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Right arrow Congenital - acyanotic

Ann Thorac Surg 2006;81:236-242
© 2006 The Society of Thoracic Surgeons

Original article: Cardiovascular

Closed Transventricular Aortic Valvotomy for Critical Aortic Stenosis in Neonates: Outcomes, Risk Factors, and Reoperations

John W. Brown, MD * , Mark Ruzmetov, MD, PhD, Palaniswamy Vijay, PhD, Mark D. Rodefeld, MD, Mark W. Turrentine, MD

Section of Cardiothoracic Surgery, Riley Hospital for Children, Indiana University School of Medicine, Indianapolis, Indiana

Accepted for publication June 27, 2005.

* Address correspondence to Dr Brown, Section of Cardiothoracic Surgery, Indiana University School of Medicine, 545 Barnhill Dr, EH 215, Indianapolis, IN 46202 (Email: jobrown{at}iupui.edu).


   Abstract
Top
 Abstract
Introduction
 Patients and Methods
 Results
 Comment
 References
 
BACKGROUND: Critical aortic stenosis (AS) in neonates necessitates urgent intervention for patient survival. The optimal treatment, however, continues to be controversial and still has high morbidity and mortality in many centers. This study examined our late outcome, risks, and reoperations after the treatment of critical AS in neonates.

METHODS: Sixty-six neonates (47 boys and 19 girls) underwent closed transventricular aortic valvotomy for critical AS between 1978 and 2000. The mean age at the first intervention was 15.1 ± 19.6 days (range, 1 to 78). Their weight ranged from 1.4 to 6.2 kg (mean, 3.5 ± 0.9 kg). Sixteen patients (23%) had isolated critical AS and normal or dilated left ventricles, and 50 neonates (77%) had associated cardiovascular anomalies (ie, aortic annular hypoplasia, hypoplasia of the left ventricle, mitral valve abnormalities, and endocardial fibroelastosis, coarctation, or interruption of aorta).

RESULTS: The hospital mortality was 29% (19 of 66). Kaplan-Meier 5- and 15-year survival was 61% and 58%, respectively. The operative mortality rates were 6% in neonates with isolated AS and 36% in patients with complex AS. The five risk factors significant for mortality on univariate analysis were (1) presence of endocardial fibroelastosis (p = 0.05), (2) presence of hypoplastic left ventricle (p = 0.003), (3) presence of associated cardiovascular anomalies (p = 0.04), (4) aortic valve annulus of less than 5.0 mm (p = 0.01), and (5) surgery before 1985 (p = 0.003). Of these five factors, only the presence of hypoplastic left ventricle (p = 0.001) and surgery before 1985 (p = 0.001) remain significant for mortality by multivariate analysis. At last follow-up (mean, 8.2 ± 6.2 years), 36 of 47 of the long-term survivors were in New York Heart Association functional class I and II. Kaplan-Meier analysis showed 5- and 15-year freedom from aortic valve reoperation to be 83% and 60%, respectively. Univariate and multivariate analysis showed the presence of multilevel stenosis (p = 0.04) as the best preoperative predictor for the need for late reoperation in survivors.

CONCLUSIONS: We conclude that critical AS in neonates continues to be associated with significant mortality. Reintervention such as surgical and balloon valvotomy are usually required within 10 years of initial surgery.


   Introduction
Top
 Abstract
 Introduction
Patients and Methods
 Results
 Comment
 References
 
Critical congenital aortic stenosis (AS) represents a serious and life-threatening condition in early infancy and in neonates. The morphologic structure in neonates with symptomatic aortic stenosis represents a wide spectrum of abnormalities and often includes patients with aortic annular hypoplasia, severe valvular dysplasia, hypoplasia of the left ventricle, mitral valve anomalities, and endocardial fibroelastosis. Owing to the increased afterload already existing during fetal circulation, these children often show severe left ventricular (LV) myocardial dysfunction and even signs of myocardial infarction. Reduced flow across the mitral valve and the LV may be responsible at least in part for the underdevelopment of the LV cavity—a prognostically unfavorable sign of a good surgical outcome. Nevertheless, early intervention is mandatory in order to reduce LV stroke load and to prevent further myocardial damage.

Various types of surgical approaches have been associated with high operative mortality (21% to 86%) in the past [1–3], but recent reports suggest that surgical results are improving [4–7]. Balloon aortic valvuloplasty has been proposed as a less invasive option, and although it was initially linked with significant procedural morbidity and mortality, particularly in neonates [8, 9]; it is now widely regarded as a safe and effective technique [10].

