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Pulmonary Stenosis and Intact Ventricular Septum
Definition
Pulmonary stenosis and intact ventricular septum is a form of right ventricular outflow tract obstruction in which the stenosis can be valvar, infundibular, or both. Isolated infundibular stenosis is unusual. This chapter concerns primarily valvar pulmonary stenosis, with or without infundibular stenosis. When neonates present with the most severe form of this defect, the term neonatal critical pulmonary stenosis is used. When patients present beyond the neonatal period or in early infancy, the term pulmonary stenosis is used.
Historical Note
In 1913, as described by Dumont, Doyen first attempted to surgically relieve pulmonary stenosis in a 20-year-old woman who, in retrospect, is thought to have had infundibular obstruction. Thirty-five years later, in December 1948, Sellors performed a successful closed transventricular instrumental pulmonary valvotomy, closely following Doyen's technique. Brock performed three successful closed valvotomies in early 1948. These patients probably all had tetralogy of Fallot. Blalock and Kieffer applied this procedure to patients with pulmonary stenosis and intact ventricular septum soon thereafter, reporting 19 patients and two hospital deaths. Swan and colleagues surgically corrected pulmonary stenosis and intact ventricular septum by an open technique in about 1953, approaching the valve through a pulmonary arteriotomy during circulatory arrest, with the patient rendered moderately hypothermic by surface cooling. Other techniques evolved.
Kirklin's experiences with closed valvotomy at Mayo Clinic led to an appreciation of the importance of acquired infundibular obstruction caused by hypertrophy and the need for a pump-oxygenator system that would allow relief by open operation. When cardiopulmonary bypass (CPB) became available in 1955, most surgeons began to use it to support patients during open valvotomy.
Surgical treatment of pulmonary stenosis was challenged in 1982 when Kan and colleagues reported successful percutaneous balloon valvuloplasty. This method of therapy is now applied to patients of all ages, and is, with the important exception of the morphologic variant called pulmonary valvar dysplasia, the initial procedure of choice.
Age Considerations
Symptoms, signs, and treatment of valvar pulmonary stenosis in the neonate presenting in severe distress during the first few days of life have long been recognized as different from those of patients presenting later in life. Interrelationships exist between neonatal valvar pulmonary stenosis and intact ventricular septum and pulmonary atresia and intact ventricular septum. Now that percutaneous techniques are used for therapy, different groups of physicians, as a rule, care for valvar pulmonary stenosis in patients presenting for treatment for the first time as adults and those presenting in early childhood. For all these reasons, this subject seems best approached according to age categories.
Section I
Critical Valvar Pulmonary Stenosis in Neonates
Morphology
Pulmonary Valve
The pulmonary valve is commonly a uniform fibrous cone with a circular, central, and stenotic orifice and two or three ridges on its pulmonary arterial side ( Fig. 39-1 ). These ridges radiate from the central orifice to the periphery and outline two or three cusps that correspond to pulmonary sinuses of Valsalva, which are usually well formed. The valvar diaphragm is considerably thicker than normal cusp tissue, particularly around the ostium, but it is mobile. Thickening is produced by an increase in myxomatous tissue. Obstruction may be due to thickened, shortened, and rigid cusp tissue with little or no commissural fusion, known as pulmonary valvar dysplasia . This was described in 1969 by Koretzky, Edwards, and colleagues and further characterized by Stamm, Anderson, and colleagues. The right ventricular–pulmonary trunk junction (anulus) may be narrowed and the pulmonary trunk wall pulled inward or tethered at the site of commissural cusp attachment. The valve is often bicuspid. Although this condition may cause critical pulmonary stenosis in neonates, stenosis is typically moderate, a finding that is characteristic of Noonan syndrome.
Pulmonary Arteries
Although it has been reported that in about 50% of neonates with critical pulmonary stenosis, right and left pulmonary arteries appear to be moderately or severely hypoplastic when imaged, this has not been confirmed by other studies ( Table 39-1 ). As a rule, the appearance of pulmonary arterial hypoplasia is probably secondary to low pulmonary blood flow, because the pulmonary arteries are usually normal in size within a few years in those who survive interventional treatment.
