- Open Access
Multimodal imaging of the tricuspid valve: normal appearance and pathological entities
© The Author(s) 2016
- Received: 8 January 2016
- Accepted: 24 May 2016
- Published: 9 June 2016
The tricuspid valve, which is the atrioventricular valve attached to the morphological right ventricle, is affected by a wide range of pathological processes. Tricuspid valve diseases are now increasingly recognized as a significant cause of morbidity and mortality. Echocardiography is the most widely available and, hence, the first-line imaging modality used in the evaluation of tricuspid valve disorders; however, CT and MRI are also increasingly used for further evaluation and characterization of these entities. In this article, we first review the normal anatomy and embryology of the tricuspid valve, followed by a discussion of the role of multiple imaging modalities in the evaluation of tricuspid valve abnormalities. We then review and illustrate the imaging appearance of several congenital and acquired tricuspid valve abnormalities.
• Tricuspid valve diseases have a significant impact on morbidity and mortality.
• CT and MRI are increasingly used in the evaluation of tricuspid disorders.
• CT and MRI help in diagnosis, functional evaluation, pre-surgical planning and post-surgical follow-up.
• The most common cause of tricuspid regurgitation is functional.
- Tricuspid valve
- Atrioventricular valve
The tricuspid valve is affected by a wide variety of pathological entities, ranging from congenital abnormalities to neoplasms. Their impact also varies widely, from the characteristic stenosis and regurgitation to the more subtle carcinoid tumours and fibroelastomas. Because tricuspid valve and right heart abnormalities are usually asymptomatic, and are often secondary to left heart disorders, they have generally received less attention than the abnormalities on the left side . However, recent studies have shown that tricuspid valve diseases have a significant impact on morbidity and mortality . Tricuspid regurgitation may be asymptomatic for long periods, but severe tricuspid regurgitation may present with edema, anasarca, hepatic congestion, loss of appetite, fatigue, atrial fibrillation, abdominal pain, dyspnea, oliguria, ascites and jaundice.
Several imaging modalities are utilized in the evaluation of tricuspid valve disorders. Echocardiography is widely available, and is often the first-line imaging modality used for evaluating these disorders; however, computed tomography (CT) and magnetic resonance imaging (MRI) are also increasingly employed, not only for initial diagnoses and functional assessments, but also for pre-surgical planning to define complex anatomy, or even for post-surgical follow-up .
In this article, we first review the normal anatomy and embryology of the tricuspid valve, followed by a discussion of the role of multiple imaging modalities in the evaluation of tricuspid valve abnormalities. We then review and illustrate the imaging appearance of several congenital and acquired tricuspid valve abnormalities.
The papillary muscles of the RV (Fig. 1b) are smaller, more numerous and more widely separated than those of the left ventricle (LV). There are two sets of papillary muscles , namely the anterior and medial, with the anterior muscle providing chordae to the anterior and posterior leaflets, and the medial muscle providing chordae to the posterior and septal leaflets. The septal papillary muscle is either absent or diminutive. However, significant variability exists in the attachment of papillary muscles to the valve cusps through the chordae. The septal wall may provide chordae to the septal and anterior leaflets [2, 4]. Often, there are smaller chordae tendineae that attach the papillary muscles to the ventricular wall or function as bow strings between adjacent papillary muscles. Both the chordae tendineae and the septal leaflet of the tricuspid valve attach to the septum, which separates the right atrium (RA) from the LV. The tricuspid annulus, on which the leaflet sits, is a horseshoe-shaped saddle-like structure with an elliptical configuration. During right ventricular filling, the annulus opens and dilates more so along the free ventricular wall, becoming more spherical and ring-like.
Functionally, the tricuspid valve prevents retrograde flow of blood from the RV into the RA. The pulsatile nature of caval flow is caused by the cyclical opening and closing of the tricuspid valve. The valve opens with ventricular diastole and closes with ventricular systole.
