Version May 2024
INTRODUCTION — Prosthetic valve dysfunction encompasses prosthetic valve obstruction (stenosis) and prosthetic valve regurgitation. Regurgitation associated with prosthetic heart valves includes regurgitation through the valve (transvalvular) as well as paravalvular regurgitation (also known as paravalvular leak). Symptomatic severe prosthetic valve regurgitation is an uncommon complication of surgical valve replacement. However, it is associated with poor outcomes with both conservative management and surgical treatment.
This topic will discuss clinical manifestations and diagnosis of surgical prosthetic aortic and mitral valve regurgitation. Transcatheter heart valve regurgitation and prognosis and management of surgical prosthetic valve regurgitation are discussed separately. (See "Transcatheter aortic valve implantation: Complications" and "Management and prognosis of surgical aortic and mitral prosthetic valve regurgitation".)
DEFINITIONS AND PREVALENCE — Normally functioning mechanical valves and some normally functioning bioprosthetic valves have trivial to mild transvalvular regurgitation, which should be distinguished from pathological regurgitation. On color Doppler echocardiographic imaging of normally functioning mechanical prosthetic valves, two types of retrograde jets are seen: a closing volume caused by motion of the occluder and true trivial or mild regurgitation at the edges of the occluder. Mechanical prosthetic valves are designed to cause trivial to mild transvalvular regurgitation when functioning normally as a safety mechanism known as leakage backflow or washing jets; this mechanism is thought to reduce the risk of valve thrombosis. Trivial regurgitation is also normal for some types of bioprosthetic valves (particularly stentless valves), due to minimal leaflet retraction once placed.
The principal types of pathologic prosthetic valve regurgitation are transvalvular regurgitation (due to structural valve deterioration [SVD] or non-structural valve dysfunction) and paravalvular leakage:
●Transvalvular regurgitation − Pathologic transvalvular regurgitation is much more common with bioprosthetic valves compared with mechanical valves. With conventional stented bioprostheses, 10 to 30 percent had significant SVD at 10 years, and 20 to 50 percent at 15 years [1]. However, SVD includes both regurgitation and stenosis, and the prevalence of patients with regurgitation is unknown. The rate of structural failure decreases with age, probably in part due to less activity in older patients.
As an additional example, 2659 patients receiving 2758 Carpentier-Edwards aortic valve bioprosthesis (98 required a second bioprosthesis and one required a third) were prospectively followed using clinical and echocardiographic criteria [2].
•SVD was defined as development of severe aortic stenosis or severe aortic regurgitation (AR). The number of patients with severe AR was not reported. SVD was reported in 157 patients (123 of whom required reintervention) over a cumulative follow-up of 18,404 valve-years. All cases of SVD were late events, and actuarial freedom from SVD at 15 and 20 years was 78.6 and 48.5 percent, respectively.
•Freedom from reoperation for SVD at 15 years was 70.8 percent for patients aged 60 years or less, 82.7 percent for those 60 to 70 years, and 98.1 percent for those over 70 years old.
●Paravalvular leak − The incidence of prosthetic paravalvular leak varies widely among registries. However, they are more commonly detected in mechanic valves and in the mitral position. Mitral paravalvular leak can be seen in 7 to 17 percent of implanted valves, while aortic paravalvular leaks occur in 2 to 10 percent of implanted valves [1,3].
CLINICAL MANIFESTATIONS
Symptoms and signs — The clinical presentation of prosthetic valve regurgitation varies depending upon its severity, its hemodynamic effects, and its cause (eg, valve thrombus or vegetations). In asymptomatic patients, prosthetic valve regurgitation may be detected as an incidental finding obtained on routine follow-up, while symptomatic patients frequently present with marked symptoms of overt heart failure (HF). (See 'Identifying the cause of prosthetic valve regurgitation' below.)
Many cases of prosthetic valve regurgitation present as an incidental finding in an asymptomatic patient, as most patients with prosthetic valve regurgitation have a normally functioning valve with trivial to mild regurgitation and a benign course without symptoms. However, significant regurgitation can lead to serious clinical consequences and adverse outcomes.
