The pulmonary valve plays a crucial role in directing blood from the right ventricle to the pulmonary arteries during systole. Its closure during diastole is equally essential to prevent the backward flow into the right ventricle caused by the decrease in right ventricular pressure. Any abnormalities in the structure or function of this valve can obstruct the forward flow.
Issues such as defective valve coaptation, annular dilation, or the presence of fibrinoid deposits can hinder flow, leading to an increase in volume. Immediate and delayed responses to this volume overload can present as clinical signs and symptoms of pulmonary regurgitation.
Epidemiology
Mild pulmonary regurgitation is frequently observed in adolescent children and is generally deemed non-threatening. The primary diagnostic tool for assessing the extent of pulmonary regurgitation and its implications is an echocardiogram.
Individuals undergoing follow-up evaluations post-tetralogy of Fallot repair have been observed to develop pulmonary regurgitation within a span of 1 to 21 years following the initial surgical intervention.
Anatomy
Pathophysiology
Pulmonary regurgitation occurs when the pulmonary valve, responsible for directing blood from the right ventricle to the pulmonary arteries, exhibits impaired function. This dysfunction can stem from various pathophysiological factors, including defective coaptation of the valve leaflets, annular dilation, or the deposition of fibrinoid material on the valve.
These structural abnormalities compromise the valve’s ability to prevent the backflow of blood into the right ventricle during diastole. As a consequence, this impedes the normal forward flow, leading to volume overload in the right ventricle. Over time, the regurgitation of blood into the right ventricle during diastole results in clinical manifestations of pulmonary regurgitation.
The pathophysiological consequences are further accentuated in cases where patients, particularly those who have undergone tetralogy of Fallot repair, experience this condition years after the initial intervention, underscoring the long-term implications of pulmonary regurgitation.
Etiology
The etiology of pulmonary regurgitation can be multifaceted, arising from various factors that affect the structure and function of the pulmonary valve and its surrounding components. One common cause is congenital heart defects, such as tetralogy of Fallot, where abnormalities in the development of the heart can lead to malformations of the pulmonary valve, resulting in regurgitation.
Acquired causes of pulmonary regurgitation may include infectious endocarditis, which can damage the valve leaflets, as well as rheumatic heart disease. Trauma to the chest or the valve itself during surgical procedures can also contribute to the development of pulmonary regurgitation. Annular dilation, a widening of the ring-like structure supporting the valve, can be another etiological factor.
This dilation may occur due to conditions like pulmonary hypertension or chronic pulmonary artery dilation. In some cases, idiopathic or unknown factors may lead to pulmonary regurgitation. Additionally, certain connective tissue disorders or genetic conditions can predispose individuals to valve abnormalities and regurgitation.
Genetics
Prognostic Factors
Clinical History
The majority of individuals with pulmonary regurgitation are typically asymptomatic. However, symptomatic cases often manifest with initial symptoms of exertional dyspnea due to diminished cardiac output resulting from the right heart’s volume overload. A gradual decline in exercise tolerance may be observed in such cases.
In instances of severe pulmonary regurgitation, symptoms indicative of right heart failure may become apparent, including congestive hepatomegaly, pedal edema, and, infrequently, elevated jugular venous distension. Additionally, patients may present with complications arising from right ventricular dilation, notably symptomatic ventricular arrhythmias.
In clinical scenarios where an underlying pathology is identified as the primary cause of pulmonary regurgitation, symptoms related to the specific underlying disease may take precedence. For instance, pulmonary regurgitation secondary to pulmonary hypertension may exhibit symptoms characteristic of the underlying condition, such as those seen in left heart disease, chronic lung disorders like OSA or COPD, or primary pulmonary arterial hypertension.
Physical Examination
Auscultation in individuals with pulmonary regurgitation typically reveals a diastolic decrescendo murmur audible in the second and third left intercostal spaces. Additionally, an S3 sound may be appreciated, signifying volume overload. This right-sided murmur tends to intensify during inspiration, attributed to heightened preload and diminishes during the Valsalva maneuver due to altered pressures.
It is noteworthy to highlight the variations in auscultatory findings based on the presence or absence of pulmonary arterial hypertension. In cases with elevated pulmonary artery pressures, creating a substantial gradient between the pulmonary artery and right ventricle, the pulmonary regurgitation murmur becomes diastolic, persisting throughout diastole (in contrast to its transient nature in cases without pulmonary hypertension).
