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Ann Thorac Surg 1997;64:1795-1802
© 1997 The Society of Thoracic Surgeons
Departments of Cardiology and Pathology, Children's Hospital and Harvard Medical School, Boston, Massachusetts
Accepted for publication July 19, 1997.
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Abstract |
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 TopFootnotes Abstract IntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Methods. To establish the causes of death and consider their therapeutic applications, we reviewed our pathology experience from 1980 to 1995, inclusive, regarding 122 patients who died after undergoing the Norwood procedure.
Results. The most important causes of death were found to be impairment of coronary perfusion (33 patients, 27%), excessive pulmonary blood flow (23 patients, 19%), obstruction of pulmonary arterial blood flow (21 patients, 17%), neoaortic obstruction (17 patients, 14%), right ventricular failure (16 patients, 13%), bleeding (9 patients, 7%), infection (6 patients, 5%), tricuspid or common atrioventricular valve dysfunction (6 patients, 5%), sudden death from presumed arrhythmias (6 patients, 5%), and necrotizing enterocolitis (3 patients, 3%). In 26 patients (21%), more than one factor appeared responsible for death.
Conclusions. The leading causes of death after the Norwood procedure were found to be largely correctable surgical technical problems associated with perfusion of the lungs (36%), of the myocardium (27%), and of the systemic organs (14%).
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Introduction |
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To clarify the causes of death and in an effort to contribute to improvement of the surgical management of such patients, we reviewed the clinical course and postmortem findings in all autopsied patients who died after undergoing the modified Norwood procedure during the past 16 years.
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Material and Methods |
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We reexamined the heart specimens of these 122 patients with special emphasis on the pathologic anatomy, all details of the surgical palliation, the myocardial histology, and the pathologic findings. These data were correlated with the clinical, cardiac catheterization, echocardiographic, intraoperative, and postoperative findings in an effort to determine the cause or causes of death.
There were 86 boys (70%) and 36 girls (30%). All patients had a ductus-dependent systemic circulation because of obstruction of the aortic outflow tract. The underlying pathologic anatomic diagnoses are summarized in Table 1
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Several modifications of the Norwood procedure were used in the reconstruction of the neoaorta:
Several modifications were used to reestablish pulmonary blood flow:
The median survival after undergoing the Norwood procedure in these 122 postmortem cases was 2.5 days, ranging from intraoperative death to 1 year and 8 months.
Statistical analysis was performed using the 
2 test and Fisher's exact test, when appropriate, a p-value less than 0.05 being regarded as statistically significant.
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Results |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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). Precoronary stenosis was present in 26 of these patients (21% of the series). At autopsy, the opening into the native aortic root, from which the coronary arteries almost always arose, was nonpatulous, ie, not widely patent. On initial inspection from within the reconstructed neoascending aorta, the coronary ostia could not be seen. Although the opening into the native aortic root was patent to a probe, it was slitlike and appeared markedly narrowed from the functional standpoint. In 17 of these patients with precoronary stenosis, a classic Norwood procedure had been performed: the ascending aorta was opened vertically down to the aortic root. In 12 patients, the surgical sutures appeared to contribute directly to the narrowing of the opening leading into the coronary compartment, or indirectly by producing some torsion of the neoaortic wall. Inward bulging of an arterial homograft contributed to precoronary narrowing in 3 patients. Progressive fibrotic narrowing of the communication leading into the coronary compartment was found 3.6 months postoperatively in 1 patient.
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In the remaining 2 patients with precoronary stenosis, the neoascending aorta was reconstructed without augmentation by anastomosing the proximal main pulmonary artery directly to the undersurface of the transverse aortic arch. In 1 patient, this was associated with narrowing of the ostium leading into the top of the native ascending aorta. In the other patient, the aforementioned unaugmented reconstruction was associated with kinking in the midportion of the native ascending aorta.
There was no significant difference between precoronary stenosis with tubular augmentation (7 of 45 patients) or patch augmentation of the neoaorta (17 of 67 patients) (p = 0.23). The material used for the reconstruction was also not significant: prosthetic material, 17% (8 of 47 patients) versus homograft or pericardium, 25% (16 of 65) (p = 0.34). Precoronary stenosis appeared to be a correctable technical problem that occurred in all years of the present study.
In addition to precoronary stenosis, additional causes of impaired coronary arterial perfusion were identified as follows: (1) thromboembolism to the right coronary artery was found in 2 patients; (2) surgical ligation of an aberrant left circumflex coronary artery from the right pulmonary artery occurred in 1 rare case, resulting in biventricular infarction; (3) extrinsic compression of an intramural right coronary artery by prosthetic patch material (Hemashield) used to augment the neoascending aorta resulted in myocardial infarction in 1 patient; (4) laceration of the right coronary artery led to myocardial infarction and death 12 hours postoperatively in 1 patient; (5) generalized coronary arterial hypoplasia was found in one rare patient; and (6) congenital stenosis of the coronary sinus involving its termination (1 cm in length) and right atrial ostium was found in 1 patient, in whom coronary arterial and venous congestion was marked. This patient also had a persistent left superior vena cava to the coronary sinus.
