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Ann Thorac Surg 1998;65:517-524
© 1998 The Society of Thoracic Surgeons

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Original Articles: Cardiovascular

Trends in the Management of Truncal Valve Insufficiency

Divisions of Cardiothoracic Surgery and Pediatric Cardiology, University of California, San Francisco, San Francisco, California, USA

Accepted for publication July 25, 1997.

Dr Reddy, 505 Parnassus Ave, M589, San Francisco, CA 94143-0118.

Presented in poster form at the Sixty-ninth Scientific Sessions of the American Heart Association, New Orleans, LA, Nov 10–13, 1996.

	Abstract

Top Abstract Introduction Patients and Methods Results Comment References

 
Background. The single semilunar valve in patients with truncus arteriosus frequently is dysplastic and dysfunctional. Truncal valve insufficiency has been associated with poor outcome. Although the management of truncal valve insufficiency has evolved over the years, approaches to this problem vary considerably and remain a serious dilemma in many cases.

Methods. We reviewed the records of 89 patients with unrepaired truncus arteriosus and mild (n = 37), moderate (n = 33), or severe (n = 19) truncal valve insufficiency who were admitted to our institution between 1975 and 1995. Eight patients (7 neonates) with moderate or severe insufficiency died before surgical intervention, and 4 patients underwent palliative pulmonary artery banding. The remaining 77 patients underwent repair. The median age at repair was 3.2 months (range, 2 days to 15 years; 83% infants), and it decreased from 4 months between 1975 and 1985 to 1 month between 1986 and 1995. Truncal valve replacement (mechanical = 6, allograft = 4) was performed in 10 patients, and 5 patients underwent valve repair.

Results. All 4 patients who underwent pulmonary artery banding died either early or late. The hospital (or 30-day) mortality rate after repair was 34% (26/77). At a median follow-up of 10 years, 11 hospital survivors had died, with overall 1- and 10-year actuarial survival rates of 56% and 48%, respectively, and poorer survival among patients with severe truncal valve insufficiency (p = 0.02). Late truncal valve replacement (n = 24) had been performed in 21 patients. Freedom from truncal valve replacement was better in patients with mild truncal insufficiency than in those with moderate or severe preoperative insufficiency (p < 0.001). Four late deaths were related directly to reoperation for truncal valve replacement or to prosthetic valve dysfunction. Three of the 4 neonates who received allograft root replacements died within 7 months of repair, and severe allograft valve insufficiency requiring replacement 1 year after operation developed in the fourth.

Conclusions. The prospects for patients with truncal valve insufficiency have been improving over time. Nevertheless, the results in patients with severe insufficiency continue to be poor.

	Introduction

Top Abstract Introduction Patients and Methods Results Comment References

 
The single semilunar valve in truncus arteriosus frequently is dysmorphic, dysfunctional, or both [1] [2] [3] [4] [5] [6] [7] [8] [9] [10] [11] [12] [13] [14] [15] [16] [17] [18]. The surgical management of truncus arteriosus often is complicated by the presence of a regurgitant truncal valve (which is present in approximately one third of cases), and truncal insufficiency has been associated with higher rates of early [15] [17] [19] [20] and late [15] [21] mortality. Although there recently have been several encouraging reports regarding techniques for repairing [22] or replacing [18] the regurgitant truncal valve, truncal valve insufficiency in young patients with unrepaired truncus arteriosus remains a difficult surgical dilemma for which an optimal solution has yet to be found. In the present report, we describe our institutional experience with and current management strategy for truncal valve insufficiency in unrepaired truncus arteriosus, discuss technical and perioperative issues, and review the literature concerning this problem.

	Patients and Methods

Top Abstract Introduction Patients and Methods Results Comment References

 
Patients
The medical records of all patients admitted to the University of California, San Francisco Medical Center between 1975 and 1995 with a diagnosis of truncus arteriosus were reviewed retrospectively. All patients who presented with unrepaired truncus arteriosus and angiographic or echocardiographic evidence of significant truncal valve insufficiency were selected for study. This did not include patients with trace or minimal insufficiency, patients who presented for reoperation after repair with new-onset truncal valve insufficiency, or patients who underwent repair at another institution. Eighty-nine patients met these criteria. Many of these patients were included in earlier reports [20] [21]. According to standard echocardiographic and angiographic criteria for grading semilunar valve insufficiency [23] [24], truncal valve insufficiency was estimated as mild in 37 patients, moderate in 33 patients, and severe in 19 patients. Eight patients had undergone previous pulmonary artery banding elsewhere. Since 1992, we have performed routine neonatal repair with no palliative procedures.

