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Ann Thorac Surg 1997;64:721-729
© 1997 The Society of Thoracic Surgeons
Division of Cardiothoracic Surgery, UCLA School of Medicine, Los Angeles, California
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Abstract |
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 TopFootnotes Abstract IntroductionPatients and MethodsResultsCommentReferences |
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Methods. Surgical results in 19 consecutive patients are presented, with a median follow-up of 8 years. Mitral stenosis was present in all, with parachute deformity in 12 patients. Supramitral rings were found in 9 patients. Other features included subaortic stenosis (15 patients), valvar aortic stenosis (9), bicuspid aortic valve (16), and coarctation (13 patients). The patients underwent 46 surgical procedures, including 18 mitral operations (9 replacements, 9 repairs).
Results. There were three in-hospital (16%) and two late (10.5%) deaths. Of the 5 nonsurvivors, 4 patients (80%) had predominant mitral disease and moderate to severe pulmonary hypertension, versus 4 (28.5%) and 5 (36%) survivors, respectively (p = not significant). Valve repair was the final procedure in 9 survivors. The other 5 patients had repeated valve replacements (1), aortoventriculoplasty with valve replacements (2), or no mitral operation (2). Freedom from mitral reoperation was 78% (7 of 9 patients) after repair procedures and 43% (3 of 7 patients) after replacement. At follow-up, 10 patients (71.4%) are in New York Heart Association functional class I and the other 4 in class II and III. Six (43%) await reoperation due to recurrent aortic (4) or subaortic (1) stenosis and recoarctation (2). Echocardiography reveals mild mitral stenosis or regurgitation in 3 patients after repair (33%). Four are considered free of residual disease (21% of all).
Conclusions. Late outcome in Shone's anomaly seems to correlate with the predominance of mitral valve involvement and the degree of pulmonary hypertension. Valve repair is indicated whenever feasible and should be considered before the occurrence of pulmonary hypertension.
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Introduction |
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TopFootnotesAbstractIntroductionPatients and MethodsResultsCommentReferences |
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Thirty-three years after Shone and colleagues [1] first described the developmental complex bearing Shone's name, the treatment of this array of congenital left heart anomalies remains a surgical challenge. Four potentially obstructive lesions constitute the original features of Shone's complex: mitral supravalvular fibrous ring, parachute deformity of the mitral valve, subaortic stenosis (SAS), and coarctation of the aorta. These anomalies tend to coexist, but the severity and predominance of each individual lesion may vary, hampering attempts to identify an optimal management strategy. In clinical practice, the definition of Shone's anomaly has been extended beyond the original Shone complex, to encompass patients with additional forms of left heart anomalies, such as mitral and aortic valvular lesions and supraaortic stenosis.
Pediatric patients with multilevel left heart obstructive lesions are by no means a rare occurrence in clinical practice, nevertheless fewer than 50 such cases have been specifically reported in the literature. They are generally considered a poor surgical risk, and are often excluded from reports dealing with each of the individual disease components. The review of 30 cases by Bolling and associates [2] represents the largest report to date, and comprises patients with a multitude of anatomic variants as well as different management approaches. Data from this study indicate that outcome is related to the predominance and severity of the mitral component of the disease, the associated pulmonary hypertension (PHT), and the need for multiple surgical interventions. However, very limited data are currently available concerning the applicability and outcome of reparative techniques for the mitral valve lesions associated with Shone's anomaly. Moreover, it is uncertain whether management decisions based on experience with isolated left ventricular inflow or outflow disease can be applied in this more complex setting. In this review of an institutional experience, we emphasize the role of mitral valve disease in patients with multilevel left heart obstructions in view of the anatomy, hemodynamics, surgical results, and late outcome.
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Patients and Methods |
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TopFootnotesAbstractIntroductionPatients and MethodsResultsCommentReferences |
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There were 11 boys and 8 girls. All had abnormal mitral valves, and at least two other left heart obstructive lesions were diagnosed in each over the duration of the study. Median age at the first operation was 4.2 months (range, 2 days to 4.5 years), with 18 of the 19 patients (95%) having the initial surgical procedure before 18 months of age. Children with hypertrophic cardiomyopathy (often candidates for transplantation) and patients with double-outlet right ventricle were excluded, as were patients with hypoplastic left heart syndrome (left ventricle less than two-thirds normal size), who may often benefit from a Norwood-type univentricular repair rather than correction of obstructive lesions.
