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Pulmonic valve stenosis in adults: Management

Pulmonic valve stenosis in adults: Management
Literature review current through: Jan 2024.
This topic last updated: Nov 22, 2023.

INTRODUCTION — Nearly all cases of pulmonic valve stenosis (PS) are congenital in origin, and most cases occur as an isolated lesion. Acquired cases of stenosis of the native pulmonary valve are encountered less commonly and may be caused by carcinoid or rheumatic heart disease (in which case PS is always associated with other valve abnormalities). (See "Carcinoid heart disease" and "Clinical manifestations and diagnosis of rheumatic heart disease" and "Management and prevention of rheumatic heart disease".)

The natural history and treatment of congenital valvular PS will be reviewed here. The diagnosis and evaluation of PS and management of pregnancy and PS are discussed separately. (See "Clinical manifestations and diagnosis of pulmonic stenosis in adults" and "Pregnancy and valve disease", section on 'Pulmonic stenosis'.)

Right ventricular (RV) outflow obstruction may also persist or occur after surgical reconstruction for congenital cardiac disorders such as tetralogy of Fallot, pulmonary atresia, truncus arteriosus, double outlet RV, or transposition of the great arteries with PS. Reconstruction often entails the placement of a pulmonary valve prosthesis, right ventricle-to-pulmonary artery homograft, or valved conduit, which will degenerate over time, and can manifest as stenosis, regurgitation, or both. Management of these conditions is discussed separately. (See "Pulmonary atresia with intact ventricular septum (PA/IVS)" and "Truncus arteriosus", section on 'Management' and "Tetralogy of Fallot (TOF): Long-term complications and follow-up after repair", section on 'Long-term complications'.)

FORMS OF PULMONIC STENOSIS — Congenital pulmonic valve stenosis (PS) occurs in three predominant forms [1]. Although these are distinct forms under direct visualization, echocardiography in adults may not distinguish leaflets well enough to clearly determine valve morphology.

Dome-shaped – Most cases involve dome-shaped PS, which is characterized by a narrow central opening with preserved valve motion. Three rudimentary raphes are generally present without clear-cut commissures. The pulmonary trunk may be dilated due to a medial abnormality and eccentric flow from the stenotic valve. Calcification of the valve is rare but is noted in some older patients.

Pulmonic valve dysplasia – Approximately 20 percent of cases involve pulmonic valve dysplasia, with thickened valve cusps and relative immobility of the valve, often associated with severe stenosis (image 1). Dysplastic pulmonic valves are often associated with hypoplasia of the pulmonary annulus and proximal pulmonary artery and are not commonly associated with pulmonary artery dilation. Dysplastic pulmonic valves are a common component of Noonan syndrome, occurring in up to half of patients in some studies. (See "Clinical manifestations and diagnosis of pulmonic stenosis in adults", section on 'Introduction' and "Noonan syndrome".)

Associated with complex congenital heart disease – More complex congenital heart disease, such as cases of tetralogy of Fallot or transposition of the great arteries, may be associated with a unicuspid or bicuspid pulmonic valve, which may be obstructive. (See "Tetralogy of Fallot (TOF): Pathophysiology, clinical features, and diagnosis", section on 'Right ventricular outflow tract obstruction' and "D-transposition of the great arteries (D-TGA): Anatomy, clinical features, and diagnosis".)

GRADING SEVERITY — The natural history and approach to therapy of pulmonic valve stenosis (PS) are determined by the hemodynamic severity of the obstruction.

The severity of PS is classified by major society guidelines using the following echocardiographic criteria [1,2]:

Mild PS is identified by a peak Doppler gradient across the valve <36 mmHg (equal to peak Doppler jet velocity <3 m/s) [1,2].

Moderate PS is identified by a peak Doppler gradient of 36 to 64 mmHg (peak jet velocity of 3 to 4 m/s) [1,2].

Severe PS is identified by a peak Doppler gradient >64 mmHg (peak jet velocity of >4 m/s) [1,2] or mean Doppler gradient >35 mmHg [2].

The above thresholds for PS apply to patients with normal RV systolic function. Patients with severe RV systolic dysfunction may have a low stroke volume, and Doppler gradients may underestimate severity of stenosis, similar to low flow, low gradient aortic stenosis.

