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Echocardiographic evaluation of the tricuspid valve

Echocardiographic evaluation of the tricuspid valve
Literature review current through: Aug 2023.
This topic last updated: Mar 08, 2022.

INTRODUCTION — Tricuspid valve disorders can be routinely identified, and their severity can be estimated by echocardiography.

ECHOCARDIOGRAPHY OF THE NORMAL TRICUSPID VALVE — Anatomically, the tricuspid valve consists of anterior, septal, and posterior leaflets. The anterior leaflet is the most anatomically constant echocardiographic feature, with the septal and posterior leaflets being variable in size and position. With study of the valve by three-dimensional (3D) echocardiography, several subtypes ranging from two to five leaflets have been recognized [1].

Transthoracic echocardiogram — On two-dimensional (2D) transthoracic echocardiography (TTE), the tricuspid valve is routinely recorded from the long (image 1) and short-axis parasternal, apical four-chamber, and subcostal views. The location of the tricuspid valve as the most rightward valve places it at or just beneath the sternal edge and requires the ultrasound beam to be angled sharply rightward while maintaining transducer contact with the chest wall. Overall, all tricuspid valve leaflets can be seen in less than 60 percent of patients with 2D TTE from the subcostal window [2]. The normal tricuspid leaflet thickness is <3 mm [3].

Identification of individual tricuspid valve leaflets in the 2D views has been controversial. Data from pathologic examination, rotational 2D tomograms, and 2D reconstructions from 3D images have facilitated correct leaflet identification in 2D views [2,4-6]:

In the 2D parasternal long-axis (right ventricular [RV] inflow) view, the anterior leaflet is consistently visualized as the more proximal leaflet arising from the anterior free wall. The leaflet furthest from the probe is usually the septal leaflet [4,6-8]. In up to 25 percent of individuals, the posterior leaflet is seen instead of the septal leaflet. Rotation to bring the interventricular septum into view will preferentially show the septal leaflet instead of the posterior leaflet [9].

In the parasternal short-axis view at the level of the aortic valve, the posterior leaflet is imaged along the RV free wall and either the septal or anterior leaflet is imaged adjacent to the aortic root [4,6,7]. Anterior angulation will generally bring the anterior leaflet into better view, and marked anterior angulation will show the anterior leaflet alone spanning the tricuspid annulus [9].

In the apical four-chamber view, the septal leaflet is consistently visualized adjacent to the septum, and usually the anterior leaflet is visualized along the free wall [3,6,8], although occasionally the posterior leaflet is seen [9]. Anterior angulation to show the left ventricular outflow tract will bring the anterior leaflets into view along the free wall of the RV.

In an apical two-chamber view focused on the RV, the anterior leaflet is seen adjacent to the anterior wall, and opposite is usually the posterior leaflet [10]. The subcostal four-chamber view usually displays the anterior and septal leaflets [10].

3D imaging of the tricuspid valve enables en face visualization of the three leaflets (movie 1) [2,6,11] in addition to facilitating leaflet identification in 2D views [6].

The tricuspid valve annulus is slightly apically displaced compared with the mitral valve annulus; the gap resulting from this displacement is occupied by the membranous septum that separates the left ventricle from the right atrium. Attention to this feature is useful in identifying the tricuspid valve in many congenital conditions (such as Ebstein anomaly) and in understanding the anatomic substrate for congenital or acquired left ventricular to right atrial shunts (via a Gerbode defect). (See "Ebstein anomaly: Clinical manifestations and diagnosis" and "Isolated ventricular septal defects (VSDs) in infants and children: Anatomy, clinical features, and diagnosis", section on 'Left ventricle to right atrium shunting'.)

Transesophageal echocardiogram — Imaging the tricuspid valve with transesophageal echocardiography (TEE) is more difficult to accomplish than imaging the mitral and aortic valves, as the tricuspid valve is generally further from the transducer than the left-sided valves. The higher frequency waves used in TEE do not penetrate deeply into the far field.

The tricuspid valve is best visualized in multiple TEE planes: the mid-esophageal four-chamber view at 0°, rotation at the mid-esophageal level to 30°, 60°, and 90° and from the transgastric view.

In the four-chamber view, the septal and anterior leaflets are usually seen, and retroflexing the probe can bring the posterior leaflet into view.

Tricuspid regurgitant jet velocity is best measured in a view in which the ultrasound beam and the regurgitant jet are most parallel, often between 30° and 90° in the mid-esophageal view.

Measurement of tricuspid regurgitant jet velocity to estimate pressure gradients is discussed below. (See 'Peak velocity of the jet' below.)

In the transgastric position, the tricuspid valve is brought into view by turning the probe clockwise from the mitral valve short-axis view (0°) or left ventricular long-axis view (90°).

Depending upon an individual patient's anatomy, slight modification of the above views may be necessary.