ANATOMY.
The diagnosis of Shone's anomaly was based on preoperative cardiac catheterization in 18 patients, and echocardiographic examination was available in all and was supplemented by Doppler ultrasound since the late 1980s. Figure 1
demonstrates the three intracardiac lesions typical of Shone's complex. Two-dimensional transthoracic echocardiography and Doppler have been shown to be highly sensitive in the diagnosis of congenital mitral stenotic lesions, but less accurate in the assessment of the severity of obstruction [3]. More recently, transesophageal echocardiography was found particularly useful for perioperative assessment of mitral anatomy and was used routinely for end-operative evaluation of surgical repair. Data thus obtained were confirmed at operation.
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. All features did not necessarily coincide at any given time point, and their relative hemodynamic severity varied considerably. As can be seen, all patients had abnormal mitral valves, with significant gradients (mean gradient >8 mm Hg) across the left ventricular inflow present in 16 children. Mitral valve anomalies were defined according to the classification by Ruckman and Van Praagh [4]. Supramitral fibrous rings were present in 9 patients (47%) and caused significant obstruction in 4 patients. Parachute deformity [5] was the most common anomaly of the valve and was present in 12 patients (63%). In 8 of these, parachute deformity caused significant left ventricular inflow obstruction. Five patients (26%) had "typical" congenital mitral stenosis (see Comment), which was always hemodynamically significant. In addition, hypoplastic mitral stenosis [4] with only minimal ventricular hypoplasia was present in 1 patient, and 1 had arcade deformity with no gradient across the valve.
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In addition to left heart obstructive lesions, the most common associated cardiac anomaly was patent ductus arteriosus, which was present in 8 patients (42%) and was associated with aortic coarctation in 6. Additional cardiac anomalies (see Table 1
) included ventricular septal defect (4 patients), atrial septal defect (2), and infundibular right ventricular outflow tract obstruction (1 patient).
HEMODYNAMIC DATA.
Right heart catheterization after repair of coarctation and before the first intracardiac operation was available in 17 patients (89%). Pulmonary artery peak systolic pressure was 61.3 ± 5.1 mm Hg and mean pressure was 40.1 ± 3.5 mm Hg. Pulmonary hypertension was severe (more than two-thirds systemic) in 9 patients, moderate in 2, mild in 2, and absent in 4 patients. No evidence of PHT was found on echocardiographic evaluation in the remaining 2 patients. Pulmonary mean wedge pressure was 20.2 ± 1.9 mm Hg. Left ventricular inflow obstructions were initially the predominant intracardiac lesions causing the most significant hemodynamic obstruction in 9 patients (47%), and 8 of these presented with significant (moderate to severe) PHT. In contrast, predominant left ventricular outflow tract (LVOT) obstructive lesions (in 10 patients) caused significant PHT in only 3 patients (p = 0.017), with severe PHT in 1 patient. Left ventricular function was normal in 14 patients (74%), mildly impaired in 1, moderately impaired in 3, and severe dysfunction was present in 1 patient. Left ventricular end-diastolic pressure was 11 ± 1.5 mm Hg; therefore, the mean gradient across the left ventricle inflow was 9 ± 1.1 mm Hg.
CLINICAL PRESENTATION.
Only 2 patients were asymptomatic at the time of the initial presentation, having audible murmurs that were attributable to coarctation of the aorta. The others presented with congestive heart failure that expressed early in the neonatal period. Mild congestive heart failure with failure to thrive, poor intake, and occasional dyspnea was present in 5 patients (26%) and was controlled medically in 3. In all 5 patients, the predominant anatomic feature was left ventricular inflow obstruction, including mitral stenosis (4) and supramitral ring (1). Five other patients had recurrent hospitalizations due to cardiac failure in spite of medical therapy that included digitalis, furosemide, and an angiotensin-converting enzyme inhibitor. Recurrent lower respiratory infections were a common feature, requiring repeat admissions in 4 patients. The predominant presenting lesion in all these patients was coarctation of the aorta. The remaining 7 patients presented within the first 10 days of life with severe decompensated congestive heart failure, requiring mechanical ventilation and intensive life support at the initial admission. Cardiogenic shock was present in 5 patients. These neonates had critical obstructive lesions that included coarctation (5) and valvar aortic stenosis (2 patients). Presenting chest roentgenograms were interpreted as normal in 6 patients (32%). Cardiomegaly was mild in 3, moderate in 6, and severe in 2 children. Pulmonary venous congestion was evident in 5 children, and 4 had frank pulmonary edema.
