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Ann Thorac Surg 1996;62:1276-1282
© 1996 The Society of Thoracic Surgeons
Divisions of Cardiothoracic Surgery and Pediatric Cardiology, University of California, San Francisco, San Francisco, California
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Abstract |
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Methods. Between October 1992 and October 1995, 7 patients presented 8 to 20 years after atriopulmonary connection with severe right atrial dilatation (7), Fontan pathway obstruction (4), progressive congestive heart failure (4), atrial tachydysrhythmias (3), right atrial thrombus (1), obstruction of right pulmonary veins by an enlarged right atrium (1), and subaortic stenosis (1). After evaluation of the options, they underwent revision of the atriopulmonary connection to extracardiac (5) or intraatrial (2) conduit cavopulmonary anastomosis.
Results. One patient with severe cachexia, in whom transplantation was contraindicated for social reasons, died in the early postoperative period of massive effusions. Two patients eventually required permanent pacing for atrial dysrhythmias (1) or complete heart block secondary to subaortic fibromuscular resection (1), and 2 demonstrated marked improvement in unstable preoperative rhythm disturbances. At a median follow-up of 17 months, 4 of the 6 survivors were functioning at higher New York Heart Association levels than preoperatively, and 1 had recently undergone heart transplantation.
Conclusions. In properly selected patients with atrial complications, revision of a prior Fontan connection to extracardiac or intraatrial conduit cavopulmonary anastomosis appears to be a viable option.
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Introduction |
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Since Fontan and Baudet [1] described their technique for correction of tricuspid atresia in 1971, the Fontan or modified Fontan physiology has become a favored reparative end point for nearly all forms of functional single ventricle. Though early and late survival rates have been improving over time, patients undergoing any of the various modifications of the Fontan operation are still subject to substantial postoperative morbidity and mortality [2, 3]. In many cases, sequelae appear to be related at least in part to the incorporation of the right atrium (RA) into the Fontan circuit: namely, RA dilatation, right pulmonary vein obstruction, thromboembolism, and supraventricular dysrhythmias [2–6]. Obstruction at the atriopulmonary connection and hepatic failure also can occur. It is thought that the modification introduced by de Leval and associates [7], according to which caval blood is routed into the pulmonary artery (PA) without incorporating the RA, will alleviate some of these common complications by reducing the turbulence of central venous flow [8, 9].
When patients with atriopulmonary Fontan connections decline in functional status, the cause must be determined. Irreversible ventricular systolic dysfunction with or without diastolic dysfunction and elevated pulmonary vascular resistance cannot be reversed without transplantation. However, other causes can, at least in theory, be reversed with operative revision. Because these patients often have complex conditions and are physiologically fragile, with chronic effusions and cachexia, the physiologic efficacy of revision is unproven, as is the ability of these patients to tolerate the procedure acutely without excessive morbidity and mortality. To complicate the issue further, ventricular dysfunction may be related to elevated coronary sinus pressure [10], which can be secondary to Fontan obstruction or right pulmonary venous obstruction, and as a result there may be a component of reversibility in such circumstances.
In this report, we present our experience with patients who underwent revision of their atriopulmonary-type Fontan connection to either extracardiac or intraatrial conduit cavopulmonary anastomosis and discuss the indications for and implications of revising atriopulmonary to total cavopulmonary connection.
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) [11]. Originally, these patients had undergone either placement of valved RA to PA conduits (n = 5), direct RA-PA anastomosis (n = 1), or anastomosis of the right atrial appendage to the right ventricle (RA-RV; n = 1). All patients had done well after their original Fontan procedure except for patient 2 (see later). Of the 5 patients with RA-PA conduits, 2 (patients 4 and 6) had their valved conduits replaced with valveless synthetic tubes 9.2 and 10.0 years before revision, and 1 (patient 2) had a conduit placed between his left and right PAs 9.4 years before revision. Preoperative status of the patients and indications for revision are summarized in Table 2; hemodynamic and oximetric data are presented in Table 3.