TRICUSPID STENOSIS — Tricuspid stenosis is rare and is almost always acquired as a result of rheumatic fever. Rheumatic tricuspid stenosis is usually associated with mitral valve stenosis as well as tricuspid regurgitation (TR). Other, less common causes of tricuspid stenosis include congenital tricuspid atresia, tricuspid valve tumors, endomyocardial fibrosis and carcinoid heart disease, which typically manifests predominantly with TR. Rare causes, such as pacemaker-related endocarditis, have also been reported. (See "Tricuspid stenosis".)

Two-dimensional echocardiography — 2D TTE or TEE [12] enables identification of the specific features of tricuspid stenosis. Similar to mitral stenosis, the hallmark for the diagnosis is doming of the tricuspid valve seen in the parasternal long-axis view or in the apical four-chamber view. Other 2D echocardiographic findings include thickened, distorted, and calcified leaflets and restrictive leaflet motion [13].

Doppler echocardiography — We classify a tricuspid valve with mean pressure half-time ≥190 ms or a valve area ≤1.0 cm2 as having hemodynamically significant (severe) stenosis as defined in the European Association of Echocardiography/American Society of Echocardiography guidelines [13]. The tricuspid gradient is highly variable depending upon heart rate, stroke volume, and phase of the respiratory cycle, though hemodynamically significant tricuspid stenosis is usually associated with a mean pressure gradient of at least 5 to 10 mmHg at a heart rate of 70 beats per minute.

Recordings for tricuspid stenosis are similar to those seen for mitral stenosis: There is turbulent diastolic inflow, higher-than-normal maximal flow during diastole, and an increased pressure half-time. The mean tricuspid diastolic gradient can be estimated from the tricuspid inflow time velocity integral by applying the modified Bernoulli equation.

Techniques for estimating tricuspid valve area using echocardiography are not as well-established as those for estimating mitral valve area. Methods for calculating mitral valve area, such as pressure half-time, the continuity equation, and proximal isovelocity surface area, can be applied to the tricuspid valve. Tricuspid valve area in cm2 may be estimated as 190 divided by the pressure half-time [14].

TRICUSPID REGURGITATION — Doppler studies have determined that about 70 percent of normal individuals have evidence of trace or functional tricuspid regurgitation (TR) and more than 90 percent with established heart disease have evidence of TR. In the normal individual, the finding of trivial or mild (1+) TR is rarely of clinical importance beyond providing a means of obtaining an accurate determination of pulmonary artery systolic pressure [15]. (See "Echocardiographic assessment of the right heart", section on 'Pulmonary artery pressure'.)

Echocardiography provides a means to estimate the severity of TR, measure the velocity of TR (to estimate the systolic RV to right atrial gradient), and identify the mechanism responsible for TR. When reporting the RV systolic pressure from measurement of the peak TR velocity, it is important to avoid underestimates from incomplete Doppler waveforms or overestimates from artifact extending beyond the true Doppler waveform. It is best to measure along the modal frequency of complete Doppler envelopes [16]. If possible, sample the TR jet from several views and, if they differ, choose the highest velocity. The four-chamber view is usually, but not always, the highest velocity. If only one view provides a complete TR jet, the velocity may be underestimated. As explained below, the magnitude of the TR gradient does not necessarily correlate with TR severity. (See 'Peak velocity of the jet' below.)

Classification — As recommended in the 2020 American College of Cardiology/American Heart Association (ACC/AHA) valve guidelines, TR is classified using a staging system based upon symptoms and severity of valvular heart disease, including valve anatomy, valve hemodynamics (largely from Doppler examination), and hemodynamic consequences reflected in the RV, right atrium, and inferior vena cava (IVC) (table 1) [17].

Severe TR is identified using hemodynamic parameters including central jet area ≥50 percent of RA, vena contracta (VC) width ≥0.7 cm, effective regurgitant orifice area (EROA) ≥0.40 cm2, regurgitant volume ≥45 mL, dense triangular Doppler continuous wave jet contour with early peak, and hepatic vein systolic flow reversal (table 1) [17,18]. Adverse prognosis associated with severe TR is discussed separately. (See "Management and prognosis of tricuspid regurgitation", section on 'Prognosis'.)

Evidence of the hemodynamic effects of TR include dilated RV, right atrium and IVC with decreased IVC respirophasic variation, elevated right atrial pressure with c-V wave, and diastolic flattening of the interventricular septum.

We agree with the following key points from the European Association of Echocardiography and the European Association of Cardiovascular Imaging recommendations on assessment of valvular regurgitation [18-20]:

Although jet area is included in the 2020 ACC/AHA guidelines, the color flow area of the regurgitant jet is used primarily for diagnosis of TR, rather than for quantifying severity of TR. However, a large eccentric jet reaching the posterior wall of the right atrium suggests significant TR, and a small central jet usually indicates mild TR.

When feasible, the measurement of the VC is recommended to quantify TR. A VC width ≥7 mm identifies severe TR. Lower values are difficult to interpret. In case of multiple jets, the respective values of the VC width are not additive.

When feasible, the measurement of the proximal isovelocity surface area (PISA) radius is reasonable to quantify the TR severity. A TR PISA radius >9 mm at a Nyquist limit of 28 cm/s indicates severe TR.