The interval between operation and death in the group with impairment of coronary perfusion was a median of 0.25 days and mean of 11.0 ± 38.95 days. The length of postoperative survival of the patients with other causes of death was a median of 11.0 days and mean of 62.37 ± 124.2 days (p < 0.01).
Impairment of coronary perfusion led to acute myocardial failure in 30 patients (91%), and to chronic myocardial failure in 3 patients (9%). (1) In the acute heart failure group, 9 deaths occurred intraoperatively—accounting for 64% of all intraoperative fatalities. Of these 30 patients, 21 died within the first 3 postoperative days (70%). (2) In the chronic heart failure group, 3 patients died of myocardial ischemia more than 2 weeks postoperatively. One of these patients also had residual coarctation of the neoaortic arch, which may have contributed to death 3 weeks postoperatively. The patient with progressive fibrotic precoronary stenosis survived for 110 days postoperatively (3.6 months). The patient with severe congenital stenosis of the coronary sinus (described above) also had stenosis of the central shunt leading to the right pulmonary artery. Both of these factors contributed to the death of this patient 6.5 months postoperatively.
Excessive Pulmonary Blood Flow
Excessive pulmonary blood flow was the second most common cause of death after undergoing the modified Norwood procedure (23 patients, 19%, Table 2
). Pulmonary blood supply was reestablished by a conduit from the right ventricle to the distal main pulmonary artery in 2 early patients using a nonvalved 8-mm Gore-Tex conduit in 1 and a 12-mm valved Hancock conduit in the other. Neither of these relatively large conduits introduced the necessary degree of pulmonary stenosis. A central shunt was associated with increased pulmonary blood flow in 4 patients (4 mm in 3, and 5 mm in 1), 3 of whom had additional sources of pulmonary blood flow: an unligated ductus arteriosus in 2, and a classic Blalock-Taussig shunt in 1. In 1 patient, the distal main pulmonary artery was sutured directly into the neoascending aorta. The other 16 patients all had modified Blalock-Taussig shunts: 7 mm in 2; 5 mm in 1; 4 mm in 12; and 3.5 mm in 1.
Postoperative deaths occurred early in 17 patients (74%): intraoperatively in 4; on the first postoperative day in 7; and 23 days or less postoperatively in 6. Of these 17 early fatalities, additional factors contributing to death were identified in 9 patients: groups 2, 14, 15, 16, 20, 21, and 22 (Table 3).
There were 6 late deaths in the excessive pulmonary blood flow group, occurring between 48 days and 13 months postoperatively. Additional factors contributing to death were found in 3 of these 6 patients: groups 17 to 19 (Table 3).
The size of the shunt was significantly related to excessive pulmonary blood flow. When the size of the modified Blalock-Taussig shunt was 4 mm or more, excessive pulmonary blood flow occurred in 22% (14 of 63 patients). But when the size was 3.5 mm or less, excessive pulmonary blood flow occurred in only 5% (2 of 39 patients) (p = 0.02). The origin of the superior stoma of the shunt was not significantly related to the prevalence of excessive pulmonary blood flow: from the innominate artery, 20% (12 of 59 patients), from the junction between the innominate and the subclavian artery, 8% (2 of 25 patients), and from the subclavian artery, 11% (2 of 18 patients) (p 
0.14). However, after 1989, when 3.5-mm shunts were used preferentially and the superior stoma was placed at the innominate–subclavian artery junction, only 3 patients died of excessive pulmonary blood flow (13% of this group).
Obstruction of Pulmonary Arterial Blood Flow
Obstruction of pulmonary arterial blood flow was the third most common cause of death after undergoing the Norwood procedure (21 patients, 17%, Table 2). Death resulted from acute thrombosis of the modified right Blalock-Taussig shunt in 14 patients (67%). Factors predisposing to acute shunt thrombosis were as follows: stenosis of the superior stoma of the shunt, 2; narrowing of the inferior stoma of the shunt, 1; upward tenting of the inferior wall of the right pulmonary artery narrowing the outlet from the shunt, 1; compression of the superior and inferior stomata because of excessive length of the shunt, 1; operative narrowing of the shunt caliber after the Norwood procedure, 1; acute low cardiac output caused by precoronary stenosis in 3 (with stenosis of the superior stoma of the shunt in 1); chronic right ventricular failure, 1; and evidence of infection in 3 (sepsis in 1, necrotizing enterocolitis in 1, and acute bronchopneumonia in 1).
Thromboembolic occlusion of the shunt related to an indwelling catheter in the right atrium accounted for 1 death. This patient had a successful thrombectomy and shunt replacement 1 hour postoperatively, but he died of a thromboembolus to the shunt on the tenth postoperative day. In another patient, the cause of the shunt thrombosis remained unclear. In 1 patient there was chronic thrombotic occlusion of the shunt that led to death 10 months postoperatively. This patient also had chronic right heart failure plus diarrhea for 5 days before death. All but 1 of the patients with acute shunt thrombosis died within 18 days postoperatively (13 of 14), 5 deaths occurring within the first 24 hours.