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Patient 2 presented with extreme Fontan failure. He had never done well after his original Fontan operation, having undergone early implantation of a permanent bipolar epicardial pacemaker and experiencing progressive congestive heart failure. Seven years after atriopulmonary anastomosis, he experienced a pulmonary embolic event, and several months before revision, his failure began to increase in severity, with progressive ascites, worsening inguinal hernias, bilateral effusions, protein-losing enteropathy, and hepatic dysfunction. In addition, a massive thrombus filled most of his RA and extended into his conduits. However, there was no obstruction; his RA and PA pressures were equal because of extensive collaterals draining into the coronary sinus. A preferable therapeutic option would have been orthotopic heart transplantation, but social factors precluded this, so Fontan revision was offered as a last resort after drainage of his ascites.
Patient 3 presented in New York Heart Association class II. Routine echocardiography had shown a huge RA, with poor forward flow and a question of mural thrombus. Fontan obstruction was also present with a gradient of 3 mm Hg. Preoperative evaluation had also demonstrated a reasonably sized RV, as well as potentially functional valve leaflets beneath the tricuspid patch that had been a component of his original Fontan procedure. On the basis of his RA dilatation and the possibility of mural thrombus, operative reintervention was recommended. There was some hope that his right-sided anatomy would be suitable for one-and-a-half ventricle repair. Intraoperatively, however, it was determined that such a solution would probably not work well, and Fontan revision to extracardiac cavopulmonary anastomosis was completed.
Patient 4 demonstrated bulboventricular foramen obstruction with a peak systolic gradient of 40 mm Hg, and was asymptomatic and without appreciable Fontan-related compromise. However, her RA was markedly dilated, with a 3 mm Hg RA to PA gradient. Because subaortic resection was necessary and Fontan pathway obstruction was present, we decided it would be logical to revise her Fontan at the same time to preempt the development of atrial dysrhythmias or the potential need for later Fontan-related reinterventions.
Patient 5 presented with pronounced obstruction of her RA-RV anastomosis (RA-PA gradient, 11 mm Hg) and declining functional status. Her RA was severely enlarged, but she had no rhythm disturbances or evidence of thrombus. Preoperatively, catheter balloon dilatation of her stenotic RA-RV anastomosis was unsuccessful, and it was decided that conversion to extracardiac conduit total cavopulmonary anastomosis was preferable to simple revision of the conduit obstruction.
Patient 6 was in progressive heart failure and had recently developed unstable atrial arrhythmias that were unresponsive to flecainide and required electrical cardioversion. Her systolic cardiac function was adequate, but the VEDP was elevated to 13 mm Hg and there was mild mitral valve insufficiency. Her RA was extremely dilated, with a 6 mm Hg gradient across her proximal right PA. We elected to revise her Fontan and reconstruct her stenotic PA.
Patient 7 presented with a severely dilated RA that was extending posteriorly and compressing both the upper and lower right pulmonary veins. This probably contributed to the calculated elevation in her pulmonary vascular resistance to 4.7 Wood units. Her inferior vena cava was also markedly dilated, and echocardiography results suggested a thrombus in the RA. She had previously had a permanent pacemaker placed for sinus bradycardia, but she also experienced atrial tachydysrhythmias. Her cardiac output was poor despite borderline normal ventricular function, and she had very low exercise tolerance, marked ascites, and mild mitral regurgitation. Revision to extracardiac conduit Fontan was elected.
Operative Procedure
Because of adhesions from multiple previous operations, the dissection can be difficult and often tedious in these patients. In 1 patient, it was necessary to initiate cardiopulmonary bypass through femorofemoral cannulation, though in the remaining patients we were able to dissect completely the aorta and both cavae and begin bypass using standard aortic and caval cannulation. In patients who are particularly fragile, it may be wise to expose the groin vessels before attempting to dissect the mediastinum, so that femorofemoral bypass can be initiated if necessary.
Because the morphology of the patients' lesions and their surgically altered anatomy differed considerably, there was some variation in the technique of Fontan revision and additional procedures performed. All patients had their previous atriopulmonary or modified atriopulmonary connections taken down and replaced with extracardiac or intraatrial conduit total cavopulmonary anastomoses.
