Ann Thorac Surg 2001;71:1358-1360
© 2001 The Society of Thoracic Surgeons
Case report
Septal dissection and rupture evolved as an inferobasal pseudoaneurysm
Isidoro Di Bella, MDa,
Gaetano Minzioni, MDa,
Daniele Maselli, MDa,
Stefano Pasquino, MDa,
Mario Viganò, MDa
a Division of Cardiac Surgery, Policlinico San Matteo, IRCCS University of Pavia, Pavia, Italy
Accepted for publication April 12, 2000.
Address reprint requests to Dr Di Bella, Divisione di Cardiochirurgia, Policlinico San Matteo, Piazzale Golgi 2, Pavia 17100 Italy
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Abstract
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We report two cases of postinfarction dissecting hematoma of the interventricular septum with restrictive ventricular septal defect that evolved as an inferobasal pseudoaneurysm. The difficult anatomical pattern was assessed by two-dimensional (2-D) echocardiography with Doppler and color analysis, left ventriculography and perioperative transoesophageal echo. Because the patient had no signs of heart failure, the surgical repair was successfully delayed until the dissecting tissue became fibrotic. Problems of diagnosis, decision making and surgical management are discussed.
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Introduction
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Rupture of the interventricular septum complicates 1% to 2% of all patients who suffer a myocardial infarction and, in most cases, requires a prompt surgical approach [1–2]. Commonly, it is acute, single and involves the full thickness of the septum. In a rare condition, blood infiltrates the spiral muscles, causing a dissecting hematoma [3]. This situation can lead to a delayed subacute septal rupture and formation of a pseudoaneurysm. We describe two cases of septal dissection and rupture that evolved as septal pseudoaneurysms with chronic clinical evolution.
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Case reports
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Patient 1
The first patient was a 67-year-old man who underwent investigations that showed electrocardiographic signs of a previously undetected inferior myocardial infarction and a pansistolic murmur. Two-dimensional echocardiography and color flow Doppler showed: an inferobasal pseudoaneurysm, a ventricular septal defect (Fig 1), light mitral incompetence with normal subvalvular apparatus and normal tricuspid valve. Left ventriculography confirmed the septal defect and the inferobasal pseudoaneurysm (Fig 2). Coronary angiography showed only the occlusion of the proximal right coronary artery. Renal and liver function were normal.
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Fig 1. Transoesophageal echo that shows turbulent flow into the false channel connecting the left ventricle (LV) with the right ventricle (RV).
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Fig 2. Left ventriculagraphy that shows the inferobasal pseudoaneurysm and the simultaneous injection of the right ventricle and pulmonary artery.
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The patient underwent surgical repair 28 days after admission. Cardiopulmonary bypass was instituted and the heart arrested with crystalloid cardioplegia. The pseudoaneurysm, located on the inferior wall of the right ventricle, was opened on the right side of the posterior descending artery. Inside this fibrotic chamber, we found three perforations: one leading to the left ventricle and two small ones leading to the right ventricle. We closed only the first perforation with a Gore-Tex patch (W. L. Gore & Associates, Flagstaff, AZ) sutured on the left side with interrupted pledgetted stitches (Ethibond 2/0). The pseudoaneurysm was closed with running sutures (Prolene 3/0). The postoperative course was uneventful and the patient was discharged home on the fifth postoperative day.
Patient 2
The second patient was a 70-year-old woman who had an inferior myocardial infarction with postinfarction stable angina. The day after that, she developed a pansystolic murmur but no clinical signs of heart failure. Two-dimensional echocardiography, color flow Doppler, and left ventriculography revealed the same patterns as the previous case. Coronary angiography showed occlusion of the right coronary artery and a critical lesion on the anterior descending artery. Renal and liver function were normal.
The patient underwent the operation 32 days after myocardial infarction. The procedure was carried out as previously described but, in this case, we found two perforations (Fig 3). The first, connected with the left ventricle, was closed with four pledgetted stiches (Ethibond 2/0). We left the second, connected with the right ventricle, open. We also performed two grafts: on the anterior descending artery with mammary artery and on the first diagonal with saphenous vein. The postoperative course was uneventful and the patient was discharged home on the seventh postoperative day.
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Fig 3. The pseudoaneurysm is opened on the right side of the posterior descending artery and retracted. Inside is shown the fibrotic communication between this chamber and the left ventricle.
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Comment
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An intramyocardial dissecting hematoma is a rare complication of myocardial infarction [3]. It is generally associated with posterior ventricular septal defect [4] that, in this case, has an "entry port" and an "exit port."
In our patients, the septal defect was quite restrictive and, consequently, clinically well tolerated. The flow through the dissection led to a progressive enlargement of the dissecting chamber that evolved as a fibrotic pseudoaneurysm, bulging on the right side of the posterior descending artery.
Transesophageal echo, Doppler analysis, revealing turbulent flow in the false channel, and color Doppler imaging are the key to a correct diagnosis [5]. Left ventriculography, in these cases, showed an inferobasal pseudoaneurysm that, on the right anterior oblique projection, bulged posteriorly to the mitral annulus.
Daily clinical evaluation, to exclude any sign of hemodynamic deterioration, allows the surgeon to delay the operation until the healing process makes the tissues less fragile.
In this situation, it is enough to close the entry port leaving the chamber on the low pressure right side [6].
We believe that, in these cases, a correct diagnosis and daily clinical evaluation allow a simple operation with good postoperative recovery.
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References
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Loisance D.Y., Cachera J.P., Poulain H., Aubry P., Juvin A.M., Galey J.J. Ventricular septal defect after acute myocardial infarction. Early repair. J Thorac Cardiovasc Surg 1980;80:61-67.[Abstract]
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