Among patients with paravalvular leak, the rate of symptomatic regurgitation varies among series between 1 to 5 percent [4,5]. The rate of symptomatic transvalvular regurgitation is difficult to estimate, as reported structural valve deterioration (SVD) includes both stenotic and regurgitant deterioration, as has been previously discussed. When symptomatic, patients present with HF in more than 90 percent of cases, with an average New York Heart Association (NYHA) functional class >III [4,6].
A change in auscultatory findings, such as a change in prosthetic valve sounds or the appearance of a new murmur, should prompt suspicion of prosthetic valve dysfunction, although such findings have low specificity [7].
Some cases of prosthetic regurgitation caused by valve thrombosis or vegetations are associated with embolic events. Other clinical manifestations of infection, such as fever, are commonly present in patients with endocarditis. (See "Mechanical prosthetic valve thrombosis or obstruction: Clinical manifestations and diagnosis" and "Prosthetic valve endocarditis: Epidemiology, clinical manifestations, and diagnosis".)
Blood tests — Blood tests are not indicated to diagnose prosthetic valve regurgitation. However, abnormal test results (eg, signs of hemolysis) may trigger evaluation of a prosthetic valve.
●Detection of hemolysis − Patients with prosthetic valves who develop significant hemolysis should undergo prosthetic valve evaluation to assess for paravalvular leak (PVL) or transvalvular regurgitation. On the other hand, hemolysis screening should be performed whenever significant (more than mild) regurgitation is detected. Patients with prosthetic valves commonly have hemolysis caused by shear stress across the prosthesis, more commonly with mechanical valves than with bioprosthetic valves [8]. However, rarely is hemolysis severe enough to cause anemia with new generation normal functioning prosthetic valves (<1 percent) [9]. Since significant hemolytic anemia is strongly associated with SVD or the appearance of PVL, pathological regurgitation should be suspected if significant hemolysis occurs. (See "Overview of the management of patients with prosthetic heart valves", section on 'Hemolytic anemia' and "Non-immune (Coombs-negative) hemolytic anemias in adults", section on 'Intravascular devices'.)
Typical findings of hemolysis include elevated lactate dehydrogenase level, anemia (reduced hemoglobin level), depressed serum haptoglobin level (eg, ≤25 mg/dL), and an elevated reticulocyte count (>2 percent). Although there are no standard criteria for quantifying prosthetic-related hemolytic anemia, it is considered severe when it results in symptomatic hemolysis, refractory anemia, high levels of urinary iron, or need for frequent red blood cell transfusions [9].
●Natriuretic peptide levels − In patients presenting with HF, natriuretic levels are expected to be elevated (eg, N-terminal pro-brain natriuretic peptide >400 pg/mL; brain natriuretic peptide >100 pg/mL). Natriuretic levels are not required to diagnose HF, but may be helpful if the diagnosis of HF is uncertain, as discussed separately. (See "Natriuretic peptide measurement in heart failure" and "Heart failure: Clinical manifestations and diagnosis in adults", section on 'Natriuretic peptide'.)
Chest radiograph — Chest radiograph is not indicated to diagnose prosthetic valve regurgitation but may be obtained as part of the evaluation of HF or dyspnea of unknown cause. There are no specific radiologic signs of prosthetic regurgitation, but signs of HF may be present. (See "Heart failure: Clinical manifestations and diagnosis in adults", section on 'Chest radiograph'.)
Electrocardiogram — An electrocardiogram (ECG) is not indicated to diagnose prosthetic regurgitation. However, an ECG is generally obtained during the diagnostic evaluation, as it can help detect other conditions that may explain the patient’s symptoms, such as ischemia or an arrhythmia.
Echocardiogram — The role of echocardiography in the diagnosis and evaluation of prosthetic valve regurgitation is discussed below. (See 'Approach to diagnosis and evaluation' below and 'Echocardiography' below.)
APPROACH TO DIAGNOSIS AND EVALUATION
When to suspect prosthetic valve regurgitation — Significant prosthetic valve regurgitation is a clinical challenge, as its diagnosis is often complicated. Patients with prosthetic heart valves should undergo routine follow-up, which is discussed separately, for early detection of any complication. Many prosthetic valve regurgitations are detected during routine follow-up visits in asymptomatic patients, as mentioned above. (See "Overview of the management of patients with prosthetic heart valves", section on 'Schedule of follow-up'.)
