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Ann Thorac Surg 1995;59:60-66
© 1995 The Society of Thoracic Surgeons

Anastomotic Pseudoaneurysm of the Ventricle After Homograft Placement in Children

Department of Cardiology and Division of Cardiac Surgery, Children's Hospital, and the Departments of Pediatrics and Surgery, Harvard Medical School, Boston, Massachusetts

Accepted for publication June 13, 1994.

	Abstract

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
A pseudoaneurysm of the right ventricle was diagnosed postoperatively in 8 patients between 1986 and 1992. One pseudoaneurysm formed after placement of a Carpentier-Edwards conduit and the other seven arose after placement of a homograft between the right ventricle and the pulmonary artery. Both aortic (n = 3) and pulmonary (n = 4) homografts had been used. In 6 patients, the homografts had been augmented proximally with Dacron, Gore-Tex, or pericardium. Pseudoaneurysms originated between the augmentation patch and the homograft in 4 patients, between the homograft or conduit and the myocardium in 3 patients (1 patient with and 2 without an augmentation patch), and between the patch and the myocardium in 1 patient. The prior operations performed were placement of a palliative conduit for tetralogy of Fallot with pulmonary atresia (n = 5), repair of truncus arteriosus (n = 2), and repair of absent pulmonary valve syndrome (n = 1). Pseudoaneurysms were discovered from 5 weeks to 4 years after the operation. Symptoms were present in 3 patients; in the others, diagnosis was made during follow-up on the basis of routine imaging studies. Symptoms, when present, were due to compression of surrounding mediastinal structures. Pseudoaneurysms ranged in diameter from 1.0 to 5.0 cm. Echocardiography and color-flow mapping reliably identified the pseudoaneurysm in the 6 patients in whom it was performed. Characteristic features included a well-defined, narrow aneurysm neck leading to an extracardiac echo-free space. Color-flow mapping demonstrated to-and-fro flow through the neck of the aneurysm. Right ventricular pressure was half the systemic pressure or less in 2 patients and was the same as or exceeded the systemic pressure in 6 patients. The pseudoaneurysm was surgically repaired in 7 patients; in the eighth patient, the neck of the pseudoaneurysm was closed with a double-umbrella, clamshell device in the catheterization laboratory. A pseudoaneurysm of the right ventricle forms infrequently after the placement of a homograft or conduit between the right ventricle and the pulmonary artery and is probably multifactorial in origin, though it is frequently associated with systemic right ventricular pressure. This defect can be diagnosed easily by echocardiography and successfully treated.

	Introduction

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
Pseudoaneurysms are a rare complication of cardiovascular surgical procedures. When present, they can be associated with catastrophic consequences, including rupture, infection, embolism, and compression of surrounding structures [1–4]. Incisional or anastomotic pseudoaneurysms most commonly arise after vascular bypass procedures. A number of variables are considered responsible, including elevated pressure at the anastomotic site, poor viability of the residual vessel bordering the graft, progressive vascular disease, infection, and the suture technique or material used, or both [5–8]. By comparison, relatively few cases of incisional anastomotic pseudoaneurysms involving the ventricle have been reported, and even fewer involving the right ventricle.

Right ventricular pseudoaneurysms usually develop after right ventriculotomy. In the few reports of right ventricular pseudoaneurysms, the most important causes suggested include systemic pressure in the right ventricle and the type of material used in the repair [9–14]. Most of the pseudoaneurysms described in the literature have occurred after right ventriculotomy and placement of a right ventricular outflow tract patch in patients with tetralogy of Fallot, although there are rare reports of pseudoaneurysms forming after a right ventriculotomy for placement of a conduit or homograft between the right ventricle and the pulmonary artery [11, 13].

We have identified incisional anastomotic pseudoaneurysm formation of the right ventricle in 8 children with congenital heart disease who had undergone right ventriculotomy. We describe our findings in these 8 patients, including their presenting symptoms, the nature of their evaluation, and their outcome.

