AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

The pulmonic valve is normally a thin tricuspid structure that prevents blood from regurgitating into the right ventricle once ejected into the low-pressure pulmonary circulation. Pulmonic regurgitation refers to retrograde flow from the pulmonary artery into the right ventricle during diastole. Physiologic (trace-to-mild) pulmonic regurgitation is present in nearly all individuals, particularly in those with advanced age. However, pathologic conditions that produce excessive and clinically significant regurgitation can result in impairment of right ventricular function and eventual clinical manifestations of right-sided volume overload and heart failure. Often, pulmonic regurgitation is not the primary process but a finding secondary to an underlying process such as pulmonary hypertension or dilated cardiomyopathy.

Pathophysiology

Incompetence of the pulmonic valve occurs by 1 of 3 basic pathologic processes: dilatation of the pulmonic valve ring, acquired alteration of pulmonic valve leaflet morphology, or congenital absence or malformation of the valve.

Frequency

United States

Physiologic pulmonic regurgitation is present in nearly all individuals and is a normal echocardiographic finding. Pulmonic regurgitation detected by physical examination is not a normal finding in healthy adults. Congenital pulmonic regurgitation and congenital absence of the pulmonic valve are rare conditions.

International

No difference in international incidence is known.

Mortality/Morbidity

The morbidity and mortality rates associated with pulmonic regurgitation vary considerably, depending on the underlying etiology.

Race

No racial or ethnic predilection exists.

Sex

Differing frequency of pulmonic regurgitation between men and women corresponds to the specific etiology resulting in pulmonic regurgitation.

Age

Except for congenital absence of the pulmonic valve, which is more likely to cause right-sided ventricular decompensation early in life, the age at which clinical symptoms of pulmonic regurgitation occur is variable and is primarily related to the underlying process causing the pulmonic regurgitation.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

Pulmonic regurgitation is seldom clinically significant. However, symptoms of right-sided heart failure can occur when the severity and duration of the regurgitation result in right ventricular enlargement and decompensation. Dyspnea on exertion is the most common complaint. Easy fatigability, light-headedness, peripheral edema, chest pain, palpitations, and frank syncope may occur in patients with any cause of right-sided heart failure and do little to elucidate the etiology of the right-sided failure. Patients who experience these symptoms may attribute them to poor physical fitness or anxiety, delaying evaluation until their condition worsens. In more advanced presentations of right-sided heart failure, abdominal distension secondary to ascites, right upper quadrant pain secondary to hepatic distension, and early satiety may occur.

Other symptoms specific to the underlying disease process causing pulmonic regurgitation may occur. Such disease processes include connective-tissue disease, infective endocarditis, carcinoid heart disease, rheumatic heart disease, and primary or secondary pulmonary hypertension. For example, hemoptysis is generally not associated with pulmonic regurgitation per se, but, in severe pulmonary hypertension causing pulmonic regurgitation, it may occur as a result of the associated pulmonary arteriole rupture and hemorrhage and/or parenchymal inflammation.

Physical

• Jugular venous pressure (JVP) is usually increased. Often, an increased A wave is present, but this may be less apparent when significant tricuspid regurgitation with a dominant V wave is also present. When right ventricular enlargement is present, a palpable impulse (lift or heave) is usually present at the left lower sternal border. Palpable pulmonary artery pulsation at the left upper sternal border may be present in the setting of significant pulmonary artery dilatation. With significant pulmonary hypertension, pulmonic valve closure can be palpated.
• The pulmonic component of the second heart sound (P₂) is inaudible in the absence of a pulmonic valve, whether congenital or secondary to surgical resection. In pulmonic regurgitation due to pulmonary hypertension, P₂ is accentuated; with increased right ventricular end-diastolic volume, the ejection time is increased, P₂ is delayed, and the S₂ split is widened. 
• A low-pressure regurgitant flow across the pulmonic valve, as occurs when the pulmonary arterial pressure is normal, is heard as a brief, decrescendo early diastolic murmur at the upper left sternal border. It is made louder by squatting or inspiration and softer by Valsalva maneuvers or expiration. An S₃ or S₄ may be noted at the left mid-to-lower sternal border because of the presence of right ventricular hypertrophy or failure and is augmented by inspiration.
• The Graham Steell murmur of pulmonary hypertension is a high-pitched, early diastolic decrescendo murmur noted over the left upper-to-left midsternal area and is a result of high-velocity regurgitant flow across an incompetent pulmonic valve. The regurgitant flow murmur may be present during the whole of diastole because there is a pulmonary-to-right ventricular pressure gradient throughout this time period. Typically, the murmur occurs in severe pulmonary hypertension when the pulmonary artery systolic pressure is more than 60 mm Hg. The quality of this high-pitched early decrescendo diastolic murmur is identical to that of aortic insufficiency. However, the peripheral manifestations of aortic insufficiency are absent. The associated findings of tricuspid regurgitation are frequently present, that is, prominent JVP with surging V waves, holosystolic murmur at the lower left sternal border (louder with inspiration), and enlarged, pulsatile liver.