Table 39-1
Critical Pulmonary Stenosis in Neonates: Relationship of Moderate or Severe Hypoplasia of Right and Left Pulmonary Arteries to Right Ventricular Cavity Size
Data from Hanley and colleagues.
| Moderate or Severe RPA and LPA Hypoplasia b | |||
|---|---|---|---|
| RV Cavity Size a | n | No. | % of n |
| Enlarged (1-5) | 3 | 0 | 0 |
| Normal (0) | 37 | 1 | 3 |
| Mildly reduced (−1, −2) | 30 | 0 | 0 |
| Moderately reduced (−3) | 11 | 1 | 9 |
| Severely reduced (−4, −5) | 3 | 1 | 33 |
| Subtotal | 84 | 3 | 4 |
| Unknown | 17 | 0 | |
| TOTAL | 101 | 3 | |
Key: LPA, Left pulmonary artery; RPA, right pulmonary artery; RV, right ventricle.
a Numbers in parentheses refer to grading of RV cavity size.
b Degree of hypoplasia of the pulmonary arteries was graded as 0 to −5. Hypoplasia was considered moderate or severe when graded −3, −4, or −5. Grading scheme was validated by comparison with actual measurements transformed to z values in patients for whom they were available.
Right Ventricle
Rarely, the right ventricular (RV) cavity is severely reduced in size. More commonly, mild or moderate reduction is present ( Fig. 39-2 ). Reduction in cavity size relates in part to the amount of concentric RV hypertrophy produced by the RV outflow tract (RVOT) obstruction ( Fig. 39-3 ).
Histologic appearance of the RV varies. Concentric RV hypertrophy is characterized by increased muscle cell size and diffuse fibrosis. The former is greater in the fibers near the endocardial surface; in some areas, muscle fibers can be seen to be disintegrating. Fibrosis is diffuse or patchy, but papillary muscles are the most severely affected. Fibrosis increases pari passu with hypertrophy and probably results from imbalance in the myocardial oxygen supply/demand ratio. Fibrosis of both endocardium and trabeculations is a marked feature when the RV is hypoplastic, contributing to poor compliance.
Neonates with critical pulmonary stenosis occasionally have severely enlarged RVs. This may represent coexisting important cardiomyopathy or (rarely) tricuspid valve disease. Prognosis is poor with or without valvotomy.
Tricuspid Valve
About 50% of neonates have normal tricuspid valve dimensions (within 2 standard deviations of the mean value for normal persons of the same size; see “Dimensions of Normal Cardiac and Great Artery Pathways” in Chapter 1 ). In the others, diameter is smaller than normal; in less than 10% the tricuspid valve is severely hypoplastic ( Fig. 39-4 ). When it is markedly hypoplastic, it is apt to be grossly abnormal as well, with abnormal chordal attachments and fused cusps. Otherwise, the cusps and chordae usually are normal.
Right Ventricular Coronary Artery Fistulae
About 10% of neonates with critical pulmonary stenosis have RV sinusoids, but only 2% have RV coronary arterial fistulae. RV-dependent coronary circulation in such hearts is rare.
Right Atrium
The right atrium is usually large. There is generally at least a patent foramen ovale, and right-to-left shunting across it is a major contributor to arterial desaturation exhibited by many of these neonates.
Morphologic Correlates
RV cavity size and tricuspid valve dimension are not highly correlated in this condition, but mild to moderate hypoplasia is the rule in both locations. This is in contrast to pulmonary atresia and intact ventricular septum (see Morphology in Chapter 40 ), suggesting that reduction in RV cavity size in critical pulmonary stenosis is secondary to RV hypertrophy and thickening from outflow obstruction, rather than from genetic or developmentally induced hypoplasia. This is in harmony with the hypothesis that critical pulmonary stenosis develops relatively late in fetal life, in contrast to some types of pulmonary atresia.
Coexisting Cardiac Conditions
Coexisting cardiac conditions are uncommon. Ebstein malformation, which occurs in about 5% of patients with pulmonary atresia and intact ventricular septum, occurs in about 1% of those with critical pulmonary stenosis.
Clinical Features and Diagnostic Criteria
Neonates presenting with critical pulmonary stenosis and intact ventricular septum are usually critically ill, irritable, tachypneic, and severely hypoxic from right-to-left shunting at the atrial level. They usually present for treatment within a few days after birth and are generally of normal birth weight. When the atrial septum is intact, which is uncommon, cyanosis is absent.
Tachycardia and severity of heart failure often make auscultatory findings nondiagnostic. Physical findings of tricuspid regurgitation may be present. Chest radiograph usually shows a normal or somewhat enlarged heart. Pulmonary stenosis with hypoplastic RV is associated with less electrocardiographic (ECG) evidence of RV hypertrophy than expected. Diminished RV potentials are due to smallness of the RV cavity rather than to diminished muscle mass.