	Material and Methods

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
We identified all patients with congenital heart disease who had undergone cardiac surgical procedures at this institution between 1986 and 1992 and in whom a pseudoaneurysm of the ventricle was diagnosed on the basis of the findings yielded by echocardiography, catheterization, or cardiac operation. Their medical records, including echocardiograms, electrocardiograms, catheterization data, and radiographs, were reviewed in detail. The surgical log was reviewed in an effort to quantitate the frequency of surgical procedures performed between 1984 and 1992 that involved a right ventriculotomy.

	Results

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
Patients
There were 8 patients during this 7-year period in whom a ventricular pseudoaneurysm developed postoperatively. The patient characteristics are summarized in Table 1. Patient ages at the time of pseudoaneurysm diagnosis ranged from 9 months to 9.5 years. The age at the initial operation which involved a right ventriculotomy ranged from 3 months to 8.5 years. In 6, a single right ventriculotomy had been performed before pseudoaneurysm formation; 2 patients had undergone two procedures each. Four of these patients had undergone closure of a ventricular septal defect at the time of homograft placement.

Clinical Findings
Symptoms of respiratory distress appeared in 2 patients and were due to compression of upper airway structures by the pseudoaneurysm. Another patient presented with respiratory distress, but there was also evidence of pneumonia as the cause of these symptoms and the finding of a pseudoaneurysm may have been incidental. The left diaphragm was also elevated in 1 of the 3 patients with respiratory symptoms, and this was probably due to phrenic nerve compression by the pseudoaneurysm. The other 5 patients were asymptomatic and the pseudoaneurysm was discovered during routine follow-up.

Catheterization
Cardiac catheterization was carried out in 7 patients. In 2, the catheterization was done for routine evaluation of hemodynamics and the pseudoaneurysm was discovered incidentally. In the other 5 patients, catheterization was performed specifically because of the finding of a pseudoaneurysm. In 1, this was done for therapeutic intervention. The other four studies were necessary because additional hemodynamic information as well as imaging of the distal pulmonary arteries were needed. One patient underwent repair based on the information yielded by the echocardiogram only. Hemodynamic data from catheterization or echocardiography, or both, revealed suprasystemic right ventricular pressure in 1 patient, systemic right ventricular pressure in 5 patients, and less than half the systemic right ventricular pressure in 2 patients. Cineangiograms were available for review in 5 patients. The neck of the pseudoaneurysm was imaged by cineangiography in 3 of these patients (Fig 1). None of the pseudoaneurysms contained obvious filling defects suggestive of thrombus. One patient had two defects, both of which were calcified.

View larger version (111K): [in this window] [in a new window]   Fig 1. . Angiographic appearance of a pseudoaneurysm in the anteroposterior (top) and lateral (bottom) projections. The narrow neck of the pseudoaneurysm originates between the homograft and the myocardium. Contrast agent is seen filling a large pseudoaneurysm that sits in the superior mediastinum.

View larger version (115K): [in this window] [in a new window]   Fig 2. . Echocardiographic appearance of a pseudoaneurysm in a high parasternal view. The arrow in the left panel points to the discrete deficiency in the endocardium. The panel on the right shows the pulsed-Doppler flow pattern produced when a cursor is placed at the point where the pseudoaneurysm communicates with the heart. The downward trace represents flow going from the defect into the heart during diastole and the upward trace represents flow going into the defect during systole. (RVOT = right ventricular outflow tract.)

View larger version (89K): [in this window] [in a new window]   Fig 3. . Chest radiograms from a patient with a pseudoaneurysm. The left panel shows the cardiac silhouette in the anteroposterior projection 5 months before a pseudoaneurysm was diagnosed. The right panel shows the change in contour seen at the time of pseudoaneurysm diagnosis. There is a new spherical shadow visible toward the right in the superior mediastinum.