The systolic hepatic flow reversal is specific for severe TR with lower sensitivity. In one small series, the specificity of systolic hepatic flow reversal was 93 percent and the sensitivity was 60 percent [21]. Systolic hepatic flow reversal represents the strongest nonvalvular parameter for evaluating TR severity.

When TR is more than mild, evaluation of RV dimensions and function, right atrial volume, IVC diameter, and the pulmonary arterial systolic pressure is mandatory. Assessment of RV systolic function using tricuspid annular plane systolic excursion (TAPSE) and systolic myocardial velocity (at the lateral tricuspid annulus) is reasonable when searching for RV dysfunction. However, TAPSE and systolic myocardial velocities are load dependent and may not reflect true RV myocardial function in patients with severe TR. (See 'Inferior vena caval flow' below.)

Two-dimensional echocardiography — On 2D TTE or TEE, the tricuspid valve can be examined, and hemodynamic effects of TR can be evaluated by inspection of RV size and function, right atrial size and function, and IVC size and motion (movie 2 and image 2A-B and table 1). We have observed that, as the TR worsens, the left-sided chambers may decrease in size, masking pathologic left-sided chamber enlargement.

Right ventricular size — Hemodynamically significant, chronic TR is generally associated with RV dilation. 2D echocardiographic methods for identifying RV enlargement are largely semiquantitative and the use of this finding as a guide to severity is limited. Three-dimensional reconstruction methods enhance RV size assessment. (See "Echocardiographic assessment of the right heart", section on 'Right ventricular size'.)

Right ventricular function — It is useful to examine the descent of the RV base toward the apex as a guide to RV systolic function. The excursion of RV base frequently becomes accentuated in acute TR and also with long-standing significant TR with normal/compensated RV function [22,23]. However, the RV may later fail with depressed RV basal motion in the setting of severe TR and chronic volume overload. RV strain measurement is generally performed only on the lateral wall because strain in the interventricular septum is constrained. (See "Echocardiographic assessment of the right heart", section on 'Right ventricular function'.)

Interventricular septum — When severe TR is present, RV volume overload causes diastolic interventricular septal flattening. The left ventricle becomes D-shaped, as increased preload in the RV displaces the septum toward the left. Septal flattening is best appreciated in the short-axis view at the level of the basal or mid-left ventricle. However, this sign of RV volume overload is not specific for severe TR. If severe TR coexists with pulmonary hypertension, combined RV pressure and volume overload results in septal flattening occurring in both systole and diastole. Since diastolic interventricular septal flattening represents relative RV and left ventricular filling, an RV overload pattern may be manifest in the setting of mitral stenosis and less severe forms of TR. (See "Echocardiographic assessment of the right heart", section on 'Interventricular septal shape'.)

Right atrial size — In the normal state, the right and left atria appear to be nearly equal in size and shape. With isolated TR, the right atrium appears enlarged and spherical when compared to the left atrium. The degree of right atrial enlargement depends upon many factors, including the duration and severity of TR, intrinsic disease of atrial muscle, and, if present, the duration of chronic atrial fibrillation. A normal-sized right atrium coexisting with severe TR suggests that the valve lesion is of recent onset [18]. (See "Echocardiographic assessment of the right heart", section on 'Right atrial size'.)

Interatrial septum — Normally, the flexible interatrial septum moves bidirectionally or slightly left to right during atrial filling, reflecting the slightly higher filling pressure of the left heart [24]. In the presence of severe TR, the normal curvature is reversed with the interatrial septum bulging towards the left atrium when the TR jet impinges on the septum and/or RV filling pressure is elevated relative to the left.

Inferior vena cava — The IVC and hepatic veins can be imaged in the subcostal view. The vena cava expands in systole in response to TR and retrograde V waves. Continuous flow from the inferior vena cava into the right atrium has been shown to be correlated with normal central venous pressure [25].

With more advanced degrees of TR, the systolic expansion of the IVC is visually apparent (image 3 and movie 3A-B). IVC size and its respiratory variation can be used to estimate right atrial pressure. (See "Echocardiographic assessment of the right heart", section on 'RA pressure'.)

Pulsed wave Doppler examination of hepatic veins is discussed below. (See 'Pulsed wave Doppler' below.)

Color flow Doppler echocardiography — Color flow Doppler echocardiography is the best way to establish the presence of TR and it is a key modality for classifying its severity (table 1) [17,18]. As with mitral regurgitation, several methods have been used to establish the severity of TR (image 4 and movie 4A-D).

Comparison of color Doppler methods — Several Doppler criteria are used for severity of TR and some but not necessarily all criteria apply to each patient. Both VC and PISA methods may be more accurate than jet area [20]. Visualization of the VC is less technically demanding than use of PISA. However, both jet area and PISA underestimate severe TR in 20 to 30 percent of patients [26].

All of these color Doppler methods are more accurate for grading severity of central compared to eccentric TR jets. It may be difficult to distinguish mild from moderate TR by either the jet area or VC methods.