In 5 patients (patients 2, 3, 5, 6, and 7), extracardiac conduit total cavopulmonary anastomosis was performed [12]. A bidirectional superior cavopulmonary shunt was performed, with transection of the superior vena cava, oversewing of the cardiac stump, and end to side anastomosis of the cranial end to the right PA. The inferior vena cava was transected at its junction with the RA, and the cardiac end was oversewn. The inferior vena cava was anastomosed to an expanded polytetrafluoroethylene conduit (range, 20 to 25 mm in diameter), which was connected end-to-side with the underside of the right PA, completing the extracardiac conduit Fontan. Reduction of the RA was performed in 4 of these patients (patients 2, 3, 5, and 7), as was atrial septectomy (patients 2, 3, 6, and 7). Reconstruction of the PA was carried out in 3 of these patients (patients 2, 6, and 7), and 1 patient (patient 2) underwent RA thrombectomy, left superior vena cava ligation, and pacemaker replacement. None of these patients had right to left atrial level "pop-off" shunts included.
Extracardiac conduit revision was our preferred policy. In 2 patients (patients 1 and 4), however, after the appropriate structures were dissected, it was determined that RA dimensions and mobility were not amenable to the creation of a suitable channel for the extracardiac conduit, and intraatrial conduit Fontan was performed instead. Superior cavopulmonary anastomosis was performed in the same manner as with extracardiac cavopulmonary anastomosis. Through a right atriotomy, a valveless 22-mm expanded polytetrafluoroethylene tube was sewn to the inferior cavoatrial junction, carried up through the RA appendage, and anastomosed at the point of previous atriopulmonary connection. In patient 4, the cavopulmonary anastomoses were not directly end to side, but slightly anterior, with an expanded polytetrafluoroethylene hood carried over the anterior aspect of the connection to enlarge the junction. Both of these patients had 5-mm conduit fenestrations placed, 1 (patient 1) because of a high preoperative Fontan pressure and transpulmonary gradient, and the other (patient 4, in whom ventricular muscle resection was performed to enlarge the bulboventricular foramen) because of concerns about early postoperative rhythm disturbances and ventricular dysfunction. In addition, atrial septectomy was performed in both of these patients, and RA reduction was done in patient 1. In patient 4, the bulboventricular foramen was enlarged in accordance with the known location of the conduction axis, with resection of a wedge of tissue from the apical trabecular septum by incising close to the obtuse margin of the ventricular mass.
Total perfusion time ranged from 82 to 320 minutes (mean, 228 minutes). In addition, 4 patients required aortic cross-clamping (mean, 87.7 minutes; range, 61 to 132 minutes) and cold crystalloid cardioplegia administration. All patients were maintained on coumadin for at least 3 months postoperatively.
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Results |
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All 6 of the remaining patients required postoperative mechanical ventilation (median, 10 hours; range, 7 to 17 hours) and inotropic support (median, 2 days; range, 1 to 4 days). They were discharged from the hospital at a median of 21 days after operation (range, 6 to 23 days). In 2 survivors (patients 3 and 6), effusions developed that required chest tube drainage for 12 and 21 days, respectively. In patient 3, who had no preoperative rhythm disturbances, early atrial flutter/fibrillation developed. Patient 4 suffered complete heart block as a result of bulboventricular foramen resection. Two patients underwent early reoperation: patient 2, as discussed earlier, and patient 4, who had a permanent dual-chambered epicardial pacemaker placed on postoperative day 8, along with debridement of her thumb secondary to extravasation during transfusion and subsequent cellulitis. None of the patients demonstrated RA thrombi by echocardiographic analysis or suffered clinically evident thromboembolic events.
In Table 3
, variables relating to postoperative hemodynamic and oxygenation status are presented, along with comparable preoperative values. Mean systemic arterial partial pressure of oxygen increased for the group as a whole. However, in 2 patients with fenestrations in the conduit, the postrevision systemic arterial partial pressure of oxygen was lower. For both PA pressure (PAP) and VEDP, there was a clear division between patients with higher preoperative pressures (n = 3; ranges: PAP, 19 to 22 mm Hg; VEDP, 10 to 13 mm Hg) and lower preoperative pressures (n = 4; ranges: PAP, 5 to 9 mm Hg; VEDP, 2 to 5 mm Hg). Pressures in the former group were lower after revision. All patients with low prerevision PAP had some degree of Fontan pathway obstruction with RA-PA gradient. Once this obstruction was relieved, the postrevision PAP increased in these patients.