Causes

Significant pulmonic regurgitation occurs variably as a complication of the following:

• Primary pulmonary hypertension (~1 instance per 500,000 cases): This diagnosis can be made only after all other causes have been excluded.
• Secondary pulmonary hypertension (multiple causes): This is the most common cause of pulmonic regurgitation in adults. 
• Tetralogy of Fallot: Especially with congenital absence of the pulmonary valve or postoperative following surgical repair of this condition (eg, pulmonary valvotomy). 
• Infective endocarditis: Rare, but may occur in an intravenous drug user or an individual with an atrial septal defect and a large left-to-right intracardiac shunt.
• Rheumatic heart disease: Pulmonary valve affected following mitral, aortic, and tricuspid valve involvement. 
• Carcinoid heart disease: See Carcinoid Lung Tumors and Carcinoid Tumor, Intestinal.
• Medications: Medications that act via serotoninergic pathways (eg, methysergide, pergolide, fenfluramine).
• Disorders that dilate the pulmonic valve ring to create valvular incompetence are the most common cause of pulmonic regurgitation.  
• • Primary or secondary pulmonary hypertension 
  • Dilatation of the pulmonary trunk in Marfan syndrome or Takayasu arteritis
  • Idiopathic 

• Acquired disorders that alter pulmonic valve morphology  
• • Rheumatic heart disease: In most cases, the other valves (ie, mitral, aortic, tricuspid) are also substantially affected. 
  • Trauma from a Swan-Ganz catheter: This cause is unusual, but it can result if the catheter tip is withdrawn across the pulmonic valve with the balloon inflated. 
  • Complications related to therapeutic balloon catheter dilatation of a stenotic pulmonic valve (eg, pulmonary balloon valvuloplasty). Such complications are not uncommon; however, in most cases, the degree of regurgitation is clinically insignificant, rendering pulmonic valve balloon catheter dilation a safe and effective treatment for moderate-to-severe pulmonic stenosis in adult and pediatric patients.
  • Complications of surgical repair of pulmonic stenosis or congenital heart disease, such as tetralogy of Fallot 
  • Syphilis infection 
  • Carcinoid heart disease: The heart is affected in up to 60% of patients in whom carcinoid has metastasized to the liver, most commonly manifesting as valvular disease. In Pellikka and colleagues' 1993 series of 74 patients, the pulmonic valve was involved in 88%. Of those, 49% exhibited significant pulmonic stenosis, and 81% had significant pulmonic regurgitation.¹

• Congenital disorders that produce an incompetent pulmonic valve
• • Complete absence of the pulmonic valve 
  • Valvular abnormalities such as fenestrations or redundant leaflets

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Other Problems to be Considered

Marfan syndrome
Rheumatic heart disease
Carcinoid heart disease
Aortic insufficiency: The Graham Steell murmur of pulmonary hypertension is identical in quality to that of the early diastolic murmur in aortic insufficiency. They must be differentiated.