Balloon aortic valvuloplasty or open valvotomy is currently advocated by several centers as the procedure of choice [10–12]. Closed transventricular valvotomy was the standard approach in the management of the critical neonatal AS at our institution until 2000. Balloon valvotomy became the initial procedure of choice after 2000, when both cardiologists and surgeons decided to give balloon valvotomy a trial as initial therapy. In this report, we present our experience in the management of critical neonatal AS over a 22-year period (1978 to 2000).


   Patients and Methods
Top
 Abstract
 Introduction
 Patients and Methods
Results
 Comment
 References
 
Between January 1978 and August 2000, a total of 66 neonates (47 male and 19 female) below the age of 3 months underwent surgical treatment of critical aortic stenosis with closed transventricular valvotomy (CTV) at the James W. Riley Hospital for Children at Indianapolis. All patients with biventricular hearts as well as atrioventricular and ventriculoarterial concordance were included for review. Patients with univentricular atrioventricular connection, double-outlet right ventricle, common atrioventricular valve orifice, or truncus arteriosus were excluded from the study. All patients included in this study had serious congestive heart failure requiring inotropic support (n = 42; 64%), ventilation (n = 29; 44%), or administration of prostaglandin E1 (n = 34; 52%) preoperatively. The diagnosis was usually made clinically and confirmed with two-dimensional echocardiogram (n = 54; 82%) or cardiac catheterization and echocardiogram (n = 12; 18%). All measurements were made with Doppler echocardiography and reported as the mean value ± SD. Intraoperative data collection forms, hospital charts, and echocardiographic and catheterization reports were reviewed. We defined early mortality as death during initial hospitalization or within 30 days of operation and late mortality as death thereafter.

The mean age at the first intervention was 15.1 ± 19.6 days (median, 5; range, 1 to 78). Their weights ranged from 1.4 to 6.2 kg (mean, 3.5 ± 0.9 kg; median, 3.4 kg). The mean preoperative aortic annulus diameter was 6.6 ± 1.4 mm (median, 7 mm; range, 3.8 to 8.5 mm). The mean peak instantaneous aortic valve gradient was 65.2 ± 27.8 mm Hg (median, 64 mm Hg; range, 20 to 138 mm Hg). Left ventricular ejection fraction ranged from 10% to 65% (mean, 33% ± 13%).

Sixteen patients had isolated critical AS (23%), and 50 neonates (77%) had associated cardiovascular anomalies (ie, aortic annular hypoplasia, hypoplasia of the left ventricle, mitral valve abnormalities, endocardial fibroelastosis, and coarctation or interrupted aortic arch; Table 1). Moderate mitral insufficiency (n = 11) due to primary mitral valve anomaly or mitral valve stenosis (n = 7) was found in 18 patients (27%). Eighteen patients (27%) subjectively had mild to severe hypoplastic left ventricle, 10 patients had coarctation of the aorta, and 4 patients had hypoplasia or interruption of the aortic arch. The definition of degree of the LV hypoplasia was proposed by Kirklin and Barratt-Boyes [13] but was somewhat subjective. Endocardial fibroelastosis was found in 12 neonates (18%). The aortic valve was bicuspid in 38 children (57%), tricuspid in 27 (41%), and unicuspid in 1 patient (2%).


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  		Table 1. Lesions Associated With Critical Aortic Stenosis in 50 Neonates
 
Surgical Technique
All neonates who had the potential to maintain a patent ductus arteriosus were kept on prostaglandin E1 to sustain a good systemic blood flow. General anesthesia was usually narcotic based (Fentanyl, Abbott Laboratories, Abbott Park, IL). Any metabolic acidosis was corrected. Most patients were maintained on a regimen of low-dose inotropes preoperatively. After median sternotomy (n = 43) or left thoracotomy (n = 23), the LV apex was gently elevated out of the pericardium, and a warm moist sponge was placed behind the heart to make the apex accessible. A pledgeted mattress suture of 4-0 polypropylene with a 3 x 7 mm pledget was placed at the left ventricle apex after lidocaine (1 mg/kg) was injected intravenously. Performance of the surgery through a left lateral thoracotomy allows for the concomitant repair of aortic coarctation and patent ductus arteriosus. A stab wound was made in the LV apex and a Grüntzig balloon catheter (B-Braun Medical Inc, Bethlehem, PA) (n = 13) or serial Hegar dilators (Johnson & Johnson Co, Piscataway, NJ) (n = 53) were passed into the left ventricle, and guided through the stenotic aortic valve using digital palpation of the aortic root (Fig 1A and B). Progressive dilation was carried out with successive dilators stopping at or 1 mm more than the aortic annulus diameter on preoperative echocardiography (range, 5 to 8 mm). The heart was allowed to recover after each pass of the dilator. Four patients who fibrillated were connected through previously placed pursestring sutures to a bypass, and the closed valvotomy was continued. After closure of the left ventriculotomy, the left ventricular-aortic gradient was assessed by invasive measurements and by transesophageal echocardiography to confirm the degree of successful relief of the gradient across the LV outflow tract (LVOT) and any degree of aortic regurgitation produced (dilating was stopped when mild aortic valvar regurgitation was produced).