The murmur retains its decrescendo quality, is associated with a pronounced P2, and is audible in the second and third left intercostal spaces, exhibiting an augmentation during inspiration.
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Constrictive pericarditis
Infective endocarditis
Restrictive cardiomyopathy
Chronic pulmonary emboli
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Surgical intervention is recommended for all symptomatic patients experiencing pulmonary regurgitation. The preferred treatment methods typically involve surgical pulmonary valve replacement, with options including a bioprosthesis or mechanical valve. Bioprosthesis valves are favored due to their durability, lower risk of valve failure, and relatively shorter period of required anticoagulation compared to mechanical valves.
Percutaneous pulmonary valve replacement is an advancing field in interventional cardiology. However, certain challenges need addressing, such as deviations in the anatomy of the right ventricular outflow tract that may limit its applicability. Tricuspid regurgitation often arises as a consequence of complications following pulmonary regurgitation and necessitates attention. In cases of tricuspid regurgitation, tricuspid annuloplasty may be performed.
Additionally, the presence of large akinetic right ventricular outflow tract segments may require resection to prevent further exacerbation of the prognosis. Medical intervention is solely advised when pulmonary regurgitation is a consequence of an underlying medical condition, such as pulmonary arterial hypertension or carcinoid disease. In cases where the cause is secondary to a primary medical condition, medical therapy becomes a consideration.
Specifically, medications aimed at managing heart failure, including diuretics, ACE inhibitors, and beta-blockers, are recommended exclusively for symptomatic individuals with severe pulmonary regurgitation. This approach is particularly relevant for patients deemed unsuitable candidates for surgery due to factors like advanced age or the presence of significant comorbidities.
Lifestyle Modifications: Adopting a healthy lifestyle can help manage pulmonary regurgitation. This includes maintaining a balanced diet, regular exercise, avoiding smoking, and managing stress.
Monitoring and Follow-up: Regular monitoring by a cardiologist is essential for individuals with pulmonary regurgitation. This may involve echocardiograms, cardiac MRI, or other imaging tests to assess the function of the heart and the severity of the regurgitation.
Pregnancy Management: For women with pulmonary regurgitation, especially those with severe cases or additional cardiac complications, careful management during pregnancy is crucial.
Endocarditis Prevention: Individuals with certain types of heart defects, including those causing pulmonary regurgitation, are at increased risk of infective endocarditis.
Role of Beta blockers
Metoprolol: It may be indicated to alleviate symptoms associated with PR, such as palpitations, chest discomfort, or shortness of breath.
By slowing the heart rate and reducing the force of contraction, metoprolol can help improve cardiac efficiency and reduce symptoms related to increased myocardial oxygen demand.
Role of Angiotensin receptor blocker
Losartan: It is indicated for the management of systemic hypertension.
By lowering blood pressure, losartan can help reduce afterload on the heart, potentially mitigating the impact of hypertension on PR and overall cardiac function.
Pulmonary Valve Replacement: If the pulmonary valve is severely damaged or dysfunctional, pulmonary valve replacement may be necessary. This can involve either a surgical procedure where the damaged valve is removed and replaced with a mechanical or biological valve or a less invasive procedure called transcatheter pulmonary valve replacement (TPVR).
Balloon Valvuloplasty: For patients with pulmonary valve stenosis, balloon valvuloplasty may be performed. This procedure involves inserting a catheter with a balloon tip into the narrowed valve and inflating the balloon to widen the valve opening.
Pulmonary Valve Repair: In some cases, particularly in congenital heart conditions where the pulmonary valve is malformed but not severely damaged, surgical repair of the valve may be possible. This can involve techniques to reshape or reconstruct the valve to improve its function.
use-of-phases-in-managing-pulmonary-regurgitation
Diagnosis and Assessment: Symptoms of PR may include shortness of breath, fatigue, palpitations, and signs of right heart failure.
Diagnostic tests: Echocardiography is typically the primary diagnostic tool to assess. Additional tests such as cardiac MRI or cardiac catheterization may be used for further evaluation if needed.
Monitoring and Follow-up: Patients with PR require ongoing monitoring to assess disease progression and the development of symptoms or complications.
Imaging studies: Periodic echocardiograms or other imaging tests may be recommended to evaluate changes in pulmonary regurgitation severity and its effects on the heart.
Intervention: Intervention may be indicated in patients with severe PR, progressive right ventricular dysfunction, or symptoms refractory to medical therapy.