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Imaging Studies

• Plain radiographs
• • Plain radiographs change little with pulmonic regurgitation unless tricuspid regurgitation also occurs, in which case cardiomegaly and enlargement of the right-sided heart contour are observed.
  • Prominent central pulmonary arteries with enlarged hilar vessels and loss of vascularity in the peripheral lung fields ("pruning") suggests severe pulmonary hypertension.
• Fluoroscopy and catheterization
• • Cardiac catheterization is usually not necessary for diagnosis but may be helpful in determining the underlying etiology and for determining coexisting conditions that may influence treatment and/or repair decisions.
  • Pulmonary artery angiography may reveal evidence of multiple pulmonary emboli as a cause of pulmonary hypertension when the degree of clinical suspicion is high. Ventilation/perfusion scanning or CT angiography is now more commonly performed in most hospitals. Pulmonary emboli must be excluded before the diagnosis of primary pulmonary hypertension is possible.
  • If pressure measurements are performed, the pulmonary artery and right ventricular pressure curves equalize in late diastole in individuals with severe pulmonary regurgitation.
• Echocardiography
• • Two-dimensional echocardiography (2DE) and M-mode echocardiography can reveal right ventricular hypertrophy and dilatation. Right ventricular volume overload may induce a characteristic abnormal septal wall motion, which appears as flattening of the septum during diastole. Conversely, right ventricular pressure overload usually appears as flattening of the septum during systole. The lack of a pulmonic valve or valve deformities can be noted with 2DE, but the pulmonic valve apparatus typically appears unremarkable. In some cases, pulmonic ring dilatation with poor valve leaflet coaptation may be observed.
  • Doppler techniques are used to visualize the regurgitant flow. These techniques are useful to directly visualize regurgitant jets, measure the flow velocities of the regurgitant jets, and accurately estimate pulmonary pressures. Regurgitation that persists throughout diastole suggests the presence of pulmonary hypertension, whereas regurgitation that diminishes earlier in diastole suggests more normal pulmonary arterial pressures. Normally, peak flow velocity across the pulmonic valve is achieved within 140 milliseconds of systole. With pulmonary hypertension, the peak flow velocity is reached faster. The shortening of the interval within which the peak velocity is reached (acceleration time) is linearly inversely proportional to the severity of the pulmonary hypertension.
  • Color flow Doppler echocardiography is the mainstay for recognizing pulmonic regurgitation. In trivial-to-mild pulmonic regurgitation, the jet is central and narrow. In moderate-to-severe pulmonic regurgitation, the width of the jet increases, as does the penetration of the jet into the right ventricular outflow tract. In free or open pulmonic regurgitation (usually due to congenitally absent pulmonic valve), color Doppler can miss the jet altogether due to the brisk and laminar regurgitant flow.
  • Using pulsed wave and continuous wave Doppler, pulmonary artery systolic and diastolic pressures can be calculated. Pulmonary artery systolic pressure can be estimated (using continuous wave Doppler) in the presence of tricuspid regurgitation by measuring the peak regurgitant flow velocity across the tricuspid valve, converting it to a pressure gradient (by use of the modified Bernoulli equation), and then adding the gradient to an estimate of the right atrial pressure.
  • Pulmonary artery diastolic pressure can be estimated by measuring the end-diastolic regurgitant flow velocity across the pulmonic valve (at the QRS complex on the ECG), converting it to a pressure gradient, and then adding the gradient to the estimated right atrial pressure. Both pulmonary artery systolic pressure and diastolic pressure are predictors of cardiac status and outcome.
  • Pulmonary arterial mean pressure can also be estimated by converting the early diastolic regurgitation velocity to a pressure gradient, and then adding it to the estimated right atrial pressure. 
• Cardiac magnetic resonance (CMR)
• • CMR has shown promise based on recent studies of pulmonary regurgitation. CMR has excellent temporal and spacial resolution and can provide accurate estimation of the severity of regurgitation, mechanism of regurgitation, and right ventricular size and function. However, size and time constraints limit the use of CMR in clinical practice.

Other Tests

• Electrocardiography
• • ECG may demonstrate findings of right ventricular dilatation (occurs either while in a compensated volume overload state or in a decompensated pressure overload state), including incomplete right bundle branch block and right axis deviation. Right ventricular hypertrophy may be present by ECG criteria.
  • In the presence of right ventricular hypertrophy (representing a compensated state of pressure overload), the following may be present:
    
    
    • Tall R wave in V₁ or qR in V₁
    • R wave greater than S wave in V₁
    • R wave progression reversal in the precordial leads
    • Inverted T wave in the anterior precordial leads
    • Right axis deviation
    • Right atrial enlargement

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical Care

Pulmonic regurgitation is seldom severe enough to warrant special treatment because the right ventricle normally adapts to low-pressure volume overload without difficulty. High-pressure volume overload leads to right-sided heart strain and, ultimately, heart failure.

