect is considered an indication
for surgical closure in most centres.
The mortality for surgical closure of a post-infarction
ventricular septal defect may be up to 50%. Cardiogenic shock is
exacerbated by the acute left ventricular volume load from the
shunt through the ventricular septal defect. There is a small but