Surgical Procedures
The 19 patients underwent a total of 46 major operations, consisting of 94 distinct reparative procedures. Coarctation repair was performed through a left thoracotomy in 11 patients (58%) and was the first surgical procedure in 10 patients. Median age at the initial coarctation repair was 1.5 months (range, 2 days to 2 years). Repair was by subclavian flap in 7 patients, by polytetrafluoroethylene patch in 2, and by resection and end-to-end anastomosis in 2, with concomitant patent ductus arteriosus closure in 5 patients. In addition, balloon aortic angioplasty was attempted five times in 4 patients, 2 of whom had recoarctation. Two patients with coarctation did not undergo surgical repair due to mild gradient (1) or successful balloon dilatation (1).
Sixteen patients (84%) had one to four operations on the left ventricular inflow (Table 2), and in the remaining 3 patients with mitral disease intervention was not necessary during the study period. Resection of a supramitral ring was the only inflow procedure in 4 patients, whereas in the other 12 the initial procedure included valve repair in 9 and replacement in 3 patients. Average age at the time of first mitral valve operation was 2.1 ± 0.5 years (range, 1 month to 7 years). Since the late 1980s, repair of the mitral valve (see Table 2) was performed whenever possible. The reasons for mitral valve replacement (in 5 patients) included early failure of valve repair (2), or valve morphology that was not considered suitable for repair (3). All initial valve replacements were performed before 18 months of age (mean age, 12 ± 3 months), using St. Jude bileaflet prosthetic valves sized 19 mm (3 patients) or 21 mm (2 patients), two of the former being implanted in supraannular position. Replacement of the mitral prosthesis was required once in 1 patient and three times in another.
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). Age at the initial LVOT procedure was 2.5 ± 1.5 years. For SAS, transaortic resection was performed initially in 14 of 15 patients with this lesion (93%) and was accompanied by ventricular septal myomectomy in 12 patients. A left ventricular apical to descending aorta valved homograft conduit was placed in 1 patient after resection and myomectomy failed to relieve LVOT gradients. A Konno-Rastan aortoventriculoplasty [7, 8] was the first LVOT procedure in 1 patient and was performed to treat recurrence in 2 other children. One 12-mm aortic homograft was initially used in the aortic position in an 8-month-old boy, and was replaced 1 year later. St. Jude bileaflet prosthetic aortic valves (19 mm) were used for the final repair. Additional procedures were performed concomitant with the operation for left heart obstructive lesions in 11 patients:
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Results |
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TopFootnotesAbstractIntroductionPatients and MethodsResultsCommentReferences |
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One patient died 1 year after mitral commissurotomy and resection of severe tunnel-type SAS, performed at 18 months of age. Systemic PHT was present preoperatively and did not recede after repair. Despite good hemodynamics, recurrent ventricular arrhythmia with severe hypotension and seizures led to multiple admissions, and sudden death occurred at home in spite of maximal medical treatment. The second underwent a Konno-Rastan aortoventriculoplasty 8 years after initial resection of a discrete subaortic membrane at 9 months of age. At this time, severe recurrent tunnel-type SAS was present with left ventricular dysfunction. A single dysplastic kidney and progressive renal failure were also noted preoperatively. The patient survived a complete cardiorespiratory arrest 2 months postoperatively, but suffered severe ischemic encephalopathy. In spite of good hemodynamics, renal failure progressed to end stage, and sepsis and death occurred 4 years after operation.
Multivariate analysis identified no risk factors for operative or late death; however, survivors tended to be older at the time of the first intracardiac repair procedure (29.8 ± 7 months versus 12 ± 3.6 months, p = not significant). At this time, severe PHT was present in 4 of 5 nonsurvivors (80%), but in only 5 of 14 survivors (36%, p = not significant). The predominant obstructive lesion was mitral stenosis in 4 nonsurvivors (80%), but in only 4 survivors (28.5%, p = not significant).
Postoperative Morbidity
Postoperative complications in 4 patients (25% of early survivors) included heart block requiring implantation of permanent pacemaker after a Konno-Rastan aortoventriculoplasy in 2 patients, and tracheal stenosis after prolonged mechanical ventilation in a patient with suprasystemic PHT, who was treated by tracheostomy.