Underlying etiologies causing severe pulmonic regurgitation, whether congenital or acquired, must be treated to prevent or reverse right-sided heart strain and failure that may further complicate the clinical picture. A discussion of therapeutic interventions in pulmonary hypertension by etiology is beyond the scope of this article. Refer to the articles for each entity under Differentials for a detailed discussion of treatment options.

• If pulmonary hypertension is identified with pulmonic regurgitation, determining the etiology is essential to institute appropriate therapy as expeditiously as possible. For instance, primary pulmonary hypertension, secondary pulmonary hypertension due to thromboembolism, severe mitral stenosis, and pulmonary carcinomatosis can all manifest as severe pulmonary hypertension with pulmonic regurgitation.
• No aspect of medical management of heart failure is uniquely applicable to pulmonic regurgitation, and the discussion of management of right-sided heart failure is beyond the scope of this article. In general, similar approaches to those used in the treatment of patients with left-sided congestive heart failure can be useful. In some circumstances, such as in patients with pulmonary hypertension, vasodilator therapies must be very carefully considered and monitored. In addition, therapies aimed toward the underlying etiology may also reduce pulmonic regurgitation (see Heart Failure).

Surgical Care

• When right-sided heart failure due to pulmonic regurgitation from an abnormal pulmonic valve cannot be ameliorated by medical management, appropriate options include surgical reconstruction or replacement of the pulmonic valve, preferably with a bioprosthetic valve.
• Although congenital pulmonic regurgitation is usually well tolerated, the much more rare congenital absence of the pulmonic valve usually requires valve replacement.

Consultations

Consider consultation with cardiologists for patients with right-sided heart failure in the presence of severe pulmonic regurgitation.

Activity

Since pulmonic regurgitation is usually of a mild-to-moderate degree, restriction of athletic activities is unnecessary. Follow-up echocardiographic studies can provide data to assess for changes in pulmonic regurgitation and right ventricular functional status in order to more objectively base activity limitation recommendations.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medications are directed according to the specific etiology resulting in pulmonic regurgitation in addition to the treatment of heart failure (if present). Complete discussions regarding medication use in the specific etiologies noted above may be found in the respective eMedicine articles (see Heart Failure). Infective endocarditis antibiotic prophylaxis should be considered for patients whose pulmonic regurgitation is due to valve leaflet abnormalities.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• Aspects of inpatient care are primarily governed by the treatment indicated for the particular disorder that causes pulmonic regurgitation. As previously mentioned, if heart failure is present that is due to or exacerbated by pulmonic regurgitation, usual heart failure management applies.

Further Outpatient Care

• Regurgitation may worsen with time. Therefore, periodic echocardiographic reassessment with Doppler color flow studies provides a longitudinal comparison of the progression of both the regurgitation and right ventricular size and function. In cases of significant pulmonic regurgitation, exercise capacity should be assessed and quantitated serially, observing for a change or decrease in function, the goal being to accurately assess the need and potential timing for surgical repair.

Transfer

• Transfer requirements are the same as in heart failure.

Deterrence/Prevention

• Specific comments on deterrence and prevention of pulmonic regurgitation in general are not found in the literature, except in the context of the specific entities, such as those listed in Causes, that can cause pulmonic regurgitation.
• Periodic echocardiographic follow-up is appropriate when significant pulmonic regurgitation is present in order to better manage the condition over the long term and to help decide when interventions may be warranted.

Complications

• Right-sided heart failure is a complication of volume overload of the right ventricle due to severe pulmonic regurgitation.
• Other complications are related to the underlying disease processes resulting in pulmonic regurgitation.