Eight patients (7 neonates) with moderate (n = 1) or severe (n = 7) truncal valve insufficiency died before any surgical intervention could be performed. Four patients with moderate truncal valve insufficiency (all less than 40 days of age) underwent pulmonary artery banding because of their small size and associated interrupted aortic arch (n = 1) or intramural left main coronary artery (n = 1). The remaining 77 patients underwent truncus arteriosus repair at a median age of 3.2 months (range, 2 days to 15 years), with 83% of patients less than 1 year of age. Patient age at the time of repair decreased dramatically over time, especially in patients with moderate or severe truncal valve insufficiency (Fig 1). Among the 56 patients (with all degrees of insufficiency) who underwent repair between 1975 and 1985, the median age was 4 months, whereas the median age of the 21 patients who underwent repair between 1986 and 1995 was 1 month. The median weight of the patients who underwent repair or pulmonary artery banding was 3.9 kg at the time of operation (range, 2 to 35 kg).

View larger version (14K): [in this window] [in a new window]   Age at admission plotted against year of admission for operation among patients with moderate or severe truncal valve insufficiency. Asterisks indicate patients who died in the hospital before operation (preop). Squares indicate patients who underwent pulmonary artery banding (PAB). Inverted triangles indicate patients who underwent repair. Solid symbols represent hospital survivors. Hollow symbols represent hospital deaths. A horizontal line is drawn at 30 days of age to delineate neonates.

View larger version (134K): [in this window] [in a new window]   Autopsy specimen from a patient who died after pulmonary artery banding and interrupted aortic arch repair at 10 days of age, showing a severely dysmorphic four-leaflet truncal valve. The leaflet toward the bottom of the picture was divided at autopsy; the two halves are indicated by small arrows. The valve was moderately regurgitant before operation.

Data Analysis
Preoperative and perioperative data were collected on retrospective review of patient records. Cross-sectional follow-up was carried out by means of physician or patient contact, and was completed by February 1996. Results classified as "early" are those that occurred before hospital discharge or within 30 days of operation if the patient was discharged from the hospital before that time. Statistical Package for the Social Sciences, Windows version 6.01 (SPPS Inc, Chicago, IL), was used to perform statistical calculations. Data are expressed as median and range. Although patient groups differed over time and surgical and perioperative techniques changed significantly over the course of this experience, analysis of the diagnostic, morphologic, and surgical variables was performed to identify factors associated with early and late death and truncal valve reoperation across this period. ² Analysis was used to compare dichotomous variables. Nonparametric analysis involving polychotomous variables was conducted with the Wilcoxon signed-rank test. Independent samples t-test was used for comparison of means. Kaplan-Meier and Cox proportional hazards models were used for actuarial survival analysis and for analysis of freedom from truncal valve replacement.

	Results

Top Abstract Introduction Patients and Methods Results Comment References

 
Survival
Of the 4 patients who underwent pulmonary artery banding at our institution, 2 died early and 2 died late, at 2 and 23 months after operation, respectively, without definitive repair. Among the patients who underwent truncus arteriosus repair, there were 26 early deaths, for an operative mortality rate of 34%. Early mortality rates were almost identical among surgical patients with mild, moderate, and severe truncal insufficiency, although it is important to keep in mind that this statistic does not take into account patients with severe insufficiency who died without undergoing operation. There were no early deaths among the 5 patients who underwent truncal valve repair, whereas 4 of the 6 patients who underwent mechanical truncal valve replacement and 1 of the 4 patients who underwent allograft truncal valve root replacement died in the early postoperative period (Table 1). Among the 10 neonates who underwent repair after 1992, there was 1 early death, which occurred in a patient who underwent allograft truncal valve root replacement.