In a critically ill neonate with clear lung fields and a large cardiac silhouette, two-dimensional echocardiography provides near-certain diagnosis. The thick stenotic pulmonary valve is visualized, the RV cavity is seen, and size and cusp thickness of the tricuspid valve can be determined. Additionally, the pulmonary artery branch diameter can be accurately estimated, and color Doppler imaging can suggest presence of coronary artery anomalies such as RV-to–coronary artery fistulae.
Cardiac catheterization is indicated in essentially all cases for both diagnostic reasons (e.g., to define coronary artery anomalies) and therapy, because balloon pulmonary valvotomy is currently the treatment of choice. Cardiac catheterization usually shows peak RV pressure higher than that in the left ventricle (LV) or systemic arteries. Rarely, and in the presence of severe heart failure, peak RV pressure is less than that in the systemic circulation, despite severe valvar stenosis.
Cineangiography provides precise information regarding site of stenosis, size of RV cavity and infundibulum, presence or absence of tricuspid regurgitation, morphology of the pulmonary trunk and right and left pulmonary arteries, and presence or absence of RV-to–coronary artery fistulae ( Fig. 39-5 ). The tricuspid valve is competent in about 10% of patients, and in the other 90% it is moderately or severely regurgitant (Hanley and colleagues and the Congenital Heart Surgeons Society: personal communication; 1992). Regurgitation, which is not well correlated with degree of RV hypertension ( Fig. 39-6 ), is probably a manifestation of RV failure.
Currently, magnetic resonance and computed tomographic imaging are not routinely used in neonatal critical pulmonary stenosis, simply because these studies provide little added value to echocardiography and the mandatory cardiac catheterization. Recently, fetal echocardiography has been used to predict the postnatal fate of patients with critical pulmonary stenosis. The aim is to predict whether a two- or single-ventricle circulation will result following postnatal therapy. These techniques are more applicable to pulmonary atresia and intact ventricular septum but also have a role, albeit a lesser one, in pulmonary stenosis. Morphologic and physiologic characteristics identified at fetal echocardiographic interrogation can accurately predict the fate of the circulation following birth. These data can be used for planning postnatal therapy, parental counseling, and possibly prenatal intervention.
Natural History
Presentation is usually within the first 2 weeks, and mean age at operation in the series at Toronto Hospital for Sick Children was 3.9 days. Most neonates in whom severe hypoxia develops, with or without heart failure, die without treatment, although some may live for a few months.
Technique Of Operation
Percutaneous Balloon Valvotomy
The technique of percutaneous balloon valvotomy has been described in detail. Briefly, a guidewire is introduced via the femoral vein across the pulmonary valve and maneuvered through the ductus arteriosus into the descending aorta. A wire-guided balloon 1.2 to 1.3 times the measured size of the anulus is placed across the pulmonary anulus. The balloon is inflated rapidly two or three times. Several case reports of fetal intervention for critical pulmonary stenosis using percutaneous balloon valvotomy have been reported, documenting technical success. Efficacy of the procedure has not yet been documented.
Open Pulmonary Valvotomy Using Cardiopulmonary Bypass
When percutaneous balloon valvotomy has not been used or is unsuccessful, open pulmonary valvotomy using CPB is recommended. The surgical procedures of closed pulmonary valvotomy and open valvotomy with simple inflow stasis have also given good results; however, they are not currently recommended in most circumstances. Operation may be performed using one or two venous cannulae and CPB with mild (32°C-34°C) or moderate (25°C-28°C) hypothermia as described in Chapter 2 . A single venous cannula and mild hypothermia are chosen when a simple patent foramen ovale is present that will not be closed; two venous cannulae and moderate hypothermia are chosen when an atrial septal defect (ASD) will be closed.
Before establishing CPB, the ductus arteriosus is dissected and ligated immediately after initiating CPB. After establishing CPB and hypothermia, the aorta is clamped and cold cardioplegia administered (see “Cold Cardioplegia, Controlled Aortic Root Reperfusion, and [When Needed] Warm Cardioplegic Induction” in Chapter 3 ). Alternatively, operation may be done on the beating heart, without aortic clamping.