The pulmonary valve plays a crucial role in directing blood from the right ventricle to the pulmonary arteries during systole. Its closure during diastole is equally essential to prevent the backward flow into the right ventricle caused by the decrease in right ventricular pressure. Any abnormalities in the structure or function of this valve can obstruct the forward flow.
Issues such as defective valve coaptation, annular dilation, or the presence of fibrinoid deposits can hinder flow, leading to an increase in volume. Immediate and delayed responses to this volume overload can present as clinical signs and symptoms of pulmonary regurgitation.
Mild pulmonary regurgitation is frequently observed in adolescent children and is generally deemed non-threatening. The primary diagnostic tool for assessing the extent of pulmonary regurgitation and its implications is an echocardiogram.
Individuals undergoing follow-up evaluations post-tetralogy of Fallot repair have been observed to develop pulmonary regurgitation within a span of 1 to 21 years following the initial surgical intervention.
Pulmonary regurgitation occurs when the pulmonary valve, responsible for directing blood from the right ventricle to the pulmonary arteries, exhibits impaired function. This dysfunction can stem from various pathophysiological factors, including defective coaptation of the valve leaflets, annular dilation, or the deposition of fibrinoid material on the valve.
These structural abnormalities compromise the valve’s ability to prevent the backflow of blood into the right ventricle during diastole. As a consequence, this impedes the normal forward flow, leading to volume overload in the right ventricle. Over time, the regurgitation of blood into the right ventricle during diastole results in clinical manifestations of pulmonary regurgitation.
The pathophysiological consequences are further accentuated in cases where patients, particularly those who have undergone tetralogy of Fallot repair, experience this condition years after the initial intervention, underscoring the long-term implications of pulmonary regurgitation.
The etiology of pulmonary regurgitation can be multifaceted, arising from various factors that affect the structure and function of the pulmonary valve and its surrounding components. One common cause is congenital heart defects, such as tetralogy of Fallot, where abnormalities in the development of the heart can lead to malformations of the pulmonary valve, resulting in regurgitation.
Acquired causes of pulmonary regurgitation may include infectious endocarditis, which can damage the valve leaflets, as well as rheumatic heart disease. Trauma to the chest or the valve itself during surgical procedures can also contribute to the development of pulmonary regurgitation. Annular dilation, a widening of the ring-like structure supporting the valve, can be another etiological factor.
This dilation may occur due to conditions like pulmonary hypertension or chronic pulmonary artery dilation. In some cases, idiopathic or unknown factors may lead to pulmonary regurgitation. Additionally, certain connective tissue disorders or genetic conditions can predispose individuals to valve abnormalities and regurgitation.
The majority of individuals with pulmonary regurgitation are typically asymptomatic. However, symptomatic cases often manifest with initial symptoms of exertional dyspnea due to diminished cardiac output resulting from the right heart’s volume overload. A gradual decline in exercise tolerance may be observed in such cases.
In instances of severe pulmonary regurgitation, symptoms indicative of right heart failure may become apparent, including congestive hepatomegaly, pedal edema, and, infrequently, elevated jugular venous distension. Additionally, patients may present with complications arising from right ventricular dilation, notably symptomatic ventricular arrhythmias.
In clinical scenarios where an underlying pathology is identified as the primary cause of pulmonary regurgitation, symptoms related to the specific underlying disease may take precedence. For instance, pulmonary regurgitation secondary to pulmonary hypertension may exhibit symptoms characteristic of the underlying condition, such as those seen in left heart disease, chronic lung disorders like OSA or COPD, or primary pulmonary arterial hypertension.
Auscultation in individuals with pulmonary regurgitation typically reveals a diastolic decrescendo murmur audible in the second and third left intercostal spaces. Additionally, an S3 sound may be appreciated, signifying volume overload. This right-sided murmur tends to intensify during inspiration, attributed to heightened preload and diminishes during the Valsalva maneuver due to altered pressures.
It is noteworthy to highlight the variations in auscultatory findings based on the presence or absence of pulmonary arterial hypertension. In cases with elevated pulmonary artery pressures, creating a substantial gradient between the pulmonary artery and right ventricle, the pulmonary regurgitation murmur becomes diastolic, persisting throughout diastole (in contrast to its transient nature in cases without pulmonary hypertension).
The murmur retains its decrescendo quality, is associated with a pronounced P2, and is audible in the second and third left intercostal spaces, exhibiting an augmentation during inspiration.