Width of the vena contracta — As noted in the 2020 ACC/AHA guidelines, a VC width >0.7 cm is one of the main criteria for severe TR [17]. The VC is the narrowest portion of the color flow regurgitant jet that occurs at or just downstream from the valve orifice. However, due to technical variability, it is often not reliable clinically.

VC width correlates with other echocardiographic measures of TR severity and with clinical evidence of TR [27,28].

Proximal flow acceleration — PISA measurement is a helpful but infrequently used method of quantifying TR. An EROA ≥40 mm2 or a regurgitant volume ≥45 mL indicates severe TR [20].

Proximal flow acceleration describes the phenomenon of increasing blood velocity as regurgitant blood approaches the regurgitant orifice from the ventricular side of the valve. By color flow imaging, this phenomenon may be visualized as a series of concentric, roughly hemispheric isovelocity shells of decreasing surface area and increasing surface velocity. The relatively low sampling rate of color flow imaging limits the peak measurable blood velocity. When flow velocity exceeds the aliasing velocity (Nyquist limit), color reversal occurs. (See "Principles of Doppler echocardiography", section on 'Color flow imaging'.)

The EROA can be calculated by dividing the flow rate through the regurgitant orifice (which is estimated as the product of the surface area of the hemisphere [2πr2] and Va) by the peak velocity of the regurgitant jet (PkVreg):

EROA  =  (2πr2  x  Va)  /  PkVreg

Limitations of PISA include difficulty in identifying the regurgitant orifice and inaccurate estimation of the convergence shape [29]. The PISA method assumes a hemispheric convergence shape that may not accurately reflect the geometry of flow convergence for eccentric jets, multiple jets, or complex or elliptical regurgitant orifices. Application of PISA to TR is limited by greater difficulty in visualizing a measurable contour of flow convergence [18].

Though PISA has been less extensively studied for TR than for mitral regurgitation, small studies support its use as a means of quantifying TR [20]. These have indicated that PISA-derived measurements correlate with angiographic grade of TR [30] and other echocardiographic measures of TR [26,31]. In a study of 95 patients with TR and 95 patients with mitral regurgitation, similar EROAs were associated with smaller regurgitant volumes for TR compared to mitral regurgitation but a similar prevalence of venous flow reversal [31]. Based upon these findings, an EROA of ≥40 mm2 was recommended as a criterion of severe regurgitation in both TR and mitral regurgitation.

Color flow jet size — Although the size of the color flow TR jet in the right atrium is generally proportional to the severity of TR (as determined by angiography [26,30,32] as well as by clinical examination [27]), this method of quantifying TR is subject to limitations [26,27,30,32]. Very small central jets are diagnostic of functional, minimal, trace, trivial, or mild TR. Color jets that fill the right atrium suggest severe TR. For central (not eccentric) jets imaged using a Nyquist limit of 50 to 60 cm/s, a jet area of <5 cm2 suggests mild, 5 to 10 cm2 suggests moderate, and >10 cm2 suggests severe TR.

However, there is significant overlap in jet area among grades of TR, particularly mild and moderate [26,30]. Jet size is also influenced by entrainment, which is described in the next section. Jet area is not recommended as the sole parameter to grade TR severity.

Entrainment of the jet — As an eccentric jet enters the right atrium, it tends to travel along adjacent surfaces and thus hugs the atrial wall; this is called entrainment or the Coanda effect. The jet area of an eccentric jet impinging upon the wall of the receiving chamber will appear smaller than a centrally directed jet with the same regurgitant volume. Once entrained on the wall, the jet may completely circle the chamber.

In mitral regurgitation, a "wall-hugging jet" entrained along an atrial wall is usually indicative of high-grade regurgitation. While this phenomenon has not been formally studied in TR, experience suggests that this sign is frequently present with lesser degrees of TR and therefore cannot be considered a reliable sign of severity. (See "Echocardiographic evaluation of the mitral valve".)

Pulsed wave Doppler

Inferior vena caval flow — Pulsed wave and color Doppler recordings of IVC and hepatic vein flow are helpful in quantifying the severity of TR. As noted in the 2017 American Society of Echocardiography (ASE) valve regurgitation guidelines, moderate TR is associated with blunting of the normally dominant systolic wave of venous return, and severe TR is associated with systolic venous flow reversal (table 1) [17,18]. Systolic hepatic flow reversal is a specific but somewhat insensitive criterion for severe TR. (See 'Classification' above.)

The direction of blood flow in these vessels is generally toward the heart during both phases of the cardiac cycle. During inspiration, the normally dominant systolic inflow signal is exaggerated. Under normal conditions, retrograde caval flow occurs only briefly after atrial contraction.

The flow reversal during systole in the hepatic veins with TR is analogous to flow reversal in pulmonary venous flow with mitral regurgitation [33]. In the presence of significant TR, the normally dominant systolic component of flow may be blunted or reversed (movie 3B) and, during inspiration, the abnormality becomes accentuated [34,35].

RV inflow — Early diastolic peak velocity (peak E) and velocity time integral of RV inflow is increased in proportion to TR severity. These findings are analogous to those seen with mitral regurgitation, although the threshold for abnormally increased peak E is lower for TR than for mitral regurgitation.