Shunt size was significantly related to shunt thrombosis. When the size of the modified Blalock-Taussig shunt was 3.5 mm in diameter or less, thrombosis occurred in 26% (10 of 39 patients). But when the shunt size was 4.0 mm in diameter or greater, then thrombosis occurred in only 8% (5 of 63 patients) (p < 0.02). In contrast, the superior origin of the modified Blalock-Taussig shunt was not significantly related to the prevalence of shunt thrombosis: from the innominate artery, 14% (8 of 59 patients); from the junction of the innominate and subclavian arteries, 16% (4 of 25 patients); and from the subclavian artery, 17% (3 of 18 patients) (p 0.50).
The majority of thromboses of the modified Blalock-Taussig shunt occurred after 1989, when shunts of smaller size and superior origins from either the innominate–subclavian junction or the subclavian artery were used preferentially: 60% (9 of 15 patients).
Other causes of lethal obstruction of pulmonary arterial blood flow included the following: severe stenosis of the superior stoma of the modified Blalock-Taussig shunt without thrombosis, 1; narrowing of the central shunt, 1; compression of the subclavian artery by excessive conduit length in 2, with associated compression of the right pulmonary artery in 1; pulmonary thromboembolism, 1; and compression of the pulmonary arteries and of the tracheobronchial tree by a large false aneurysm of the neoascending aorta, 1.
Three of the above-mentioned patients had additional factors contributing to death (groups 12, 25, and 26, Table 3).
Neoaortic Obstruction
The fourth most common cause of death was obstruction of the neoaorta (17 patients, 14%, Table 2). Obstruction of the ascending neoaorta was produced by kinking and inward bulging of the wall or suture line involving the amplifying patch, the proximal main pulmonary artery, or both (6 of 17 patients, 35%). In 1, a ligated but undivided ductus arteriosus appeared to contribute to the deformity by pulling the neoaorta leftward. In another, the wall of the proximal main pulmonary artery formed a low roof above the pulmonary valve, leaving only a small opening to the right between the supravalvar compartment and the remainder of the neoascending aorta. In 1 patient, additional factors contributing to death were identified (group 15, Table 3). Stenosis of the neoascending aorta occurred only with patch augmentation (6 of 67 patients, 9%), but never with tube augmentation (0 of 45 patients, 0%), this being a significant difference (p = 0.04). However, there was no significant difference between stenosis associated with a prosthetic patch (4 of 47, 8.5%) versus stenosis associated with a homograft or pericardial patch (2 of 65, 3%) (p = 0.16).
Stenosis of the distal end or of the transverse arch of the neoaorta was found in 10 of 17 patients (59%). This type of complication occurred with tubular amplification of the neoascending aorta and with patch amplification when either technique did not extend distal to the site of the native aortic isthmus. In 1 of these patients with tubular amplification, the tube was compressed by chest closure. Additional factors contributed to the death of 5 other patients (groups 3, 14, 25, and 32, Table 3). Stenosis of the transverse aortic arch or of the distal end of the neoaorta was associated significantly more frequently with tubular augmentation (7 of 45 patients, 16%) than with patch augmentation (3 of 67 patients, 4.5%) (p = 0.04). In this group as well, there was no significant difference between patients receiving reconstructions of prosthetic material (5 of 47 patients, 11%) and patients receiving reconstructions of homograft or pericardium (5 of 65 patients, 8%) (p = 0.22).
Chest wall compression of a conduit from the ascending neoaorta to the descending aorta occurred in 1 patient (6%). This conduit was placed in an attempt to bypass a stenosis in the neoascending aorta.
Right Ventricular Failure
Right ventricular myocardial failure appeared to be the primary immediate cause of death in 16 patients (13%, Table 2). Preoperative right ventricular failure with low cardiac output predisposed to an unfavorable postoperative outcome in 5 of 16 patients (31%). Postoperative right ventricular failure with low cardiac output occurred in 6 of 16 patients (37.5%). In none of these patients was any technical factor predisposing to right ventricular failure identified. A right ventriculotomy (to create a right ventricle-to-pulmonary artery conduit) was performed in 3 patients and was thought to contribute importantly to right ventricular failure. All 3 patients had additional factors leading to death (groups 15, 16, and 34, Table 3). These patients died 11 hours or less postoperatively. An "unprepared" right ventricle led to death in 1 patient who underwent a modified Norwood procedure very late (21 days of age), a balloon aortic valvuloplasty having been performed at 1 day of age. In addition to severe congenital aortic stenosis, this patient also had left ventricular hypertrophy and enlargement, endocardial fibroelastosis of the left ventricle, and congenital mitral stenosis. However, the right ventricle was relatively thin-walled (3 to 5 mm) compared with the left ventricle (9 to 13 mm). Chronic right ventricular failure of uncertain cause was found in 1 patient who also had chronic shunt thrombosis and an episode of diarrhea during the final 5 days of life (group 26, Table 3).
Bleeding
Hemorrhage leading to shock or pericardial tamponade was the immediate cause of death in 9 patients (7%). Of these 9 patients, 7 (78%) died early postoperatively (
23 hours postoperatively).
There were 2 late deaths caused by bleeding. One patient died 9 days postoperatively, with the autopsy revealing a 10-mm dehiscence in the suture line between the native main pulmonary artery and the native ascending aorta. The other patient died 34 days postoperatively of chronic tamponade that was thought to be caused by the oozing of blood through the Gore-Tex patch that was used to amplify the neoascending aorta. No discrete bleeding point was identified at reoperation or at autopsy.