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  		Fig 1. Operative technique demonstrating antegrade transventricular aortic valvotomy using blunt Hegar's dilator (A) or Grüntzig balloon catheter (B).

 
Of the 50 patients with associated cardiovascular anomalies, two defects were repaired before CTV, 12 had other repairs as a concomitant procedure, and 2 had associated defects repaired as a second procedure during the same hospitalization (Table 2). Three other patients required reoperation in the immediate postoperative period, 1 for atrial and ventricular septal defect closure, and 2 for heart transplantation after valvotomy failed to improve low cardiac output.


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  		Table 2. Operations Performed Previously, Concomitantly or During Same Hospitalization as Closed Transventricular Aortic Valvotomy
 
Statistical Analysis
Measured and calculated data are expressed as mean ± SD. Comparison between two groups was performed by using Student's t test. A p value of less than 0.05 was considered significant. Specific statistical software, SPSS for Windows, version 10 (SPSS, Chicago, Illinois) was used for data analysis.

Hospital mortality and freedom from reoperation were studied for the following possible risk factors: age, age less than 1 month, weight, sex, preoperative ventilatory support, endocardial fibroelastosis, presence of hypoplastic left ventricle, presence of ductus arteriosus, presence of mitral anomaly, aortic valve annulus of less than 5.0 mm, presence of other associated cardiovascular anomalies, presence of multilevel stenosis, LV ejection fraction, peak transaortic valve gradient, postoperative pulmonary hypertension, postoperative extracorporeal membrane oxygenation (ECMO) support, and postoperative aortic insufficiency (AI).

The Kaplan-Meier product limit method and Cox proportional hazards regression methods were used for the analysis of survival and freedom from reoperation. Multiple regression analysis was performed as conditional backward stepwise proportional hazards regression.

In the analysis of risk factors for mortality, freedom from reoperation, variables with significance levels of 0.1 in univariate analysis were submitted to a multivariate logistic regression model. Factors with p values of less than 0.05 were considered significantly related to mortality and freedom from reoperation.


   Results
Top
 Abstract
 Introduction
 Patients and Methods
 Results
Comment
 References
 
Postoperative Results
The mean preoperative LVOT peak gradient decreased from 65.2 ± 27.8 mm Hg (range, 20 to 138 mm Hg) to 17.2 ± 11.2 mm Hg (range, 0 to 40 mm Hg) intraoperatively (p = 0.002). Nine patients (9 of 47; 19%) had peak intraoperative gradients ranging between 30 to 40 mm Hg, and no patient had significant aortic gradient more than 50 mm Hg. There were no significant differences in aortic gradients between bicuspid and tricuspid aortic valves (preoperative, 68.1 ± 22.3 versus 63.9 ± 26.2, p = 0.26; intraoperative, 22.6 ± 8.4 versus 15.2 ± 12.6, p = 0.93). Intraoperatively 12 patients (18%) had mild aortic incompetence without moderate or severe AI. Six neonates had postoperative ECMO support (mean, 3.8 days; range, 1 to 9). Four patients during CTV fibrillated and were placed on bypass and then on ECMO; 2 children were placed on ECMO 2 and 6 days after CTV owing to LV diastolic dysfunction and poor cardiac output.

Survival
Overall, there were 19 early deaths (19 of 66; 29%) in neonates with CTV (Fig 2). Ten of the 13 early deaths were of infants operated on before 1985 (10 of 13; 77%). The mortality rate for CTV since 1985 has been 17% (9 of 53; 77% versus 17%, p = 0.003). The babies with isolated AS with or without patent ductus arteriosus had a 6% of operative mortality (1 of 16) and patients with complex AS had a 36% of operative mortality (18 of 50; p = 0.02). Details of early postoperative deaths are shown in Table 3.