Although mean gradients have been less commonly used to quantify PS, the 2018 American Heart Association/American College of Cardiology guidelines for adults with congenital heart disease include a mean gradient criterion for severe PS since this may reflect the catheter-derived peak-to-peak gradients more accurately than do peak Doppler gradients [2]. A study of 90 patients with isolated PS found that the mean Doppler gradient more accurately reflected the catheter-derived peak-to-peak gradient [3]. The peak Doppler gradient averaged 24 mmHg higher than the catheter-derived peak-to-peak gradient. Additionally, the studies that demonstrated the effectiveness of transcatheter pulmonary valve replacement in patients with prosthetic pulmonic valves or pulmonary homografts used mean gradients as an inclusion criterion. Consequently, mean gradient is commonly used when deciding treatment timing for patients with RV outflow obstruction. (See "Transcatheter pulmonary valve implantation".)

Of note, most patients with congenital PS do not have significant pulmonic regurgitation (PR); mixed PS and PR is more commonly seen with acquired pulmonary valve disease or after intervention for PS. (See 'Management of postvalvotomy PR' below.)

MONITORING

Frequency — The frequency of recommended routine follow-up for patients with pulmonic valve stenosis (PS) is based upon the patient's clinical status [1,2], which can be defined by the physiologic stage, as described in the 2018 American Heart Association/American College of Cardiology adult congenital heart disease guideline [2]. (See 'Physiologic stage' below.)

For physiologic stage A – For patients with trivial (less than mild) PS with no symptoms and normal exercise capacity, follow-up with an adult congenital heart disease cardiologist, electrocardiogram (ECG), and transthoracic echocardiography (TTE) with Doppler is recommended at three- to five-year intervals, with exercise testing performed as needed.

For physiologic stage B – For patients with mild PS with New York Heart Association (NYHA) functional class I or II (table 1), follow-up with an adult congenital heart disease cardiologist, ECG, TTE, and exercise testing is recommended at two-year intervals.

For physiologic stage C – For patients with moderate or greater PS with NYHA functional class I, II, or III (table 1), follow-up with an adult congenital heart disease cardiologist is recommended at 6- to 12-month intervals, with routine ECG and TTE at 12-month intervals and exercise testing at two-year intervals.

For physiologic stage D – For patients with PS with NYHA functional class IV (table 1) who are not candidates for intervention, follow-up with an adult congenital heart disease cardiologist is recommended at three- to six-month intervals, with routine ECG, TTE, and exercise testing at 12-month intervals.

The same principles for monitoring apply to patients with PS who have undergone intervention. Patients with PS frequently have RV outflow tract obstruction (infundibular and PS) and/or pulmonic regurgitation after pulmonary valvotomy.

Physiologic stage — The physiologic stage is categorized as follows (patients are classified based upon the highest [most severe] relevant physiologic feature) [2]:

Stage A

NYHA functional class I (table 1)

No hemodynamic or anatomic sequelae

No arrhythmias

Normal exercise capacity

Normal renal/hepatic/pulmonary function

Stage B

NYHA class II symptoms (table 1)

Mild hemodynamic sequelae (mild aortic enlargement, mild ventricular enlargement, mild ventricular dysfunction)

Mild valvular disease

Trivial or small shunt (not hemodynamically significant)

Arrhythmia not requiring treatment

Abnormal objective cardiac limitation to exercise

Stage C

NYHA class III symptoms (table 1)

Significant (moderate or greater) valvular disease

Moderate or greater ventricular dysfunction (systemic, pulmonic, or both)

Moderate aortic enlargement

Venous or arterial stenosis

Mild or moderate hypoxemia/cyanosis

Hemodynamically significant shunt

Arrhythmias controlled with treatment

Pulmonary hypertension (less than severe)

End-organ dysfunction responsive to therapy

Stage D

NYHA class IV symptoms (table 1)

Severe aortic enlargement

Arrhythmias refractory to treatment

Severe hypoxemia (almost always associated with cyanosis)

Severe pulmonary hypertension

Eisenmenger syndrome

Refractory end-organ dysfunction

NATURAL HISTORY — Pulmonic valve stenosis (PS) in children is usually associated with a benign clinical course, and excellent treatment options are available for severe cases. Thus, there is a high rate of survival into adulthood.

