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Ann Thorac Surg 1996;62:519-524
© 1996 The Society of Thoracic Surgeons
Department of Thoracic and Cardiovascular Surgery and Department of Pediatric Cardiology, German Heart Institute Berlin, Berlin, Germany
Accepted for publication March 19, 1996.
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Abstract |
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 TopFootnotes Abstract IntroductionPatients and MethodsResultsCommentAcknowledgmentsReferences |
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Methods. Between January 1988 and November 1995, 120 patients with complete atrioventricular septal defect underwent total correction at the German Heart Institute Berlin. Sixty-nine of the patients were infants and 51 were children or adolescents. Eleven patients had previously undergone pulmonary artery banding. One hundred three patients had Down's syndrome. In all 120 patients complete atrioventricular septal defect repair was performed using the two-patch technique. The mitral cleft was closed with interrupted sutures in 119 cases.
Results. Thirty-four patients required aggressive treatment of postoperative pulmonary hypertensive crises (including nitric oxide inhalation). There were 12 hospital deaths (10%). Mortality was highest in patients with persistently high postoperative pulmonary arterial pressure (pulmonary artery pressure/systemic artery pressure > 0.6) (7 of 17 patients died; 41%). Associated atrioventricular valve anomalies, especially dysplastic valve tissue and severe preoperative cardiopulmonary instability necessitating catecholamine support and artificial ventilation, represented other risk factors. There were six late deaths (5%); cumulative mortality was 15%. Four patients suffered a complete heart block and sick sinus node syndrome necessitating pacemaker implantation 1 to 6 months after operation. During the follow-up period (3 to 80 months after operation), 7 patients (6.8% of survivors) were successfully reoperated on after significant mitral valve incompetence due to an open "cleft" (suture failure) developed.
Conclusions. Correcting complete atrioventricular septal defect using the two-patch technique, routine cleft closure, and atrial septal incision led to a low incidence of residual mitral valve incompetence. Mortality was primarily influenced by severe cardiopulmonary instability and additional atrioventricular valve anomalies preoperatively and the persistence of high pulmonary arterial hypertension postoperatively.
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Introduction |
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TopFootnotesAbstractIntroductionPatients and MethodsResultsCommentAcknowledgmentsReferences |
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Today complete atrioventricular septal defects (CAVSDs) can be corrected with acceptable mortality and postoperative morbidity. Nevertheless, opinions differ regarding the method of repair (one- versus two-patch technique) [1–5] and the necessity of mitral "cleft" closure [1, 6–10] and mitral valve annuloplasty [5, 9].
The following is an analysis of the surgical treatment of complete atrioventricular septal defects over an 8-year period at the German Heart Institute Berlin.
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Patients and Methods |
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TopFootnotesAbstractIntroductionPatients and MethodsResultsCommentAcknowledgmentsReferences |
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A total of 69 infants (mean age, 4.3 months; range, 21 days to 12 months) and 51 children and adolescents (mean age, 4 years; range, 1 to 19 years) underwent total CAVSD correction. Their weight at the time of operation ranged from 2.0 to 56 kg. Down's syndrome was present in 103 patients (86%). All of the patients underwent cardiac catheterization and angiography. Preoperative pulmonary vascular resistance was not calculated. The preoperative pulmonary-to-systemic flow ratio ranged from 0.8 to 8.8 (mean, 2.7), and the relative pulmonary-to-systemic resistance ratio from 0.06 to 1.3 (mean, 0.4). The pulmonary-to-systemic resistance ratio was greater than 0.5 in 22 patients. Preoperative angiographic examinations revealed systemic atrioventricular valve incompetence in 28 patients (23.3%), which was mild in 13 (11%), moderate in 14 (12%), and severe in 2 (1.7%).
There were 65 additional cardiovascular anomalies in 56 patients (Table 1
). The incidence of mitral valve anomalies (double-orifice mitral valve, single left ventricular papillary muscle, dysplastic valve with extreme deficiency of mitral tissue) was determined in 14 patients and found to be 10.6% in patients with Down's syndrome (11 of 103 patients) and 17.6% in those without (3 of 17 patients; p > 0.05). The incidence of other cardiovascular anomalies was similar in both groups (45.6% and 41.6%, respectively; p > 0.05). Significant extracardial anomalies were observed in 8 patients (6.6%).
