Echocardiographic evaluation of prosthetic heart valves

INTRODUCTION — Echocardiography is the key noninvasive modality for evaluation of prosthetic valve structure and function [1]. Transthoracic echocardiography (TTE) is the mainstay for monitoring prosthetic valves and can generally identify normal function as well as evidence of valve dysfunction (stenosis). Transesophageal echocardiography (TEE) is helpful particularly for assessment of valve structure and prosthetic valve regurgitation (figure 1), especially involving mechanical mitral and tricuspid prostheses as well as assessment of endocarditis for all valves (figure 2).

This topic will review echocardiography of prosthetic heart valves. Management of patients with prosthetic heart valves and prosthetic valve complications are discussed separately. (See "Mechanical prosthetic valve thrombosis or obstruction: Clinical manifestations and diagnosis" and "Prosthetic valve endocarditis: Epidemiology, clinical manifestations, and diagnosis" and "Antithrombotic therapy for mechanical heart valves" and "Overview of the management of patients with prosthetic heart valves".)

MONITORING GUIDELINES

Baseline transthoracic echocardiogram — We agree with the American College of Cardiology/American Heart Association (ACC/AHA) guideline recommendation to perform transthoracic echocardiogram (TTE) six weeks to three months after valve implantation (when the hemoglobin has normalized) to evaluate valve hemodynamics and to establish a baseline for future comparison [2]. The TTE should include Doppler measurements of transvalvular velocities as well as assessment of valvular and paravalvular regurgitation. Adequate Doppler velocity recordings can generally be obtained despite acoustic shadowing from valve prostheses.

Transvalvular gradients for normally functioning prosthetic valves are dependent upon valve type, location, and size (as compiled in the 2009 American Society of Echocardiography guidelines) as well as patient-specific factors [1]. A higher than expected initial gradient is often due to a high output state (eg, due to anemia) or patient-prosthetic mismatch and is only rarely due to early dysfunction of the prosthesis (eg, thrombus formation or hemodynamically significant valvular regurgitation). We suggest obtaining the postoperative baseline study after the patient’s hemoglobin has returned to baseline to avoid recording a gradient that is transiently higher than expected due to anemia.

Change in clinical status — The echocardiographer should be alert to the range of complications that can occur with prosthetic devices, including the following (see "Mechanical prosthetic valve thrombosis or obstruction: Clinical manifestations and diagnosis"):

●Prosthetic obstruction due to thrombus, pannus ingrowth, leaflet thickening, or calcification of biologic prostheses.

●Prosthetic regurgitation due to paravalvular leak, prosthetic leaflet interference by thrombus, or vegetation (movie 1C) or leaflet tear of a bioprosthesis.

●Prosthetic valve endocarditis with findings including vegetations and abscess formation (movie 1A and movie 1B).

●Prosthetic valve dehiscence with valve ring instability/"rocking."

●Mechanical structural failure (eg, strut fracture and component escape), which is rare with current valve types.

A TTE is recommended as the initial test in patients with prosthetic valves with a change in clinical status suggestive of valve dysfunction and/or endocarditis [2]. Symptoms and signs of bioprosthetic valve degeneration, pannus formation, or endocarditis include new exertional dyspnea, a louder murmur, or a new murmur. Symptoms and signs of mechanical valve dysfunction due to thrombosis, pannus formation, or endocarditis include a new or louder murmur, new onset of dyspnea, and signs of heart failure, thromboembolism, and hemolysis. For patients with a prosthetic valve, a TTE may also be useful since it provides proper alignment for Doppler assessment of transvalvular velocities, gradient, and valve area. In patients with aortic prostheses, valvular regurgitation can be reliably detected on TTE. For all patients with a prosthetic valve, TTE may be useful for assessment of biventricular cavity size and systolic function as well as an estimate of pulmonary artery systolic pressure. Transesophageal echocardiography has much higher sensitivity for detection of prosthetic valve thrombi, vegetations, and extravalvular extension of infection as well as prosthetic mitral regurgitation.