On the other hand, prosthetic regurgitation diagnostic work-up should be undertaken in patients with:
●Unexplained, refractory, or new onset HF
●Significant hemolysis (with or without anemia)
●Auscultatory changes
Overview of diagnosis and evaluation — The goals of the diagnostic evaluation of patients with suspected significant prosthetic valve regurgitation are as follows:
●Identify (or exclude) prosthetic regurgitation, its type (transvalvular or paravalvular), and severity.
●Assess its hemodynamic effects (eg, symptoms and signs of HF such as dyspnea and elevated jugular venous pressure and increased ventricular size and filling pressures on echocardiography). (See "Echocardiographic evaluation of left ventricular diastolic function in adults", section on 'Estimation of left atrial pressure' and "Echocardiographic assessment of the right heart".)
●Determine the cause of prosthetic regurgitation. (See 'Identifying the cause of prosthetic valve regurgitation' below.)
To achieve these goals, we recommend the following approach to diagnosis and evaluation of prosthetic regurgitation [10]:
●Assess for symptoms or signs of prosthetic valve regurgitation (eg, symptoms and signs of HF) or associated conditions (eg, embolism as a sequelae of endocarditis or valve thromboembolism).
●Transthoracic echocardiography (TTE) is the key initial test to accomplish the above goals of diagnosis and evaluation.
●Transesophageal echocardiography (TEE) is recommended next in the following clinical settings since it generally provides superior imaging for transvalvular and paravalvular prosthetic regurgitation:
•For patients with suspected significant transvalvular prosthetic regurgitation, if the severity or cause has not been established by TTE. (See 'Aortic transvalvular regurgitation' below and 'Mitral transvalvular regurgitation' below.)
•For patients with a suspected significant paravalvular leak [4,11], to determine the severity and cause. (See 'Paravalvular AR' below and 'Paravalvular MR' below.)
Approach according to prosthetic regurgitation type — The approach to diagnostic evaluation varies according to prosthetic regurgitation valve site (eg, aortic or mitral) and type (transvalvular or paravalvular) [10]. The 2020 American College of Cardiology/American Heart Association (ACC/AHA) valve guidelines note that often both TTE and TEE are required to determine the cause and severity of prosthetic valve regurgitation [12].
Aortic transvalvular regurgitation — Prosthetic transvalvular aortic regurgitation (AR) is generally well visualized from multiple views by TTE since the effects of prosthetic acoustic shadowing are usually limited. TTE is often adequate to identify and quantify AR severity. The severity of prosthetic transvalvular AR is graded using the same principles used for quantitation of native AR [13,14], although limited data are available on the validation of the established parameters in the context of prosthetic regurgitation [10].
The following parameters are used to semiquantitatively assess prosthetic AR:
●Valve structure and motion
●Left ventricular (LV) size
●Jet width (vena contracta), particularly for central jets
●Jet density
●Jet deceleration rate
●Diastolic flow reversal in the descending aorta
As an example, the jet width is compared to the LV outflow tract diameter: ≤25 percent suggests mild AR, and ≥65 percent suggests severe. However, the jet width method has a lower accuracy for eccentric jets. The accuracy of 3D vena contracta and estimated regurgitant orifice area are limited in the setting of multiple jets and those with great radial extension [15]. (See "Echocardiographic evaluation of the aortic valve", section on 'Aortic regurgitation' and "Echocardiographic evaluation of prosthetic heart valves", section on 'Prosthetic aortic regurgitation'.)
In the evaluation of prosthetic aortic transvalvular regurgitation, TEE is recommended when TTE results are suboptimal or inconclusive and is particularly helpful for assessing causes of regurgitation such as endocarditis (with vegetations and/or abscess formation), thrombus, other masses, and dehiscence (a cause of paravalvular leak) [10].