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). Eleven patients had previously undergone pulmonary artery banding.
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Mitral valve annuloplasty was performed in 2 patients, aged 8 and 12 years old. After intracardiac repair had been completed, pulmonary and left atrial lines were inserted, the patients were rewarmed, and cardiopulmonary bypass was discontinued. Transesophageal echocardiography was used to evaluate the quality of surgical repair in the last 35 patients in the series. Type A CAVSD [13] was observed in 96 patients (80%), type B in 4 patients (3.3%), and type C in 10 patients (8.3%). Distinct CAVSD classification could not be made in the remaining 10 patients. A 10-month-old patient who also had pulmonary vein stenosis underwent a second period of cardiopulmonary bypass and atrial patch fenestration because of suprasystemic pulmonary artery pressure, whereas a 12-year-old patient underwent closed atrial patchstomy 12 hours after the initial operation. Additional surgical procedures included closure of patent ductus arteriosus in 19 patients, closure of additional ventricular septal defects in 5 patients, debanding and reconstruction of the pulmonary artery in 11 patients, right ventricular infundibular patch in 3 patients, patch enlargement of the stenotic right pulmonary artery in 2 patients, ligation of the left superior caval vein in 1 patient, and splitting of the single papillary muscle in 1 patient. A delayed sternal closure procedure was used in 18 patients.
Statistical Analysis
The computer program Statigraphics (version 2.01, Statistical Graphics Inc, Minneapolis, MN) was used for multivariate correlation analysis. Variables were analyzed to determine risk factors for early death. The paired t test was used to compare the different groups. The difference was considered statistically significant when the p value was 0.05 or less.
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Results |
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TopFootnotesAbstractIntroductionPatients and MethodsResultsCommentAcknowledgmentsReferences |
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Altogether there were 12 early deaths (10%). A total of 9 of 69 infants (13.0%) and 3 of 51 older children and adolescents (5.8%) died postoperatively. There was no significant difference in mortality between patients with or without Down's syndrome (9.7% and 11.1%, respectively; p > 0.05). All 3 patients with advanced preoperative cardiopulmonary instability and pneumonia died (see Table 2
), as did 7 of the 17 patients (41%) with persistently high pulmonary arterial pressure (pulmonary pressure/systemic pressure > 0.7). One infant died due to a pulmonary hypertensive crisis; another infant with preoperative cardiac arrest died due to low cardiac output.
Mortality in 56 patients with surgically significant cardiovascular anomalies was 14.2% (8 of 56 patients) compared with 6% in patients without (4 of 64 patients; p > 0.05), whereas it was 28.5% (4 of 14 patients) in patients with additional mitral valve anomalies compared with 7.5% in patients without (8 of 106 patients; p < 0.05) (Table 3). Mortality correlated highly with additional mitral valve anomalies, persistently high postoperative pulmonary arterial pressure, and preoperative cardiopulmonary instability (Table 4). A combination of these risk factors was observed in the majority of the patients who ultimately died. None of the 11 patients who underwent pulmonary artery debanding died.
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Late Reoperation
Echocardiographic examinations were used to evaluate mitral valve function in 93 patients (93% of late survivors) 3 to 80 months postoperatively; mitral valve incompetence was absent in 76 patients (81.7%) and mild in 9 (9.7%). Severe mitral valve incompetence (MVI) was observed in 7 patients (7.5%), in 6 of whom the mitral cleft was found to be partially or completely open, which was caused by suture failure in 5 (Table 5). Subsequent complete cleft closure eliminated MVI in 5 patients. Mitral annuloplasty was necessary in the other patient, a child with preoperative dysplastic valve tissue, and was performed in conjunction with cleft closure. As this intervention resulted in mitral valve stenosis, the patient underwent mitral valve replacement with a mechanical prosthesis 7 days later. Isolated annuloplasty eliminated MVI in another patient, a 6-year-old child. There was no difference in the rate of late reoperations in patients with or without Down's syndrome (6.8% and 6.6%, respectively; p > 0.05). Also, no correlation was determined between the severity of preoperative MVI and the incidence of reoperation (n = 95; r = 0.1192; p = 0.2501). Small residual ventricular septal defects had to be closed in only 5 patients. This was performed concomitantly with cleft closure in 3 patients, with mitral valve annuloplasty in 1, and with pulmonary artery enlargement in another.