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  		Fig 2. Surgical results of closed transventricular aortic valvotomy in neonates. (Postop = postoperative.)

 

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  		Table 3. Etiology of Early and Late Mortality
 
There were 6 late deaths during the first 4 months after initial surgery: 1 death was due to chronic liver failure, 2 were due to pulmonary hypertension, and 3 deaths were sudden of unknown cause. The seventh patient was a 2-day old neonate with a small LV who underwent CTV that was complicated by perforation of the posterior aspect of the aortic root. Bleeding in this patient required placement on cardiopulmonary bypass and repair of the aortic root. The patient required ECMO support because of severe LV diastolic dysfunction before and after the procedure. This patient was weaned from ECMO, but could not be weaned of ventilatory support. An echocardiogram showed a residual gradient of approximately 25 mm Hg across the aortic valve and moderate aortic regurgitation. Orthotopic cardiac transplantation was performed, but this child died of low cardiac output several days later secondary to pulmonary hypertension and graft failure.

Two other late deaths occurred 10 and 14 years after the initial operation. One of patient was a 2-week old neonate with a moderately small left ventricle, hypoplasia of the ascending aorta, mild mitral valve dysplasia, and endocardial fibroelastosis who underwent orthotopic heart transplantation 2 months later after initial CTV owing to poor LV function. Ten years later, this patient had worsening graft function and underwent diagnostic cardiac catheterization. The catheterization was uncomplicated; however, after emerging from general anesthesia, the patient had a sudden decline in cardiopulmonary function for unknown reasons. The patient required ECMO but died 2 days later secondary to massive right cerebral infarct. The other patient died 6 years after apical aortic conduit implantation for tunnel subaortic stenosis and 8 years after initial CTV, had multilevel LVOT obstruction, and had cardiomyopathy and heart failure. Overall survival estimated by the Kaplan-Meier method including early mortality was 61% at 1 and 5 years, 59% at 10 years, and 58% at 15 and 20 years (Fig 3). In our series, all the early deaths occurred during the initial hospitalization, and all the late deaths occurred after discharge from the initial hospitalization.



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  		Fig 3. Kaplan-Meier estimate of survival (diamonds) and freedom from reoperation (squares) in patients undergoing transventricular aortic valvotomy. (yr. = years.)

 
Echocardiographic Results
Recent echocardiography has been performed in 37 patients. The peak aortic pressure gradient at latest follow-up was 30.5 ± 25.8 mm Hg (p = 0.01) by Doppler at a mean of 6.8 ± 4.8 years (range, 1 to 19) after CTV in all survivors. Survivors who have not required reintervention (n = 23) have all undergone late echocardiographic examination, and the peak LVOT gradient was 38.6 ± 17.9 mm Hg (range, 8 to 78 mm Hg). Three of these patients have moderate degrees of AI, and the rest have mild or no AI. Patients who required reintervention (n = 14) underwent echocardiographic examination before reoperation, and the peak gradient was 59.5 ± 15.4 mm Hg (range, 30 to 80 mm Hg). At latest follow-up, the peak gradient in these patients was 16.4 ± 12.5 mm Hg (range, 5 to 22 mm Hg). All of these patients have mild or no AI.

Late Complications and Reoperations
Fourteen patients (35%; 14 of 40) have required 20 reoperations during follow-up (6 months and more). Fourteen patients have undergone one reoperation, 4 have required two, and 1 has required three reoperations. The mean interval between the first and second procedure was 6.0 ± 3.8 years (range, 1 to 14). The indications for the reoperation was recurrent valvar AS in 1 patient, and recurrent valvar AS and moderate (n = 4) or severe (n = 4) AI in 8 patients. The development of AI was gradual and progressive over the follow-up period. Complex LVOT obstruction (valvar, supravalvar, and tunnel subvalvar AS) developed in 2 patients, and discrete subaortic stenosis developed in 3 patients. The first reoperation consisted of open aortic valvotomy in 1 patient, and resection of discrete subaortic membrane in 3 patients (1 with additional myotomy), whereas aortic valve replacement was necessary in 8 patients (eight Ross procedures, including one Konno modification). In the early part of the experience, 2 patients had an apical aortic conduit implantation. Four children underwent second reoperation for recurrent subaortic membrane resection (n = 1), repeat open valvotomy (n = 1), and Ross-Konno procedure (n = 2). One patient (with two previous open valvotomies) underwent a third reoperation, a Ross procedure. Overall, 11 children have had a Ross procedure. Two patients with Shone's anomaly underwent an addition mitral valve replacement with a mechanical prosthesis. None of the initial hospital survivors died during reoperations. Overall freedom from aortic valve reoperation estimated by the Kaplan-Meier method was 83% at 5 years, 73% at 10 years, 64% at 15 years, and 60% at 20 years (Fig 3).