Operative Results
COARCTATION.
Surgical coarctation repair (in 11 patients) effectively reduced the gradient across the lesion from 40 ± 4 mm Hg to 9 ± 2 mm Hg (p = 0.008, paired t test). However, residual gradients of 15 to 25 mm Hg were present postoperatively in 3 patients (27%). Two of these and 2 additional patients had severe recoarctation within 3 months to 11 years postoperatively. Recurrence was not related to the method of repair (subclavian flap in 3 and polytetrafluoroethylene patch in 1). Balloon angioplasty (in 4 patients) was attempted as the initial therapy for coarctation in 2 and for recoarctation in 2 patients. Angioplasty was successful in eliminating the need for operation in 1 patient, and significant gradient reduction was achieved in three of five procedures. However, recurrence occurred in 2 patients within 1 to 3 years, and in 2 other patients there was no hemodynamic benefit from balloon angioplasty.
MITRAL VALVE OPERATION.
There was no recurrence of resected supramitral rings (in 8 surviving patients). Mitral valve repair was performed in 9 patients (see Table 2). Early postoperative (30 days) failure of the repair occurred in 2 infants (22%), aged 7 and 10 months, and was manifested by severe regurgitation requiring replacement of the valve. Both had severely reduced annular size and thick undeveloped chordae tendineae and required commissurotomy, chordal separation, and splitting of papillary muscles. The others had excellent surgical results, with one late death that was unrelated to valve repair. Residual mitral gradients (in 3 patients) were mild. Six long-term survivors were followed up for 6.8 ± 2.2 years (41 patient-years) after the initial repair procedure. There were no reoperations on the mitral valve during follow-up, and recent echocardiographic examination shows no more than mild mitral stenosis or regurgitation in all.
Mitral valve replacement was performed in 5 patients, two procedures being part of a Konno aortoventriculoplasty with double valve replacements. Two early postoperative deaths occurred in this group, and the 3 survivors were followed for 5 to 12 years (23.3 patient-years) after the initial replacement. One patient required three subsequent replacements after initial supraannular replacement at 4 months of age. These were due to panus formation 1 month after the initial operation, obstruction of pulmonary venous inflow 4 months later, then replacement with a larger sized valve at 6 years of age. The second had one re-replacement 5 years after the first procedure, which was done at 8 months of age. Both had a 19-mm St. Jude prosthesis implanted initially. The third patient, who had a 21-mm valve implanted at 1.5 years of age, did not require reoperation over 6 years of follow-up. Freedom from mitral valve reoperation after repair and replacement procedures is shown in Figure 3.
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Commissurotomy and resuspension of the aortic valve was successful in an 8-year-old patient but failed in a 2-day-old neonate, who underwent a Konno aortoventriculoplasty with a 12-mm homograft aortic valve after two repairs and a balloon angioplasty failed to relieve the valvar obstruction. One early death occurred in the third patient who underwent open aortic valvotomy.
Late Outcome
Survivors (n = 14) were followed up for 7.9 ± 1 years after the initial operation (up to 14 years). Ten patients (71%) are in New York Heart Association functional class I, 2 (14%) are in functional class II, and 2 (14%) are in functional class III. Recent echocardiographic findings are as follows:
As can be seen, significant hemodynamic abnormalities are present in 10 of 14 survivors (71%), whereas the remaining 4 are considered free of disease (21% of all patients). Six of these await reoperation for mitral stenosis (1), aortic stenosis (3), and recoarctation (2), whereas the others are being followed up conservatively. Interestingly, right ventricular pressures at follow-up are normal or mildly elevated in all but 1 patient, including 5 patients with preoperative severe PHT.
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Comment |
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TopFootnotesAbstractIntroductionPatients and MethodsResultsCommentReferences |
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The finding in Shone's original description that the extent of mitral valve involvement seems to be the predominant factor determining outcome is supported by the largest reported experience to date by Bolling and colleagues [2] and by data from the present study. Although Bolling and colleagues' report included 26 patients with mitral valve anomalies, only seven had mitral operations and three operative deaths (43%) occurred in this subgroup. Preoperative pulmonary pressures were significantly elevated in nonsurvivors, rendering PHT a considerable surgical risk factor. In the current series, 4 of 16 patients who underwent mitral operation died postoperatively (25%), all having predominant mitral disease and severe PHT. Thus, surgical mortality in patients with Shone's complex and severe mitral disease is comparable with existing experience with isolated congenital mitral stenosis [11, 12], and patients with critical obstruction and severe secondary PHT generally carry the worst prognosis. Nevertheless, our finding that even severe PHT is reversible in a vast majority of long-term survivors is encouraging, and as perioperative care continues to improve this may lead to lower overall mortality in these high-risk patients.