Surveillance of old bioprosthetic valves — Since the incidence of bioprosthetic valve dysfunction markedly increases 10 years after implantation, we agree with the 2020 ACC/AHA valve guidelines, which state that a TTE is reasonable in patients with a bioprosthetic valve after the first five years and then again at 10 years, even in the absence of change in clinical status [2]. The guideline suggested annual TTE thereafter. However, in individuals at increased risk of early valvular degeneration, such as those with chronic renal failure, diabetes, and younger age at implantation, it is reasonable to perform echocardiography at five years postimplantation and then yearly thereafter [3].

Routine annual echocardiographic evaluation is not indicated in patients with mechanical valve prostheses with normal postoperative baseline examination and no signs or symptoms of valve dysfunction [2]. However, follow-up echocardiography is indicated if there are signs or symptoms that suggest valve or ventricular dysfunction.

KEY COMPONENTS OF THE ECHOCARDIOGRAM

Overview — Echocardiographic evaluation of patients with prosthetic valves includes imaging of the valve and its seating; assessment of valve hemodynamics, including transvalvular velocities; identification and quantification of valve regurgitation (intravalvular and paravalvular); and measurement of cardiac chamber sizes, left ventricular wall thicknesses, and assessment of left ventricular systolic and diastolic function.

Prosthetic valves are generally inherently stenotic, so Doppler velocity recordings across normally functioning valves are similar to those of mild native valve stenosis [1]. Normal function of the valve is confirmed by evaluation of the contour of the jet velocity, including the acceleration time (the time from onset of flow to maximal velocity), the effective orifice area (EOA), and the Doppler velocity index (DVI). Expected ranges for gradients and EOA for normally functioning prosthetic valves are included in appendices to the 2009 American Society of Echocardiography prosthetic valve guidelines.

An increase in the transprosthetic velocity could be due to valvular obstruction, regurgitation, or an increase in cardiac output, whereas a decrease in either the EOA or the DVI is more specific for prosthetic obstruction. A Doppler velocity pattern demonstrating normal transprosthetic flow gradient and flow duration is usually sufficient to exclude a stenotic valve [1]. However, the gradient may not be elevated in the setting of obstruction with low stroke volume.

The EOA is calculated using the continuity equation:

where VTI_PrV is the velocity time integral through the prosthesis determined by continuous wave Doppler. The stroke volume is generally derived from an adjacent site as cross-sectional area (estimated from the associated diameter and assuming a circular area) multiplied by the VTI of flow measured by pulsed wave Doppler at that site. For prosthetic aortic and pulmonic valves, site for calculation of stroke volume is at the site of flow just proximal to the valve. For prosthetic mitral valves, stroke volume may be calculated at the aortic or pulmonary annulus if no significant regurgitation is present.

The DVI is a simplified method for evaluating aortic valve obstruction. The DVI is the ratio of the velocity proximal to the valve by pulsed wave Doppler to the velocity through the valve by continuous wave Doppler. Use of this index avoids the need to measure stroke volume [4]. A DVI <0.25 suggests significant valve obstruction.

Prosthetic aortic regurgitation (intravalvular or paravalvular) can generally be identified by transthoracic echocardiography (TTE). Prosthetic mitral regurgitation and tricuspid regurgitation are usually difficult to assess on TTE due to acoustic shadowing and thus transesophageal echocardiography (TEE) is preferred.

Role of TTE and TEE — TTE and TEE are complementary in the evaluation of prosthetic valves. As mentioned, acoustic shadowing caused by prosthetic material may limit TTE visualization of prosthetic discs/leaflets, vegetations, abscesses, and thrombi. In addition, while prosthetic aortic valve regurgitation is usually well visualized on TTE color Doppler imaging, prosthetic mitral regurgitation is frequently undetectable [5]. As a result, TEE is the imaging method of choice when the TTE is technically inadequate or when there are borderline findings on the TTE in a patient in whom there is a strong clinical suspicion of prosthetic malfunction [6]. As an example, one study of 170 patients who underwent surgery for valve dysfunction found that diagnostic errors (ie, findings on the TTE that were not confirmed at surgery) occurred in 12 percent and were primarily related to paravalvular regurgitation [7].