Clinical Follow-Up in Surviving Patients
Forty-five of the 47 initial hospital survivors (97%) included in the neonatal critical AS group have had a mean follow-up of 8.2 ± 6.2 years (median, 9; range, 2 months to 23 years). Two patients were lost at follow-up. All 36 late survivors are currently in New York Heart Association functional class I or II. Electrocardiograms show that all patients are in sinus rhythm (100%). There was no atrioventricular block and pacemaker implantation in this series.

Risk Factors Analysis
There were five risk factors significant for mortality by univariate analysis: (1) the presence of endocardial fibroelastosis (p = 0.05), (2) the presence of hypoplastic LV (p = 0.003), (3) the presence of associated cardiovascular anomalies (p = 0.04), (4) aortic valve annulus of less than 5.0 mm (p = 0.01), and (5) surgery before 1985 (p = 0.003). Of these 5 factors, only the presence of a hypoplastic LV (p = 0.001), and surgery before 1985 (p = 0.001) remain significant by multivariate analysis.

Univariate and multivariate analysis showed the presence of multilevel stenosis (p = 0.04) as the best preoperative predictor for the need for late reoperation.


   Comment
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
References
 
Because critical AS in neonates is uniformly fatal without treatment, a variety of surgical and catheter approaches have been proposed for the treatment of critical AS. In 1955, a direct surgical approach to the aortic valve with the use of transventricular dilation was accomplished by Marquis and Logan [14]. Trinkle and colleagues [15] in 1974 also proposed CTV. In 1956, the first open surgical valvotomy with surface cooling and inflow occlusion was performed [16]. These operations remained the only therapeutic options until 1983, when Lababidi [17] reported the use of aortic balloon valvotomy.

In the early 1990s, McKay and colleagues [18] examined the morphology of the ventriculoarterial junction in critical AS in 21 patients at autopsy. These authors suggested that early aortic root replacement with a pulmonary autograft might be the best way of achieving a biventricular correction. There have been sporadic case reports of the pulmonary autograft aortic valve replacement, or Ross-Konno approach, performed in early infancy for critical AS [19, 20].

The optimal management of critical AS in the neonatal age remains highly controversial. Surgical and balloon techniques certainly have their merits and drawbacks, and the variability in the anatomy and physiology of this group of the patients makes comparisons of different techniques difficult. The choice of the most appropriate treatment depends on the skills of the surgeons and the interventional cardiologist at each institution.

Balloon aortic valvuloplasty has been introduced as a less invasive and safer treatment modality, partly as a response to high surgical mortality reported by some groups [2, 10, 12]. In the first years of its application, the balloon valvuloplasty was associated with major procedure-related morbidity, including transection of the femoral and iliac arteries, perforation of the aorta, massive aortic regurgitation, and perforation of the left ventricle, pericardial tamponade, perforation of the mitral valve, and complete avulsion of the aortic valve. Mortality rates in excess of 50% have been reported [8, 9]. Increasing experience and patient selection has led to a marked reduction in procedural mortality, but not in reduction of morbidity. Vascular complications remained common in neonates [10, 12]. Balloon aortic valvuloplasty has become the technique of choice in most institutions, including ours, for the primary treatment for neonatal AS owing to its increasing safety and effectiveness [10, 11].

Neonates who present with critical AS present a formidable challenge because of their frequent associated unstable hemodynamic status. They are prone to ventricular arrhythmias and have limited myocardial reserve. Additional cardiac lesions such as left ventricular endocardial fibroelastosis, mitral stenosis, a hypoplastic aortic annulus, and LV hypoplasia add to the complexity of operative and postoperative management. We were fortunate to have encountered minimal sustained ventricular arrhythmias during CTV because of our delicate manipulation of the heart and the administration of lidocaine before cardiac manipulation. We also attempted to maintain ductal patency when possible with prostaglandin E1.