Constrictive pericarditis
Infective endocarditis
Restrictive cardiomyopathy
Chronic pulmonary emboli
Surgical intervention is recommended for all symptomatic patients experiencing pulmonary regurgitation. The preferred treatment methods typically involve surgical pulmonary valve replacement, with options including a bioprosthesis or mechanical valve. Bioprosthesis valves are favored due to their durability, lower risk of valve failure, and relatively shorter period of required anticoagulation compared to mechanical valves.
Percutaneous pulmonary valve replacement is an advancing field in interventional cardiology. However, certain challenges need addressing, such as deviations in the anatomy of the right ventricular outflow tract that may limit its applicability. Tricuspid regurgitation often arises as a consequence of complications following pulmonary regurgitation and necessitates attention. In cases of tricuspid regurgitation, tricuspid annuloplasty may be performed.
Additionally, the presence of large akinetic right ventricular outflow tract segments may require resection to prevent further exacerbation of the prognosis. Medical intervention is solely advised when pulmonary regurgitation is a consequence of an underlying medical condition, such as pulmonary arterial hypertension or carcinoid disease. In cases where the cause is secondary to a primary medical condition, medical therapy becomes a consideration.
Specifically, medications aimed at managing heart failure, including diuretics, ACE inhibitors, and beta-blockers, are recommended exclusively for symptomatic individuals with severe pulmonary regurgitation. This approach is particularly relevant for patients deemed unsuitable candidates for surgery due to factors like advanced age or the presence of significant comorbidities.
Cardiology, General
Physical Medicine and Rehabilitation
Pulmonary Medicine
Lifestyle Modifications: Adopting a healthy lifestyle can help manage pulmonary regurgitation. This includes maintaining a balanced diet, regular exercise, avoiding smoking, and managing stress.
Monitoring and Follow-up: Regular monitoring by a cardiologist is essential for individuals with pulmonary regurgitation. This may involve echocardiograms, cardiac MRI, or other imaging tests to assess the function of the heart and the severity of the regurgitation.
Pregnancy Management: For women with pulmonary regurgitation, especially those with severe cases or additional cardiac complications, careful management during pregnancy is crucial.
Endocarditis Prevention: Individuals with certain types of heart defects, including those causing pulmonary regurgitation, are at increased risk of infective endocarditis.
Cardiology, General
Critical Care/Intensive Care
Metoprolol: It may be indicated to alleviate symptoms associated with PR, such as palpitations, chest discomfort, or shortness of breath.
By slowing the heart rate and reducing the force of contraction, metoprolol can help improve cardiac efficiency and reduce symptoms related to increased myocardial oxygen demand.
Cardiology, General
Critical Care/Intensive Care
Losartan: It is indicated for the management of systemic hypertension.
By lowering blood pressure, losartan can help reduce afterload on the heart, potentially mitigating the impact of hypertension on PR and overall cardiac function.
Cardiology, General
Pulmonary Valve Replacement: If the pulmonary valve is severely damaged or dysfunctional, pulmonary valve replacement may be necessary. This can involve either a surgical procedure where the damaged valve is removed and replaced with a mechanical or biological valve or a less invasive procedure called transcatheter pulmonary valve replacement (TPVR).
Balloon Valvuloplasty: For patients with pulmonary valve stenosis, balloon valvuloplasty may be performed. This procedure involves inserting a catheter with a balloon tip into the narrowed valve and inflating the balloon to widen the valve opening.
Pulmonary Valve Repair: In some cases, particularly in congenital heart conditions where the pulmonary valve is malformed but not severely damaged, surgical repair of the valve may be possible. This can involve techniques to reshape or reconstruct the valve to improve its function.
Cardiology, General
Physical Medicine and Rehabilitation
Diagnosis and Assessment: Symptoms of PR may include shortness of breath, fatigue, palpitations, and signs of right heart failure.
Diagnostic tests: Echocardiography is typically the primary diagnostic tool to assess. Additional tests such as cardiac MRI or cardiac catheterization may be used for further evaluation if needed.
Monitoring and Follow-up: Patients with PR require ongoing monitoring to assess disease progression and the development of symptoms or complications.
Imaging studies: Periodic echocardiograms or other imaging tests may be recommended to evaluate changes in pulmonary regurgitation severity and its effects on the heart.
Intervention: Intervention may be indicated in patients with severe PR, progressive right ventricular dysfunction, or symptoms refractory to medical therapy.