Most patients with PS are asymptomatic [4]. The life-expectancy in patients with isolated PS is similar to that of the general population [4].

Mild stenosis — Mild PS causes no symptoms. If a patient with mild PS has symptoms, the symptoms should not be attributed to PS. Some adults with mild stenosis will have been diagnosed during childhood [5], but many cases will have gone undetected. (See "Pulmonic stenosis in infants and children: Clinical manifestations and diagnosis", section on 'Mild or moderate pulmonic stenosis'.)

The course during adulthood is generally benign with little progression of stenosis and a persistently high functional status in most patients. In the Natural History Study of Congenital Heart Defects (NHS), for example, among patients with baseline peak systolic valve gradient <25 mmHg, 96 percent were free of operation at 10-year follow-up [4].

Moderate stenosis — Moderate PS is often detected in childhood and is frequently symptomatic. Dyspnea on exertion and fatigue may occur due to the limitation of RV cardiac output. (See "Pulmonic stenosis in infants and children: Clinical manifestations and diagnosis", section on 'Mild or moderate pulmonic stenosis'.)

A minority of patients with moderate PS receive a pulmonic valve procedure during childhood, as discussed separately. These individuals generally survive into adulthood with life expectancies that are not different from the general population [4]. Long-term follow-up of patients in the NHS found that only 4 percent who had surgical valvotomy or balloon valvotomy in childhood required reoperation [4]. (See "Pulmonic stenosis in infants and children: Management and outcome", section on 'Moderate pulmonic stenosis (gradient 40 to 60 mmHg)'.)

Patients with moderate stenosis treated medically in childhood may fare well into adulthood, although some may show evidence of progression of stenosis and require an intervention [5,6]. Overall, there were few differences between surgically and medically treated patients with moderate PS in the NHS [4]. Both groups had low levels of cardiac drug use (4 percent) and excellent clinical status as defined by New York Heart Association criteria (97 percent were in class I) (table 1).

Severe stenosis — Severe PS most often presents in childhood with right ventricular failure and cyanosis. Severe valvular PS does not spontaneously remit and may progress over time, resulting in elevated RV end-diastolic pressure and risk of irreversible RV dysfunction. (See "Pulmonic stenosis in infants and children: Clinical manifestations and diagnosis", section on 'Clinical manifestations' and "Pulmonic stenosis in infants and children: Management and outcome", section on 'Natural history' and "Pulmonic stenosis in infants and children: Management and outcome", section on 'Management'.)

Adults will have usually been treated early in life with either balloon valvotomy or surgery, regardless of symptomatology [5]. The prognosis continues to be good into adulthood after successful treatment [4].

INDICATIONS FOR INTERVENTION — The decision to perform a valve intervention depends on the valve anatomy, severity (gradient), and symptoms. In most cases, the valve is amenable to balloon valvotomy (dome-shaped or selected dysplastic valves that are amenable to balloon valvotomy). Surgical valve intervention may be preferred or required if the anatomy is not favorable (dysplastic pulmonic valves not amenable to balloon valvotomy, an associated hypoplastic pulmonary annulus, severe pulmonic regurgitation (PR), or subvalvular or supravalvular pulmonic stenosis [PS]), if balloon valvotomy fails to relieve the stenosis, or if the patient is undergoing cardiac surgery for another indication (eg, severe tricuspid regurgitation) (algorithm 1). (See 'Balloon valvotomy' below and 'Surgical intervention' below.)

For pulmonic valve stenosis — Indications for intervention include:

Severe stenosis – For patients with severe PS (Doppler peak gradient >64 mmHg or mean Doppler gradient >35 mmHg), we recommend intervention. Most patients are treated by balloon valvotomy. Patients with severe PS are usually symptomatic and are likely to develop progressive RV hypertrophy and irreversible RV dysfunction if not corrected. (See 'Severe stenosis' above.)

Moderate stenosis with associated symptoms – For patients with moderate PS (36 to 64 mmHg) with associated symptoms (eg, dyspnea, cyanosis from interatrial right-to-left communication, and/or exercise intolerance), we suggest intervention (generally balloon valvotomy). (See 'Moderate stenosis' above.)