Follow-up
Follow-up was obtained at a median of 17 months postoperatively (range, 3 to 24 months) for the 6 hospital survivors. Selected follow-up data are presented in Table 4. There had been no late deaths at the time of follow-up. Two patients had undergone late reoperation: Patient 1 had her Fontan fenestration closed 19 months after revision, and patient 3 had a permanent unipolar ventricular epicardial pacemaker placed 8 months postoperatively and underwent heart transplantation 18 months after Fontan revision. Relative to their prerevision New York Heart Association classification status, 4 patients had improved, 1 was unchanged, and 1 had deteriorated (Fig 1). All 6 patients were taking cardiac medications. Four patients, including the 2 with intraatrial conduits (patients 1 and 4), were taking coumadin as part of their medical regimen. Five patients were taking antiarrhythmia drugs, 3 of whom (patients 3, 4, 5) had had no preoperative rhythm disturbances. Two patients (patients 1 and 6) with prerevision arrhythmias were improved or stabilized in this respect at the time of follow-up. All surviving patients had discharge echocardiograms performed, and 5 patients had had recent follow-up echocardiograms performed, 3 to 23 months (median, 19 months) after revision. Of these, 1 patient (patient 1) demonstrated an improvement in ventricular function relative to her prerevision state, along with a decrease in tricuspid valve regurgitation from mild to none, whereas 2 patients (patients 5 and 7) with normal preoperative ventricular function were unchanged in that respect after revision. Patient 4 experienced a decline in ventricular function from normal to mildly depressed after suffering complete heart block following bulboventricular foramen enlargement. Patient 3, who had normal preoperative ventricular function, remained stable, with fair to normal cardiac function, for almost a year after revision to total cavopulmonary connection. However, he had progressive deterioration by 17 months after revision and development of a severely dilated ventricle with an ejection fraction of 0.18. At the most recent follow-up, 18 months postoperatively, he was 2 weeks out from a successful cardiac transplantation. Only 1 patient has undergone cardiac catheterization since the Fontan revision.
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Comment |
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A third option in selected Fontan patients with deteriorating functional status is revision to a total cavopulmonary anastomosis [16]. Specific indications for this approach are not clearly defined; however, patients in whom a specific complication or condition is directly addressed by the procedure are the most obvious candidates. Examples include a giant atrium with thrombus, arrhythmias refractory to medical or electrophysiologic treatment, or pulmonary venous obstruction, and possibly patients with ventricular dysfunction secondary to elevated coronary sinus pressure. Other conditions, such as obstruction of the atriopulmonary connection, restrictive bulboventricular foramen, atrioventricular valve regurgitation, and others can be treated operatively, but do not per se require conversion to a cavopulmonary connection. Such patients may benefit from the improved hemodynamic status of the cavopulmonary connection performed at the time of the operation for the specific lesion. We have performed a cavopulmonary conversion on patients in both of these general categories: Patients 1, 6, and 7 had conditions that could best be addressed by revision of the Fontan connection to total cavopulmonary anastomosis; in patients 3, 4, and 5, cavopulmonary revision was performed as a supplementary procedure.
The most questionable indication for revision involves the patient with deteriorating functional status who has no specific target conditions; for example, the patient who is functionally very limited and has moderately elevated pulmonary vascular resistance, moderately depressed ventricular function, a large RA without specific complications, and no obstructive lesions. The improvement gained by conversion to a cavopulmonary connection might well be outweighed by the risks of the procedure itself. In our series, patient 2 fell into this category, and he represented the only death among our 7 patients.