Paravalvular AR — Paravalvular AR is often well visualized from multiple views by TTE since the effects of prosthetic acoustic shadowing are limited [10]. Thus, TTE may be adequate to identify and quantify paravalvular AR severity. The severity of paravalvular AR is defined using the parameters and methods described above for transvalvular AR [10]. However, paravalvular AR jets are frequently eccentric, and jet width is less accurate for eccentric jets. In 2018, a five-class grading scheme was proposed by the Valve Academic Research Consortium, which was later adapted by the PVL Research Consortium [16]. (See "Echocardiographic evaluation of the aortic valve", section on 'Aortic regurgitation' and "Echocardiographic evaluation of prosthetic heart valves", section on 'Prosthetic aortic regurgitation'.)
For patients with suspected significant paravalvular AR, TEE is recommended to further assess the severity of AR and to aid in identifying the cause. The recommended TEE views for the aortic paravalvular leak analysis are [17]:
●Midesophageal long and short axis views
●Transgastric view with 100 to 120° and leftward flexion
●0° deep transgastric view
In order to describe the jet position, it is recommended to use a clockwise orientation: 5 o'clock correlates to the commissure between the right and left coronary sinuses, 8 o'clock to the commissure between the right and non-coronary sinuses, and 11 o'clock to the commissure between the non-coronary and left coronary sinuses. The most frequent location for aortic paravalvular leaks are the right and noncoronary cusps [18].
During the TEE examination, it is essential to report the coronary arteries' position and their relationship with the paravalvular leak, as it can be limiting for an eventual intervention.
Mitral transvalvular regurgitation — On TTE, mitral prosthetic transvalvular regurgitation is generally not well visualized, as the left atrium is generally shadowed by the prosthesis, especially with mechanical mitral prosthetic valves. Thus, color Doppler imaging of a mitral prosthetic regurgitant jet is generally suboptimal. Similarly, paravalvular mitral regurgitation (MR) is generally not well visualized by TTE, as the jets are usually eccentric, thin, and adjacent to the ring. (See "Echocardiographic evaluation of prosthetic heart valves", section on 'Prosthetic mitral regurgitation'.)
However, TTE is helpful in assessing the characteristics of the flow across the mitral prosthetic valve, which can provide indirect evidence of significant MR. The presence of "occult" significant mitral prosthetic regurgitation should be suspected when one or more of the following signs are present [13,19]:
●Abnormalities of valve structure and motion.
●Dilated and hyperkinetic LV.
●Systolic flow convergence seen in the LV toward the prosthesis.
●Peak mitral E-wave velocity ≥1.9 m/s.
●Mean mitral gradient ≥5 mmHg.
●Doppler velocity index = VTIPMV/VTILVOT >2.2 (where VTI is the velocity time integral, PMV is the prosthetic mitral valve, and LVOT is the LV outflow tract).
●Unexplained or new worsening of pulmonary arterial hypertension.
In addition, TTE sometimes provides additional indicators of significant prosthesis regurgitation (eg, systolic pulmonary flow reversal in the case of severe MR). (See "Echocardiographic evaluation of the mitral valve", section on 'Abnormalities associated with mitral regurgitation'.)
Given the limitations of TTE in visualizing the regurgitant jet, TEE is generally recommended to evaluate patients with suspected prosthetic transvalvular MR.
The severity of prosthetic transvalvular MR is generally assessed using a composite of TTE and TEE findings including the following parameters [10,14]:
●Valve structure and motion.
●Color flow jet area.
●Flow convergence or proximal isovelocity surface area (PISA).
●Jet density.
●Jet contour.
●Pulmonary venous flow.
●Quantitative parameters (not as well validated with prosthetic MR as for native MR): vena contracta width, regurgitant volume, regurgitant fraction, and effective regurgitant orifice area.
Paravalvular MR — Paravalvular MR is generally not well visualized on TTE. The left atrium is generally obscured by acoustic shadowing, particularly with a mechanical mitral prosthetic valve, and paravalvular MR jets are usually eccentric, thin, and adjacent to the ring. Thus, for patients with suspected paravalvular MR, TEE is generally recommended.