When deciding on the optimal surgical approach to patients with multilevel left heart obstructions, one must consider the morphology and predicted course of individual obstructive lesions and their relative hemodynamic significance as well as associated risk factors. We found PHT to be associated mainly with left ventricular inflow obstructions, whereas predominant LVOT lesions, although severe, rarely caused more than moderate elevation in right heart pressures. Because relief of LVOT obstructions was undertaken early, mitral incompetence did not develop in these patients, which may explain this finding.
A majority of patients in this series presented initially in the neonatal period with coarctation of the aorta as the predominant obstructive lesion. Coarctation may mask the presence and severity of associated intracardiac lesions, and indeed the diagnosis of Shone's anomaly in several patients was made on the basis of persistent symptoms of heart failure after coarctation repair. Therefore, additional left heart obstructions should be excluded in such patients, or in cases when symptoms are disproportionate to the severity of coarctation. However, intracardiac lesions were rarely severe at the time of coarctation repair, and in most patients tended to become clinically significant only later in the course of the disease (beyond 2 years of age in this study), which may explain the low operative risk associated with the initial thoracotomy in our patients and in Bolling's report. In the setting of Shone's anomaly, an especially aggressive form of aortic coarctation is suggested by the early neonatal presentation, the severity of symptoms, and the high recurrence rate (36%). Moreover, repair in neonates has been associated with higher incidence of restenosis regardless of operative technique [13, 14]. Recently, the use of an extended end-to-end anastomosis of the mobilized descending aorta to the inferior curvature of the aortic arch [15] and even inclusion of the ascending aorta [16] has shown considerable promise and is currently recommended by us.
Recent advances in operative technique and the routine use of intraoperative transesophageal echocardiography tend to favor a reconstructive approach over initial replacement for mitral stenosis. Reports from this institution [17] as well as others [12] suggest that late results of valve repair are superior to replacement in patients with isolated congenital mitral anomalies. Successful repair may allow for annular growth and delay or obviate the need for valve replacement and anticoagulation, whereas in this and other reports [11] early replacement frequently required subsequent reoperation for placement of larger prostheses. Although the comparison of the results of mitral repair and prosthetic replacement indicated no significant differences in terms of survival or reoperation rates because of the limited number of patients in this study, we noted a trend toward lower risk of late events in patients undergoing repair (see Fig 3). Early failure of repair occurred in 2 patients, but excellent results were observed in the others, and persisted over an average follow-up of 6.8 years. When initially successful, repair was durable and reoperation was not required. And, because the failed repair procedures were performed before the availability of transesophageal echocardiography, it can be assumed that this outcome is currently preventable. Initial valve replacement was performed in 2 patients in the early 1980s, both requiring subsequent replacements of the prosthesis. More recently, repair may have been attempted in both cases. These results support the conclusion that a repair procedure based on understanding of the common anatomic variants is warranted whenever possible for treatment of the obstructive mitral lesions associated with Shone's anomaly. Currently, we believe that most such lesions are initially amenable to repair rather than primary replacement, chiefly because the main obstructive element in this condition is subvalvar, rather than the small annular orifice associated with hypoplastic left heart and the hypoplasic mitral valve. The availability of smaller mitral prostheses (16 mm) now provides a "safety net" in case of failed repair, making early operation a viable option. Because PHT adversely affects surgical outcome, repair should not be delayed even in very young patients.
The morphology of the mitral valve in Shone's anomaly is critical to determine the reconstructive surgical approach. Precise preoperative evaluation of the anatomy can now be obtained by high resolution two-dimensional echocardiography [3]. The most prevalent variants of mitral obstructive lesions in this disease (parachute deformity and supramitral ring) are not readily amenable to balloon angioplasty due to unbalanced chordal attachment and supravalvar obstruction, respectively, rendering operation the only viable option [11, 18].