Patients with mild stenosis are generally asymptomatic and do not require intervention. Asymptomatic patients with moderate stenosis also generally do not require intervention, although they should be monitored for worsening of the gradient and/or development of symptoms. (See 'Monitoring' above and 'Mild stenosis' above and 'Moderate stenosis' above.)

The above recommendations for intervention in adults with PS are similar to those in major society guidelines [1,2].

Patients treated with balloon valvotomy or surgical valvotomy require ongoing follow-up for PR and residual or recurrent stenosis. (See 'Monitoring' above and 'Management of postvalvotomy PR' below.)

For asymptomatic dilated pulmonary artery — There are no definite indications for intervening for an asymptomatic dilated pulmonary artery, as these are low-pressure aneurysms with an extremely low risk of dissection or rupture. Repair for evidence of symptomatic compression of neighboring structures and repair at the time of valve replacement are reasonable approaches. Some suggest elective repair for pulmonary artery aneurysms over 80 mm and individualized management for all other patients [7].

INTERVENTIONS — Most patients with pulmonic valve stenosis (PS) requiring intervention are candidates for balloon valvotomy. For patients with PS who are not candidates for balloon valvotomy, options include surgical intervention (valvotomy or replacement) and transcatheter pulmonary valve implantation. Surgical intervention may be preferred in patients with a concurrent indication for cardiac surgery. (See 'Surgical intervention' below.)

Balloon valvotomy — When intervention is indicated for PS and pulmonary valve anatomy is suitable (ie, domed, or dysplastic but amenable to balloon valvotomy), percutaneous balloon valvotomy (figure 1) is the procedure of choice, with excellent short- and long-term results. (See 'Indications for intervention' above.)

Balloon valvotomy causes commissural splitting [8]. Use of an oversized balloon (approximately 1.2 to 1.25 times the measured pulmonic annulus) aids in achieving a successful result (defined as a final peak valvular gradient of <20 mmHg) [9].

Exclusions — Patients with the following conditions are generally not optimal candidates for balloon valvotomy:

Valve anatomy not amenable to balloon valvotomy (some dysplastic valves)

Hypoplastic pulmonary valve annulus

Moderate or severe pulmonic regurgitation (PR)

Concurrent subvalvular PS

Concurrent supravalvular PS

Acute outcomes — The balloon valvotomy procedure for PS is generally well tolerated. A mortality rate of 0.2 percent and major complication rate of 0.6 percent were reported by the Valvuloplasty and Angioplasty of Congenital Anomalies registry [10]. Among 784 patients of all ages, clinical success was achieved with balloon valvotomy in 98 percent, with a fall in the systolic outflow gradient from 71 to 28 mmHg [10]. Among the 196 patients in whom such data could be obtained, transvalvular and infundibular obstruction were each responsible for approximately one-half of the total residual gradient.

Acute complications are generally minor and include a vagal response, catheter induced ventricular ectopy, right bundle branch block, and transient or permanent high-grade atrioventricular nodal block [9]. Transient severe RV outflow tract (RVOT) obstruction ("suicidal right ventricle") has been reported after the pulmonic valvular obstruction has been relieved [9,11,12]. This may be treated by volume expansion and beta blocker therapy.

Other complications include development of PR, tricuspid regurgitation, stroke, syncope, pulmonary artery rupture, pulmonary edema, cardiac perforation, and tamponade.

Long-term outcomes — After balloon valvotomy, infundibular gradients generally decline over months and years with regression of RV hypertrophy [10,12-16]. Improvement in RVOT gradients and PR over time was illustrated by a series of 53 adolescent and adult patients 13 to 55 years of age treated between 1985 and 1995 [13]. The systolic pressure gradient across the pulmonic valve fell from 91 to 38 mmHg after the procedure and had fallen further at late follow-up an average of seven years later.

Restenosis is uncommon (eg, 1.5 or 5 percent at a mean of 6 years follow-up [8,14]) after balloon valvotomy and may be more likely in patients with dysplastic valves [14].

PR commonly develops after balloon valvotomy, is often mild [17-19] and may spontaneously resolve in some patients [13].