View larger version (11K): [in this window] [in a new window]   Overall actuarial survival curve for patients with truncal valve insufficiency who underwent complete truncus arteriosus repair.

View larger version (17K): [in this window] [in a new window]   Overall actuarial freedom from truncal valve replacement among patients with mild, moderate, and severe truncal valve insufficiency before repair.

View larger version (168K): [in this window] [in a new window]   Ascending aortogram performed 11 months after truncus arteriosus repair with aortic allograft truncal valve root replacement in a 2-day-old patient with moderate truncal valve insufficiency. This diastolic frame demonstrates severe insufficiency of the allograft valve, which was replaced 2 months later with a mechanical valve.

Truncal valve insufficiency at the time of hospital discharge in the 5 patients who had undergone truncal valvuloplasty or annuloplasty ranged from none to mild, and was improved in all patients. Two of these patients eventually required late truncal valve replacement 10 and 11 years after operation, respectively. One patient had moderate insufficiency at a follow-up of 14 years, and the most recent 2 patients had trace or no insufficiency 1 and 2 years, respectively, after repair (Table 1). Information regarding truncal valve function at the time of hospital discharge was available for the 10 neonates who underwent repair after 1992. The 3 early survivors who underwent truncal valve root replacement had trivial (n = 1) or mild (n = 2) allograft insufficiency, whereas the patient who underwent mechanical valve replacement had trivial paravalvular leak. Truncal valve insufficiency at hospital discharge in 2 patients decreased from moderate (before operation) to mild and from mild to none, respectively, whereas it remained unchanged in 1 patient with mild insufficiency and progressed from mild to moderate in 1 patient.

	Comment

Top Abstract Introduction Patients and Methods Results Comment References

 
Trends in Management: Evolving Approaches, Improving Outcomes?
In 1968, McGoon and colleagues [25] introduced a repair procedure for truncus arteriosus in which a conduit was used to connect the right ventricle with the pulmonary arteries. For many years, the primary beneficiaries of this new procedure were children older than 1 year of age [15]. The surgical predecessor to conduit repair, which continued to be used in infants long after McGoon and colleagues’ report, was banding of the pulmonary arteries to reduce pulmonary overcirculation. However, as a review of the literature from 1964 and 1974 by Applebaum and associates [19] showed, the early mortality rate after pulmonary artery banding for truncus arteriosus was around 50%, with significant additional mortality in the first few years after banding. Thus, for many years, treatment options for patients less than 1 year of age with truncus arteriosus were limited and outcomes were poor. The prognosis was particularly dismal in neonates with significant truncal valve insufficiency, who were likely to die before ever making it to the operating room, as autopsy studies [5] [6] [7] [8] [9] [10] [11] [12] and the first 10 years of our institutional experience demonstrate.

Aside from the neonates with severe insufficiency who typically did not survive, there was another subset of patients with moderate to severe truncal valve insufficiency who generally were older at the time of repair. Although the older group of patients represented a challenge in this earlier era, they cannot be compared readily with neonates with a similar degree of truncal valve insufficiency. In the 1985 report by Di Donato and co-workers [15], 37% of 167 patients undergoing truncus arteriosus repair had moderate (n = 52) or severe (n = 10) truncal valve insufficiency. All 10 of the patients with severe truncal valve insufficiency were older than 5 years of age at the time of operation, and most of the remaining patients were beyond infancy. Similarly, in our series, approximately 30% of the 26 patients with moderate to severe truncal valve insufficiency who underwent repair between 1975 and 1985 were older than 6 months of age. Truncal valve thickening and insufficiency in the neonatal period are thought to develop in utero, a theory that is supported by experimental evidence [26]. However, truncal valve insufficiency in these older patients, which may have been present to a lesser degree early in life, most likely progressed or developed over time as the function of dysplastic or otherwise abnormal semilunar valve leaflets became compromised in the face of prolonged turbulence. It is interesting to note that Di Donato and co-workers [15] reported that early mortality rates among this subset of patients did not differ significantly from those in all patients. Similarly, we found that surgical mortality rates among patients with truncal valve insufficiency did not correlate with the degree of insufficiency, especially among patients who underwent repair after the neonatal period, although it is important to keep in mind that most neonates before 1985 did not even undergo operation and thus were not entered into the analysis of surgical mortality.

