Ann Thorac Surg 2005;79:701-703
© 2005 The Society of Thoracic Surgeons
Case report
Postinfarction Ventricular Septal Defect With Pseudoaneurysm Repair After Failed Percutaneous Closure
Subroto Paul, MDa,
Tomislav Mihaljevic, MD*,b,
Marzia Leacche, MDa,b,
Michael Landzberg, MDa,b,
Carolyn Y. Ho, MDa,b,
Gavin J. Blake, MDa,b,
John G. Byrne, MDa,b
a Department of Surgery, Boston, Massachusetts, USA
b Division of Cardiac Surgery, Department of Medicine, Division of Cardiovascular Medicine, Brigham and Women's Hospital, and Department of Cardiology, Boston Adult Congenital Heart Service, Children's Hospital, Boston, Massachusetts, USA
Accepted for publication August 28, 2003.
* Address reprint requests to Dr Mihaljevic, Brigham and Women's Hospital, Division of Cardiac Surgery, 75 Francis St, Boston, MA 02115, USA
tmihaljevic{at}partners.org
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Abstract
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Ventricular septal defect with intramyocardial dissection of the ventricular free wall is a rare complication of myocardial infarction associated with poor prognosis. We describe a patient who developed a ventricular septal defect with intramyocardial dissection of the right ventricular free wall. Initially the patient was successfully stabilized by the placement of a percutaneous closure device. The placement of the device allowed initial hemodynamic recovery of the patient and subsequent definitive surgical repair. This case illustrates the importance of collaboration between interventional cardiologists and cardiac surgeons in the treatment of complex postinfarction ventricular septal defects.
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Introduction
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A ventricular septal defect is a known serious mechanical complication of myocardial infarction. A VSD with intramyocardial dissection through the formation of a complex dissection tract connecting the right and left ventricles is a rare complication of inferior myocardial infarction with a poor prognosis despite urgent operative repair [1]. We describe a patient who developed a VSD with intramyocardial dissection of the right ventricular (RV) free wall. The patient was initially treated with percutaneous closure of the VSD, and he was stabilized before definitive operative repair. This case illustrates the advantage of a combined interventional and surgical approach in the treatment of this complex postinfarction VSD, which would otherwise be a fatal complication of myocardial infarction.
We report a 63-year-old male patient with coronary artery disease who had undergone coronary artery bypass grafting in 1993. The patient presented to the hospital with increasing shortness of breath approximately 5 weeks after sustaining an inferior wall myocardial infarction treated with medical therapy. The patient was hemodynamically stable with a heart rate of 90 beats per minute and a systolic blood pressure of 100 mm Hg with a systolic murmur. On admission, electrocardiogram showed inferior Q waves with persistent segment elevations. Transthoracic echocardiography (TTE) revealed a hypokinetic inferior wall with an ejection fraction of 25%. Transthoracic echocardiography also demonstrated a VSD with communication between the ventricles through a defect in the RV free wall, which was thought to be RV free wall dissection and consequent pooled blood. A gradient between 25 mm Hg and 42 mm Hg was measured between the defect and the pooled blood within the dissection plane of the RV myocardium. Cardiac catheterization showed severe native three-vessel disease, a patent left internal mammary artery to the left anterior descending coronary artery bypass, and occlusion of three of the four saphenous vein grafts. Left ventriculography also confirmed the presence of the VSD suspected on TTE with an increase in oxygen saturation from 48% O2 saturation in the superior vena cava to 73% O2 saturation in the right ventricle. The VSD was found to communicate with a right ventricular pseudoaneurysm with pooled blood created by the RV wall dissection. A thrombotic left circumflex lesion was then stented. The VSD was treated by the deployment of a percutaneous closure device (STARFish [NMT Medical, Boston, MA]) with marked improvement of the patient's New York Heart Association functional class III heart failure symptoms.
Follow-up transthoracic echocardiography and computed tomographic angiography showed a significant residual VSD (Fig 1). The VSD was followed by transthoracic echocardiography and appeared to have an increasing gradient with time. Repeat deployment of an additional percutaneous device failed to resolve the VSD. Given the failure of repeated percutaneous treatment and the documented ongoing impact of the VSD, the decision was made to proceed with surgical repair. The patient was taken to the operating room and cardiopulmonary bypass was initiated. A redo sternotomy was performed. The patient was subsequently cooled to 22°C and the heart was allowed to fibrillate. The diaphragmatic portion of the right ventricle was sharply dissected. There was no evidence of contained rupture with the RV wall intact. The STARFlex device (NMT Medical) was palpable in the inferior aspect of the RV wall. The anterior layer of the right ventricle was incised at the diaphragmatic surface and the VSD was exposed. The area of the dissection of the RV wall formed a pseudoaneurysm containing a moderate amount of blood (3 mm thick) and one of the STARFlex devices (NMT Medical). Visualization of the left ventricular cavity and the partial ventricular septal defect was possible through the incision without entering the RV cavity. The second device had been placed into the area of communication between the left ventricle and the RV free wall dissection with a rim of necrotic myocardium surrounding the device. The devices were removed, the necrotic myocardium was debrided, and the VSD was repaired with a Dacron patch (Hemashield Finesse, Boston Scientific, Boston, MA) using 2-0 Ethibond sutures (Ethicon, Somerville, NJ). The patch was then oversewn with felt strips. Intraoperative transesophageal echocardiogram showed no residual communication between the left and right ventricle. Hemostasis was achieved, cardiopulmonary bypass was weaned, the patient was decannulated, and the chest was closed. The patient was taken to the intensive care unit in stable condition and was eventually discharged to rehabilitation. On follow up the patient was clinically stable with a transthoracic echocardiogram demonstrating no residual VSD with an ejection fraction of 25%.