In a study of 118 patients with varying degrees of TR [36], tricuspid peak E was compared to TR graded according to ASE-recommended parameters [37]. Tricuspid peak E of ≥0.65 m/s had a sensitivity of 73 percent and specificity of 88 percent for the detection of severe TR.

Since peak E is augmented in the presence of regurgitation, an E-wave dominant (E>A) mitral inflow pattern is observed in the presence of significant mitral regurgitation [33]. The presence of an A-wave dominant mitral inflow pattern excludes the presence of severe mitral regurgitation. Although the predictive value of an A-wave dominant tricuspid inflow pattern for excluding TR has not been reported, clinical experience indicates that an A-wave dominant pattern eliminates significant TR.

Although TR volume can theoretically be calculated by subtracting the flow across a non-regurgitant valve from antegrade tricuspid flow, this approach is generally not used, partially due to difficulty estimating tricuspid annular area [18].

Continuous wave Doppler — There are several features of the continuous wave Doppler spectral recording that are useful in grading or staging TR, including the shape, density, and peak velocity of the jet (image 5A-B) [18].

Shape of the jet — The shape of the TR jet as recorded by continuous wave Doppler is usually symmetrically parabolic, reflecting the relative equality of rates of flow acceleration and deceleration. In severe TR, the intrusion of a large regurgitant volume into the right atrium during systole exceeds the ability of atrial capacitance or compliance to maintain low pressure and a rapid rise in atrial late systolic pressure occurs. This rise or V-wave produces early equilibration of right atrial and RV pressures, creating an asymmetric early peaking triangular regurgitant wave form.

The 2020 ACC/AHA valve guidelines and 2017 ASE valve regurgitation guidelines include jet contour as a parameter to grade TR [17,18]. Mild TR is associated with a parabolic shape, moderate TR is associated with a variable contour, and severe TR is associated with a triangular early peaking jet. In our experience, the V-wave cut-off sign produced by early deceleration of the TR jet is one of the most useful and reliable signs of severe TR (table 1) [38].

Density of the jet — With mild TR, it may be difficult to obtain a complete Doppler wave form (envelope) without the use of contrast enhancement of the signal; with more severe degrees of TR, the jet is completely outlined and the signal is dense. As the degree of severity increases, the jet progressively darkens and approaches the density of the tricuspid inflow jet.

The strength of the Doppler signal is proportional to the number of red blood cells serving as reflecting targets. As a result, the tricuspid inflow signal is proportional to the volume of systemic flow and the relative density of the TR signal indicates the magnitude of the regurgitant fraction [39]. "Soft" TR jets are graded as mild and "dense" TR jets are graded as moderate or severe (table 1) [17,18,37].

Peak velocity of the jet — The peak TR gradient can be estimated by applying the modified Bernoulli equation (ΔP = 4v2 where ΔP is the difference between right atrial pressure [RAP] and RV systolic pressure [RVSP] in mmHg and v is the peak velocity of the TR jet in m/s). Accurate measurement of peak velocity requires a low intercept angle between the TR jet and the ultrasound beam. If the intercept angle is high, the velocity may be underestimated. (See "Echocardiographic assessment of the right heart", section on 'Pulmonary artery pressure'.)

Peak RVSP can be estimated by summing estimated RAP and the estimated peak TR gradient (RVSP = RAP + ΔP) [40]. The RVSP is equal to the pulmonary artery systolic pressure (PASP) minus any pulmonic valve systolic gradient. If pulmonic stenosis (or other cause of RV outflow obstruction) is absent, RVSP equals PASP. Reference hemodynamic values are displayed in the table (table 2). It should be noted that up to 50 percent of individuals with pulmonary hypertension do not have a measurable TR waveform [41]. When a measurable TR waveform is present, the mean TR gradient has been shown to have better catheterization laboratory correlation than the standard peak TR gradient [42].

Peak velocity of the continuous wave Doppler TR jet is determined by RV systolic pressure, not the severity of TR [43]. Since TR velocity is determined by ΔP, TR velocity is not an indicator of regurgitant fraction or volume (ie, TR severity) [15].

Thus, the presence of severe pulmonary hypertension is not an indicator of severe TR. In the presence of wide-open severe TR, the peak velocity of the TR jet is generally only mildly to moderately elevated, reflecting a mild to moderate systolic gradient between the right atrium and RV. In this setting, accurate estimation of right atrial pressure (which may be markedly elevated) as well as tricuspid systolic gradient is required to accurately estimate pulmonary artery systolic pressure.

Contrast echocardiography — Use of agitated saline or other ultrasound contrast agents can enhance the TR jet signal (image 5B) [44]. Since contrast administration requires intravenous access, its use for enhancing TR jets may be limited to situations in which access is readily available or contrast is being employed for another purpose. Contrast enhancement of weak TR velocity signal may permit more accurate determination of right heart hemodynamics.

A right-sided contrast agent such as agitated saline may also enhance visualization of hepatic vein flow reversal. Following administration of contrast into an upper extremity vein, the IVC and hepatic veins are monitored for systolic appearance of contrast. Normally, only minimal contrast enters the hepatic veins but in the presence of significant TR, abnormal reflux can be detected by 2D imaging, pulsed Doppler, color Doppler, or M-mode.