Since TTE images are obtained anteriorly, they are usually sufficient for evaluation of aortic prostheses. However, since the atria are situated in the far field where resolution is low, they are shadowed by mechanical and to lesser extent, biological mitral prostheses, so the evaluation of mitral prosthetic function is limited. On the other hand, TEE images are taken from a position posterior to the heart, so the atrial side of the mitral and tricuspid valves can be well seen. TTE demonstrates the ventricular side of the valve that lies in its near field, whereas TEE does not. The presence of mitral and aortic devices in the same patient may make the task of the echocardiographer more difficult and may require both TTE and TEE.

The physician evaluating a prosthetic device with TEE should be aware of the range of abnormalities that are possible in these devices and should match those possibilities to the patient's presentation (figure 2). Complications of prosthetic valves detected by TEE include:

●Paravalvular leak

●Endocarditis (movie 1A-B)

●Extrinsic interference of function (pannus, thrombus, vegetation) resulting in obstruction and/or regurgitation (movie 1C)

●Leaflet tears of bioprosthesis

●Leaflet calcification/stenosis of bioprosthesis

●Ball variance, now rare as ball in cage valves are no longer implanted

●Strut fracture and component escape, also now rare with newer-generation valves

It is worth mentioning the finding of microbubbles, which can be seen in an otherwise normally functioning mechanical prosthesis and are not associated with valve pathology. They are usually seen with mitral prostheses within the left ventricular inflow and are likely due to degassing of carbon dioxide [8].

The role of the TEE for evaluating the abnormalities associated with prosthetic valves will be reviewed here. The major complications encountered with these valves and the role of echocardiography in the evaluation of infective endocarditis are discussed fully elsewhere. (See "Mechanical prosthetic valve thrombosis or obstruction: Clinical manifestations and diagnosis" and "Role of echocardiography in infective endocarditis".)

FEATURES OF VALVE DYSFUNCTION

Prosthetic valve obstruction — Prosthetic valve obstruction should be suspected in a newly symptomatic patient with a rise in transprosthetic gradient from a baseline determination or from established normal values for valves of that type and size. The expected range of Doppler gradients and effective orifice area encountered in properly functioning valves are included in appendices to the ASE prosthetic valve guidelines (table 1) [1]. (See 'Prosthetic aortic stenosis' below.)

Causes of obstruction include pannus ingrowth, thrombus, and vegetation (movie 1A-C). Clinical clues to this possibility include the age of the valve and the adequacy of anticoagulation. In a bioprosthesis or heterograft, the leaflets themselves may become calcified and immobile. There has been an increasing recognition of subclinical thrombus formation on bioprosthetic valves, which appears to be more common in percutaneous valves than in surgically placed valves as discussed separately. (See "Bioprosthetic valve thrombosis, thromboembolism, and obstruction: Management" and "Transcatheter aortic valve implantation: Complications", section on 'Valve thrombosis'.)

Once there is a high suspicion of obstruction, transesophageal echocardiography (TEE) should be performed for etiologic definition with both mechanical and bioprosthetic valves, especially for mitral prostheses. Doppler transthoracic echocardiography (TTE) is the primary means to diagnose prosthetic valve obstruction; hemodynamic cardiac catheterization is not routinely needed [9]. 3D-TEE may be helpful in identifying pannus, although its utility has not been well defined [10]. Computed tomography (CT) scan is an important adjunctive imaging modality.

●In the case of suspected aortic pannus, the distal end of the left ventricular outflow tract should be examined both with imaging and with color flow Doppler. Pannus tends to lie close to the valve ring and can be easily overlooked. There can be proximal flow acceleration present on color flow Doppler that suggests pannus, which, on further searching with a variety of frequencies, angles, and gain settings, will be detected.