Infection
Infection caused death in 6 patients (5%) as follows: (1) acute mediastinitis in 2 patients; (2) sepsis (positive blood cultures) in 2 patients, immediately preoperatively in 1 and in association with increased pulmonary blood flow in the other; (3) peritonitis with increased pulmonary blood flow in 1; and (4) acute tricuspid endocarditis caused by Staphylococcus aureus, with destruction of the septal leaflet leading to an increase in tricuspid regurgitation in 1.
Tricuspid or Common Atrioventricular Valve Dysfunction
Dysfunction of the tricuspid valve (n = 5) or of a common atrioventricular valve (n = 1) was an important immediate cause of death in 6 patients (5%, Table 2). Tricuspid regurgitation or regurgitation of a common atrioventricular valve occurred in 5 patients. Three had right ventricular failure and 2 had excessive pulmonary blood flow. Tricuspid stenosis, after tricuspid valve replacement, was found in 1 patient. Autopsy 8.5 months after tricuspid valve replacement revealed pannus formation on the atrial and ventricular prosthetic surfaces, restricting leaflet mobility.
Sudden Arrhythmic Death
Sudden death, presumably as a result of arrhythmia, occurred in 6 patients (5%, Table 2). Three died early (11 days postoperatively). One of these patients had a history of Wolff-Parkinson-White syndrome and autopsy also revealed precoronary stenosis. The second patient died after cardiac arrest during airway suctioning. However, in the third early death, autopsy revealed no specific cause predisposing toward arrhythmia.
Three patients died late (from 2 to 20 months postoperatively), and autopsy disclosed no specific reason for the sudden arrhythmic death.
Necrotizing Enterocolitis
Necrotizing enterocolitis was the cause of death in 3 patients. Two of them had reduced systemic perfusion (stenosis at the distal end of the neoaorta in 1, and excessive pulmonary blood flow with reduced systemic perfusion distal to the shunt in 1), and the third patient had necrotizing enterocolitis in association with chronic mediastinitis and sepsis.
Obstruction of Pulmonary Venous Return
A restrictive interatrial septum resulted in obstruction of the pulmonary venous return in 2 patients (2%, Table 2). In 1 patient, additional problems coexisted (group 28, Table 3), whereas in the other patient, the main postmortem finding was an intact atrial septum with a 3-mm diameter patent foramen ovale.
Miscellaneous
Six other immediate causes of death were identified in this study and are summarized in groups 5, 6, and 43 to 45 in Table 3.
Myocardial Histology
Histologic slides were available for review in 98 of the 122 patients. Myocardial histology was normal except for hypertrophy (group 1, Table 4) in 25 patients (26%), and showed evidence of ischemia in the remaining 73 patients (74%). The majority of patients with abnormal findings showed coagulation necrosis (group 2, Table 4): 62 patients, 63% of the series. Myocyte dropout with granulation tissue and variable replacement fibrosis (group 3, Table 4) was observed in 11 patients (11%). The relationship between the duration of postoperative survival and the myocardial histologic findings is summarized in Table 5.
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= 0.22).
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Comment |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Consequently, the present study was undertaken in an effort to identify the causes of death after undergoing the modified Norwood procedure (stage I palliation), to contribute to the improvement of the medical and surgical management of these patients. Eleven main causes of death were identified by this study, many of which appeared to be largely correctable surgical technical problems.
Impairment of coronary arterial perfusion occurred in 33 patients (27%, Table 2). In the classic Norwood procedure in which the aorticopulmonary septum is incised vertically, it is important that the approaches to the coronary ostia remain patulous. The surgeon should be able to see the (typically) atretic aortic valve and the adjacent coronary arterial ostia after completion of the reconstruction of the ascending neoaorta.
If tubular amplification of the neoaorta is used, it is important that the superior stoma leading into the native ascending aorta be widely patent. Stretching, flattening, or kinking of this superior aortic stoma should be avoided because the small native ascending aorta functions as a common coronary artery that leads down to the aortic root and the coronary ostia.
Impairment of coronary perfusion may not be evident in myocardial histology at postmortem examination because significant ischemia may lead to death before myocardial necrosis can develop. The presence of histologic findings of myocardial ischemia by light microscopy appeared to correlate with the duration of postoperative survival rather than with the severity of myocardial ischemia. For example, among patients with normal myocardial histology, ie, no evidence of ischemia, the median postoperative survival was only 0.5 days (group 1, Table 5). Patients with histologic evidence of coagulation necrosis (partial or complete) had a median postoperative survival time of 5.5 days (group 2, Table 5). Patients with the most advanced histologic evidence of myocardial ischemia had a median postoperative survival interval of 15.0 days (group 3, Table 5). Histologic findings indicative of myocardial ischemia in patients with impairment of coronary perfusion were not significantly different from those found in patients without impairment of coronary perfusion (Table 6).
Although light microscopy did not discriminate between the impaired and the unimpaired coronary perfusion groups (as above), the duration of postoperative survival was very different in these two groups: impaired coronary perfusion, median survival of 0.25 days; and unimpaired coronary perfusion, median survival of 11.0 days.