LESIONS AND CONDITIONS CAUSING TRICUSPID REGURGITATION — The echocardiogram in conjunction with other clinical data can help establish the etiology of tricuspid regurgitation (TR).

The most common cause of TR is functional, defined as regurgitation with apparently structurally normal leaflets and chords. The cause of functional TR appears to be tricuspid annular dilatation (due to RV or right atrial enlargement) and tethering of the tricuspid valve leaflets, although the mechanisms of valve dysfunction have not been fully defined. Causes of functional TR include disease states that can cause RV dilatation and failure, such as left heart failure, pulmonary hypertension, left-to-right shunt, and RV infarction. (See "Etiology, clinical features, and evaluation of tricuspid regurgitation", section on 'Etiology'.)

Primary disorders of the tricuspid valve causing TR are much less common than functional TR. Causes of primary TR include rheumatic heart disease, tricuspid endocarditis, tricuspid valve prolapse, Ebstein anomaly, carcinoid heart disease, and traumatic injury of the tricuspid valve apparatus [45]. (See "Etiology, clinical features, and evaluation of tricuspid regurgitation", section on 'Primary TR'.)

The etiology of TR may be evident only by TEE. Possible settings in which this might occur include vegetations with leaflet destruction, a flail tricuspid leaflet due to traumatic chordal rupture (occurring, for example, as a complication of diagnostic or follow-up transcatheter endomyocardial biopsy), periprosthetic regurgitation, leaflet fixation due to a RV pacing lead, or adherence of the septal leaflet in the formation of a ventricular septal aneurysm spontaneously closing a ventricular septal defect [46].

Unusual tricuspid regurgitant jet direction is also encountered. As an example, eccentric TR jets can contribute to the severity of right-to-left shunting via an atrial septal defect by direct streaming through the defect [47].

Functional tricuspid regurgitation — Conditions that may contribute to progressive functional TR include atrial fibrillation and pulmonary arterial hypertension (precapillary or caused by left heart failure). In a case-control study of 100 patients with progressive functional TR, independent predictors of TR progression were pulmonary artery systolic pressure (odds ratio [OR] 1.14 per 1 mmHg of pulmonary artery systolic pressure increase), permanent atrial fibrillation (OR 14.3), and coronary artery disease (OR 5.7) [48].

Atrial fibrillation — Chronic atrial fibrillation is associated with progressive left and right atrial enlargement. In some patients, the tricuspid valve annulus dilates with the atrium and begets atrioventricular valve regurgitation. Regurgitation engenders further dilation of the valve rings and steady worsening of mitral regurgitation and TR. In the background, worsening left ventricular diastolic function also may contribute to progressive regurgitation. Eventually, severe right heart failure may complicate this picture [49,50].

Evidence is lacking on the effect of rhythm versus rate control on TR progression. The role of rhythm versus rate control in managing atrial fibrillation is discussed separately. (See "Management of atrial fibrillation: Rhythm control versus rate control".)

Pulmonary hypertension — TR commonly complicates pulmonary hypertension, regardless of type and cause (eg, pulmonary arterial hypertension, pulmonary hypertension due to left heart disease, pulmonary hypertension due to chronic lung disease and/or hypoxemia). (See "Clinical features and diagnosis of pulmonary hypertension of unclear etiology in adults" and "Treatment and prognosis of pulmonary arterial hypertension in adults (group 1)".)

When TR is present, it contributes to RV and right atrial dilation and right-sided heart failure. The leaflets are usually anatomically normal in their echocardiographic appearance.

Left heart failure — The most common cause of significant TR is right heart failure secondary to left heart failure. In this situation, left ventricular dysfunction of any cause raises left atrial pressure and pulmonary artery pressure, and induces RV and right atrial dilatation [51].

The severity of TR parallels the severity of right chamber enlargement. As the annulus dilates, the leaflets, fixed in length, overlap progressively less at their tips. With time, TR causes further chamber dilation and less leaflet coaptation. In this vicious cycle, TR begets more TR. The leaflets appear normal in thickness, annular attachment, and excursion, but the dwindling coaptation surface migrates apically.

RV function may be depressed and this reduced function is recognized by diminished systolic descent of the anterior RV base (tricuspid annular plane systolic excursion). Effective treatment of left ventricular failure often results in a decrease or disappearance of TR, thereby confirming the diagnosis of functional TR.

Primary tricuspid regurgitation

Rheumatic disease — Rheumatic disease, where prevalent, is a common cause of TR. In patients with rheumatic heart disease, significant TR almost never exists as an isolated lesion and generally accompanies rheumatic mitral involvement [52]. The degree of anatomic change affecting the tricuspid valve is almost always less than that affecting the mitral valve. Among patients with rheumatic mitral disease, TR occurs with normal as well as deformed leaflets [53].