If two venous cannulae are used and an ASD is to be repaired, a small-caliber vent can be placed into the left side of the heart through a purse-string suture in the right pulmonary vein. Alternatively, the right atrium is opened through a small oblique incision, and a pump sump-sucker is placed across the foramen ovale and into the left atrium.
The pulmonary trunk is opened through a vertical incision, and fine stay sutures are placed on the edge of the incision for exposure. Two or three fused commissures can usually be seen, and these are opened with a knife, extending the incisions to the RV–pulmonary trunk junction. Because regurgitation is of less concern than residual narrowing, the incisions may be tailored to some extent to ensure that the valve has a wide opening. Portions of the valve are excised only when other methods fail to achieve a wide opening. Less commonly, the valve is dysplastic with three fully formed commissures and markedly thickened, even bulky, cusps. In this case, cusp debulking by partial resection of tissue is necessary to relieve obstruction. Rarely in neonates is there need to resect RV infundibular musculature. The pulmonary trunk is closed with one row of continuous 7-0 polypropylene suture. Usually, operation requires less than 15 minutes, and the aortic clamp, if used, is simply removed and de-airing accomplished. Remainder of the operation is completed in the usual manner (see “Completing Cardiopulmonary Bypass” in Section III of Chapter 2 ).
A patent foramen ovale, if present, is usually left open because the RV is very hypertrophied. The patient will benefit from allowing right-to-left atrial shunting until the RV remodels. If an ASD coexists, the decision is more complex because it is likely the patient will eventually develop significant left-to-right shunting through it once RV remodeling is complete. Judgment must be used in this setting. If there is concern that RV size and hypertrophy will result in perioperative RV failure, the ASD should be left open; it can be addressed at a later time once the RV has remodeled. If the RV is judged to be adequate, the ASD should be closed. Regardless of the initial decision, the physiology should be assessed carefully in the operating room following separation from CPB, and surgical readjustments (either opening or closing the ASD) made as necessary. Remainder of the operation is completed in the usual manner.
A concomitant systemic–pulmonary artery shunt may be added if Pa o 2 is severely reduced (<30 mmHg) after discontinuing CPB. The neonate usually comes to the operating room well resuscitated by prostaglandin E 1 (PGE 1 ). However, in the rare circumstance in which this is not the case, methods employed for seriously ill adult patients will probably improve results (see “Cold Cardioplegia, Controlled Aortic Root Reperfusion, and [When Needed] Warm Cardioplegic Induction” in Chapter 3 ).
Consideration should be given to placing a fine polyvinyl catheter into the RV, inserted through the right atrium across the tricuspid valve. It is used perioperatively to monitor RV pressure and typically is removed 48 hours later in the intensive care unit (see Special Features of Postoperative Care later). Measurements in the operating room after repair are not as informative and cannot serve as a guide to concomitant infundibular resection (see Results ).
Transesophageal echocardiography should be used routinely to assess the outflow tract after separation from CPB, paying particular attention to gradients at the valvar and infundibular level, degree of pulmonary and tricuspid valve regurgitation, RV function, and presence and degree of intraatrial shunting.
Transanular Patch
Although the likelihood of needing a transanular patch is greater when the RV cavity is small, the decision to place one at the initial surgical procedure is generally best made during operation. When surgery is performed as a secondary procedure, the decision is usually made preoperatively. Operation proceeds as described earlier for open pulmonary valvotomy. The interior of the RV infundibulum is inspected by looking through the pulmonary valve orifice. If it appears to be narrowed and if the diameter of the opened pulmonary valve (and thus presumably the “anulus”) has a z value of −3 or less (see discussion of z value in “Standardization of Dimensions” under Dimensions of Normal Cardiac and Great Artery Pathways in Chapter 1 ), and particularly when the RV cavity is very small, a transanular patch is probably indicated.
Incision in the pulmonary trunk is carried across the anulus and down to the junction of the sinus and infundibular portions of the RV. The pulmonary valve cusps are excised. Conservative resection of hypertrophied muscular trabeculae in the infundibulum may be accomplished, but this is often impractical in neonates (see Fig. 38-11 in Chapter 38 ). An enlarging patch is fashioned from glutaraldehyde-treated or untreated autologous pericardium and sewn into place with continuous 6-0 or 7-0 polypropylene sutures (see “Decision and Technique for Transanular Patching” in Section I of Chapter 38 ). Remainder of the procedure, including placing the polyvinyl catheter, is as described in the preceding text. A systemic–pulmonary artery shunt is added only if Pa o 2 is severely reduced after discontinuing CPB.