Surgical intervention — Surgical intervention (valvotomy or valve replacement) is performed in patients with PS requiring intervention who are not candidates for balloon valvotomy or who have a concurrent indication for cardiac surgery (algorithm 1). (See 'Indications for intervention' above.)

Surgical valvotomy is generally well tolerated, although operative mortality (eg, 2.5 percent [20]) may be higher than with balloon valvotomy due to differences in patient populations and interventions. Surgery tends to produce lower long-term pulmonary valve gradients but higher rates of PR compared with balloon valvotomy (45 versus 11 percent in one series) [21]. Of note, PR requiring pulmonic valve replacement was the indication for the majority of reinterventions in surgical series [22,23]. (See 'Management of postvalvotomy PR' below.)

Long-term follow-up of surgical intervention from the era of the Natural History Study of Congenital Heart Defects (NHS) cohort, which was before the use of percutaneous balloon valvotomy, comes from a report of 53 patients who were initially treated between 1951 and 1982 at a mean age of 10 years; their status was determined 33 years later [22]. Forty of the patients were treated with open valvotomy, with infundibular resection in 13. The following findings were noted:

Thirty-five reinterventions were performed in 28 patients (53 percent), including pulmonary valve replacement for regurgitation in 21, open valvotomy in five, and balloon valvotomy in three. Most of the reinterventions were performed more than 25 years after the initial procedure. The only predictor of the need for reintervention was closed valvotomy.

Twenty patients developed an atrial arrhythmia, six of whom had radiofrequency ablation, and three patients developed a ventricular arrhythmia.

Similar outcomes were noted at 22- to 33-year follow-up in a later cohort of 90 consecutive patients who underwent surgery between 1968 and 1980 [23]:

Survival was 93 percent at 25 years. At last follow-up, 67 percent of patients were in New York Heart Association class I (table 1) and maximal exercise capacity was 90 percent of normal.

Reintervention was required in 15 percent, primarily for PR. Reoperation for PR was required in 9 percent, particularly after use of the transannular patch technique. At last follow-up, moderate to severe PR was present in 37 percent.

Supraventricular arrhythmias occurred only in patients with severe PR and disappeared after reoperation. There were no major ventricular arrhythmias.

Transcatheter pulmonary valve implantation — Transcatheter pulmonary valve implantation is an option for patients with PS requiring intervention. The procedure, exclusions, and complications are discussed separately. (See "Transcatheter pulmonary valve implantation".)

MANAGEMENT OF POSTVALVOTOMY PR — Pulmonic regurgitation (PR) commonly develops after balloon valvotomy or surgical valvotomy for pulmonic valve stenosis (PS), with higher rates of significant PR observed after surgical valvotomy. While mild degrees of PR are well tolerated, more significant PR may result in RV enlargement and dysfunction sufficient to consider pulmonary valve replacement. Imaging criteria (eg, echocardiographic or cardiovascular magnetic resonance imaging criteria for RV dilation or dysfunction) for intervention for PR in asymptomatic patients post-balloon valvotomy or surgical valvotomy for isolated PS have not been established. While some practitioners may utilize criteria for other diseases for which PR is a common sequela, such as tetralogy of Fallot, data are lacking to support such an approach.

In patients with PR following valvotomy, we assess PR severity and RV size (algorithm 2) [2].

In patients with no or mild PR, we perform routine follow-up. For patients with mild PR, clinical and imaging follow-up every two to four years is reasonable.

In patients with moderate or greater PR and RV enlargement, we assess for the presence of symptoms caused by PR.

We refer patients with symptomatic PR for pulmonic valve replacement, either surgical or transcatheter. (See 'Indications for intervention' above.)

For patients with RV dysfunction, progressive RV dilation, or progressive decrease in exercise capacity, we refer to a comprehensive adult congenital heart disease program for individualized assessment of the benefit/risk of pulmonary valve replacement. Optimal criteria for intervention for pulmonary valve replacement have not been established, and practice varies. (See "Pulmonic regurgitation" and "Tetralogy of Fallot (TOF): Long-term complications and follow-up after repair".)

For patients without symptoms or the above changes, we perform serial imaging and cardiopulmonary exercise testing according to the patient's physiologic stage (at least every 12 months). (See 'Physiologic stage' above.)

