Netherlands Journal

netherlands journal of critical care
Figure 1: Apical, 4-chamber, trans-thoracic echocardiographic view showing VSR (arrow).
(MV = mitral valve, TV = tricuspid valve, IVS = interventricular septum, RV = right ventricle)
Figure 2: Per-operative image showing massive hemorrhagic anterior wall myocardial infarction),
and VSR (at the tip of suction device / speculum).
to be 1: 2.2. Emergency surgery was performed immediately.
After sternotomy the anterior wall of the left ventricle was seen
to be haemorrhagic and infarcted. This extended into the right
ventricular wall and there was blood in the pericardium indicating
imminent ventricular free wall rupture (Figure 2). By means of
ventriculotomy in the infarcted anterior region, both the impending
ventricular free wall rupture and the VSR were covered by an
autologous pericardial patch. mitral valve annuloplasty was not performed
because of moderate mitral valve regurgitation.
Temporary epicardial atrial and ventricular pacemaker leads
were attached although the patient had persistent sinus tachycardia
without any conduction disturbances.
Transoesophageal echocardiography performed directly after
surgery showed no signs of pericardial effusion but there was still a
minor residual VSR. Both left ventricular function and mitral valve
regurgitation remained unchanged.
Postoperatively, however, mixed venous oxygen saturation progressively
increased, indicating progressive VSR with a calculated
shunt fraction up to 1: 2.9, indicating patch dehiscence
Because of hypotension, progressive renal failure and ongoing
myocardial ischaemia it was decided that further surgical intervention
was not feasible. Active treatment was suspended and the patient
died soon after. Permission for autopsy was refused.
Discussion
VSR after AMI is associated with female gender, advanced age, anterior
wall myocardial infarction, one-vessel coronary artery disease,
absence of collateral circulation and no coronary reperfusion [1,2].
Our patient, although a man, fulfilled most of these risk factors for
VSR. We do not have any clinical indication or data from literature
that Buerger’s Disease is involved in the occurrence of VSR after
AMI.
With the advent of the more appropriate reperfusion treatment
the incidence of VSR has declined over the years. In the era before
thrombolytic therapy, VSR complicated 1 to 3 percent of cases of
AMI, occurring within one day or after 3 to 5 days [1]. In the GUS-
TO-I trial the incidence of VSR was 0.2 percent [2]. Remarkably,
most of the VSR occurred in the first 24 hours after onset of AMI.
It was concluded from these observations that thrombolysis, although
reducing infarct size and VSR occurrence rate, may promote
haemorrhagic dissection in the myocardium, thereby accelerating
the onset of VSR.
The effects of percutaneous coronary intervention (PCI) with respect
to the occurrence of VSR after AMI are not well established.
However, Yip et al report a significantly lower occurrence rate of
VSR after AMI in PCI-treated patients, although in this study no
data are available with respect to final angiographic results [3].
Mortality rates among patients with VSR who do not have surgery
are approximately 24% in the first 24 hours, 46% in the first
week, and 67 to 82% over two months. However, the 30-day mortality
of medically and surgically treated patients with VSR was 76
and 53% respectively, indicating the potential benefit of surgical
treatment [4]. In the study of Lemery and co-workers it was shown
that in patients who go into cardiogenic shock after VSR, the prognosis
was uniformly fatal unless they undergo prompt surgery. In
the same study it was found that a higher age correlated with an
adverse outcome. So, early surgery should be considered for every
patient with VSR after AMI in the knowledge that elderly patients
in cardiogenic shock have the worst prognosis [4]. The operation
involves excluding rather than excising the infarcted septum and
ventricular wall. A left ventriculotomy is made through the infarcted
area of muscle and a pericardial patch is sewn over the endocardium
of the left ventricle around the infarcted area of myocardium. The
ventriculotomy is then closed over the pericardial patch.[5]
Patients with VSR are regularly treated with an IABP which improves
survival by augmenting coronary blood flow as well as reducing
left ventricular afterload and wall tension. Indeed, IABP support
results in lower immediate postoperative mortality rates, although
IABP treatment was not found to be associated with improved longterm
survival [6]. In our patient it was decided not to insert an IABP
because of severe atherosclerosis of the femoral arteries.
Alternative insertion sites (e.g. intra-thoracic) were not feasible
because of severe atherosclerosis and elongation of the aorta. The
development of residual or recurrent VSR is reported in up to 28%
of patients who survive surgical repair, and is associated with high
mortality [7].
Nowadays VSR is an extremely rare complication of AMI. VSR
should be considered in all patients who deteriorate rapidly after an
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neth j crit care • volume 10 • no 5 • october 2006