The tricuspid valve apparatus is derived from the endothelial cells of the endocardial AV cushion tissue that separates the atria and ventricles and that contributes to the formation of the AV septum. The septal leaflet develops mainly from the inferior endocardial cushion, with a small contribution from the superior cushion. The leaflet subsequently delaminates from the myocardium. The anterior and posterior leaflets develop by invagination of a portion of the ventricular myocardium, including the lateral mesenchymal cushion, subepicardial mesenchyme and myocardium of the AV groove. This tunneling invagination process starts inferiorly and continues superiorly until the AV junction is reached. Thereafter, there is controlled resorption of the adjacent surrounding muscle tissue, which finally gives the valvular leaflets. This degenerative receding ventricular wall tissue also contributes to the chordae tendineae .
Comparison of different imaging modalities used in the evaluation of the tricuspid valve
• Gray scale
• Cine SSFP
• RV long-axis, RV horizontal long-axis, axial, short-axis, 4-chamber
• Velocity-encoded phase contrast
• Black-blood T1W, T2W, fat-saturated
• Early contrast enhancement
• Delayed contrast enhancement
• Widely available
• Good spatial resolution
• Good spatial resolution
• Low cost
• Good temporal resolution
• Good temporal resolution
• Multiplanar reconstruction capabilities
• Multiplanar imaging capabilities
• Can be performed at bedside
• Morphological information
• Can be performed even in hemodynamically unstable patients
• Evaluation of associated extracardiac disorders
• Tissue characterization
• Morphological and functional evaluation
• Pre-surgical planning
• Accurate functional quantification of valve and ventricles
• Ionizing radiation
• Not widely available
• Limited windows, especially for right heart
• Potentially nephrotoxic contrast media
• Higher cost
• More limited in obesity, COPD, immediately post-surgery
• Dynamic evaluation/ventricular functional evaluation possible only in retrospective ECG-gated scans which is associated with higher radiation dose
• Limited tissue characterization
• Valve function cannot be evaluated
• Contraindicated in some devices, claustrophobia
• Limited in patients with high/irregular heart rates
• Calcifications not well seen
• Limited tissue characterization
• Risk of nephrogenic systemic fibrosis in patients with severe renal dysfunction.
• Only in hemodynamically stable patients
• Cannot be performed in hemodynamically unstable patients.
• Requires breath-hold and steady heart rates
Because of its widespread availability and low cost, echocardiography is often the first-line modality for the evaluation of tricuspid valve pathologies. It can be performed safely even at the bedside in hemodynamically unstable patients. Echocardiography provides morphological information as well as functional evaluation of the tricuspid valve, using grayscale, 2D or 3D, and Doppler technique. However, echocardiography is operator-dependent, and may be limited in obese patients and those with emphysema, due to a restricted field of view.
CT is also valuable in the evaluation of the tricuspid valve, particularly for providing morphological information due to its good spatial and temporal resolutions and ability to do multiplanar reconstruction with isotropic resolution. Localization of a mass and its impact on the valve can be evaluated using CT. Calcifications are better evaluated with CT than MRI. Functional dynamic cine imaging can also be performed using retrospective ECG gating, albeit at a higher radiation dose. The scan protocol has to be optimized to ensure adequate contrast opacification around the valve and minimize artefacts. Typically, CT is performed using a prospective ECG-triggered acquisition to minimize motion and radiation, but retrospective ECG gating is chosen if cine images are required. Intravenous administration of 50–70 ml of contrast agent, followed by a 50/50 mixture of contrast and saline, is used to reduce streak artefacts from the superior vena cava (SVC). An alternate option is to use dual-route injection, with simultaneous injection of the upper and lower extremities. However, CT is associated with radiation and the use of potentially nephrotoxic contrast agents.