The severity of paravalvular MR is assessed as described above for transvalvular MR. The maximal width of the vena contracta is a particularly helpful parameter in assessment of paravalvular MR [10]. The PISA has not been validated as a quantitative tool to estimate the severity of paravalvular MR, although a large PISA shell is consistently related with more severe regurgitation [20]. The use of quantitative Doppler methods to measure regurgitant volume and regurgitant fraction is not generally recommended, since this method has not been validated for paravalvular regurgitation [21]. Systolic flow reversal in the pulmonary veins can be useful, as it is a specific (but not sensitive) sign of severe MR [10]. As for aortic paravalvular leak, the PVL Research Consortium has proposed a five-class grading scheme for paravalvular MR [16].
To specify the location of paravalvular leak, a clock face system is recommended, assigning the 12 o'clock position to the anterior mitral ring at the level of the aortic valve and 9 o'clock at the level of the left atrial appendage. The most common location of mitral prosthetic valve leaks are between 10 and 11 o'clock (aortic-mitral curtain), and 5 and 6 o'clock (posterior wall) [6,22].
Multiple leak approach — Analysis of severity of regurgitation in the presence of multiple aortic or mitral paravalvular leaks is challenging. Color Doppler can be useful in the initial analysis, but is clearly limited in the presence of eccentric jets, and the simple addition of all the venae contractae or PISAs has not been validated.
Guidelines suggest using the proportion of regurgitant areas to the circumference of the prosthesis, indicating severe regurgitation when >20 percent [10,15].
Another possibility is the use of volumetric methods, calculating the regurgitant volume from the subtraction of the volumes across the regurgitant and the non-regurgitant valves for semiquantitative assessment. However, this method is prone to errors and is of limited usefulness.
Identifying the cause of prosthetic valve regurgitation
Transvalvular regurgitation — Causes of significant mechanical prosthetic transvalvular regurgitation include non-structural causes such as pannus or thrombus and, rarely, structural causes (mechanical failure/deterioration). Causes of significant bioprosthetic transvalvular regurgitation include leaflet deterioration and calcification, endocarditis, thrombus, and pannus formation.
●Structural failure – Valve deterioration should be suspected as a significant cause of regurgitation in patients with a bioprosthesis older than 10 years. It is extremely rare with a bioprosthesis during the first five years after the implantation or with a mechanical prosthesis.
●Nonstructural causes
•Infectious endocarditis – This entity is usually easily recognizable, as patients present with febrile syndrome and elevated acute phase reactants, usually followed by HF symptoms, as acute severe regurgitation is poorly tolerated. As discussed separately, confirmation is based upon a combination of clinical, microbiological, and imaging criteria. TTE imaging of prosthetic valves is frequently suboptimal; TEE is generally indicated to identify prosthetic valve vegetations and identify complications such as paravalvular abscess or fistula. (See "Prosthetic valve endocarditis: Epidemiology, clinical manifestations, and diagnosis".)
•Thrombus – Prosthetic valve thrombosis can cause valve obstruction or regurgitation. The risk of mechanical valve thrombosis is particularly high in patients who have not been therapeutically anticoagulated. A growing body of evidence has shown that patients with bioprosthetic valve (surgical or transcatheter implants) are also at risk for valve thrombosis, but this appears to be a rare cause of bioprosthetic valve regurgitation [23]. (See "Mechanical prosthetic valve thrombosis or obstruction: Clinical manifestations and diagnosis".)
•Pannus – Pannus (fibrous or granulation tissue) can interpose within the prosthetic valve and interfere with prosthetic valve function, causing regurgitation or obstruction. Differentiating between pannus and thrombus is often difficult based on the echocardiographic imaging, as they both present as new onset prosthesis related masses. However, pannus growth differs from thrombus in being unrelated to the intensity of anticoagulation. (See "Bioprosthetic valve thrombosis, thromboembolism, and obstruction: Management".)
Paravalvular regurgitation — Paravalvular regurgitation occurs with both mechanical and bioprosthetic valves. Paravalvular leaks early after surgery, as detected with intraoperative TEE or postoperative TTE, are common; the majority of leaks are trivial or mild and do not progress over a two- to five-year follow-up [4,11]. In contrast, the later development of new paravalvular regurgitation may result from valve dehiscence, most commonly caused by infective endocarditis, with infrequent cases occurring without infection (eg, with an inflammatory process such as Behçet syndrome [24]).