Supramitral fibrous rings are a characteristic feature of Shone's anomaly [1], never occur as isolated lesions [3], and are rarely severely obstructive [4]. Present in 47% of patients in this series, they caused significant obstruction in 44% of cases. Resection is straightforward and although recurrence has been described in one report [19], in our experience and that of others [11] these lesions do not tend to recur.
Of the mitral valvular anomalies, parachute deformity was present most often (in 65% of patients). In this lesion, all chordae tendineae connect to one papillary muscle. The chordae are usually shortened and thickened, and although the anterolateral papillary muscle is most often absent, there is considerable anatomic variability in the arrangement of the papillary muscles. Rarely (in 2 patients in this series) both papillary muscles are present with chordal attachments to one. In 9 of 13 patients, parachute deformity caused significant left ventricular inflow obstruction. The common association of this deformity with supramitral rings and coarctation of the aorta has been documented [3–5]. Parachute mitral valves can cause varying degrees of hemodynamic compromise depending on chordal development and annular size, and satisfactory hemodynamic results have been achieved in this series by a reconstructive approach consisting of splitting the papillary muscle and release and separation of chordae tendinae so as to open the obliterated chordal spaces and increase the effective mitral orifice. Another morphologic type, the "typical" congenital mitral stenosis as defined by Ruckman and van Praagh [4], was seen in 25% of our patients. In this anomaly annular size is small, the leaflet margins are thickened and rolled, the chordae tendinae are short and thick, and there is variably reduced interpapillary distance. In this variant, commissurotomy with separation of the chordae may postpone or even eliminate the need for valve replacement.
Left ventricular outflow tract obstructive lesions in patients with Shone's anomaly may be subvalvar, valvar, or supravalvar (65%, 30%, and 10% respectively in this series). Subaortic stenotic lesions are rarely present at birth and are usually progressive, albeit at a variable rate [20, 21]. Discrete membranous lesions can be effectively treated by transaortic resection, which usually eliminates the obstruction, and by ventricular septal myomectomy, which has been recommended to prevent recurrence [22]. However, the incidence of recurrence is still considerable (20% in our experience [23] and as high as 55% in some reports [24]). Long segment fibromuscular tunnel lesions represent a less common but more severe form of SAS. In tunnel SAS, residual postoperative gradients are often present and recurrence following isolated local resection is common [21]. In the present series of patients with Shone's anomaly the tunnel variant was the presenting type of SAS in 27% of patients with LVOT lesions, over three times the incidence observed in patients with isolated SAS at this institution [23]. Moreover, rapid progression of the obstruction was observed in all patients with SAS, as reflected by the mean patient age at the time of the first SAS operation (2.5 years), which was significantly lower than the mean age for SAS surgery in patients with no other anomalies [22, 23, 25]. In addition, the recurrence rate after transaortic resection of discrete lesions was 56% (5 patients) in 9 survivors after one to nine years. These data suggest that a more aggressive form of SAS is present in the setting of Shone's anomaly, and may require more extensive surgery to provide long term relief of LVOT obstruction. We found that a Konno–Rastan aortoventriculoplasty [7, 8] using mechanical aortic valve prostheses effectively eliminated subaortic and aortic valvular obstruction in 3 patients over 5 years of follow-up. This procedure, using prosthetic or homograft aortic valves was recommended by others for the treatment of tunnel type SAS [22]. Although aortoventriculoplasty was used mostly for recurrent SAS at this institution, it may be the optimal initial operation for long segment lesions or in the presence of significant aortic valve disease. More recently, the pulmonary valve autograft has been successfully used in the aortic position as part of a Ross-Konno operation [26], and showed growth potential in addition to excellent competence. This new technique may emerge as the best option for definitive repair of LVOT obstructive lesions in children with Shone's anomaly.
It is apparent that the diversity and complex nature of cardiac anomalies in children with Shone's disease make it necessary to tailor the surgical interventions and management of each individual patient. Despite high surgical risk and considerable early mortality, late outcome in the majority of patients is favorable. We believe that an aggressive reconstructive approach to both left ventricular inflow and outflow lesions may further extend event-free survival in these critically ill patients.
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Address reprint requests to Dr Laks, Division of Cardiothoracic Surgery, UCLA Medical Center, 62-182A Center for the Health Sciences, 10833 Le Conte Ave, Los Angeles, CA 90095.
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