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Ann Thorac Surg 2004;78:204-208
© 2004 The Society of Thoracic Surgeons
a Pediatric and Congenital Heart Surgery, The Children's Hospital at The Cleveland Clinic, Cleveland, Ohio, USA
Accepted for publication December 29, 2003.
* Address reprint requests to Dr Duncan, Pediatric and Congenital Heart Surgery/M41, The Cleveland Clinic Foundation, 9500 Euclid Ave, Cleveland, OH 44195, USA
e-mail: duncanb{at}ccf.org
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Abstract |
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METHODS: From November 1994 through April 2002, nine children, median age 8 months (range, 74 days to 2.5 years) underwent 10 operations for VSD closure via apical right ventriculotomy (one patient with a residual defect underwent successful VSD closure via a second apical right ventriculotomy). Two patients were status post pulmonary artery banding and two patients had previous unsuccessful attempts at closure via a transatrial approach.
RESULTS: There was no hospital mortality; there were 2 late deaths (78% survival; 95% confidence interval [CI], 45% to 94%), 3 months and 4 years postoperatively. Postoperative echocardiography demonstrated no residual VSDs in 3 and insignificant residual VSDs in 4 of the survivors. All survivors currently exhibit normal biventricular function during a median follow-up of 25 months (range, 11 to 104 months).
CONCLUSIONS: Apical right ventriculotomy provides excellent exposure allowing safe and effective closure of apical VSDs. The observed late morbidity and mortality reflects the complexity that often exists in these cases due to additional irreparable lesions.
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Patients and methods |
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Results |
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There was no in-hospital mortality. In-hospital complications included one patient who required reoperation for a recurrent apical VSD. This 2-year old with heterotaxy syndrome, situs inversus, pulmonary hypertension, small left-sided cardiac structures, and multiple VSDs, initially underwent attempted transatrial closure of a perimembranous defect at another hospital. This patient continued to have severe congestive heart failure, and at the time of the initial operation here, underwent an apical right ventriculotomy with patch closure of an apical VSD and transatrial patch closures of a large anterior VSD and a small residual perimembranous lesion. Postoperatively, the patient had evidence of a significant residual ventricular level left-to-right shunt (QP/QS 2:1 at cardiac catheterization) and underwent reoperation 17 days later. Of interest, this patient had two distinct apical right ventricular chambers divided by a prominent muscle bundle corresponding to the apex of the right ventricular sinus posteriorly and the right ventricular infundibulum anteriorly as described by Van Praagh and colleagues [7] and Stellin and colleagues [8]. Takedown of this muscle bundle through the apical incision revealed a large defect that was closed with a patch and a small leak around the original apical VSD patch that was closed primarily. A supramitral membrane was also resected through a transatrial approach. The second procedure was complicated by temporary junctional rhythm that recovered without the need for pacemaker placement and the patient was subsequently discharged with no residual VSD or evidence of pulmonary hypertension on echocardiogram. Other complications included culture proven septicemia in four patients and a superficial wound infection in one patient.
The in-hospital echocardiogram demonstrated no residual leak in four patients or only a trivial residual leak in five patients. Two patients exhibited mild to moderate right ventricular dysfunction on the immediate postoperative echocardiogram; there was no significant left ventricular dysfunction in any patient.
There were two late deaths (78% long-term survival; 95% CI, 45% to 94%). One death occurred in a 14-month old who had undergone tetralogy of Fallot repair complicated by complete heart block requiring pacemaker implantation. Postoperatively, the patient demonstrated significant congestive heart failure and was found to have multiple anterior muscular VSDs and a large apical VSD. The patient underwent apical right ventriculotomy with patch closure of the apical lesion and transatrial primary closure of the anterior muscular VSDs along with revision of the right ventricular outflow tract reconstruction using a homograft conduit. Before discharge, the patient demonstrated moderate right ventricular dysfunction, a small residual VSD, and moderate tricuspid regurgitation with evidence of mild pulmonary hypertension. The patient lived in another country and died 98 days after discharge to home; further details regarding the death are unknown. The other death occurred in the patient described above who required a second procedure for a recurrent apical lesion. During follow-up the patient initially demonstrated sinus rhythm with significant periods of junctional rhythm and retrograde conduction of P waves, while the echocardiogram demonstrated normal biventricular function and no residual VSD. This patient suffered a presumed arrhythmogenic cardiac arrest more than three years after discharge with significant resultant anoxic brain injury and eventually died of overwhelming sepsis four years after surgery.
The median duration of follow-up for the seven survivors is 25 months (range, 11 to 104 months). Echocardiography in the seven survivors demonstrates no residual defect in three patients and small, hemodynamically insignificant residual VSDs in four patients. All survivors exhibit normal biventricular function. Figure 2 demonstrates the survival curve for this group of patients.