Gundry and Behrendt [21] reported their experience in 24 patients undergoing aortic valvotomy in the first 6 months of life. They found a low ejection fraction, high left ventricular end-diastolic pressure, and presence of endocardial fibroelastosis were all predictive indexes of poor outcome. Hammon and associates [22] examined a group of 19 patients undergoing aortic valvotomy in the first 6 months of life and found that preoperative elevated mean pulmonary artery pressure and low left ventricular end-diastolic volume were predictive of poor outcome. Rhodes and associates [23] examined a group of 65 patients with critical AS after they had undergone a biventricular repair. These authors found that the best predictors of survival included a large aortic root dimension indexed to body surface area, a high ratio of the long-axis dimension of the left ventricle to the long-axis dimension of the heart, and a normal or large mitral valve area indexed to body surface area.

Robinson and colleagues [24] found that an aortic valve diameter less than 6 mm, the presence of mitral valve stenosis, and a nonapex-forming LV were all risk factors for a poor outcome in both univariate and multivariate analyses of the ductal-dependent infants. The nonductal-dependent infants in their series who had intervention at approximately 1 month of age had a significantly larger body surface area and had a better long-term survival and less reoperation than the ductal-dependent infants.

We currently (since 2000) employ a diverse therapeutic approach to the heterogeneous spectrum of critical neonatal AS. Preoperatively, patients receive aggressive medical therapy, prompt initiation of prostaglandin E1 infusion to open the patent ductus arteriosus and to augment systemic blood flow [2]. Echocardiogram is used to access structure and function after medical stabilization. Neonates with two or more of these characteristics—(1) aortic annulus less than 5.0 mm; (2) a subjective estimate of left ventricular volume less than 70% of normal; (3) mitral annulus less than 8.0 mm; or (4) a dense LV endocardial fibroelastosis—are considered for Norwood palliation. In those neonates with favorable or borderline anatomy (no major associated cardiac anomalies or only one of the mentioned criteria) and either poor LV function and persistent acidosis, we would advocate a prompt catheterization laboratory balloon aortic valvotomy under echocardiography guidance. We frequently are asked by our interventional cardiologist to provide surgical access to the right internal carotid artery for a retrograde balloon dilatation of the aortic valve in the catheterization laboratory. We do not advocate a neonatal Ross or Ross-Konno except for patients who have failed a closed approach.

Reoperation after CTV was high in our study (12 of 42 survivors). Actuarial freedom from reoperation for hospital survivors was 83% at 5 years and 64% at 15 years, almost identical to those reported by Karl and associates [25] and Hawkins and coworkers [7]. Like others, we found that reoperation was largely for recurrent LV outflow tract obstruction and only rarely for severe aortic regurgitation [26]. In most patients who require reoperation and who have little or no AI we have opted to perform open aortic valvuloplasty as the first reintervention. In patients with moderate or severe aortic valve insufficiency or with a significant degree of subaortic stenosis, we proceeded to a Ross or Ross-Konno procedure, as is favored by several other groups [19, 20]. We have avoided allograft or mechanical valve insertion in young children as much as possible. We have found that the Ross and Ross-Konno procedure to be a reliable, low-risk, and perhaps the best long-term alternative in the growing infant or child who requires reoperation after a failed surgical or balloon valvotomy in the neonatal period.

In conclusion, transventricular closed aortic valvotomy was a valuable tool in the treatment of neonates and young infants with critical AS from 1978 to 2000 at our institution. The long-term results with respect to survival and reoperation were acceptable and compare favorably with other forms of treatment for neonatal critical AS. Neonates and young infants with evidence of severe aortic annulus hypoplasia and low ejection fraction are not good candidates for surgical valvotomy and should be considered for a univentricular repair (namely, Norwood). We consider that all procedures in neonates are palliative procedures, and reintervention will usually be required within 10 years. Since 2000, our interventional pediatric cardiologists have been increasingly successful in retrograde balloon dilatation of the aortic valve through surgical access to the right carotid. Surgical CTV is currently reserved for those neonates in whom the aortic valve cannot be crossed in a retrograde manner [27].


   References
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 

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Eur. J. Cardiothorac. Surg., June 1, 2007; 31(6): 1013 - 1021.
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R. S. Mosca
Invited commentary
Ann. Thorac. Surg., January 1, 2006; 81(1): 242 - 242.
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