●In the mitral position, the same procedure should be followed. Finding a high grade of spontaneous contrast in the left atrium, with or without thrombi, or finding thrombus around the sewing ring in the setting of adequate anticoagulation should heighten suspicion of pannus formation. Thin fibrillar strands may also be encountered adjacent to the mitral annulus and on the sewing ring of the valve. These structures are brightly reflective and highly mobile and may or may not be associated with a pathologic process.

Diagnosis and management of valve obstruction due to thrombus or pannus are discussed separately. (See "Bioprosthetic valve thrombosis, thromboembolism, and obstruction: Management".)

Distinction between thrombus and pannus — The most common etiology for prosthetic valve obstruction is thrombus formation; pannus formation due to fibrous tissue ingrowth is far less common. In one surgical study of 112 obstructed mechanical valves, pannus formation was the underlying cause in 11 percent of valves, pannus formation in combination with thrombus was present in 12 percent, while thrombus alone was the etiology in the remaining cases [11]. Since treatment options for thrombus and pannus differ, it is important to distinguish between these two causes. (See "Bioprosthetic valve thrombosis, thromboembolism, and obstruction: Management".)

Echocardiographic differentiation of pannus and thrombus may be difficult. In general:

●Thrombus tends to be larger, mobile, be somewhat less echo-dense, and more commonly associated with spontaneous echo contrast.

●Pannus is highly echogenic, consistent with its fibrous composition; is usually firmly fixed (minimal mobility) to the valve apparatus; and mostly involves the sewing ring, which may make it difficult to distinguish from the ring [1].

In order to establish factors associated with the presence of thrombus, one study evaluated the findings on a preoperative TEE in 53 patients with an intraoperative diagnosis of pannus or thrombus [12]. Predictors of thrombus or a mixed presentation (pannus and thrombus) included:

●Mobile mass

●Attachment of mass to valve occluder

●Elevated gradients

●An international normalized ratio ≤2.5

All patients with thrombus or a mixed presentation had one or more of these features. The prevalence of thrombus with ≤1, 2, and ≥3 features was 14, 69, and 91 percent, respectively.

Color flow aliasing with proximal acceleration of the flow jet in the vicinity of the mass may aid in the identification of pannus. In one study of 23 patients who presented with 24 obstructed valves, clinical, TTE, and TEE data were compared with pathology at surgery in order to determine the clinical and echocardiographic characteristics that differentiate thrombus from pannus formation [13]. Thrombus was established in 14 valves and pannus in 10. Pannus formation was more common in the aortic position. From the standpoint of echocardiography, thrombus was more likely to be associated with soft ultrasound density (92 versus 29 percent) [8].

The role of other imaging modalities (eg, multidetector CT) in distinguishing thrombus from pannus is discussed separately. (See "Mechanical prosthetic valve thrombosis or obstruction: Clinical manifestations and diagnosis".)

Prosthetic valve regurgitation — Physiologic regurgitation, the so-called "seating puff" of angiography, is universally encountered with mechanical valves and dependent in degree on the type of prosthesis used. However, severe regurgitation may result from bioprosthetic valve leaflet degeneration or destruction from endocarditis, mechanical valve pannus, thrombus, or vegetation that interferes with mechanical leaflet function.

Physiologic regurgitation — All mechanical valves exhibit some degree of obligatory regurgitation of up to 15 mL of blood [14]. The physiologic regurgitation associated with prosthetic valves appears only briefly and is due to retrograde volume displacement as the valve leaflets close. This type of regurgitation is detected by highly sensitive color flow Doppler imaging on TEE. In addition, a certain amount of more prolonged "leakage backflow" regurgitation occurs after the valve closes [15]. These are often referred to as "washing jets," believed to inhibit the formation of thrombi.