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Comment |
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TopFootnotesAbstractIntroductionPatients and MethodsResultsCommentAcknowledgmentsReferences |
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Associated cardiovascular anomalies were observed in half the patients; however, neither they nor the presence of Down's syndrome generally had a significant influence on morbidity or mortality, thus confirming the findings by others [1, 7, 15]. Although more associated mitral anomalies were present in patients without Down's syndrome than in those with, this difference was not statistically significant. Double-orifice mitral valves were observed in 5.8% of the patients. It has been suggested that performing cleft closure in cases involving double-orifice mitral valves may occasionally cause mitral valve stenosis [16]. In this present study cleft closure completely eliminated MVI in all 7 patients, although 1 patient with preoperative cardiac arrest died of myocardial failure. Valve stenosis was not noted in the 6 survivors in this patient subgroup, nor was late reoperation for residual MVI necessary, contrary to observations in other groups [5, 17, 18].
The most important associated mitral valve anomaly was dysplastic atrioventricular valves with tissue deficiency. This was often observed in small infants and precluded adequate valve reconstruction [10, 18, 19]. Two of 5 such patients died early after operation; 1 infant had been scheduled to undergo early reoperation because of repair dehiscence and the other had undergone successful mitral valve replacement with a mechanical prosthesis after two unsuccessful attempts to reconstruct the systemic atrioventricular valve.
Another high risk factor identified in this study was severe cardiopulmonary instability necessitating preoperative catecholamine and respiratory support. All 3 affected patients died during the early postoperative period because of continuing cardiopulmonary deterioration despite adequate repair. Similar experiences have been reported by others [1, 20]. Pulmonary artery banding may be more appropriate in such patients to prevent the deleterious effect of cardiopulmonary bypass.
Persistently high postoperative pulmonary arterial pressure was also a high risk factor in this series. The high proportion of patients aged more than 2 years is explained by the fact that most of them were from the eastern part of Germany, where in the recent past the possibility for early repair was very limited. Mortality in patients with persistently high postoperative pulmonary arterial pressure was 41% (7 of 17 patients), 4 of whom were small infants with additional risk factors such as pulmonary vein stenosis, a hypoplastic left ventricle, or preoperative cardiopulmonary instability. Atrial patch fenestration was performed in 2 of these 17 patients (during the initial operation in 1 and several days afterwards in the other) resulting in one death. Although modern diagnostic methods were used, including nitric oxide test during heart catheterization, we, as did others [18], found it very difficult to adequately assess the operability of patients with severely elevated pulmonary vascular resistance. In some cases preoperative lung biopsy may be considered.
The most controversial issue in the surgical treatment of CAVSD is the necessity of closing the so-called mitral cleft. The opinion that the cleft should be left intact is not new and was proposed for patients with incomplete atrioventricular septal defect as long as 35 years ago [21, 22]. In the late 1970s the three-leaflet concept of mitral valve CAVSD was introduced [6, 23], which led to some surgeons leaving the cleft open during total repair of CAVSD [8, 24]. At the same time, some proponents of the three-leaflet mitral valve concept maintained that "although it was impossible to produce a bi-leaflet valve which structurally approximated the mitral valve of a normal heart, closure of the `cleft' in some cases may be the only way to produce a component atrioventricular valve" [23].
The main goal of mitral valve reconstruction in patients with CAVSD is to produce a competent and nonstenotic systemic atrioventricular valve [25]. Criticism of the three-leaflet concept has increased over the last decade as surgeons have noted the high rate of reoperations necessitated by late MVI after total correction of CAVSD and have surmised that the major causes for an incompetent mitral valve were nonclosure or incomplete closure of the cleft or separation of a previously sutured cleft [1, 2, 5, 7, 9, 14, 20, 24]. Considering the surgical point of view, we do not find it particularly important to consider the cleft as a normal commissure in CAVSD [6, 23]. It is more important to note that a partially or completely open cleft is the main cause of subsequent valve incompetence and that cleft closure represents the only means for achieving long-term valve competence in such cases [24]. The incidence of late operation for late severe MVI in patients with nonclosed cleft approaches 14% to 26% [8, 20, 24].