Excessive pulmonary blood flow occurred in 23 patients (19%, Table 2). Our findings support the view that the modified Blalock-Taussig conduit should be 3.5 mm in diameter in the newborn, and that conduits of 4.0 mm or greater are too large, resulting in excessive pulmonary blood flow. In these 23 patients with excessive pulmonary blood flow, the hypothetical possibility exists that myocardial ischemia may have resulted, in part, from a coronary steal phenomenon secondary to an excessive left-to-right shunt through the Blalock-Taussig anastomosis. However, we have no physiologic data that support or refute this speculative possibility.
Obstruction of pulmonary arterial blood flow occurred in 21 patients (17%, Table 2). Shunt thrombosis or thromboembolism usually appeared to be related to surgical technical factors, or to the presence of significant associated problems such as infection or low cardiac output.
Neoaortic obstruction involving the proximal and distal portions of the aortic reconstruction occurred in a total of 17 patients (14%, Table 2). When patch amplification of the ascending neoaorta is used, care should be taken to avoid inward bulging of the reconstruction. When tubular amplification is employed, narrowing of the distal aortic arch can occur because of failure of the amplification to extend sufficiently distally. Obstruction of the ascending neoaorta was found to be a cause of death in 6 of our 122 patients (5%). Weinberg and associates [8] documented moderate to severe proximal aortic narrowing in 5 of 27 patients (19%) examined by postmortem two-dimensional echocardiography. Moderate to severe obstruction at the distal end of the neoaorta was a lethal factor in 10 of our 122 patients (8%), compared with 2 of 27 patients (7%) in the series of Weinberg and associates [8].
Right ventricular failure occurred in 16 patients (13%, Table 2). Failure of the systemic right ventricle occurred preoperatively (in 5 patients) and postoperatively (in 6 additional patients) unrelated to any surgical technical factors that we were able to identify. These patients who had "primary" right ventricular failure raise the question of the adequacy of the morphologically right ventricle as a systemic pump. All of the factors that favor the arterial switch procedure for transposition of the great arteries to make the morphologically left ventricle the systemic pump [9] are conversely of concern regarding the morphologically right ventricle as the systemic pump in patients undergoing the modified Norwood procedure. In addition, surgical technical factors were found to be important in leading to right ventricular failure in some cases (right ventriculotomy and "unprepared" right ventricle).
Bleeding occurred in 9 patients (7%, Table 2). Hemorrhage usually appeared to be a preventable surgical technical problem.
Infection occurred in 6 patients (5%, Table 2). Infection was often an associated factor in patients with other surgical technical problems, such as increased pulmonary blood flow.
Tricuspid or common atrioventricular valvar dysfunction occurred in 6 patients (5%, Table 2). Tricuspid regurgitation often appeared to be related to the deficiencies of the tricuspid valve as a systemic atrioventricular valve—the mitral valve being much better designed to occlude an approximately circular systemic atrioventricular orifice [9].
Sudden arrhythmic death occurred in 6 patients (5%, Table 2). Although autopsy did not reveal a specific cause of death in these patients—except for 1 with precoronary stenosis—it is noteworthy that the severe endocardial fibroelastosis typically associated with aortic valvar atresia is considered to be "old" global subendocardial myocardial ischemic necrosis or infarction, with myocardial replacement by fibrous and elastic tissue; hence, the gross and histologic appearance of endocardial fibroelastosis. When the left ventricular intracavitary pressure remains greater than the coronary perfusion pressure in diastole, the subendocardial layer of the myocardium cannot be adequately perfused, leading to subendocardial myocardial ischemia and infarction—which in turn are well-established risk factors for ventricular arrhythmias. Marked ventricular hypertrophy (as of the right ventricle with aortic valvar atresia) also is an independent risk factor for sudden arrhythmic death [10].
Necrotizing enterocolitis occurred in 3 patients (3%, Table 2). Necrotizing enterocolitis appeared to be secondary to reduced organ perfusion in association with excessive pulmonary blood flow, systemic outflow tract obstruction, or infection.
Obstruction of pulmonary venous return occurred in 2 patients (2%, Table 2). Because the atrial septum is frequently thickened in the hypoplastic left heart syndrome, balloon atrial septostomy is often unsuccessful, making adequate surgical atrial septectomy mandatory.
Death was the result of more than one main cause in 26 patients (21%, Table 3).
One of the limitations of this study is that functional factors (such as pulmonary hypertensive crises) may be underrepresented in this analysis.
In this study the preoperative, intraoperative, postoperative, and postmortem data have been carefully analyzed and correlated. Unfortunately, there are few available data at the present time with which our findings can be compared. Clearly, more studies of this type are needed. It is our hope that the findings of the current study will help to further improve the surgical results after undergoing the modified Norwood procedure.