Rheumatic features including diffuse leaflet thickening, restriction of opening motion by commissural fusion, calcification of the leaflets, and chordal shortening [53]. Restriction of leaflet mobility produces characteristic leaflets motion with failure to move apart and "doming" as a unit into the RV during diastole.

Rheumatic TR is frequently accompanied by tricuspid stenosis. Because the tricuspid valve annulus is large, tricuspid stenosis without regurgitation is considerably less common. In a study of 788 consecutive patients aged 9 to 64 with rheumatic heart disease in India, 9 percent had echocardiographic evidence of tricuspid valve involvement and all had mitral valve stenosis [52]. Of these patients, 50 percent had TR, 7 percent had tricuspid stenosis, and 43 percent had combined TR and stenosis.

Tricuspid valve prolapse — Myxomatous disease of the mitral valve is often accompanied by tricuspid involvement but isolated tricuspid prolapse has rarely been reported [7]. Among patients with mitral valve prolapse, the likelihood that the tricuspid valve will develop this form of degeneration increases with age [54].

Ischemic tricuspid regurgitation — Myocardial infarction of the RV free wall or interventricular septum may involve the wall supporting the papillary muscle with resulting tension on the chordae causing TR. The 2D echocardiogram demonstrates incomplete and often asymmetric closure of the tricuspid leaflets with apical displacement of the coaptation point. This phenomenon is similar to that seen with left ventricular myocardial infarction with resulting loss of support of mitral papillary muscle, resulting in ischemic mitral regurgitation. (See "Chronic secondary mitral regurgitation: General management and prognosis".)

Endocarditis — Endocarditis of the tricuspid valve most frequently occurs as a complication of illicit intravenous drug use. Right-sided endocarditis affects the tricuspid valve far more commonly than the pulmonic valve.

Echocardiographic findings include mobile, often bulky vegetations that prolapse into the right atrium, distort valve leaflets and may be accompanied by flail leaflet resulting from chordal destruction (image 6 and movie 5A-B) [55]. When there is a flail leaflet, the degree of regurgitation is marked.

TTE or TEE? — When tricuspid endocarditis is suspected, TTE should be attempted first. If the clinical question is unanswered, then it is reasonable to proceed to TEE. (See "Clinical manifestations and evaluation of adults with suspected left-sided native valve endocarditis".)

The improved image quality that TEE usually offers over TTE is not as apparent in imaging tricuspid valve disease as mitral valve disease unless precordial images cannot be obtained (eg, soon after open heart surgery). Hemodynamic information derived from measurement of the TR jet is generally more readily obtained from the TTE approach.

The sensitivity of TTE for detection of tricuspid valve vegetations was illustrated by a study of 48 intravenous drug users, who were young and perhaps more easily imaged [56]. Vegetations were detected by TTE in all 22 patients with vegetations detected by TEE. The grading of TR was also identical with the two techniques, although TEE did give more detailed images of the vegetations.

However, TTE will miss some tricuspid vegetations that are detectable by TEE [57]. (See "Role of echocardiography in infective endocarditis".)

TEE is essential for the diagnosis of endocarditis in some situations, such as infection of central venous catheters and pacemaker or implantable cardioverter-defibrillator leads. One example is that of immunocompromised patients receiving chemotherapy or hyperalimentation who develop vegetations on chronically-placed, central venous catheters. TTE is often nondiagnostic in this setting. This was illustrated in a review of 19 patients in which TTE had a sensitivity of only 26 percent; in nine of these patients, TEE led to a major change in management, such as surgery, line removal, or antibiotic or anticoagulant therapy [58].

3D TEE may aid diagnosis of endocarditis affecting the tricuspid valve, particularly when artifact from prosthetic devices, such as pacemaker and defibrillator leads, and prosthetic valves limits 2D TTE and TEE image quality [59].

Carcinoid tumors — Carcinoid tumors that have metastasized to the liver and produce large amounts of 5-hydroxyindoleacetic acid are associated with TR. The valve leaflets have a unique appearance in carcinoid heart disease, being shortened, thickened, and rigid with little change in position from systole to diastole [60] (image 2A and movie 4D-E). (See "Clinical features of carcinoid syndrome".)

With advanced deformity, the leaflets appear to neither open nor close. Although small diastolic gradients occur in carcinoid, the predominant lesion is almost always severe regurgitation.

Ebstein anomaly — Ebstein anomaly is a congenital malformation characterized by exaggerated apical displacement of the functional tricuspid valve annulus relative to the mitral annulus. Echocardiography establishes the diagnosis and demonstrates its salient features. The diagnosis and management of Ebstein anomaly are discussed separately. (See "Ebstein anomaly: Clinical manifestations and diagnosis".)

In Ebstein anomaly, the septal and posterior leaflets are adherent to underlying myocardium so that their hinge points are apically displaced (figure 1). The septal leaflet hinge point is apically displaced by ≥8 mm/m2 body surface area compared to the position of the mitral valve annulus in the apical four-chamber view [61,62]. Ebstein anomaly affects the septal leaflet most and the anterior the least but, in the more severe cases, the entire apparatus may be situated in or near the apex [63]. Right atrial enlargement and TR (with origin at the most apically-displaced point of the valve) are usually present and may be severe.