Magnetic resonance imaging
MRI can provide comprehensive morphological and functional information on the tricuspid valve, with good spatiotemporal resolution, a large field of view and multiplanar imaging capabilities. MRI also provides functional assessment without the use of radiation and potentially nephrotoxic contrast media. It is ideal for evaluating the consequences of valvular abnormalities, such as the volume, mass and function of the ventricles. The tricuspid can be evaluated on MRI using steady-state free precession (SSFP) sequences in multiple planes, particularly the four-chamber, RV long-axis and short-axis views through the tricuspid annulus and valve. Right ventricular volumes can be measured in either the short-axis or axial plane, but the axial plane is associated with lower inter-observer variability . Flow can be evaluated using a velocity-encoded flow quantification sequence. This can be measured either directly using short axis images through the tricuspid valve or indirectly from RV volumes of the short axis and forward flow obtained from the pulmonary artery. MRI also has superior tissue characterization capabilities, and lesions such as masses can be characterized using a combination of T1-weighted (T1W), T2-weighted (T2W) and fat saturation sequences and contrast enhancement, both early (perfusion) and delayed.
Tricuspid valve dysfunction is seen in several primary and secondary abnormalities, both congenital and acquired. This can manifest as valvular stenosis, regurgitation or both.
Trace tricuspid regurgitation (TR) is seen in 80–90 % of healthy individuals. The most common cause (75 %) of pathological regurgitation is functional [7, 9], due to dilation of the annulus and valvular tenting, seen either due to RV dysfunction (left heart disease, ischemia, arrhythmogenic right ventricular dysplasia [ARVD], systemic RV in transposition of the great arteries [TGA)]), RV overload (pulmonary hypertension, systemic RV in TGA) or other causes (physiologic, atrial fibrillation, tumours). Left heart failure is the most common cause of TR. Structural TR is seen in 25 % and can either be congenital or acquired. Congenital causes include Ebstein’s anomaly, dysplasia, hypoplasia, cleft, prolapse, double orifice or bicuspid valve, whereas acquired causes include rheumatic fever, infective endocarditis, carcinoid, Loeffler endocarditis, trauma, tumours, or iatrogenic causes. Rheumatic fever is the most common cause of primary TR and is seen in 38 % of those with rheumatic mitral valve stenosis, with the valve appearing thickened and a with hockey stick-shaped appearance .
Grades of tricuspid regurgitation in echocardiography 
Effective regurgitant orifice (mm2)
Regurgitation volume (ml)
Vena contracta width (mm)
PISA radius (mm)
Hepatic vein inflow
Abnormal/flail/large coaptation defect
Large central/eccentric and wall-impinging
Continuous-wave Doppler jet signal
Dense/triangular with early peaking
Surgery is performed with severe symptomatic TR or less severe TR with concomitant mitral valve disease, infective endocarditis, tetralogy of Fallot or annular diameter > 40 mm. If the functional TR is caused by annular dilation, it is treated by annuloplasty using rigid or flexible annular bands which decreases the annular size and restores the shape. If there is valvular tethering and RV dysfunction, a bioprosthetic or mechanical valve replacement is performed.
On echocardiography, CT and MRI, the tricuspid valve is absent or abnormally closed. The areolar sulcal tissue occupying the gap where the AV connection and valve should have been present results in high signal in T1W and T2W MRI sequences. This distinguishes an absent AV connection from an imperforate valve. The RV is hypoplastic. Flow can be seen from the RA into the left atrium (LA) through the ASD and then through the mitral valve into the LV. The RA and systemic veins are dilated. All the types of tricuspid atresia are surgically treated by a three-stage repair with initial creation of an aortopulmonary shunt followed by the Glenn and Fontan procedure. Critical features for surgical management are the size of the VSD, ventriculoarterial concordance and pulmonary/subpulmonary stenosis/atresia.
Ebstein’s anomaly is characterized by apical displacement of the tricuspid valve leaflets into the RV, which divides the RV into an ”atrialized” portion and a “functional” portion with intrinsic musculature, both of which show varying degrees of dysplasia, fibrosis and thinning. This anomaly is caused by failure of delamination of leaflets or incomplete extension medially of the valvular leaflet tissue from its origin from the ventricular wall. Ebstein’s anomaly primarily affects the septal and posterior leaflets of the tricuspid valve and their anomalous attachment to the valvular annular apparatus. The leaflets can be hypoplastic, aplastic, irregular or completely fused. The anterior leaflet may also be redundant, tethered, or exhibit fenestrations, or may be voluminous with a sail-like configuration. The tricuspid annulus has varying levels of rotation and obliquity. The chordae tendineae and papillary muscles have dysplasia and varying levels of myocardial insertion. Associated anomalies include patent foramen ovale (PFO), ASD and VSD.
