CARDIOVASCULAR JOURNAL OF AFRICA • Vol 23, No 9, October 2012
AFRICA
e3
percutaneous interventions.
1-3
VSR is more rare than a rupture
of the ventricular free wall. Women are affected more often than
men. Age, smoking and hypertension are other risk factors.
4
A VSR usually occurs two to eight days after the infarction
and often precipitates cardiogenic shock. The magnitude of
the left-to-right shunt is determined by the size of the defect
and hence causes haemodynamic deterioration, which affects
survival. Spontaneous closure of this defect is extremely rare.
5
There are three types of VSR: in type I there is an abrupt tear
in the wall without thinning; in type II, the infarcted myocardium
erodes before rupture and is covered by a thrombus; and type III
represents the perforation of a previously formed aneurysm.
6
The
blood supply to the septum originates from branches of the left
anterior descending coronary artery, the posterior descending
branch of the right coronary artery or the circumflex artery.
A VSR has equal frequency in anterior and non-anterior
infarctions.
7
An anterior MI is associated with rupture of the
apical septum. In an inferior MI, the base of the heart is often
affected. An MI associated with a VSR is usually extensive.
Early treatment of the MI with thrombolytic therapy or primary
percutaneous intervention may reduce the incidence of the VSR
by reducing the infarct area. Restoring the blood flow therefore
improves the outcome.
Ventricular free-wall rupture is a catastrophic complication of
MI. Its prevalence is 4% in patients with MI and 23% in those
who die of MI.
8
Rarely the rupture is contained by an adherent
pericardium, creating a pseudoaneurysm that needs emergency
surgery.
Our case is unique, illustrating an acute anterior MI,
complicated by a VSR and ventricular pseudoaneurysm
formation, which are both lethal. The patient survived with
moderate symptoms until successful intervention.
Conclusion
Early coronary angiography and primary percutaneous
intervention in acute coronary syndromes is life-saving and
may prevent lethal complications, including VSR and free-wall
rupture.
References
1.
Birnbaum Y, Fishbein MC, Blanche C, Siegel RJ. Ventricular septal
rupture after acute myocardial infarction.
N Engl J Med
2002;
347
:
1426–1432.
2.
Gueret P, Khalife K, Jobic Y,
et al
.
Echocardiographic assessment
of the incidence of mechanical complications during the early phase
of myocardial infarction in the reperfusion era: a French multicentre
prospective registry.
Arch Cardiovasc Dis
2008;
101
: 41–47.
3.
Murday A. Optimal management of acute ventricular septal rupture.
Heart
2003;
89
(12): 1462–1466.
4.
Crenshaw BS, Granger CB, Birnbaum Y,
et al
.
Risk factors, angio-
graphic patterns, and outcomes in patients with ventricular septal defect
complicating acute myocardial infarction. GUSTO-I (Global Utilization
of Streptokinase and TPA for Occluded Coronary Arteries) trial investi-
gators.
Circulation
2000;
101
: 27–32.
5.
Ilia R, Goldfarb B, Wanderman KL, Gueron M. Spontaneous closure
of a traumatic ventricular septal defect after blunt trauma documented
by serial echocardiography.
J Am Soc Echocardiogr
1992;
5
: 203–205.
6.
Becker AE, van Mantgem JP. Cardiac tamponade: a study of 50 hearts.
Eur J Cardiol
1975;
3
: 349–358.
7.
Batts KP, Ackerman DM, Edwards WD. Postinfarction rupture of the
left ventricular free wall: clinicopathologic correlates in 100 consecu-
tive autopsy cases.
Hum Pathol
1990;
21
: 530–535.
8.
Pollak H, Nobis H, Miczoc J. Frequency of left ventricular free wall
ruptures complicating acute myocardial infarction since the advent of
thrombolysis. Am J Cardiol 1994;
74
:
184–186.