In an evaluation of 136 mechanical prosthetic valves, TEE color flow Doppler imaging revealed regurgitant jets in 95 percent of the mitral prostheses and 44 percent of the aortic prostheses [16]. In contrast, TTE documented regurgitant jets in only 28 percent and 29 percent, respectively. The lower incidence of detected regurgitation in the aortic position may be explained by the shadowing of the left ventricular outflow tract in TEE imaging [17].

Normally functioning mechanical valves, such as the bileaflet St. Jude prosthesis, usually have two to four centrally directed regurgitant jets. Features associated with these jets include a low intensity and only minimal penetration into the atrium, generally less than 3 cm [15,18,19]. The monodisc Medtronic-Hall valve has two jets, one of which is prominent and longer [19,20]. Normally functioning bioprosthetic and heterografts are less likely to have these small regurgitant signals; when mild regurgitation is present, there is usually one central jet [16,21].

Pathologic regurgitation — Most pathologic regurgitation associated with mechanical valves is perivalvular. However, occasionally, disc closure may be impeded by a vegetation or thrombus leading to combined stenosis and regurgitation. If TTE does not reveal the offending mass or tissue, TEE should be performed.

Bioprostheses with leaflet degeneration may exhibit central pathologic regurgitation that is broad-based when severe. The bioprosthetic leaflets can usually be seen and are often thickened and calcified with possible perforation or disruption leading to a flail leaflet. Forward flow velocities measured by spectral Doppler may be increased due to the larger flow volume associated with regurgitation as well as concurrent obstruction.

A review of 134 patients with a prosthetic mitral valve attempted to derive echocardiographic indices of valvular dysfunction [22]. The results suggested that a peak transmitral E wave velocity exceeding 1.9 m/sec or a ratio of peak diastolic transmitral flow to left ventricular outflow tract velocity greater than 2.2 identifies prosthetic valve regurgitation (sensitivity 92 percent, specificity 78 percent), provided that the valve is not stenotic (pressure half-time less than 130 msec) [22]. On the other hand, a prosthetic valve with a peak E wave Doppler velocity of less than 1.9 m/sec, a ratio of peak diastolic transmitral flow velocity to left ventricular outflow velocity of less than 2.2, and a pressure half-time of less than 130 msec has a 98 percent chance of being normal (neither stenotic nor regurgitant).

Paravalvular regurgitation — Trace or mild paravalvular regurgitation immediately following valve replacement is common with both mechanical and bioprosthetic prostheses and generally not progressive. Paravalvular regurgitation can develop late after valve replacement due to suture dehiscence, from a poorly seated ring, or from endocarditis leading to valve dehiscence. Hemolysis is a common complication of these leaks, especially when they occur with a mitral valve prosthesis [23,24]. Paravalvular regurgitation should be suspected when a patient with a prosthetic valve presents with hemolytic anemia. Severe hemolysis can also occur after mitral valve repair, when regurgitation develops around the annuloplasty ring. A TEE is frequently required to detect paravalvular leakage. (See "Non-immune (Coombs-negative) hemolytic anemias in adults", section on 'Intravascular devices'.)

To recognize a paravalvular leak, TEE must be performed with a high color frame rate in several views from several angles outside the sewing ring [25]. There should be a careful search for periprosthetic leaks around as much of the valve circumference as possible and an attempt made to define the extent of the regurgitation once it is identified. The origin of a periprosthetic leak may appear deceptively narrow when caused by disruption of a limited number of sutures. Three-dimensional echocardiography is helpful in mapping the extent of the paravalvular leak and has proven efficacious for guiding percutaneous device closure of these leaks.

The most severe form of paravalvular regurgitation is seen when there is dehiscence of a substantial portion of the sewing ring [26]. In this setting, there may be such severe regurgitation that the regurgitant flow is almost laminar. The sewing ring on echocardiography may be seen to rock with each cardiac cycle; mobile echo densities representing the liberated suture material often can be visualized.