Systemic–Pulmonary Artery Shunt
If a systemic–pulmonary artery shunt is required as an isolated procedure (see Special Features of Postoperative Care later), a polytetrafluoroethylene (PTFE) interposition aortopulmonary shunt is made using a 3.5- or 4-mm tube via a median sternotomy. Whether shunting is an isolated procedure or concomitant to valvotomy or transanular patching, the PTFE tube is placed between the brachiocephalic trunk–right subclavian artery junction and the right pulmonary artery (see Technique of Operation in Section I of Chapter 38 ).
Special Features Of Postoperative Care
Proper perioperative management of neonates is essential for success. Generally these deeply cyanotic and critically ill infants are started on PGE 1 intravenously in doses of 0.05 to 0.4 µg · kg −1 · min −1 even before any studies are done; the resulting enlargement of the ductus arteriosus increases pulmonary blood flow and Pa o 2 by the time of operation. PGE 1 is continued during percutaneous valvotomy and early thereafter until the RV has a chance to remodel.
Caution must be used lest pulmonary overcirculation develop in a neonate whose pulmonary valve has been widely opened. The infant is left intubated and ventilated. As PGE 1 is discontinued in the hours after the procedure, Sa o 2 is monitored by pulse oximeter, or Pa o 2 is measured frequently. If after 24 hours, Pa o 2 remains well above 30 mmHg and the hemodynamic state is good, the neonate is gradually weaned from the ventilator and extubated. Even though some arterial desaturation persists, so long as Pa o 2 stays above about 30 mmHg and the clinical condition remains good, the neonate is patiently followed in anticipation of continued improvement as the RV remodels and the pulmonary vascular resistance decreases. If Pa o 2 falls to 30 mmHg or less, and if residual stenosis is mild or absent, a PTFE systemic–pulmonary artery shunt is performed. If important RVOT obstruction is present along with important hypoxia, a transanular patch as well as a systemic–pulmonary artery shunt is probably necessary.
If a primary surgical procedure is performed on the RVOT, the ductus has typically been ligated, and an appropriately sized systemic–pulmonary artery shunt may also have been placed. When a systemic–pulmonary artery shunt has been performed, the infant should be restudied at about age 6 to 12 months; plans should then be made for shunt closure by percutaneous or surgical means. In some surgical patients who do not receive a shunt at the time of the initial RVOT procedure, persistent cyanosis will occur, requiring return to surgery for placement of a shunt. Patients should be followed after hospital discharge until there is assurance that the RV–pulmonary artery peak pressure gradient is within acceptable limits. If it is not but can be remedied by further valvotomy, percutaneous techniques are generally recommended. In about 10% of patients, follow-up evaluation indicates important residual RV hypertension from “anular” or persistent infundibular narrowing; placing a transanular patch is then required to achieve the desired result.
Results
Survival
Early (Hospital) Death
About 10% of heterogeneous groups of neonates die during initial hospitalization ( Fig. 39-7 ). Risk-adjusted analysis indicates that early death occurs in only 6% of neonates treated by the surgical methods described in this chapter ( Fig. 39-8 ). This very good result in critically ill patients is directly traceable to introduction of PGE 1 , general improvement in neonatal cardiac surgery, and advent of percutaneous balloon valvotomy. Results of balloon valvotomy in neonates compare favorably with those of surgical valvotomy. Tabatabaei and colleagues were able to accomplish balloon dilatation in 35 of 37 neonates with critical valvar pulmonary stenosis (generally with suprasystemic RV pressure), with only 3 deaths (8%; CL 0%-16%). Others have reported similarly good survival.
Time-Related Survival
Survival for at least 4 years after birth in heterogeneous groups of treated neonates is about 80% (see Fig. 39-7 ). The rapidly declining appreciable early rate of death (hazard function) begins to flatten out considerably about 3 months after intervention. Risk-adjusted survival for at least 4 years can be presumed to be 94% (see Fig. 39-8 ), because death rarely occurred between 6 months and 4 years postoperatively in a large study. Gudausky and Beekman have reviewed mid- and long-term outcomes following balloon valvotomy in neonates, citing 6 studies since 1995 in addition to their own experience, totaling 221 patients. There were a total of 249 patients, with successful dilatation in 224 (90%). Follow-up ranged from 1 to 116 months. Twelve serious complications resulted from the procedure, and 13 total deaths; 5 of the deaths were early and 8 were late.