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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This article has been selected for the open discussion forum on the STS Web site: http://www.sts.org/annals
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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B. D. Kussman, K. Gauvreau, J. A. DiNardo, J. W. Newburger, A. S. Mackie, K. L. Booth, P. J. del Nido, S. J. Roth, and P. C. Laussen Cerebral perfusion and oxygenation after the Norwood procedure: Comparison of right ventricle-pulmonary artery conduit with modified Blalock-Taussig shunt J. Thorac. Cardiovasc. Surg., March 1, 2007; 133(3): 648 - 655. [Abstract] [Full Text] [PDF]
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 B. Alsoufi, J. Bennetts, S. Verma, and C. A. Caldarone New Developments in the Treatment of Hypoplastic Left Heart Syndrome Pediatrics, January 1, 2007; 119(1): 109 - 117. [Abstract] [Full Text] [PDF]
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M. Nathan, D. Rimmer, P. J. del Nido, J. E. Mayer, E. A. Bacha, A. Shin, W. Regan, R. Gonzalez, and F. Pigula Aortic Atresia or Severe Left Ventricular Outflow Tract Obstruction with Ventricular Septal Defect: Results of Primary Biventricular Repair in Neonates Ann. Thorac. Surg., December 1, 2006; 82(6): 2227 - 2232. [Abstract] [Full Text] [PDF]
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M. Ricci, P. Lombardi, A. Galindo, S. Schultz, A. Vasquez, and E. Rosenkranz Effects of single-ventricle physiology with aortopulmonary shunt on regional myocardial blood flow in a piglet model. J. Thorac. Cardiovasc. Surg., August 1, 2006; 132(2): 252 - 259.e2. [Abstract] [Full Text] [PDF]
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E. M. Graham, G. A. Forbus, S. M. Bradley, G. S. Shirali, and A. M. Atz Incidence and outcome of cardiopulmonary resuscitation in patients with shunted single ventricle: Advantage of right ventricle to pulmonary artery shunt J. Thorac. Cardiovasc. Surg., May 1, 2006; 131(5): e7 - e8. [Full Text] [PDF]
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E. Villa, G. Brancaccio, A. Carotti, P. Francalanci, and R. M. Di Donato Circumflex Coronary Artery From Right Pulmonary Artery in Hypoplastic Left Heart Syndrome Ann. Thorac. Surg., November 1, 2005; 80(5): 1919 - 1920. [Abstract] [Full Text] [PDF]
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 M. Nosal', I. C. Omeje, and R. Poruban Hypoplastic left heart syndrome with anomalous origin of left coronary artery from the right pulmonary artery: successful surgical treatment in a neonate Eur. J. Cardiothorac. Surg., September 1, 2005; 28(3): 497 - 498. [Abstract] [Full Text] [PDF]
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C. L. Cua, R. R. Thiagarajan, R. Taeed, T. M. Hoffman, L. Lai, J. Hayes, P. C. Laussen, and T. F. Feltes Improved Interstage Mortality With the Modified Norwood Procedure: A Meta-Analysis Ann. Thorac. Surg., July 1, 2005; 80(1): 44 - 49. [Abstract] [Full Text] [PDF]
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H. M. Burkhart, D. A. Ashburn, I. E. Konstantinov, N. C. De Oliviera, L. Benson, W. G. Williams, and G. S. Van Arsdell Interdigitating arch reconstruction eliminates recurrent coarctation after the Norwood procedure J. Thorac. Cardiovasc. Surg., July 1, 2005; 130(1): 61 - 65. [Abstract] [Full Text] [PDF]
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 I. Zeltser, J. Menteer, J. W. Gaynor, T. L. Spray, B. J. Clark, J. Kreutzer, and J. J. Rome Impact of Re-Coarctation Following the Norwood Operation on Survival in the Balloon Angioplasty Era J. Am. Coll. Cardiol., June 7, 2005; 45(11): 1844 - 1848. [Abstract] [Full Text] [PDF]
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S. Takabayashi, H. Kado, Y. Shiokawa, K. Fukae, and T. Nakano Comparison of hemodynamics between Norwood procedure and systemic-to-pulmonary artery shunt for single right ventricle patients Eur. J. Cardiothorac. Surg., June 1, 2005; 27(6): 968 - 974. [Abstract] [Full Text] [PDF]
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C. Pizarro, T. Mroczek, E. Malec, and W. I. Norwood Right Ventricle to Pulmonary Artery Conduit Reduces Interim Mortality After Stage 1 Norwood for Hypoplastic Left Heart Syndrome Ann. Thorac. Surg., December 1, 2004; 78(6): 1959 - 1964. [Abstract] [Full Text] [PDF]
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 N. C. De Oliveira, D. A. Ashburn, F. Khalid, H. M. Burkhart, I. T. Adatia, H. M. Holtby, W. G. Williams, and G. S. Van Arsdell Prevention of Early Sudden Circulatory Collapse After the Norwood Operation Circulation, September 14, 2004; 110(11_suppl_1): II-133 - II-138. [Abstract] [Full Text] [PDF]