Trauma — Causes of TR from mechanical damage or interference affecting the tricuspid valve or subvalvar apparatus include iatrogenic injury during transcatheter right heart endomyocardial biopsy [64-66], injury or impingement from endocardial pacemaker or defibrillator leads, and blunt chest trauma resulting in a chordal rupture or annular tear [67,68]. (See "Endomyocardial biopsy", section on 'Complications'.)

When tricuspid chordal rupture occurs, systolic fluttering of the leaflets, similar to what is observed with mitral chordal rupture, can be detected by M-mode. If the leaflet is flail, it may be displaced (along with the severed chord) into the right atrium during systole and appear as a prolapsing mass. The echocardiographic appearance of a severed chord with flail leaflet can be difficult to distinguish from a vegetation.

PACEMAKER OR DEFIBRILLATOR LEAD IMPINGEMENT — RV pacing can cause dyssynchrony, RV dysfunction, and tricuspid regurgitation [69]. RV pacemaker or defibrillator lead placement can cause TR due to leaflet perforation, lead impingement on the tricuspid valve, lead entanglement with the tricuspid valvular apparatus, and lead adherence to the valve [70,71]. Observational data indicate that significant TR associated with pacemaker leads is associated with worse long-term-prognosis [72]. Shadowing from a pacemaker lead may occasionally obscure TR so imaging from multiple planes is essential. Damage to the tricuspid valve apparatus with transvenous lead extraction can cause increased TR, though the TR is rarely clinical significant [73]. Similar complications have been reported with placement or removal of pulmonary artery catheters.

SURGICAL AND INTERVENTIONAL CONSIDERATIONS — Symptomatic severe tricuspid valve disease is a standard indication for surgery. Surgery for severe tricuspid regurgitation may improve survival [74]. Tricuspid valve surgery can also be considered if annular dilatation is >4 cm, which can be measured in the apical four-chamber view. Postoperatively, if valve repair has been performed, annuloplasty rings can be seen as symmetric echodensities on either side of the valve leaflet, and are more central than the anatomic annulus. If valve replacement has been performed, a follow-up echocardiogram should be performed to establish baseline valve gradient measurements for the new prosthesis. Echocardiographic findings of increase in the mean gradient by more than 50 percent in three years, increased cusp thickness, and reduced cusp mobility are signs of bioprosthetic valve thrombosis [75]. (See "Management and prognosis of tricuspid regurgitation", section on 'Indications'.)

Echocardiography is a key component of planning and executing structural interventions. Percutaneous tricuspid valve intervention requires special training in a high volume center and is beyond the scope of this topic [76-78].

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

The tricuspid valve consists of anterior, septal, and posterior leaflets, although variations are common. The anterior leaflet is the most anatomically constant echocardiographic feature and is seen in the apical four-chamber view on transthoracic echocardiography, with the septal and posterior leaflets being variable in size, number, and position. (See 'Echocardiography of the normal tricuspid valve' above.)

The tricuspid valve annulus is slightly apically displaced compared with the mitral valve annulus; the gap resulting from this displacement is occupied by the membranous septum that separates the left ventricle from the right atrium. Attention to this feature is useful in identifying the tricuspid valve in congenital conditions such as Ebstein anomaly and in understanding the anatomic substrate for congenital or acquired left ventricular to right atrial shunts (via a Gerbode defect). (See 'Transthoracic echocardiogram' above.)

Tricuspid stenosis is rare and is almost always due to rheumatic disease, which is usually associated with mitral valve stenosis as well as tricuspid regurgitation (TR). Other causes of tricuspid stenosis include congenital tricuspid atresia, tricuspid valve tumors, endomyocardial fibrosis and carcinoid heart disease, which typically manifests predominantly with TR. (See 'Tricuspid stenosis' above.)

About 70 percent of normal individuals have evidence of trace or functional TR and more than 90 percent with established heart disease have evidence of TR. (See 'Tricuspid regurgitation' above.)

The severity of TR can be evaluated using proximal isovelocity surface area, vena contracta width, color Doppler jet area (with limitations), continuous wave jet density and contours, and hepatic vein flow. (See 'Classification' above.)

The peak TR gradient can be estimated by applying the modified Bernoulli equation (ΔP = 4v2 where ΔP is the difference between right atrial pressure and right ventricular systolic pressure and v is the peak velocity of the TR jet). (See 'Peak velocity of the jet' above.)

In the presence of "wide-open" severe TR, the peak velocity of the TR jet is generally only mildly to moderately elevated, reflecting a mild to moderate systolic gradient between the right atrium and right ventricle. (See 'Peak velocity of the jet' above.)

Causes of TR include tricuspid annular dilatation (eg, functional TR from left heart failure), rheumatic heart disease, tricuspid endocarditis, tricuspid prolapse, Ebstein anomaly, carcinoid heart disease, pacemaker or implantable cardioverter defibrillator leads, and trauma from endomyocardial biopsy. (See 'Lesions and conditions causing tricuspid regurgitation' above.)

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References

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