In patients 3, 4, and 5, Fontan revision was performed as a supplementary procedure. Complications arose in 2 of these patients after revision. Patient 4 required early implantation of a permanent pacemaker for complete heart block, and is also taking rhythm medications. However, these complications resulted not from Fontan revision per se, but from bulboventricular foramen enlargement. Though the location of the atrioventricular conduction bundle in {S,L,L} hearts is well understood, it is sometimes difficult to avoid injury to the conduction system in these circumstances. The bundle is intrinsically fragile in {S,L,L} hearts, a fact that can be compounded by the need to resect a large wedge of tissue in more severely obstructed cases and by the considerable manipulation required to expose the bulboventricular foramen through the hypoplastic chamber. Otherwise, the functional status of patient 4 was unchanged from the preoperative status. It should be noted that she probably would not have undergone revision to cavopulmonary anastomosis at the time she did had it not been for her subaortic stenosis. Patient 3 continued to have arrhythmias that required medication and eventually permanent pacing, and deteriorated from New York Heart Association class II preoperatively to class IV at a follow-up of 17 months. One month later (18 months after Fontan revision), he underwent successful cardiac transplantation. He, along with 3 of the other patients, underwent extensive RA resection at the time of revision. This may have influenced the development of postoperative atrial flutter, although the 1 other patient who had RA resection but no preoperative atrial dysrhythmias remained in normal sinus rhythm perioperatively and at follow-up. Patient 5 had severe Fontan conduit obstruction. Although in theory a simple conduit change could have been performed, we elected to revise her Fontan. This patient had a good functional result, but paroxysmal atrial tachycardia developed after operation. This was controlled with antiarrhythmia medication, and there has been no recurrence.
The indications for revision in the remaining 3 patients-patients 1, 6, and 7-were clear: worsening or unstable arrhythmias with or without conduit obstruction with RA dilatation and increasing systemic congestion, along with PA hypoplasia in 1 patient and compression of the right pulmonary veins by the enlarged RA in another. Postoperatively and at follow-up, they were all markedly improved. Functional status improved in patients 1 and 6, along with improvement or stabilization of their atrial arrhythmias postoperatively. In terms of functional status, patient 7 improved two New York Heart Association classes and was relieved of the preoperative right-sided congestion and pulmonary venous obstruction. This patient was on a permanent pacemaker preoperatively, and no new rhythm disturbances have been noted since the operation.
For a number of years, it has been theorized that elevated coronary sinus pressure in the atriopulmonary Fontan might contribute to myocardial dysfunction by reducing coronary perfusion pressure, and data from recent studies support this hypothesis [10]. In all 3 patients in our series with elevated RA pressure (and therefore coronary sinus pressure), the VEDP was elevated. In all of these cases, the VEDP was significantly reduced after conversion to the cavopulmonary anastomosis, suggesting that lowering coronary sinus pressure does in fact improve ventricular function.
There is evidence that total cavopulmonary anastomosis, insofar as it takes a substantial load off the RA and improves right-sided flow patterns, may improve survival, with a decreased incidence of arrhythmias relative to Fontan modifications that incorporate the RA [8, 9]. From a technical standpoint, we prefer to perform an extracardiac conduit cavopulmonary anastomosis. Like other forms of total cavopulmonary connection, the extracardiac Fontan provides a maximally streamlined cavopulmonary communication, but requires substantially less atrial suturing and avoids trauma to the sinoatrial node region.
Although the impact of total cavopulmonary connection on thromboembolic events or hepatic dysfunction is not yet certain [5, 6], it is likely to reduce rhythm disturbance, which is generally thought to be a more common and more serious source of morbidity. Of course, revising a previously placed atriopulmonary Fontan cannot be expected to yield the same results as constructing a cavopulmonary anastomosis primarily or after staged palliation. Nevertheless, relieving central venous obstruction and RA dilatation is a reasonable therapeutic maneuver from the point of view of both hemodynamic management and the prevention or alleviation of atriopulmonary Fontan-related sequelae.
Fontan revision to extracardiac or intraatrial conduit total cavopulmonary anastomosis can be performed with success, and sometimes with dramatic improvement, in properly selected patients with complications referable to RA-PA or modified RA-PA connection, such as thrombosis, pulmonary venous obstruction, or arrhythmias. Revision may also be beneficial in patients with no complications directly related to the RA-PA connection but with other indications for operation. However, it is not clear at present whether RA reduction is necessary with Fontan revision, especially in patients who have no preoperative arrhythmias. Finally, in the failing patient who both lacks complications specifically related to the RA-PA connection and has other specific indications for operation (eg, bulboventricular foramen obstruction, atrioventricular valve regurgitation), revision to total cavopulmonary anastomosis may be ill advised. At present, such patients with severe exercise intolerance, effusions or ascites, and protein-losing enteropathy are not considered candidates for revision.
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Address reprint requests to Dr Reddy, 505 Parnassus Ave, M593, San Francisco, CA 94143-0118.
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