Modes of Death
The mode of virtually all deaths is either hypoxia or acute cardiac failure.
Incremental Risk Factors for Premature Death
Although uncommon, RV enlargement of an appreciable degree is a highly lethal coexisting cardiac anomaly. This is probably a special situation in which there is a coexisting cardiomyopathy or tricuspid valve lesion (e.g., Ebstein malformation) already present in fetal life because of genetic or developmental factors. Aside from these rare cases, no general patient-specific risk factors for death are identifiable in neonates. This is unusual in patients with congenital heart disease.
For open pulmonary valvotomy without inflow stasis or CPB and for certain morphologic variants (see text that follows), transanular patching without a shunt is a risk factor, and these procedures should not be used ( Table 39-2 ). Other procedures give good results, with few differences between them ( Fig. 39-9 ). In neonates and young infants, transanular patching unaccompanied by a systemic–pulmonary artery shunt is an incremental risk factor when the pulmonary “anulus” is severely hypoplastic or when there is important tricuspid regurgitation. Patients in this situation usually have severe RV hypertrophy and reduced cavity size; without a shunt, they tend to have marked hypoxia from right-to-left shunting across a patent foramen ovale secondary to acute RV failure.
Table 39-2
Incremental Risk Factors for Death at Any Time after Initial Accomplished Procedure a
Data from Hanley and colleagues.
| Risk Factor | Single Hazard Phase P Value | |
|---|---|---|
| Procedural | ||
| Open pulmonary valvotomy without inflow stasis | <.0001 | |
| Transanular patching without a shunt b | ||
| (Smaller) | +Dimension ( z value) of RV-PT junction | .01 |
| (Greater) | +Degree of tricuspid regurgitation | .0002 |
| (Earlier) | +Date of procedure | .04 |
Key: PT, Pulmonary trunk; RV, right ventricle.
a Database consists of 101 neonates with critical pulmonary stenosis entered into a multiinstitutional study between January 1987 and 1991. Median age of entry was 3 days. Analysis was of 93 patients, excluding five with Ebstein anomaly, a large right ventricle, or both, and three (two are deceased) in which no procedure was performed.
b The three factors listed under transanular patching without a shunt are interaction terms; that is, they pertain only to patients in whom transanular patching without a shunt was performed, not to patients undergoing other types of procedure. Transanular patching without a shunt, when examined without interaction terms, had a low P value of .9.
Reintervention
About 75% of neonates successfully undergoing pulmonary valvotomy require no further procedure for at least 4 years. About 10% remain hypoxic and require a systemic–pulmonary artery shunt. In a few, repeat balloon valvotomy is needed. About 10% of those not initially receiving a transanular patch will need one at some point. Rarely (<2%), a two-ventricle system cannot be attained, and a superior cavopulmonary anastomosis or Fontan-type operation is ultimately required. Similarly, Rao reports occurrence of reintervention was 25% following initial balloon valvotomy.
Occasionally, closure of an ASD is required as the RV remodels and important left-to-right shunting develops in patients in whom the ASD was purposefully left open at the time of the neonatal procedure. The long-term implications of severe pulmonary regurgitation, primarily in those patients who received a transanular patch, remain unclear. In patients who fail to develop adequate Sa o 2 (>85% at rest) and right atrial pressure (<12-15 mmHg at rest) with the atrial septum and any systemic–pulmonary artery shunt temporarily closed, a superior cavopulmonary anastomosis can be considered to reduce the workload of the RV, allowing closure of the ASD and systemic–pulmonary shunt. Occasionally, a Fontan-type operation is ultimately indicated.
Residual Right Ventricular Outflow Tract Obstruction
Limited information is available concerning residual gradients. In about 90%, any important residual gradient has disappeared or been overcome by repeat percutaneous valvotomy within 6 to 12 months of the initial procedure. Ultimately, the RV–pulmonary trunk gradient is usually about 20 mmHg. In unusual cases in which the gradient remains above about 50 mmHg, transanular patching is warranted. The mechanism by which percutaneous balloon valvotomy effects its good results is generally the ideal one of commissural splitting; tearing of pulmonary valve tissue is uncommon. The exception may be the dysplastic pulmonary valve, in which commissural fusion is not the dominant problem causing obstruction. Although Stamm, Anderson, and colleagues emphasize that balloon valvotomy is ineffective, based on morphologic characteristics of dysplastic valves, reports vary as to effectiveness of this procedure in this setting.
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