Download Myocardial Infarction-induced Ventricular Septal Defect

OCTOBER 2012
ISSUE 49
Myocardial Infarction-induced Ventricular Septal Defect
Lorenzo Azzalini MD1,2, Zoraida Moreno-Weidmann MD3, Rubén Leta MD3, Alessandro Sionis MD3, Suhny Abbara MD1
Clinical History
A 63-year-old man presented to an outside hospital with a two-week
history of recurring chest pain. His presenting ECG was consistent
with an evolving inferior wall myocardial infarction (MI). On physical
exam he was tachycardic with a holosystolic 3/6 murmur on his
left sternal border. He was transferred for emergent percutaneous
coronary intervention (PCI) and further management.
Findings
Coronary angiography showed one vessel disease, with
subacute thrombotic occlusion of the distal right coronary artery
(Fig. 1). An echocardiogram (not shown) revealed a large basal
ventricular septal defect (VSD) with left-to-right shunt, a small
inferior basal pseudoaneurysm, normal biventricular function
and valve morphology and function. The VSD was surgically
repaired with a pericardial patch, and the pseudoaneurysm was
excluded (David technique). The patient did initially well, but
represented three months later with right-sided heart failure. An
echocardiogram showed a residual VSD (Fig. 2), a large inferior
basal pseudoaneurysm, reduced left ventricular ejection fraction
(LVEF 38%) and right ventricular global hypokinesis. A cardiac CT
(Fig. 3 and 4) was requested for surgical planning prior to repeat
cardiac surgery and confirmed a residual VSD and a recurrent
large inferior basal pseudoaneurysm. Unfortunately, surgical
repair of the residual VSD, pseudoaneurysm or the implantation
of a ventricular assist device were considered to be technically
unfeasible. The patient underwent cardiac transplantation, but
eventually died of the complications of an invasive pulmonary
aspergillosis.
Discussion
VSD is a mechanical complication of myocardial infarction and
typically occurs three to five days after an acute MI. Nevertheless
it has been observed also within the first 24 hours or as late as two
weeks [1]. In a study of 6678 consecutive MI patients during the last
30 years, it accounted for about 2% of the total population [2]. The
incidence has been diminishing over the last decades thanks to the
introduction of timely reperfusion therapy [2]. VSD is observed with
equal frequency in anterior and non-anterior infarctions [3]. In case
of an anterior MI, the defect is most commonly found in the apical
septum; in inferior MI, it usually occurs in the basal segments.
Rupture develops at the limit between the necrotic and nonnecrotic myocardium. The defect can be either a direct throughand-through hole, or have a more irregular and serpiginous path
[4]. The size of the VSD determines the magnitude of left-to-right
shunt, which in turn correlates with survival. Cardiac CT has
excellent spatial resolution, and is well suited to delineate the
morphology and extent of pseudoaneurysm and septal defects.
Cardiac Imaging, Department of Radiology and 2Interventional Cardiology,
Heart Center, Massachusetts General Hospital, Boston, MA, USA;
3
Cardiology, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain
1
Editors:
Suhny Abbara, MD, MGH Department of Radiology
Figure 1
Figure 2
Figure 3
Figure 4
Figure 1: Coronary angiography showing a subacute thrombotic occlusion of
the distal right coronary artery, which has lead to acute VSD (not shown).
Figure 2: Echocardiogram with and without color Doppler (two-chamber
view) shows a large inferior pseudoaneurysm with typical “yin and yang”
flow pattern. LV: left ventricle. LA: left atrium. PsAn: pseudoaneurysm.
Figure 3: Cardiac CT (short-axis view) three months after surgical repair of
infarct-related VSD shows degenerated surgical patch with residual VSD
(arrow) and a large inferior pseudoaneurysm. LV: left ventricle. RV: right
ventricle. PsAn: pseudoaneurysm.
Figure 4: Cardiac CT (long-axis view) shows a large inferior
pseudoaneurysm. LV: left ventricle. LA: left atrium. PsAn: pseudoaneurysm.
REFERENCES
1. Marion, DW. Mechanical complications of acute myocardial infarction. In:
UpToDate, Basow, DS (Ed), UpToDate, Waltham, MA, 2012.
2. Figueras J, Alcalde O, Barrabés JA, Serra V, Alguersuari J, Cortadellas
J, Lidón RM. Changes in hospital mortality rates in 425 patients with acute
ST-elevation myocardial infarction and cardiac rupture over a 30-year period.
Circulation. 2008;118(25):2783.
3. Batts KP, Ackermann DM, Edwards WD. Postinfarction rupture of the left
ventricular free wall: clinicopathologic correlates in 100 consecutive autopsy
cases. Hum Pathol. 1990;21(5):530.
4. Mann JM, Roberts WC. Acquired ventricular septal defect during acute
myocardial infarction: analysis of 38 unoperated necropsy patients and
comparison with 50 unoperated necropsy patients without rupture. Am J
Cardiol. 1988;62(1):8.
Wilfred Mamuya, MD, PhD, MGH Division of Cardiology