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Comment |
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Large numbers of both surgical and nonsurgical approaches have been reported for this relatively rare condition emphasizing the limitations for any one of these therapies [1, 3–5, 9–16]. Techniques for device closure of apical VSDs in the cardiac catheterization laboratory or for intraoperative deployment have been utilized [3–5, 15]. Percutaneous transcatheter techniques require relatively large sheaths for introduction, which may not be suitable for the smallest infants. In addition, complications such as device embolization, tricuspid or aortic valve damage, and recurrent defects, although rare, do occur with transcatheter techniques. Intraoperative device closure is also possible but possesses risks as well; Okubo and colleagues [3] reported the use of intraoperative devices in 14 patients with a hospital mortality rate of 14% and the need for subsequent pulmonary artery banding for significant residual defects in three patients.
Visualization and closure of most muscular VSDs is usually possible via a right atriotomy; however, access to lesions in the apex is difficult via the right atrium although reports exist that utilize this approach exclusively [12, 13]. Black and colleagues [13] described the septal obliteration technique, which was used to treat isolated multiple VSDs, including apical lesions. This technique utilized large autologous pericardial patches, sutured circumferentially around the apical septum that effectively sealed off the apical portion of the right ventricle. This technique was successful in all treated patients with minimal morbidity and allowed repair without interval pulmonary artery (PA) banding even in small infants. Although this is an effective approach, we believe that direct patch closure of the VSD afforded by a small apical right ventriculotomy better preserves right ventricular volume and compliance.
Left ventriculotomy provides excellent exposure for apical lesions and greatly simplifies patch application in that multiple channels through coarse trabeculations in the right ventricle often lead to a single defect on the left ventricular side of the septum. Kitagawa and colleagues [16] described the use of left ventriculotomy for the closure of apical lesions with excellent short-term and long-term results. These authors concluded that use of a limited left ventriculotomy might be expected to have little impact on ventricular function. Concerns remain, however, regarding the long-term outlook for children who have undergone apical VSD closure via left ventriculotomy. McDaniel and colleagues [14] reported the use of left ventriculotomy for apical VSD closure in four infants with good results during short-term follow-up; however, during long-term follow-up of these children (4 to 11 years), all three patients who underwent cardiac catheterization demonstrated apical dyskinesia [17]. Serraf and colleagues [1] reported that left ventriculotomy for apical lesions was a risk factor for both recurrent VSD and death. Children's Hospital, Boston reported that 50% of patients who underwent left ventriculotomy for VSD closure had significant residual lesions including residual VSD, apical aneurysm, left ventricular dysfunction, need for transplantation, or death [2]. Mechanisms resulting in left ventricular dysfunction and aneurysm formation include damage to epicardial coronary arteries, direct myocardial damage, and damage to the Purkinje network of the left ventricular conduction system [8].
We have found that an apical right ventriculotomy reliably provides access to apical and anterior muscular VSDs while avoiding complications related to alternative methods of closure. Other series utilizing apical right ventriculotomy have also demonstrated the safety and effectiveness of this approach [7–9]. Technical features that we have found useful include performing a limited right ventricular incision that is close to the left anterior descending coronary artery without endangering this vessel. As described by Tsang and colleagues [9], location of the ventriculotomy in this area allows access to the space between the papillary muscles and the septum. Septal trabeculations are then resected which usually clarifies the exact location of the defect margins and facilitates secure closure. Placement of the sutures on the left ventricular aspect of the defect in larger lesions facilitates closure and avoids the conduction system. Secure primary closure of the right ventriculotomy is routine due to the low pressure that is present in the ventricular chamber. In the present series, hemodynamically insignificant residual VSDs persisted in four of the seven survivors and probably occurred through pinhole "satellite" lesions remote from the apical VSD. Transesophageal echocardiography is essential to diagnose larger residual VSDs; however, cardiac catheterization to provide definitive diagnosis of hemodynamically significant lesions and early reoperation should be performed as was necessary in one of the present cases.
The benefits of right ventriculotomy for isolated apical VSD closure are especially important when apical defects are present in combination with other lesions. Secure closure is mandatory in that residual defects are often poorly tolerated in these instances. This technique may also be combined with a transatrial approach to address the highly deficient ("Swiss-cheese") interventricular septum with multiple lesions in perimembranous, midmuscular, anterior, and apical locations; a combined transatrial-transapical approach was utilized in three cases in the present series. In addition, closure techniques should be able to be performed without significantly adding to the ischemic time required to repair associated lesions. We have found apical right ventriculotomy to satisfy these requirements by providing reliable VSD closure while minimizing additional ischemic time. In the present study, this approach resulted in 100% hospital survival despite the presence of severe associated lesions in a number of these patients. The substantial long-term mortality emphasizes the severity of coexisting disease and appears to be unrelated to the use of a right ventriculotomy for VSD closure. However, careful follow-up of larger numbers of patients managed with this technique will be necessary before claims of the total safety of this approach can be made. Apical VSDs are difficult lesions to treat and institutional biases may lead to the successful use of any of the described surgical or transcatheter methods of closure. The goal of the present report is to describe the benefits of apical right ventriculotomy in terms of successful closure of apical lesions with preservation of ventricular function.
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