If pulmonary valve replacement is indicated, options include surgical pulmonic valve replacement and transcatheter pulmonary valve implantation. (See "Pulmonic regurgitation" and "Transcatheter pulmonary valve implantation".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Cardiac valve disease".)

SUMMARY AND RECOMMENDATIONS

Forms of congenital pulmonic stenosis – Congenital pulmonic valve stenosis (PS) occurs in three predominant forms: dome-shaped (the most common form), pulmonic valve dysplasia, and PS associated with complex congenital heart disease in which the valve may be unicuspid or bicuspid. (See 'Forms of pulmonic stenosis' above.)

Grading PS – The severity of PS is classified according to either the peak or mean Doppler echocardiographic gradients across the valve. Although peak gradients have been more commonly used, the mean gradients may more accurately reflect catheter-derived peak-to-peak gradients. The pulmonary valve gradient may be affected by right ventricular (RV) systolic dysfunction. (See 'Grading severity' above.)

Natural history – The majority of adult patients with PS have mild stenosis and are asymptomatic. Patients with moderate PS may develop symptoms such as dyspnea and fatigue. Patients with severe stenosis commonly have symptoms and are at risk for developing progressive RV hypertrophy and both systolic and diastolic dysfunction if the PS is left untreated (See 'Natural history' above.)

Indications for valve intervention – The decision to perform a valve intervention depends on the valve anatomy, severity (gradient), and symptom status (algorithm 1). Indications for intervention (generally balloon valvotomy) for PS include (see 'Indications for intervention' above):

Severe stenosis – For patients with severe PS (Doppler peak gradient >64 mmHg or mean Doppler gradient >35 mmHg), we recommend pulmonic valve intervention (Grade 1B). Patients with severe PS are usually symptomatic and are likely to develop progressive RV hypertrophy with systolic and diastolic RV dysfunction if not corrected. For patients with asymptomatic severe PS who are not candidates for balloon valvotomy, timing of intervention is based upon an individualized assessment weighing the risks and benefits of valve replacement. (See 'Severe stenosis' above.)

Moderate stenosis with associated symptoms – For patients with moderate PS (36 to 64 mmHg) with associated symptoms (eg, dyspnea, exercise intolerance), we suggest pulmonic valve intervention (Grade 2C). (See 'Moderate stenosis' above.)

Patients with mild stenosis are generally asymptomatic and do not require intervention. Asymptomatic patients with moderate stenosis also generally do not require intervention although they should be monitored for worsening of the gradient and/or development of symptoms. (See 'Monitoring' above and 'Mild stenosis' above and 'Moderate stenosis' above.)

Choice of intervention – Most patients with PS requiring intervention are candidates for balloon valvotomy (algorithm 1). (See 'Balloon valvotomy' above.)

Patients with the following conditions are generally not optimal candidates for balloon valvotomy (see 'Exclusions' above):

Valve anatomy not amenable to balloon valvotomy (some dysplastic valves)

Hypoplastic pulmonary valve annulus

Moderate or severe pulmonic regurgitation (PR)

Concurrent subvalvular PS

Concurrent supravalvular PS

For patients who are not optimal candidates for balloon valvotomy, options include surgical intervention (valvotomy or replacement) or transcatheter pulmonary valve replacement. Surgical intervention is usually preferred in patients undergoing concurrent cardiac surgery. (See 'Surgical intervention' above and "Transcatheter pulmonary valve implantation".)

Complications of intervention for PS Balloon valvotomy, surgical pulmonary valve replacement, surgical valvotomy, and transcatheter pulmonary valve replacement procedures are generally well tolerated, with higher procedural risk associated with surgical intervention. (See 'Balloon valvotomy' above and 'Surgical intervention' above and "Transcatheter pulmonary valve implantation".)

The main long-term complication of balloon or surgical valvotomy is PR, which may be more prominent after surgical valvotomy. Patients with moderate or greater PR may develop RV enlargement and/or dysfunction. Options for management of PR include transcatheter or surgical pulmonary valve replacement. (algorithm 2). (See 'Management of postvalvotomy PR' above and "Pulmonic regurgitation".)

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References

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