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P. Monagle, A. Chan, P. Massicotte, E. Chalmers, and A. D. Michelson Antithrombotic Therapy in Children*: The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy Chest, September 1, 2004; 126(3_suppl): 645S - 687S. [Abstract] [Full Text] [PDF]
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T. Nakano, H. Kado, Y. Shiokawa, K. Fukae, Y. Nishimura, K. Miyamoto, Y. Tanoue, H. Tatewaki, and N. Fusazaki The low resistance strategy for the perioperative management of the Norwood procedure Ann. Thorac. Surg., March 1, 2004; 77(3): 908 - 912. [Abstract] [Full Text] [PDF]
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M. D. Rodefeld, J. H. Boyd, C. D. Myers, R. G. Presson Jr, W. W. Wagner Jr, and J. W. Brown Cavopulmonary assist in the neonate: an alternative strategy for single-ventricle palliation J. Thorac. Cardiovasc. Surg., March 1, 2004; 127(3): 705 - 711. [Abstract] [Full Text] [PDF]
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P. A. Checchia, R. Larsen, R. Sehra, N. Daher, S. R. Gundry, A. J. Razzouk, and L. L. Bailey Effect of a selection and postoperative care protocol on survival of infants with hypoplastic left heart syndrome Ann. Thorac. Surg., February 1, 2004; 77(2): 477 - 483. [Abstract] [Full Text] [PDF]
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G. E. Wright, D. C. Crowley, J. R. Charpie, R. G. Ohye, E. L. Bove, and T. J. Kulik High systemic vascular resistance and sudden cardiovascular collapse in recovering norwood patients Ann. Thorac. Surg., January 1, 2004; 77(1): 48 - 52. [Abstract] [Full Text] [PDF]
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N.S. Ghanayem, G.M. Hoffman, K.A. Mussatto, J.R. Cava, P.C. Frommelt, N.A. Rudd, M.M. Steltzer, S.M. Bevandic, S.J. Frisbee, R.D.B. Jaquiss, et al. Home surveillance program prevents interstage mortality after the Norwood procedure J. Thorac. Cardiovasc. Surg., November 1, 2003; 126(5): 1367 - 1375. [Abstract] [Full Text] [PDF]
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W. T. Mahle, A. R. Cuadrado, and V. K. H. Tam Early experience with a modified norwood procedure using right ventricle to pulmonary artery conduit Ann. Thorac. Surg., October 1, 2003; 76(4): 1084 - 1088. [Abstract] [Full Text] [PDF]
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K. O. Maher, C. Pizarro, S. S. Gidding, K. Januszewska, E. Malec, W. I. Norwood Jr, and J. D. Murphy Hemodynamic Profile After the Norwood Procedure With Right Ventricle to Pulmonary Artery Conduit Circulation, August 19, 2003; 108(7): 782 - 784. [Abstract] [Full Text] [PDF]
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S. Sano, K. Ishino, M. Kawada, S. Arai, S. Kasahara, T. Asai, Z.-i. Masuda, M. Takeuchi, and S.-i. Ohtsuki Right ventricle-pulmonary artery shunt in first-stage palliation of hypoplastic left heart syndrome J. Thorac. Cardiovasc. Surg., August 1, 2003; 126(2): 504 - 510. [Abstract] [Full Text] [PDF]
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K. N. Fenton, R. D. Siewers, B. Rebovich, and F. A. Pigula Interim mortality in infants with systemic-to-pulmonary artery shunts Ann. Thorac. Surg., July 1, 2003; 76(1): 152 - 156. [Abstract] [Full Text] [PDF]
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E. Malec, K. Januszewska, J. Kolcz, and T. Mroczek Right ventricle-to-pulmonary artery shunt versus modified Blalock-Taussig shunt in the Norwood procedure for hypoplastic left heart syndrome - influence on early and late haemodynamic status Eur. J. Cardiothorac. Surg., May 1, 2003; 23(5): 728 - 734. [Abstract] [Full Text] [PDF]
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D. A. Ashburn, B. W. McCrindle, C. I. Tchervenkov, M. L. Jacobs, G. K. Lofland, E. L. Bove, T. L. Spray, W. G. Williams, and E. H. Blackstone Outcomes after the Norwood operation in neonates with critical aortic stenosis or aortic valve atresia J. Thorac. Cardiovasc. Surg., May 1, 2003; 125(5): 1070 - 1082. [Abstract] [Full Text] [PDF]
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M. L. Jacobs Aortic reconstruction in hypoplastic left heart syndrome--A reappraisal J. Thorac. Cardiovasc. Surg., March 1, 2003; 125(90030): S82 - 84. [Full Text] [PDF]
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T. Kitaichi, F. Chikugo, T. Kawahito, T. Hori, Y. Masuda, and T. Kitagawa Suitable shunt size for regulation of pulmonary blood flow in a canine model of univentricular parallel circulations J. Thorac. Cardiovasc. Surg., January 1, 2003; 125(1): 71 - 78. [Abstract] [Full Text] [PDF]
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J. J. DeRose Jr, R. Corda, M. R. Dische, J. Eleazar, and R. S. Mosca Isolated left ventricular ischemia after the Norwood procedure Ann. Thorac. Surg., February 1, 2002; 73(2): 657 - 659. [Abstract] [Full Text] [PDF]