Prosthetic valve dehiscence — Prosthetic valve dehiscence is identified on echocardiography as a separation of the prosthetic ring from the native valvular annulus and is usually accompanied by paravalvular regurgitation. Valve dehiscence is most frequently caused by endocarditis. Rocking of a prosthetic valve is a sign of dehiscence, particularly in the aortic position. Rocking of a prosthetic mitral valve can be caused by dehiscence or by retained native posterior leaflet or posterior and anterior leaflets, with the latter generally not accompanied by paravalvular regurgitation [1]. Prosthetic valve dehiscence may be identified by TTE but is frequently better visualized with TEE [27].

Thromboembolism — In patients with a suspected cardiac cause for embolism, the source may be a thrombus from a nonobstructed or obstructed prosthetic heart valve. TEE is often necessary to establish this diagnosis. In a series of 52 patients with a prosthetic heart valve who underwent TEE after a suspected systemic embolic event, 12 percent had a definitive prosthetic valve thrombus and 10 percent had fibrous strands on the valve, which were suggestive of thrombus [28]. While strands appear to be more common in patients who have had an embolic event, they can be present in up to 40 percent of patients with prosthetic valves, so their significance remains uncertain [8]. (See "Mechanical prosthetic valve thrombosis or obstruction: Clinical manifestations and diagnosis".)

SPECIFIC PROSTHETIC VALVE DISORDERS

Prosthetic aortic stenosis — Aortic prosthetic obstruction may be due to thrombus or vegetation, pannus ingrowth, or progressive leaflet degeneration in the case of a bioprosthetic valve.

We agree with the American Society of Echocardiography algorithm for diagnosis of prosthetic aortic stenosis (algorithm 1) [1].

●If the peak velocity across the aortic prosthesis is greater than 3 m/sec or if there is a significant increase over baseline, the Doppler velocity index (DVI) should be calculated.

●Further analysis should include measurement of the acceleration time (AT), which is the time from transvalvular flow onset to maximal velocity [1]. An AT <100 msec is consistent with normal function, whereas an AT >100 msec is concerning for obstruction and further evaluation is warranted.

A DVI <0.25 suggests prosthetic aortic valve stenosis if accompanied by an AT >100 msec.

●Finally, the effective orifice area (EOA) indexed by body surface area can provide evidence of patient-prosthetic mismatch when the transprosthetic velocity is high but the DVI is >0.25 and the AT is <100 msec. Patient-prosthetic mismatch is suggested by an EOA index of <0.8 cm²/m² and is considered severe when the EOA index is <0.65 cm²/m² [29]. (See "Choice of prosthetic heart valve for surgical aortic or mitral valve replacement", section on 'Prosthetic valve-patient mismatch'.)

When prosthetic aortic valve stenosis is suspected, the transthoracic echocardiography (TTE) is usually not adequate for visualization of the leaflet motion or presence of thrombus and thus warrants further investigation with fluoroscopy of a mechanical valve and/or transesophageal echocardiography (TEE) as described below.

The role of other imaging (eg, multidetector computed tomography [CT]) in assessing prosthetic valve obstruction is discussed separately. (See "Transcatheter aortic valve implantation: Complications", section on 'Valve thrombosis' and "Bioprosthetic valve thrombosis, thromboembolism, and obstruction: Clinical manifestations and diagnosis", section on 'Diagnosis of obstruction'.)

Prosthetic aortic regurgitation — Using color flow Doppler, TTE can usually detect prosthetic aortic valve regurgitation, since the prosthesis position is anterior (close to the anterior chest wall) and visualizes the ventricular aspect of the valve. It is important to differentiate pathologic prosthetic regurgitation, which is often perivalvular from the normal "physiologic" prosthetic regurgitation. Mechanical prosthetic valves displace blood when the occluder disc closes and may also have small holes in the occluders and at hinge points; the pattern is characteristic for the valve type [1]. Biologic valves may have minor degrees of central regurgitation, which are detectable due to the high sensitivity of color flow Doppler.