Beginning in the late 1970s, repair in infancy started to become more common [19] [20], and since the late 1980s and early 1990s, neonatal repair has become the standard of care for patients with truncus arteriosus at many centers [17] [18]. Thus, many of the neonates with truncal valve insufficiency who previously died before undergoing operation are undergoing repair, raising management issues that differ from those faced by surgeons in years past. In earlier series in which the majority of patients were beyond infancy, mechanical valve replacement using available prosthesis sizes was possible [15]. As truncus arteriosus repair moved into the neonatal period, however, size restrictions of available mechanical valves (among other things) led to the use of allograft valves for truncal valve replacement. Several surgeons have reported good results with the aortic allograft in truncal valve replacement [16] [18], but we have been disappointed with allografts in this capacity, primarily with their intermediate-term function. Severe allograft insufficiency developed less than a year after operation in 2 of our 3 early survivors with allograft truncal valve replacement (1 died as a result), and the other survivor died suddenly 2 months after operation. Another option for truncal valve replacement, when adequate repair is not possible, may be the use of an oversized mechanical valve along with annular enlargement [18]. Although results with mechanical truncal valve replacement early in our institutional experience were at least as disappointing as outcomes in recent patients treated with allograft root replacement, comparison across periods and patient groups is difficult, given the changes in management that have taken place. Thus, previous poor results with mechanical prostheses for truncal valve replacement are not prognostic for mechanical valves used in this position in the current era. Other reported techniques, such as using a cylindric valve fashioned from two segments of polytetrafluoroethylene tube graft, may be options, but little is known about their function and durability [27].

Our Institutional Experience
Although early infant repair of truncus arteriosus was performed more aggressively at our institution than at most others in the late 1970s and early 1980s [20], our experience with truncal valve insufficiency has paralleled that summarized above. The median age of patients with truncal valve insufficiency who underwent repair decreased from 4 months between 1975 and 1985 to 1 month between 1986 and 1995. Among 8 neonates who presented with moderate to severe insufficiency before 1985, 7 died before operation was performed, and most of the patients treated with valve replacement for severe insufficiency during this period did not survive. During these 20 years, the management of truncal valve insufficiency has evolved considerably, and prospects for neonates with this difficult lesion clearly have improved. The major gains have come in advances that allow for preoperative stabilization and management of neonates in congestive heart failure, and surgical progress that makes it possible to perform repair even in neonates with low and very low birth weights [17] [18]. This fact is demonstrated in Fig 1, which shows that 7 of 8 neonates with moderate or severe truncal valve insufficiency who were admitted to our institution between 1975 and 1985 died before operation was undertaken. In contrast, all 7 neonates who were admitted with moderate or severe truncal valve insufficiency after 1992 underwent operation, with only 1 early death. However, even though more young patients are undergoing surgical repair, severe truncal valve insufficiency remains a difficult problem, especially in neonates—2 of the 3 neonates who were discharged after allograft truncal valve root replacement after 1992 died within 8 months. Although hospital survival after surgical repair has improved over time in our series, there has been a substantial mortality rate during the first year of life among patients with moderate to severe truncal insufficiency throughout these two decades, which suggests that 1-year survival may be a more appropriate indicator of successful repair. This is supported by the stabilization of the actuarial survival curve beyond 1 year after operation (Fig 3).

Critiques of the Study
One of the shortcomings of the present study is that data regarding the morphology of the truncal valve in our patients are limited. It has been shown that patients who die in the neonatal period are more likely to have severe valve dysmorphism than patients who die later [11]. It also is believed that nodular or dysmorphic valves are more likely to be insufficient [5] [11] and to have an abnormal number of leaflets [4]. Accordingly, it also is thought that valves with four leaflets (Fig 2) are more frequently regurgitant than those with three leaflets [12]. Morphologic information about the 57 patients in this study for whom the number of valve leaflets was known seems to be consistent with these findings. Preoperative valve function among these patients was significantly worse in patients with four-leaflet valves than in those with three-leaflet valves (p = 0.001), although it is possible that this analysis may be confounded by reporting bias.