The pulmonary valve plays a crucial role in directing blood from the right ventricle to the pulmonary arteries during systole. Its closure during diastole is equally essential to prevent the backward flow into the right ventricle caused by the decrease in right ventricular pressure. Any abnormalities in the structure or function of this valve can obstruct the forward flow.
Issues such as defective valve coaptation, annular dilation, or the presence of fibrinoid deposits can hinder flow, leading to an increase in volume. Immediate and delayed responses to this volume overload can present as clinical signs and symptoms of pulmonary regurgitation.
Mild pulmonary regurgitation is frequently observed in adolescent children and is generally deemed non-threatening. The primary diagnostic tool for assessing the extent of pulmonary regurgitation and its implications is an echocardiogram.
Individuals undergoing follow-up evaluations post-tetralogy of Fallot repair have been observed to develop pulmonary regurgitation within a span of 1 to 21 years following the initial surgical intervention.
Pulmonary regurgitation occurs when the pulmonary valve, responsible for directing blood from the right ventricle to the pulmonary arteries, exhibits impaired function. This dysfunction can stem from various pathophysiological factors, including defective coaptation of the valve leaflets, annular dilation, or the deposition of fibrinoid material on the valve.
These structural abnormalities compromise the valve’s ability to prevent the backflow of blood into the right ventricle during diastole. As a consequence, this impedes the normal forward flow, leading to volume overload in the right ventricle. Over time, the regurgitation of blood into the right ventricle during diastole results in clinical manifestations of pulmonary regurgitation.
The pathophysiological consequences are further accentuated in cases where patients, particularly those who have undergone tetralogy of Fallot repair, experience this condition years after the initial intervention, underscoring the long-term implications of pulmonary regurgitation.
The etiology of pulmonary regurgitation can be multifaceted, arising from various factors that affect the structure and function of the pulmonary valve and its surrounding components. One common cause is congenital heart defects, such as tetralogy of Fallot, where abnormalities in the development of the heart can lead to malformations of the pulmonary valve, resulting in regurgitation.
Acquired causes of pulmonary regurgitation may include infectious endocarditis, which can damage the valve leaflets, as well as rheumatic heart disease. Trauma to the chest or the valve itself during surgical procedures can also contribute to the development of pulmonary regurgitation. Annular dilation, a widening of the ring-like structure supporting the valve, can be another etiological factor.
This dilation may occur due to conditions like pulmonary hypertension or chronic pulmonary artery dilation. In some cases, idiopathic or unknown factors may lead to pulmonary regurgitation. Additionally, certain connective tissue disorders or genetic conditions can predispose individuals to valve abnormalities and regurgitation.
The majority of individuals with pulmonary regurgitation are typically asymptomatic. However, symptomatic cases often manifest with initial symptoms of exertional dyspnea due to diminished cardiac output resulting from the right heart’s volume overload. A gradual decline in exercise tolerance may be observed in such cases.
In instances of severe pulmonary regurgitation, symptoms indicative of right heart failure may become apparent, including congestive hepatomegaly, pedal edema, and, infrequently, elevated jugular venous distension. Additionally, patients may present with complications arising from right ventricular dilation, notably symptomatic ventricular arrhythmias.
In clinical scenarios where an underlying pathology is identified as the primary cause of pulmonary regurgitation, symptoms related to the specific underlying disease may take precedence. For instance, pulmonary regurgitation secondary to pulmonary hypertension may exhibit symptoms characteristic of the underlying condition, such as those seen in left heart disease, chronic lung disorders like OSA or COPD, or primary pulmonary arterial hypertension.
Auscultation in individuals with pulmonary regurgitation typically reveals a diastolic decrescendo murmur audible in the second and third left intercostal spaces. Additionally, an S3 sound may be appreciated, signifying volume overload. This right-sided murmur tends to intensify during inspiration, attributed to heightened preload and diminishes during the Valsalva maneuver due to altered pressures.
It is noteworthy to highlight the variations in auscultatory findings based on the presence or absence of pulmonary arterial hypertension. In cases with elevated pulmonary artery pressures, creating a substantial gradient between the pulmonary artery and right ventricle, the pulmonary regurgitation murmur becomes diastolic, persisting throughout diastole (in contrast to its transient nature in cases without pulmonary hypertension).
The murmur retains its decrescendo quality, is associated with a pronounced P2, and is audible in the second and third left intercostal spaces, exhibiting an augmentation during inspiration.