Tests
Echocardiography — Echocardiography is the key test to identify prosthetic valve regurgitation and assess its severity, type (transvalvular or paravalvular), hemodynamic effects, and cause. The interpretation of TTE and TEE for the evaluation of the severity of pathologic prosthetic valve regurgitation is performed based upon largely the same criteria as for native valve regurgitation, although few data are available about the application and the validity of the routine parameters in the context of a prosthetic valve [10,13,14,16].
Transthoracic echocardiography — The initial diagnostic test is generally TTE, which provides helpful information about flow velocities across the prosthetic valve and an initial assessment of regurgitant jets. However, TTE color Doppler assessment of regurgitant jets (particularly with mitral prostheses) is often limited by the presence of acoustic artifacts generated by the prosthesis, which can mask the severity of the regurgitation. The role of TTE in assessing prosthetic regurgitation varies depending upon the valve site and type of regurgitation, as described above. (See 'Approach according to prosthetic regurgitation type' above and "Echocardiographic evaluation of prosthetic heart valves", section on 'Prosthetic valve regurgitation'.)
Transesophageal echocardiography — Since TEE is superior to TTE in the evaluation of paravalvular prosthetic regurgitation, as well as for prosthetic transvalvular MR, it should be performed systematically in patients with suspected significant paravalvular leaks or suspected significant prosthetic transvalvular MR or AR to aid in determining the severity and cause of regurgitation. (See 'Overview of diagnosis and evaluation' above.)
In the case of significant paravalvular leaks, TEE is essential to evaluate the localization and severity of the regurgitation. Three-dimensional (3D) TEE has proven to be superior to two-dimensional (2D) TEE in the localization and analysis of the paravalvular regurgitant jet, especially in the case of multiple jets [17,25]. 3D color Doppler can localize the jet and assess its severity, and 3D planimetry can be used to estimate the regurgitant orifice. The 2020 ACC/AHA guidelines for valve disease recommend 3D TEE guidance for patients with paravalvular prosthetic regurgitation undergoing transcatheter procedures [12].
Cardiovascular magnetic resonance — For patients in whom the severity of prosthetic regurgitation is not adequately defined by a combination of TTE and TEE, we suggest cardiovascular magnetic resonance (CMR) imaging. For mechanical and stented bioprosthesis, the applied magnetic field is usually distorted in the vicinity of the prosthetic ring, so signal loss can occur. These artifacts are magnified in cine images, degrading the quality significantly. However, CMR is able to perform accurate flow-imaging and volume-based measurements, which is especially relevant in patients with multiple jets, whose evaluation with TEE is complex [26]. CMR is the gold standard for chamber quantification, and allows a detailed view of the periprosthesis anatomy in stentless valves.
Computed tomography — For patients with suspected significant prosthetic valve regurgitation with inconclusive TTE and TEE results, the main indications for computed tomography (CT) are to differentiate between pannus and thrombus and to assess calcification, deterioration, and occluder motion [14].
Acquisition protocols resemble those used for coronary CT angiography, performed in multiple phases. ECG-gated CT with 3D/four-dimensional (4D) reconstruction images using volume rendering techniques is also useful in the evaluation of paravalvular leak [27]. Retrospective reconstruction with adjustment for opacity and color visualizes paravalvular leaks with a great level of detail, and can assist in the process of percutaneous closure.
Nuclear imaging — For the evaluation of prosthetic heart valves, the use of nuclear imaging is limited to selected cases of suspected endocarditis. The use of nuclear imaging as a complement to echocardiography in the diagnosis and evaluation of prosthetic valve endocarditis is discussed separately. (See "Prosthetic valve endocarditis: Epidemiology, clinical manifestations, and diagnosis", section on 'Diagnosis'.)
Cardiac catheterization — Cardiac catheterization (with measurement of filling pressures and angiographic assessment of regurgitant jets) is not generally required to assess prosthetic valve regurgitation and entails risk related to crossing a prosthetic valve. Coronary angiography is helpful in selected patients with significant prosthetic regurgitation who are candidates for redo valve surgery.