Operative Findings
Seven of the pseudoaneurysms were directly inspected during repair. In 1 patient, the pseudoaneurysm was found to originate between the augmentation patch and the myocardium. In 3 patients, the pseudoaneurysm originated between the augmentation patch and the homograft, and, in 2, it originated between the homograft and the myocardium. One of these patients had received an augmentation patch and one had not. The patient with the Carpentier-Edwards conduit had two small defects that originated at the anastomosis of the conduit with the myocardium. In 5 patients, there was no clear cause of pseudoaneurysm formation. In 1 patient whose defect was between the homograft and the patch, the muscle had degraded at the proximal end of the homograft, leading to dehiscence of the anastomosis with the pericardial patch. In the seventh patient, there was obvious dehiscence of the suture line between the patch and the right ventricle. All pseudoaneurysms were clearly associated with a suture line and not due to defects in the myocardium surrounding the operative site.

Treatment and Outcome
Seven of the 8 patients underwent surgical repair of the pseudoaneurysm. Of these, 4 patients were placed on bypass after the midline sternotomy was made. Two patients were placed on peripheral bypass before the chest was opened. One patient underwent a midline sternotomy and cannulation of the right atrium, but, because the heart adhered to the anterior chest wall, the aorta could not be safely cannulated. Bypass was initiated after placement of the arterial cannula into the femoral artery. The heart was then dissected away from the chest wall. There was no incidence of injury to the pseudoaneurysm or cardiac structures while the chest was being opened. The neck of the defect was repaired with a small patch in 3 patients. In 1 patient, the wall of the pseudoaneurysm was resected and the neck of the defect was closed with sutures. In 2 patients who had considerable homograft obstruction, the stenotic homograft was incised, the pseudoaneurysm was resected, and then the homograft was augmented with a patch for its entire length. The patient with the Carpentier-Edwards conduit had the conduit removed and two small pseudoaneurysms resected. The right ventricular outflow tract was then roofed over with a Gore-Tex patch that encompassed the origins of the pseudoaneurysm. All 7 patients were hemodynamically well in the immediate postoperative period.

Three of these patients subsequently died. One patient died 8 months after the pseudoaneurysm repair from respiratory failure thought to be related to pneumonia. Another patient died 1 week after repair due to respiratory failure stemming from respiratory syncytial virus pneumonitis. The third patient died 8 months after repair during reoperation to replace a stenotic homograft and close the ventricular septal defect. This death was probably related to the patient's diminutive pulmonary arteries and residual aortopulmonary collateral flow. Four patients are in good health approximately 4 to 6 years after pseudoaneurysm repair.

The final patient underwent closure of the pseudoaneurysm neck with a 23-mm double-umbrella, clamshell device in the catheterization laboratory. The procedure was uncomplicated and he was discharged from the hospital within 48 hours. Echocardiographic evaluation 1 year after the procedure confirmed that the clamshell device is in a good position and that there is no evidence of a residual pseudoaneurysm. Chest radiography now shows a normal cardiac contour.

	Comment

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
Presentation
Pseudoaneurysms and true aneurysms are an unusual complication of cardiac surgical procedures done for the treatment of congenital heart disease. Both lesions can arise in patients who have undergone a right ventricular outflow tract procedure. Aneurysms are the more frequent lesion but pseudoaneurysms are more worrisome, in that they are the result of a small disruption in the wall of a vessel or cardiac chamber that allows blood to leak into the surrounding space. The walls of these defects are composed of fibrin and pericardium, and by definition contain no myocardial elements [4]. Conversely, true aneurysms contain all the elements of the myocardial wall, or of the homograft or patch material at the aneurysm site, or both, which may make them much stronger than pseudoaneurysms. Aneurysms usually have a wide entry from the ventricle into the defect, as opposed to the narrow neck of the pseudoaneurysm. These distinctions should make it relatively easy to tell them apart with imaging techniques. The indications for repairing a true aneurysm depend on its location. In patients with a true aneurysm that has formed after repair of the right ventricular outflow tract, aneurysm repair can often be delayed because the defect is usually asymptomatic. Symptoms rarely occur due to compression of local structures, embolism, or thrombus, and are very rarely due to rupture.