Late after CAVSD correction, the mechanism of severe MVI in patients with an open cleft resembles that occasionally observed in older patients who have not been operated on in whom thickening of the leaflet tissue along the cleft occurs due to long-lasting, even initially minor, insufficiency through the cleft opening [22]. We found routine cleft closure to be safe, even in patients with a double-orifice mitral valve, resulting in a low incidence of severe MVI in the late postoperative period. Mitral valve stenosis did not develop in any of the patients. This was probably the case because an age-related minimal normal mitral valve diameter was used as a guide in all cases during cleft closure to prevent valve stenosis. The cleft was left open only once, ie, in a patient who presented with a dysplastic valve that lacked sufficient mitral valve tissue for performing cleft closure. Only 7 of the survivors (6.8%) had to be reoperated on during the late postoperative period for severe mitral valve incompetence; an open cleft, caused by suture failure, was responsible for MVI in 5 of them. Complete cleft closure eliminated MVI in all 5 patients. One patient with a dysplastic valve, mentioned above, had to undergo mitral valve replacement.
Five of the 6 patients whose cleft was found to be open during the late postoperative period had undergone operation during infancy. Because pliable valve tissue might have been responsible for the separation of a previously sutured cleft, reinforcing the cleft sutures with pericardial patches may be beneficial in such cases. Ten other patients who underwent surgical correction of atrioventricular septal defects in other facilities had to be reoperated on because of severe MVI. An open cleft was the main cause of MVI in all of them. Subsequent cleft closure completely eliminated valve incompetence in 9 patients. The remaining patient, whose atrial septal defect had been closed directly during initial repair, required mitral valve replacement due to severe valve deformity.
Recently Wetter and colleagues [14] showed that the reoperation rate for MVI was 9 times higher in patients in whom the cleft initially had been left open than in those in whom it had been sutured. Indeed, some surgeons have begun closing the cleft routinely after observing that severe MVI often developed in patients in whom the cleft had been left open during the initial operation [1, 14, 20, 24]. Other causes of late severe MVI, eg, a dilated mitral valve ring or repair dehiscence, are rare [5]. Repair dehiscence was observed only during the early postoperative period in 3 patients (all small infants) in this series, similar to reported by others [1, 7]. All 3 patients were reoperated on successfully. Residual ventricular septal defects were an insignificant problem in this series, possibly because interrupted sutures were used to affix the ventricular septal patch in all cases. We believe that the low incidence of late MVI observed in this series may be attributed to routinely suturing the cleft up to the minimal valve diameter and transecting the residual atrial septum. We conjecture that this latter procedure increased the mobility of the mitral valve ring and improved the suspension of the newly reconstructed valve leaflets after the atrial septal defect had been closed with a larger patch. It has been suggested that inaccurate closure of an atrial septal defect can cause distortion of mitral valve leaflets in atrioventricular septal defect [22].
In summary, a low incidence of residual MVI can be expected after CAVSD correction using the two-patch technique and routine cleft closure of the atrial septal defect enlargement. Severe preoperative cardiopulmonary instability, dysplastic and deficient mitral tissue, and persistently high pulmonary arterial pressure remain the major causes of mortality. Reinforcing the cleft sutures with pericardial patches is recommended in small infants with pliable and delicate valvular tissue to prevent early repair dehiscence.
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Acknowledgments |
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TopFootnotesAbstractIntroductionPatients and MethodsResultsCommentAcknowledgmentsReferences |
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Footnotes |
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TopFootnotesAbstractIntroductionPatients and MethodsResultsCommentAcknowledgmentsReferences |
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TopFootnotesAbstractIntroductionPatients and MethodsResultsCommentAcknowledgmentsReferences |
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