Constrictive pericarditis
Infective endocarditis
Restrictive cardiomyopathy
Chronic pulmonary emboli
Surgical intervention is recommended for all symptomatic patients experiencing pulmonary regurgitation. The preferred treatment methods typically involve surgical pulmonary valve replacement, with options including a bioprosthesis or mechanical valve. Bioprosthesis valves are favored due to their durability, lower risk of valve failure, and relatively shorter period of required anticoagulation compared to mechanical valves.
Percutaneous pulmonary valve replacement is an advancing field in interventional cardiology. However, certain challenges need addressing, such as deviations in the anatomy of the right ventricular outflow tract that may limit its applicability. Tricuspid regurgitation often arises as a consequence of complications following pulmonary regurgitation and necessitates attention. In cases of tricuspid regurgitation, tricuspid annuloplasty may be performed.
Additionally, the presence of large akinetic right ventricular outflow tract segments may require resection to prevent further exacerbation of the prognosis. Medical intervention is solely advised when pulmonary regurgitation is a consequence of an underlying medical condition, such as pulmonary arterial hypertension or carcinoid disease. In cases where the cause is secondary to a primary medical condition, medical therapy becomes a consideration.
Specifically, medications aimed at managing heart failure, including diuretics, ACE inhibitors, and beta-blockers, are recommended exclusively for symptomatic individuals with severe pulmonary regurgitation. This approach is particularly relevant for patients deemed unsuitable candidates for surgery due to factors like advanced age or the presence of significant comorbidities.
Cardiology, General
Physical Medicine and Rehabilitation
Pulmonary Medicine
Lifestyle Modifications: Adopting a healthy lifestyle can help manage pulmonary regurgitation. This includes maintaining a balanced diet, regular exercise, avoiding smoking, and managing stress.
Monitoring and Follow-up: Regular monitoring by a cardiologist is essential for individuals with pulmonary regurgitation. This may involve echocardiograms, cardiac MRI, or other imaging tests to assess the function of the heart and the severity of the regurgitation.
Pregnancy Management: For women with pulmonary regurgitation, especially those with severe cases or additional cardiac complications, careful management during pregnancy is crucial.
Endocarditis Prevention: Individuals with certain types of heart defects, including those causing pulmonary regurgitation, are at increased risk of infective endocarditis.
Cardiology, General
Critical Care/Intensive Care
Metoprolol: It may be indicated to alleviate symptoms associated with PR, such as palpitations, chest discomfort, or shortness of breath.
By slowing the heart rate and reducing the force of contraction, metoprolol can help improve cardiac efficiency and reduce symptoms related to increased myocardial oxygen demand.
Cardiology, General
Critical Care/Intensive Care
Losartan: It is indicated for the management of systemic hypertension.
By lowering blood pressure, losartan can help reduce afterload on the heart, potentially mitigating the impact of hypertension on PR and overall cardiac function.
Cardiology, General
Pulmonary Valve Replacement: If the pulmonary valve is severely damaged or dysfunctional, pulmonary valve replacement may be necessary. This can involve either a surgical procedure where the damaged valve is removed and replaced with a mechanical or biological valve or a less invasive procedure called transcatheter pulmonary valve replacement (TPVR).
Balloon Valvuloplasty: For patients with pulmonary valve stenosis, balloon valvuloplasty may be performed. This procedure involves inserting a catheter with a balloon tip into the narrowed valve and inflating the balloon to widen the valve opening.
Pulmonary Valve Repair: In some cases, particularly in congenital heart conditions where the pulmonary valve is malformed but not severely damaged, surgical repair of the valve may be possible. This can involve techniques to reshape or reconstruct the valve to improve its function.
Cardiology, General
Physical Medicine and Rehabilitation
Diagnosis and Assessment: Symptoms of PR may include shortness of breath, fatigue, palpitations, and signs of right heart failure.
Diagnostic tests: Echocardiography is typically the primary diagnostic tool to assess. Additional tests such as cardiac MRI or cardiac catheterization may be used for further evaluation if needed.
Monitoring and Follow-up: Patients with PR require ongoing monitoring to assess disease progression and the development of symptoms or complications.
Imaging studies: Periodic echocardiograms or other imaging tests may be recommended to evaluate changes in pulmonary regurgitation severity and its effects on the heart.
Intervention: Intervention may be indicated in patients with severe PR, progressive right ventricular dysfunction, or symptoms refractory to medical therapy.
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