Pseudoaneurysms can become symptomatic through the working of a number of mechanisms. These are thin-walled structures and, therefore, are much more likely to rupture than a true aneurysm. None of the pseudoaneurysms in our patients ruptured, but treatment was implemented soon after their discovery. The pseudoaneurysm can become quite large and produce symptoms due to a mass effect, as was evident in 3 of our patients. As expected, these symptoms were related to the compression of structures near the pseudoaneurysm, such as the large airways and the phrenic nerve. Finally, the pseudoaneurysm can be a source of emboli. There was no evidence of embolic phenomena in this series of patients; however, none of them underwent a rigorous search for pulmonary embolism beyond a chest radiograph.

Etiology
The data presented in this report suggest that the pathogenesis of pseudoaneurysms is likely to be a multifactorial process. In previous reports, authors have suggested that the formation of right-sided pseudoaneurysms is related to elevated right ventricular pressure [9–14]. The initial reports involved children with tetralogy of Fallot who had undergone right ventriculotomy and who, at the time of pseudoaneurysm discovery, had near-systemic right ventricular pressure [9, 10, 12, 14]. Four patients similar to those described here have been described; all had pseudoaneurysms at the proximal end of a homograft [11, 13]. These patients also had elevated right ventricular pressure. Most of the patients in our report had approximately systemic right ventricular pressure, supporting the implication that the mechanical stress created by systemic pressure at the proximal homograft suture line is likely to be an important factor contributing to the formation of pseudoaneurysms, although it does not appear to be a necessary condition.

Other factors implicated in the etiology of incisional pseudoaneurysms are the suture technique [2, 13, 15, 16], the suture material [6, 7], local infection leading to the degradation of sutures [12, 14], and devitalization of surrounding myocardium leading to defects in the myocardium adjacent to the suture line [12, 14]. None of these factors were identified consistently in the 8 patients described here. There was not enough information about the suture material used to allow us to evaluate this variable; however, direct inspection during repair of the pseudoaneurysm revealed no instance of suture degradation or unraveling of a suture line. Infection appears to be an unlikely explanation, in that none of the patients appeared to have an infection at the homograft site and there were no positive culture results in the perioperative period. All aneurysms were associated with a suture line and no defects were found in the adjacent myocardium.

Type and Location of Homograft
The most consistent finding in the patients in this series was that all pseudoaneurysms occurred at the proximal end of a homograft or conduit placed between the right ventricle and the pulmonary artery, and none arose after any other procedure involving right ventriculotomy. In this series, patients with homografts seemed to be at a slightly greater risk of pseudoaneurysm formation than did patients with conduits. In the period between 1984 and 1992, pseudoaneurysms developed in 6 of approximately 375 patients who received homografts (1 of the patients described here was initially operated on elsewhere). Possible contributing factors include the type of homograft used or the placement of an augmentation patch at the proximal end of the homograft. A recent study in animals has shown that there is a high incidence of pseudoaneurysm and aneurysm formation associated with the placement of pulmonary homografts into the systemic circulation [17]. This study revealed that there were significantly more pseudoaneurysms associated with pulmonary homografts then with aortic homografts. It also showed that the suture line between the Dacron patch augmentation and the homograft was more vulnerable to pseudoaneurysm formation than was the suture line between the Dacron patch and the aorta. In our series, there were patients with both pulmonary and aortic homografts as well as three types of augmentation patch and there was 1 patient without an augmentation patch. The type of homograft did not seem to be a factor consistently associated with pseudoaneurysm formation, but, given that about two-thirds of the homografts used during this time were aortic homografts, pseudoaneurysms developed in association with a higher percentage of pulmonary homografts than of aortic homografts. Pseudoaneurysms tended to form between the augmentation patch and the homograft when there was a patch, supporting the idea that mechanical stress is greater at this suture line than at the suture line between the patch and the myocardium.

In at least 1 patient, the subvalvar muscle of the homograft had degraded, leading to dehiscence. Degradation of the homograft itself has been reported before, but the methods of preserving the homografts at that time differed from those used in the current era [11]. This may explain why pseudoaneurysms form in some patients and why these defects were more often associated with homografts than with conduits or right ventricular outflow tract patches. Though it is unclear how much degradation of the muscle contributes to this phenomenon, we do believe that, when placing sutures into the homograft from either the myocardium or an augmentation patch, these sutures should be placed into the fibrous tissue of the valve (ie, the ventricular-arterial junction) and not only into the subvalvar muscle of the homograft.