Grading the severity of pathological prosthetic aortic regurgitation can be challenging and an integrative approach is recommended (table 2) [1]. When there is significant dehiscence of the valve (more than 40 percent), a rocking motion is detected, which is usually associated with severe regurgitation. The following features suggest severe regurgitation: jet width >65 percent, pressure half-time <200 msec, holodiastolic flow reversal in the descending aorta, regurgitant volume >60 mL, and a regurgitant fraction >50 percent. In addition, chronic severe aortic regurgitation is a cause of left ventricular dilation.

While TTE can detect and often grade prosthetic aortic regurgitation, the cause is often not apparent. TEE should be performed in order to diagnose endocarditis with or without abscess, thrombus interfering with disc closure, and bioprosthetic leaflet tears.

Prosthetic mitral stenosis — Prosthetic mitral valve obstruction can also occur because of thrombus, pannus, vegetation, and bioprosthetic leaflet thickening or calcification. The peak transmitral velocity, the mean gradient, and pressure half-time should all be considered in the context of the heart rate and compared with previous echocardiographic studies.

The prosthetic mitral peak E wave velocity is usually <1.9 m/sec at "normal" heart rates, but may be as high as 2.4 m/sec. Higher velocities are seen with bioprostheses. The mean gradient is usually <6 mmHg. The pressure half-time is usually <130 msec. EOA can be calculated using the continuity equation but is not as frequently used. DVI is calculated as the VTI_PrMV/VTI_LVOT and is normally <2.2 for mechanical valves [1]. The DVI will be normal in high output states, but elevated in both the case of either mitral prosthetic stenosis or regurgitation [22]. When the DVI is increased, the pressure half-time can help differentiate between stenosis and regurgitation. A pressure half-time >200 msec is most consistent with stenosis; whereas a pressure half-time <130 msec would suggest regurgitation. Intermediate values are inconclusive [1].

TEE for mechanical valves or bioprosthetic valves can further define the pathology and elucidate the mechanism for dysfunction. When TEE is unavailable or cannot be performed, fluoroscopy and/or gated CT can be useful for assessing mechanical valve motion.

Prosthetic mitral regurgitation — Since the color Doppler jet is usually obscured because of acoustic shadowing caused by the prosthesis, other clues to regurgitation must be heeded (table 3). There may be increased rocking of the prosthesis associated with dehiscence of the sewing ring. The peak transmitral E wave velocity is increased as is the mean gradient, although the pressure half-time remains within normal range. The left ventricular volume may be increased and the ejection fraction is usually preserved. However, in the presence of significant mitral regurgitation, the forward stroke volume falls, which can be inferred by a decrease in the left ventricular outflow tract VTI. The pulmonary artery pressure may be increased. Suspicion of prosthetic mitral regurgitation should prompt a TEE, which is diagnostic.

Prosthetic pulmonary valves dysfunction — Mechanical valves are rarely used in the pulmonary position because of a higher risk of valve thrombosis. Most frequently bioprosthetic valves, homografts, or heterografts are used. Assessment of prosthetic pulmonary valve stenosis is similar to aortic prostheses. An initial assessment with TTE for velocity/gradient and assessment of pulmonic regurgitation is reasonable.

The peak velocity through a homograft is usually <2.5 m/sec and through a heterograft <3.2 m/sec. There are limited data on the use of DVI or EOA for prosthetic pulmonary valves. An otherwise unexplained increase in transvalvular velocity on serial studies may be the most reliable method of detecting stenosis. An increase in the right ventricular systolic pressure, which can be estimated from the tricuspid regurgitation jet velocity, may indirectly indicate prosthetic pulmonary valve stenosis [1].

Prosthetic pulmonary valve regurgitation is usually detected by a low velocity pulmonary regurgitant jet on color flow Doppler in the parasternal short axis view on TTE. Severe prosthetic pulmonary regurgitation can be inferred by broad color flow jet, a dense continuous wave spectral Doppler signal, and rapid deceleration of the pulmonary regurgitant signal. A dilated right ventricle also suggests severe regurgitation.