Aside from prognostic implications, the specific morphology of the truncal valve, including the number of leaflets, may be important in the surgical management of patients with truncal valve insufficiency. A recent study in patients with critical aortic stenosis has suggested that aortic valves with more or less than three leaflets are less amenable to repair than are those with three leaflets [28]. Likewise, it often is more difficult to repair truncal valves that are extremely thickened or nodular, have an abnormal commissural support structure, or have an abnormal number or configuration of leaflets, especially in very young patients. Several investigators have reported successful approaches to the repair of abnormal truncal valves [22] [29] [30], but few of these repairs have been made in neonates. Primary repair techniques may vary, as does the morphology of the truncal valve and root, and can include valvuloplasty, commissural buttressing, annuloplasty, and truncal valve reduction. These have become more attractive options because the routine use of intraoperative transesophageal echocardiography now makes it possible to attempt truncal valve repair and then proceed to valve replacement if the repair is inadequate. Clearly, this is an important advance in the surgical management of truncal valve insufficiency, although the role of truncal valve repair, especially as a long-term solution, remains to be established.

Another shortcoming of the present study is that our data regarding the function of the truncal valve early after repair are limited. This inadequacy is unfortunate, given the fact that preoperative truncal valve insufficiency may not reflect accurately the postoperative situation. In unrepaired truncus arteriosus, pulmonary runoff leads to reduced diastolic pressure, which consequently may minimize the degree of truncal valve insufficiency [6] [11]. Alternatively, a reduction in flow volume through the truncal valve after repair is likely to alter the distention of the truncal root, which can lead to either improved or worsened valve function. It has been observed that truncal valve insufficiency often develops anew or progresses after truncus arteriosus repair without valve intervention [11] [19] [31], and that truncal insufficiency can improve in the same circumstances [31]. Among the limited number of patients for whom early postoperative data are available in the present study, as well as among the larger cohort for whom follow-up data on valve function are available, both these patterns were found to occur. Morphometric studies may be helpful in developing criteria that can be used to predict circumstances in which truncal valve insufficiency is more likely to develop or progress.

Coronary artery abnormalities are common in patients with truncus arteriosus [32] and have been found to correlate with poor early outcome [17]. Data on coronary anatomy before 1992 were not reliably available, which prevents us from analyzing the effect of this variable on truncal valve management. In some cases, for example, coronary arteries with an intramural course or anomalous origin may interfere with annuloplasty or valve replacement. Among the 10 neonates with significant truncal valve insufficiency who underwent repair after 1992, anomalous coronary anatomy was present in 4 patients, but in none of them did this interfere with the surgical approach used. We routinely evaluate coronary arterial anatomy before operation, and we feel confident that preoperative echocardiography can define adequately the proximal coronary arterial anatomy in almost all cases [23].

Conclusions
Despite steadily evolving approaches to the management of truncal valve insufficiency, this is still a challenging lesion. The 1-year mortality rate remains high, especially among patients with severe insufficiency. However, the survival rate levels off beyond 1 year, with most late deaths related to reoperations. Although it generally is not necessary to address mild truncal valve insufficiency at the time of truncus arteriosus repair, this insufficiency eventually may progress to the point at which truncal valve repair or replacement is required in a significant number of patients. Especially in patients with mild to moderate or moderate insufficiency, truncal valve repair may be a desirable first option, because it can lead to decreased volume load on the recovering ventricle without the early risk of neonatal truncal valve replacement. In addition, late truncal valve replacement can be performed with lower risk than primary replacement in the neonate, although there remains a high mortality rate among infants who require truncal valve replacement in the first 6 months after repair. Extremely dysmorphic leaflets may make truncal valvuloplasty untenable, but we believe that valve repair is a preferable first option in most neonates with less than severe truncal valve insufficiency. Allograft truncal valve root replacement, although initially promising [16], has been disappointing in our experience and has proved not to be an adequate answer to this problem. Late survival is steady among patients who survive the operation.

	References

Top Abstract Introduction Patients and Methods Results Comment References

 

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