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Fig 1. Computed tomographic angiography showing ventricular septal defect with communication through right ventricular wall dissection and resulting pseudoaneurysm. Arrow = ventricular septal defect; * = right ventricular wall pseudoaneurysm; ** = STARFish device (NMT Medical, Boston, MA). (LV = left ventricle; RV= right ventricle.)
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Comment
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Intramyocardial dissection of the RV wall through a septal VSD is an uncommon complication of inferoposterior wall infarction associated with a poor prognosis. It is characterized by right and left ventricular communication through a VSD originating through an area of necrotic septum and through a channel of blood formed by RV free wall dissection [1].
In our report, we describe a 63-year-old man who had RV wall intramyocardial dissection develop after an inferoposterior myocardial infarction. The novel approach in the treatment of this difficult clinical problem is represented by staged percutaneous and surgical therapy. Percutaneous closure of VSDs have been described in the literature for postinfarction VSDs [2], but never in a patient with a VSD complicated with an intramyocardial dissection of the ventricular wall. The decision to initially treat the patient with a percutaneous approach was dictated by his poor clinical condition and favorable intracardiac pathology. Operative repair of VSDs has been associated with a 30-day mortality of 20% to 40% [1]. Preoperative cardiogenic shock and early postinfarction septal rupture has been shown to be associated with poor prognosis, as was the case with our patient [1]. Our patient would have poorly tolerated emergent reoperative coronary revascularization and VSD closure because of his longstanding history of coronary artery disease, prior coronary artery bypass grafting, poor ventricular function, and presentation to us in florid congestive heart failure. The percutaneous intervention with stenting of the circumflex artery and VSD closure allowed improvement of heart failure symptoms, thereby allowing for optimal chances of a successful surgical outcome. The persistence of VSD flow with peri-device leak and reestablishment of left to right shunting can be viewed as intrinsic limitation of the percutaneous approach. Postinfarction VSD is a dynamic lesion that enlarges over time due to the progressive necrosis around the site of infarction. The initially small defect, which usually requires the placement of a single device, can enlarge over time and result in residual defects. Staged surgical repair, which includes the debridement of all necrotic myocardium, eliminates this problem.
The unique morphology of this VSD that allowed repair with only one patch through the RV free wall is that infarction of only septal tissue without RV injury caused only one defect. Previous reports describe repairs involving the resection of the right and left ventricular walls using multiple patches.
The use of computed tomographic angiography in preoperative workup complements the standard imaging techniques (ie, echocardiography and cardiac catheterization) in providing essential information regarding anatomical relationships of the postinfarction VSD. The thorough understanding of the anatomy of the defect allowed conduction of the simplest and most efficient operative repair [1, 3, 4].
In conclusion, we present a patient with postinfarction VSD with intramyocardial dissection of the RV free wall who was successfully treated by a staged approach that included coronary stenting and percutaneous VSD closure followed by delayed definitive operative closure. This report illustrates the growing importance of "hybrid" procedures and the continued interplay between cardiologists and cardiac surgeons.
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References
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- Tighe DA, et al. Survival in infarct related intramyocardial dissection: importance of early echocardiography and prompt surgery. Echocardiography. 1997;14(4):403–408[Medline]
- Pienvichit P, Piemonte TC. Percutaneous closure of postmyocardial infarction ventricular septal defect with the CardioSEAL septal occluder implant. Catheter Cardiovasc Interv. 2001;54(4):490–494[Medline]
- Edwards BS, Edwards WD, Edwards JE. Ventricular septal rupture complicating acute myocardial infarction: identification of simple and complex types in 53 autopsied hearts. Am J Cardiol. 1984;54:1201–1205[Medline]
- Fayad ZA, et al. Computed tomography and magnetic resonance imaging for noninvasive coronary angiography and plaque imaging: current and potential future concepts. Circulation. 2002;106:2026–2034[Free Full Text]
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Abstract
Introduction
