CARDIOVASCULAR JOURNAL OF AFRICA • Vol 21, No 6, November/December 2010
AFRICA
331
started and after stabilising her haemodynamic status, a coronary
angiogram was performed the following day. It showed total
occlusion in the mid segment of a dominant right coronary artery
and a discrete 60% narrowing in the mid-portion of the left ante-
rior descending artery (Fig. 1e, f). She had recurrent hypotension
and dyspnoea after catheterisation, and an intra-aortic balloon
pump (IABP) was inserted. Early surgical repair was planned.
The patient underwent an operation two days after success-
ful IABP insertion in the coronary care unit. The operation was
performed with aorto-bicaval cannulation under extra-corporeal
circulation (ECC). The heart was arrested by anterograde and
retrograde blood cardioplegia. Exploration of the ventricular
septum showed an inferior aneurysm in the right ventricular side
approach (Fig. 2). Inspection showed no other aneurysm forma-
tion, necrosis or ischaemic region.
The ventricular septal defect that was near the apex of the
septum was closed with the trans-aneurysmal approach. It was
infixed to the left ventricular free wall to be repaired by teflon
strip with pladgeted prolene sutures. The aneurysmotomy was
closed in a buttress of strips of teflon felt and sutured with
pladgeted prolene sutures (Fig. 2). After a right coronary artery
bypass with a saphenous vein graft, anostomosis of the left
internal mammary artery to the left anterior descending artery
was performed.
There was no difficulty weaning the patient from the ECC
with 2:1 IABP assistance in sinus rhythm. The postoperative
course was uncomplicated. Early transthoracic echocardiography
revealed no shunt. The patient was weaned from the IABP on the
first postoperative day and inotropic drugs were reduced on the
third postoperative day with stable haemodynamic parameters.
Discussion
Post-infarction VSD was first shown by Latham in an autopsy
in 1845, and clinical diagnostic criteria were first introduced by
Sager in 1934.
5
Reported studies defined risk factors for devel-
oping post-infarction VSD to be advanced age, female gender,
hypertension, non-smoker, higher Killip score at admission, no
known coronary heart disease and first MI.
6,7
Post-infarction VSD is usually located in the anterior or apical
portion of the ventricular septum (about 60% of cases) as a result
of an anterior MI. Twenty to 40% of patients have a defect in
the posterior portion of the ventricular septum as a result of an
inferior MI.
2
However, unexpected locations for ruptures also
appear in the literature.
1
VSD is usually associated with complete
obstruction of a coronary artery.
6
Symptoms are mostly chest pain, dyspnoea, and symptoms
due to low output and cardiogenic shock.
2
Almost all patients
have a new harsh, loud, pansystolic murmur located at the left
sternal border, spreading to the apex. A thrill usually accompa-
nies this. Doppler echocardiography has 100% sensitivity and
specificity for diagnosis.
1
Transoesophageal echocardiography
and right heart catheterisation are further techniques when
transthoracic echocardiography is inconclusive but with a high
clinical suspicion.
1
In patients who do not receive thrombolytic therapy, coagu-
lation necrosis begins within three to five days of infarction.
Neutrophils penetrate into the necrotic zone. By triggering apop-
tosis, released lytic enzymes cause the necrotic myocardium to
rupture.
1
With the rupture of the septum, a shunt from the left to
the right ventricle occurs, which increases volume load of the
right ventricle and also pulmonary blood flow, left atrial and
left ventricular volumes. The magnitude of VSD, pulmonary–
systemic vascular resistance, Qp/Qs ratio and left–right ventricu-
lar functions determine the amount of shunt.
1
If left ventricular
systolic functions deteriorate, forward flow would decrease and
compensatory vasoconstriction would raise systemic vascular
resistance, leading to increased shunt flow.
Although the exact mechanism of rupture was not known,
we presume that on the sixth day post MI, after our patient
performed several forceful Valsalva manoeuvres, the thinned,
necrotic septum was affected by the sudden volume and pres-
sure changes created by the Valsalva manoeuvres. This may have
caused the septum to rupture.
It has been shown that an approximately 20-mmHg fall in the
systemic blood pressure occurs during early phase 2, which is
followed by an abrupt rise in phase 4 of the Valsalva manoeuvre
(about 43 mmHg) in a patient who is sitting and performing it.
8
An overshoot of arteriolar vasoconstriction during late phase 2
and a 42% transient increase of the cardiac output above resting
state are believed to be the reason for the blood pressure rise
during phase 4.
9
ACC/AHA practice guidelines recommend daily
stool softeners in the hospital management of ST-elevation MI
and our opinion is that this recommendation should be closely
followed.
10
Previously reported studies have shown that mortality is
higher with: early VSD with surgery in the first 24 hours, inferior
MI, the need for inotropic agents, cardiogenic shock, low mean
pulmonary arterial pressure (PAP) and pulmonary capillary
wedge pressure (PCWP), low cardiac index (CI
<
1.75 ml/min/
m
2
), serious right ventricular dysfunction and low systolic blood
pressure.
4,11
If the right ventricle can handle the volume overload,
the mean PAP and PCWP increases, as well as the survival rate.
11
The first repair by Cooley
et al
. in 1957, a case of acquired
ventricular septal defect, was accomplished using an approach
through the right ventricle with incision of the right ventricular
outflow tract.
12
This approach, which was adapted from surgical
techniques for closure of congenital ventricular septal defects,
proved to be disadvantageous for many reasons. Subsequently,
Heimbecker
et al
. introduced and others adopted a left-sided
approach (left ventriculotomy) with incision through the area
of infarction. Such an approach frequently incorporates
infarc-
tectomy and aneurysmectomy, together with repair of the septal
rupture.
12
Our choice was to attach the apical-septal VSD to the left
ventricular free wall and repair with teflon strips and pladgeted
prolene sutures. The aneurysmotomy was closed and buttressed
with strips of teflon felt and sutured with pladgeted prolene
sutures after RCA bypass with a saphenous vein. The left internal
mammary artery to the left anterior descending anastomosis was
performed at the last stage.
It was recently reported that a small or medium-sized post-
infarction VSD could be treated successfully with a ventricular
septal occluder. This intervention may be permanent or it may
stabilise the patient and allow myocardial fibrosis, thus facilitat-
ing delayed subsequent surgical correction.
13
Conclusion
Post-infarction VSD is a serious mechanical complication of MI.
Close monitoring of the non-reperfused patients is mandatory
and a forceful Valsalva manoeuvre may facilitate the rupture of