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 A P SALMON Hypoplastic left heart syndrome---outcome and management Arch. Dis. Child., December 1, 2001; 85(6): 450 - 451. [Full Text] [PDF]
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A. Azakie, S. L. Merklinger, B. W. McCrindle, G. S. Van Arsdell, K.-J. Lee, L. N. Benson, J. G. Coles, and W. G. Williams Evolving strategies and improving outcomes of the modified Norwood procedure: a 10-year single-institution experience Ann. Thorac. Surg., October 1, 2001; 72(4): 1349 - 1353. [Abstract] [Full Text] [PDF]
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R. R. Clancy, S. A. McGaurn, J. E. Goin, D. G. Hirtz, W. I. Norwood, J. W. Gaynor, M. L. Jacobs, G. Wernovsky, W. T. Mahle, J. D. Murphy, et al. Allopurinol Neurocardiac Protection Trial in Infants Undergoing Heart Surgery Using Deep Hypothermic Circulatory Arrest Pediatrics, July 1, 2001; 108(1): 61 - 70. [Abstract] [Full Text] [PDF]
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T. V. Brennan, M. D. Rodefeld, T. A. Tacy, V. M. Reddy, and F. L. Hanley Late thrombosis of the native aortic root after Norwood reconstruction for hypoplastic left heart syndrome J. Thorac. Cardiovasc. Surg., March 1, 2001; 121(3): 580 - 582. [Full Text] [PDF]
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P. Suominen, R. Palo, H. Sairanen, K.T. Olkkola, and J. Rasanen Perioperative determinants and outcome of cardiopulmonary arrest in children after heart surgery Eur. J. Cardiothorac. Surg., February 1, 2001; 19(2): 127 - 134. [Abstract] [Full Text] [PDF]
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W. T. Mahle, T. L. Spray, J. W. Gaynor, and B. J. Clark III Unexpected death after reconstructive surgery for hypoplastic left heart syndrome Ann. Thorac. Surg., January 1, 2001; 71(1): 61 - 65. [Abstract] [Full Text] [PDF]
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M. H. Abdullah, G. S. Van Arsdell, L. K. Hornberger, and I. Adatia Precoronary stenosis after stage I palliation for hypoplastic left heart syndrome Ann. Thorac. Surg., December 1, 2000; 70(6): 2147 - 2149. [Abstract] [Full Text] [PDF]
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M. L. Jacobs Editorial: Aortic reconstruction in hypoplastic left heart syndrome--A reappraisal J. Thorac. Cardiovasc. Surg., November 1, 2000; 120(5): 872 - 874. [Full Text] [PDF]
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N. C. Poirier, J. J. Drummond-Webb, K. Hisamochi, M. Imamura, A. M. Harrison, and R. B. B. Mee Modified Norwood procedure with a high-flow cardiopulmonary bypass strategy results in low mortality without late arch obstruction J. Thorac. Cardiovasc. Surg., November 1, 2000; 120(5): 875 - 884. [Abstract] [Full Text] [PDF]
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J. S. Tweddell, G. M. Hoffman, R. T. Fedderly, N. S. Ghanayem, J. M. Kampine, S. Berger, K. A. Mussatto, and S. B. Litwin Patients at risk for low systemic oxygen delivery after the Norwood procedure Ann. Thorac. Surg., June 1, 2000; 69(6): 1893 - 1899. [Abstract] [Full Text] [PDF]
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R. R. Clancy, S. A. McGaurn, G. Wernovsky, T. L. Spray, W. I. Norwood, M. L. Jacobs, J. D. Murphy, J. W. Gaynor, and J. E. Goin PREOPERATIVE RISK-OF-DEATH PREDICTION MODEL IN HEART SURGERY WITH DEEP HYPOTHERMIC CIRCULATORY ARREST IN THE NEONATE J. Thorac. Cardiovasc. Surg., February 1, 2000; 119(2): 347 - 357. [Abstract] [Full Text] [PDF]
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S. H. Daebritz, G. D.A. Nollert, D. Zurakowski, P. N. Khalil, P. Lang, P. J. del Nido, J. E. Mayer Jr, and R. A. Jonas RESULTS OF NORWOOD STAGE I OPERATION: COMPARISON OF HYPOPLASTIC LEFT HEART SYNDROME WITH OTHER MALFORMATIONS J. Thorac. Cardiovasc. Surg., February 1, 2000; 119(2): 358 - 367. [Abstract] [Full Text] [PDF]
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K. Ishino, O. Stumper, J. J. V. De Giovanni, E. D. Silove, J. G. C. Wright, B. Sethia, W. J. Brawn, and S. M. de Leval THE MODIFIED NORWOOD PROCEDURE FOR HYPOPLASTIC LEFT HEART SYNDROME: EARLY TO INTERMEDIATE RESULTS OF 120 PATIENTS WITH PARTICULAR REFERENCE TO AORTIC ARCH REPAIR J. Thorac. Cardiovasc. Surg., May 1, 1999; 117(5): 920 - 930. [Abstract] [Full Text] [PDF]
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H. Akintuerk, I. Michel-Behnke, K. Valeske, M. Mueller, J. Thul, J. Bauer, K.-J. Hagel, J. Kreuder, P. Vogt, and D. Schranz Stenting of the Arterial Duct and Banding of the Pulmonary Arteries: Basis for Combined Norwood Stage I and II Repair in Hypoplastic Left Heart Circulation, March 5, 2002; 105(9): 1099 - 1103. [Abstract] [Full Text] [PDF]
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