Prognosis

• In general, survival is not significantly affected by mild-to-moderate pulmonic regurgitation. If pulmonic regurgitation is severe, the right ventricle is initially able to compensate for the volume overload state, and the state may remain well compensated for years. Persistently elevated right ventricular volumes may eventually cause right ventricular dilatation, and, finally, failure.
• As previously stated, the various disorders causing pulmonary hypertension are the most common causes of clinically significant pulmonic regurgitation. The principal prognostic indicators of mortality in pulmonic regurgitation associated with pulmonary hypertension are (1) the severity and duration of the pulmonary hypertension at the time of diagnosis and (2) the right ventricular response to the state of volume overload.
• • In all etiologies of pulmonary hypertension, early diagnosis that allows for intervention to slow or reverse the cause of pulmonary hypertension is essential, although, in many cases, diagnosis is difficult and requires a high degree of clinical suspicion.
  • In primary pulmonary hypertension, the pathologic process is often insidious, and symptoms manifest at an advanced disease state, resulting in an average survival period of 2.5 years from the time of diagnosis.
• In congenital regurgitation of the pulmonic valve, the prognosis depends upon the initial severity, progression of the regurgitation, and the ability of the right ventricle to adapt to volume overload. Usually, the degree of regurgitation in this condition is no more than moderate, so no clinical sequelae occur. Congenital absence of the pulmonic valve, a much rarer condition, confers an increased risk of morbidity and mortality because of more severe regurgitation and usually warrants pulmonic valve replacement for improved prognosis.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• As with any cardiovascular diagnosis, it is important to document the presence and extent of pulmonic regurgitation, the treatment options considered and undertaken (including antibiotic prophylaxis for dental and other procedures), and the plans for follow-up care.

Special Concerns

• Pregnancy: Pregnancy is usually well tolerated in patients with pulmonic regurgitation, including those who have had surgical repairs for tetralogy of Fallot, except when right-sided heart failure is present that cannot be medically controlled.
• Infective endocarditis
• • Pulmonic valve endocarditis is almost always associated with immunosuppressed states, intravenous drug abuse, and/or congenital heart disease. The risk of endocarditis is thought to chiefly depend upon 2 factors: the presence of high-velocity flow that injures endothelium by shear forces or jet impact and exposure to infective organisms. In a series of 186 patients from a congenital heart disease registry with varying degrees of pulmonary and/or tricuspid regurgitation and normal pulmonic and tricuspid valves, the investigators observed that the occurrence of pulmonic and tricuspid valve endocarditis was extremely low. The study, however, was not large enough to resolve the question of endocarditis risk in this group, and the authors still advised antibiotic prophylaxis against endocarditis.²
  • The current American Heart Association recommendations on prevention of invective endocarditis do not support the necessity for antibiotic prophylaxis in pulmonic regurgitation for otherwise structurally normal pulmonic valves, especially if no diastolic murmur is audible (see Infective Endocarditis). However, pulmonic regurgitation in congenital heart malformations, acquired valvular dysfunction as in rheumatic heart disease, complex cyanotic heart disease, prosthetic valves, and prior bacterial endocarditis comprise moderate-to-high–risk conditions that warrant antibiotic prophylaxis.

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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16. Miller-Hance WC, Silverman NH. Transesophageal echocardiography (TEE) in congenital heart disease with focus on the adult. Cardiol Clin. Nov 2000;18(4):861-92. [Medline].
17. Nagueh SF. Assessment of valvular regurgitation with Doppler echocardiography. Cardiol Clin. Aug 1998;16(3):405-19, vii. [Medline].
18. Perloff Joseph K, Child JS. Congenital Heart Disease in Adults. 2^nd ed. W B Saunders Co; 1998.
19. Ristow B, Ahmed S, Wang L, Liu H, Angeja BG, Whooley MA. Pulmonary regurgitation end-diastolic gradient is a Doppler marker of cardiac status: data from the Heart and Soul Study. J Am Soc Echocardiogr. Sep 2005;18(9):885-91. [Medline].
20. Ristow B, Ali S, Ren X, Whooley MA, Schiller NB. Elevated pulmonary artery pressure by Doppler echocardiography predicts hospitalization for heart failure and mortality in ambulatory stable coronary artery disease: the Heart and Soul Study. J Am Coll Cardiol. Jan 2 2007;49(1):43-9. [Medline].
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Article Last Updated: Apr 15, 2008