Cardiac catheterization is rarely required to assess filling pressures in patients with prosthetic valve regurgitation. Since the hemodynamic effects of prosthetic regurgitation are generally assessed by clinical evaluation along with echocardiography (TTE and/or TEE), invasive measurement of filling pressures is seldom required.
Invasive angiography is rarely required to assess the presence and severity of prosthetic valve regurgitation. Due to the inherent risks of invasive techniques, invasive angiography should be restricted to situations where noninvasive evaluation is inconclusive or discordant.
Coronary artery disease (CAD) should be evaluated before cardiac surgery, as recommended in major society guidelines [12,28]. However, most patients with prosthetic valve regurgitation have been previously screened for CAD with a coronary angiogram before the prosthesis implantation. and the proper criteria for selecting patients in whom a repeat coronary angiography should be done is controversial. We suggest repeat coronary angiography for patients in the following clinical settings:
●For patients who underwent coronary artery bypass graft surgery during the same surgery as prosthesis implantation.
●For patients who have developed angina or ventricular dysfunction.
●For patients with moderate lesions on prior coronary angiography (performed >6 months prior).
●For patients with moderate to high risk of CAD if >1 year after prior coronary angiography with no or mild lesions.
In patients at low risk for CAD who previously underwent a screening for CAD with either coronary CT or invasive coronary angiography, we suggest not screening again if they do not meet any of the above criteria and their previous test was performed less than five years ago.
DIFFERENTIAL DIAGNOSIS — Symptoms and signs of HF caused by prosthetic valve regurgitation are nonspecific and are the same as those for other causes of HF. Thus, careful clinical evaluation (including echocardiography) is required to identify alternate or concurrent causes of HF. (See "Determining the etiology and severity of heart failure or cardiomyopathy".)
In patients presenting with prosthetic regurgitation, benign trace to mild regurgitation should be distinguished from significant regurgitation based on the TTE and TEE evaluation of the valve and the severity of regurgitation.
In the patient presenting with high transvalvular gradients, prosthetic valve regurgitation should be distinguished from other causes such as high gradients due to high stroke volume, patient-prosthesis mismatch, pressure recovery, and valve obstruction.
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
●Prosthetic heart valve regurgitation includes regurgitation through the valve (transvalvular) as well as paravalvular regurgitation (also known as paravalvular leak). (See 'Definitions and prevalence' above.)
●Normally functioning mechanical valves and some normally functioning bioprosthetic valves have trivial to mild transvalvular regurgitation, which should be distinguished from pathologic regurgitation. (See 'Definitions and prevalence' above.)
●The clinical presentation of prosthetic valve regurgitation varies widely depending upon its severity, its hemodynamic effects, and its cause. In asymptomatic patients, prosthetic valve regurgitation may be detected as an incidental finding obtained on routine follow-up while symptomatic patients frequently present with moderate to severe heart failure. (See 'Clinical manifestations' above.)
●The goals of diagnostic evaluation of prosthetic valve regurgitation are to identify the type (transvalvular or paravalvular) and severity of regurgitation, its hemodynamic effects, and its cause. (See 'Overview of diagnosis and evaluation' above.)
●The approach to diagnostic evaluation of prosthetic valve regurgitation includes assessment of symptoms and signs, and transthoracic echocardiography (TTE) as the key initial test. Transesophageal echocardiography is recommended next in the following clinical settings:
•For patients with suspected significant transvalvular (aortic or mitral) prosthetic regurgitation, when TTE has not determined the severity or cause.
•For all patients with a suspected significant paravalvular leak, to determine the severity and cause.
●Causes of pathological mechanical valve regurgitation include structural prosthetic valve deterioration and nonstructural valve dysfunction due to pannus, or thrombus. Causes of bioprosthetic valve regurgitation include leaflet deterioration and calcification, endocarditis, thrombus, and pannus formation. (See 'Identifying the cause of prosthetic valve regurgitation' above.)
ACKNOWLEDGMENTS
The UpToDate editorial staff acknowledges William H Gaasch, MD (deceased), who contributed to earlier versions of this topic review.
The UpToDate editorial staff also acknowledges Catherine Otto, MD, who contributed to an earlier version of this topic.
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