Prosthetic tricuspid valve dysfunction — The principles for evaluating the prosthetic tricuspid valve are similar to that of the mitral valve. Bioprostheses are more commonly used than mechanical prostheses in the tricuspid position due to issues of valve thrombosis. Because of the respirophasic variation in transtricuspid velocities, at least five beats should be measured.

Based on a series of echocardiograms performed shortly after tricuspid bioprosthetic valve implantation in 285 patients, the peak E wave velocity should be less than 2.1 m/sec, the mean gradient <9 mmHg, and the pressure half-time <200 msec [30]. Echocardiograms performed early post-implantation in 78 patients with a mechanical tricuspid valve prosthesis (St. Jude or CardioMedics Standard prostheses) demonstrated the following: peak E velocity <1.9 m/sec, mean gradient <6 mmHg, and pressure half-time <130 msec [31]. Values greater than these suggest stenosis.

When the peak E wave velocity and mean gradient are increased with a low pressure half-time, regurgitation is suggested. Acoustic shadowing may impede detection of prosthetic tricuspid valve regurgitation as it does with mitral prosthetic regurgitation. Clinical and echocardiographic findings suggestive of prosthetic tricuspid regurgitation should prompt TEE.

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

●Transthoracic echocardiography (TTE) is helpful in evaluating prosthetic valve function, particularly valve gradients, but views are frequently limited for assessment of vegetations, thrombus, and regurgitation, especially for mitral and tricuspid prostheses. (See 'Features of valve dysfunction' above.)

●Transesophageal echocardiography (TEE) is particularly helpful in detecting paravalvular leak, prosthetic mitral and tricuspid regurgitation, vegetation, abscess, valve obstruction, ball variance, strut fracture and component escape, bioprosthetic leaflet tears, and bioprosthetic calcification/stenosis. As a result, initial TEE is often preferred. A TTE may be more useful to assess chamber sizes and ventricular function. (See 'Role of TTE and TEE' above.)

●A TTE with Doppler measurements of transvalvular velocities obtained six weeks to three months after prosthetic valve implantation (when the hemoglobin has normalized) is helpful to establish a baseline for future comparison. (See 'Baseline transthoracic echocardiogram' above.)

●Complications of prosthetic valves include prosthetic valve obstruction, regurgitation, endocarditis, dehiscence, and mechanical structural failure (rare with current valve types). (See 'Change in clinical status' above.)

●We suggest monitoring by TTE starting five years after implantation of a bioprosthetic valve due to the risk of valve degeneration. If the valve function is normal, it can be repeated at 10 years and then yearly thereafter. However, in patients with risk factors for early deterioration, such as those with renal failure, diabetes, and implantation at younger ages, it is reasonable to start monitoring at five years. (See 'Surveillance of old bioprosthetic valves' above.)

●Trace or mild paravalvular regurgitation immediately following valve replacement is common and generally not progressive. Paravalvular regurgitation can develop late after valve replacement due to broken or dehisced sutures, from a poorly seated ring, or from endocarditis (dehiscence). (See 'Paravalvular regurgitation' above.)

●Prosthetic valve obstruction should be suspected when a patient develops symptoms of heart failure and increased transprosthetic gradient. TEE is the primary means to confirm prosthetic valve obstruction and investigate its causes (pannus, thrombus, or vegetation). (See 'Prosthetic valve obstruction' above and "Mechanical prosthetic valve thrombosis or obstruction: Clinical manifestations and diagnosis" and "Bioprosthetic valve thrombosis, thromboembolism, and obstruction: Management".)

●Pathologic, intense prosthetic valve regurgitation can result from bioprosthetic valve degeneration, mechanical valve pannus, thrombus, or vegetation. (See 'Prosthetic valve regurgitation' above.)

●Systemic emboli can arise from nonobstructive or obstructive valve thrombosis. (See 'Thromboembolism' above.)