CARDIOVASCULAR JOURNAL OF AFRICA • Volume 25, No 3, May/June 2014
e2
AFRICA
has evolved and percutaneous closure of ASDs has been proven
to be safe and effective. It has become the standard treatment for
secondum-type ASD. Nowadays, percutaneous ASD closure has
largely replaced surgical treatment of secundum ASD, except in
the case of large defects (
≤
38-mm diameter), insufficient septal
rims, or insufficient left atrial size to accommodate a device.
An adequate septal rim requires 5 mm of septal tissue from the
ASD to the superior and inferior vena cava, right upper and lower
pulmonary veins, coronary sinus and mitral/tricuspid valves.
1
The reported complication rate of percutaneous ASD closure
is relatively low; several reports reveal a 1.2 to 2.5% major
complication rate and a 3.4 to 6.1% minor complication rate.
4-6
Major complications include device embolisation, erosion,
pericardial effusion with tamponade, device thrombus, stroke
and endocarditis. Minor complications include excessive
inflammatory reactions, cardiac arrhythmias and complications
of the femoral access site.
The reason for device embolisation has not been clarified,
however, suggestions are the type of device used, larger size of
defect, thin rim of atrial tissue, mobility of the implanted device,
use of an undersized device, and deficiency or absence of the
aortic rim.
7-9
The aortic rim is important and a margin less than
5 mm may predispose to both early and late device embolisation.
Another potential cause of late device embolism is acute
change in intracardiac pressure due to physical activity. A
sudden increase in afterload to the left heart in conjunction with
diminished right heart filling (Valsalva) may cause the migration
of the device to the right, and subsequently to the pulmonary
artery. Devices usually embolise in the main pulmonary artery.
9
Some physicians recommend six months of abstinence from
strenuous exercise to avoid device embolisation.
10
However in our case, the device embolised to the left side
and the patient had not done strenuous exercise during the
follow-up period. We could not determine the exact reason for
delayed embolisation of our patient, however, since our patient
had received his ASD at a relatively advanced age, he had
already developed complications such as atrial fibrillation with
an enlarged right atrium, increased right ventricular systolic
pressure and severe tricuspid regurgitation. In our opinion, the
severe tricuspid regurgitation led to an increase in right atrial
pressure and this increase may have been one of the mechanisms
for device displacement to the left side.
Fig. 1.
The well-positioned ASD closure device (arrow). Transoesophageal echocardiography immediately after the procedure (A),
and transthoracic echocardiography the following day (B).
Fig. 2.
Chest radiograph of the displaced Amplatzer closure
device (arrow), compared with the usual position of
the closure device (circle).
A
B