Choosing between a homograft and other prosthetic or biologic materials in a given case involves multiple considerations, including the ease of handling, the likelihood of creating distortion at the distal anastomosis (particularly in patients with diminutive pulmonary arteries), the risk for compression of coronary vessels by prosthetic valve rings, and the availability of various sizes of conduits. A detailed discussion of this topic is beyond the scope of this manuscript, but we currently believe that, in most cases, the advantages of the homograft seem to outweigh the disadvantage of pseudoaneurysm formation, with its low incidence.

Detection
A chest radiogram should probably be the first step in the evaluation of these patients. Our 8 patients had no consistent laboratory or physical findings, but all had some abnormality on the chest x-ray study (see Fig 3). Two patients did not have evidence of a pseudoaneurysm on chest x-ray films until years after their initial surgery. It may be that in at least 1 patient the defect was too small to sufficiently change the cardiac silhouette to allow detection, but, as the pseudoaneurysm calcified, it became obvious on a radiogram. In the other patient, it may be that the defect did not occur until late or that the defect arose early but did not get large enough to change the cardiac silhouette until later. Further evaluation needs to be tailored to the individual situation but can be done with echocardiography [18–23] or cineangiography [14, 15, 24, 25], or both methods.

Two-dimensional echocardiography was very reliable in the detection and evaluation of these defects in our patients. The hallmark of a pseudoaneurysm is the sharp disruption of the endocardium at the defect origin, with a narrow communication between the pseudoaneurysm and the ventricle [4, 20, 24, 25]. Imaging this narrow communication has been the most reliable way to distinguish a pseudoaneurysm from a true aneurysm. As these two lesions have very different prognoses, this differentiation is crucial. In our experience, echocardiography reliably defined the pseudoaneurysm as well as the narrow communication with the ventricle (see Fig 2). Further, color-flow mapping can be used to document the continuity between the structures [21]. In our patients, color-flow mapping demonstrated flow into the pseudoaneurysm during systole and out of the pseudoaneurysm during diastole. The defect size and location and the degree of compression of other cardiac structures were easily delineated.

Cineangiography can be used for imaging these defects, although the narrow neck of the pseudoaneurysm can be difficult to image because of the superimposition of the cardiac silhouette on the defect [22, 23]. Furthermore, as shown in 1 of our patients, catheterization offers an alternative way to repair the defect through the use of a double-umbrella device, thereby obviating repeat sternotomy and cardiopulmonary bypass.

Treatment
Treatment of the pseudoaneurysm was successful in all 8 patients, although 1 patient died in the immediate postoperative period from respiratory syncytial virus. Because of the risk of catastrophic complications, intervention is necessary and should not be unduly delayed. The experience in this series suggests that this can be done safely in the operating room or, in some cases, in the catheterization laboratory with low morbidity and mortality. When repairing the defect surgically, special attention needs to be given to the approach used to perform the bypass procedure. Although a midline sternotomy can be safe in these patients, femoral bypass should be considered when echocardiography or angiography shows the homograft or conduit, or the pseudoaneurysm adheres to the back of the sternum. Often the pseudoaneurysm is not in the midline because of lack of space, but is off to the right or left of the sternum. However, the location should be well delineated before the chest is opened so that this thin-walled structure is not entered. Although experience with the clamshell device closure of pseudoaneurysms is limited, this approach has been successful to date. It is a technique that may be considered when available, if the patient has an uncomplicated defect, weighs more then 10 kg, and has no associated hemodynamic problems that need to be addressed surgically. In this situation, it offers an effective and less costly alternative.

	Footnotes

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
Address reprint requests to Dr Mayer, Division of Cardiovascular Surgery, Children's Hospital, 300 Longwood Ave, Boston, MA 02115.

	References

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 

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This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Levine, J. C. Articles by Sanders, S. P. Search for Related Content PubMed PubMed Citation Articles by Levine, J. C. Articles by Sanders, S. P.