Aneurysm of the membranous ventricular septum
Transposition of the great arteries
AV canal defect
A complete AV canal defect (endocardial cushion defects, common AV canal) is a defect of the AV septum, with a common AV valve, atrial and ventricular septal defects. Embryologically, there is a failure of the AV junction to develop into two distinct AV valves, as well as failure to form atrial and ventricular septa. AV canal defects are seen in 40 % of Down syndrome patients, and 30 % of AV canal defects are associated with Down syndrome . There is left-to-right shunting, depending on the size of the defect, with biventricular volume overload. Heart failure ensues if this is not surgically corrected in the first few months of life.
Carcinoid plaques composed of smooth muscle cells, myofibroblasts and fibrous elastic tissue are seen on the ventricular side of the leaflets, forming a lining on the surface of the native valve, without involving the endocardium. In the early stages of carcinoid involvement, the leaflets are splayed open, resulting in regurgitation; however, with time, fibrotic reaction involving the mural wall endocardium and the valve annulus leads to thickening of the chordae and leaflets, resulting in valvular stenosis. TR is seen in 90 % of cases, eventually resulting in heart failure (Fig. 16b, Movie S3), whereas stenosis is seen in 10 % of cases. On CT and MRI, thickening of the tricuspid valvular and subvalvular apparatus is seen, with decreased motion of leaflets. Features of TR and stenosis are also seen, which are quantified as described above.
The tricuspid valve is affected by several masses, both neoplastic and non-neoplastic. Non-neoplastic masses include thrombus, vegetation, abscess, and caseous necrosis. Benign neoplasms include fibroelastoma, myxoma, hemangioma and lipoma. Malignant neoplasms include metastasis, lymphoma and sarcomas such as angiosarcoma and leiomyosarcoma. Thrombus is the most common non-neoplastic mass, myxoma is the most common benign mass, and metastasis is the most common malignant mass.
Tricuspid valve prolapse
Tricuspid valve prolapse is characterized by posterior bulging of the leaflets of the tricuspid valve beyond its annulus, into the RA in systole, due to sufficient elongation of the chordae and expansion of the cusp area. It is less common than mitral valve prolapse, occurs in an older age group, and may be a marker of diffuse connective tissue diseases. It is associated with mitral valve prolapse in 5–52 % of cases , and these patients are older and more symptomatic. Pathologically, the leaflets are tortuous and thickened, with myxomatous degeneration, loss of fibrous tissue, fragmentation and coiling of collagen bundles.
Although echocardiography is the most frequently used modality for the evaluation of tricuspid valve disorders, CT and MRI are also increasingly used. MRI provides not only morphological information, but also functional information on the quantification of tricuspid valvular disorders as well the secondary consequences on the ventricles.
Compliance with ethical standards
Conflict of interest
The authors have no financial disclosure and no conflict of interest.
Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
- Bruce CJ, Connolly HM (2009) Valvular heart disease: changing concepts in disease management. Circulation 119:2726–2734View ArticlePubMedGoogle Scholar
- Rogers JH, Boiling SF (2009) The tricuspid valve. Current perspective and evolving management of tricuspid regurgitation. Circulation 119:2718–2725View ArticlePubMedGoogle Scholar
- Cawley PJ, Maki JH, Otto C (2009) Valvular heart disease: changing concepts in disease management. Circulation 119:468–478View ArticlePubMedGoogle Scholar
- Shah PM, Raney AA (2008) Tricuspid valve disease. Curr Probl Cardiol 33(2):47–84View ArticlePubMedGoogle Scholar
- Sylva M, van den Hoff MJB, Moorman AFM (2014) Development of the human heart. Am J Med Genet A 164A(6):1347–1371View ArticlePubMedGoogle Scholar
- Alakih K, Plein S, Bloomer T et al (2003) Comparison of right ventricular volume measurements between axial and short axis orientation using steady-state free precession magnetic resonance imaging. J Magn Reson Imaging 18(1):25–32View ArticleGoogle Scholar
- Hung J (2010) The pathogenesis of functional tricuspid regurgitation. Semin Thorac Surg 22:76–78Google Scholar
- Baumgartner H, Hung H, Bermejo J et al (2009) Echocardiographic assessment of valve stenosis: EASE/ASE recommendations for clinical practice. J Am Soc Echocardiogr 22(1):1–23View ArticlePubMedGoogle Scholar
- Saremi F, Hassani C, Millan-Nunez V, Sánchez-Quintana D (2015) Imaging evaluation of tricuspid valve: analysis of morphology and function with CT and MRI. AJR Am J Roentgenol 204(5):W531–W542View ArticlePubMedGoogle Scholar
- Lancellotti P, Moura L, Pierard LA et al (2010) European Association of Echocardiography. European Association of Echocardiography recommendations for the assessment of valvular regurgitation. Part 2: mitral and tricuspid regurgitation (native valve disease). Eur J Echocardiogr 11(4):307–332View ArticlePubMedGoogle Scholar
- Zoghbi WA, Enrquiez-Sarano M, Foster E et al (2003) Recommendations for evaluation of severity of native valvular regurgitation with two-dimensional and Doppler echocardiography. J Am Soc Echocardiogr 16:777–802View ArticlePubMedGoogle Scholar
- Fukuda S, Saracino G, Matsumura Y et al (2006) Three-dimensional geometry of the tricuspid annulus in healthy subjects and in patients with functional tricuspid regurgitation. A real-time three-dimensional echocardiographic study. Circulation 114:1492–1498Google Scholar
- Helbing WA, Bosch HG, Maiepaard C et al (1995) Comparison of echocardiographic methods with magnetic resonance imaging for the assessment of right ventricular function in children. Am J Cardiol 76:589–595View ArticlePubMedGoogle Scholar
- Chiles C et al (2001) Metastatic involvement of the heart and pericardium. CT and MR imaging. Radiographics 21(2):439–449View ArticlePubMedGoogle Scholar
- Speiser U, Hirschberger M, Pitz G et al (2012) Tricuspid annular plane systolic excursion assessed using MRI for semi quantification of right ventricular ejection fraction. Br J Radiol 85(1017):e716–e721View ArticlePubMedPubMed CentralGoogle Scholar
- Usoro E, Soslow JH, Parra D (2013) Tricuspid annular plane systolic excursion by cardiac MRI has poor correlation with RV EF in pediatric patients. J Cardiovasc Magn Reson 15(Suppl 1):040View ArticleGoogle Scholar
- Ginns J et al (2014) The tricuspid valve in adult congenital heart disease. Heart Fail Clin 10(1):131–153View ArticlePubMedGoogle Scholar
- Warnes CA (2009) Adult congenital heart disease and importance of right ventricle. J Am Coll Cardiol 54(21):1903–1910View ArticlePubMedGoogle Scholar
- Negoi RI et al (2013) Complex Ebstein’s malformation: defining pre-operative cardiac anatomy and function. J Card Surg 28(1):70–81View ArticlePubMedGoogle Scholar
- Naidu A, Ricketts M, Goela A, et al. (2012) Incidental discovery of a membranous ventricular septal aneurysm in two dissimilar patients. Case Rep Cardiol 2012:324326. doi:10.1155/2012/324326Google Scholar
- Kelle AM, Young L, Kaushal S et al (2009) The gerbode defect the significance of a left ventricular to right atrial shunt. Cardiol Young 19(Suppl 2):96–99View ArticlePubMedGoogle Scholar
- Lamers WH et al (1995) Formation of tricuspid valve in the human heart. Circulation 91(1):111–121View ArticlePubMedGoogle Scholar
- Ming Z, Yumin Z (2008) Magnetic resonance evaluation of criss-cross heart. Pediatr Cardiol 29(2):359–365View ArticlePubMedGoogle Scholar
- Narine KK et al (2000) Tricuspid and pulmonary valve involvement in carcinoid disease. Tex Heart Inst J 27(4):405–407PubMedPubMed CentralGoogle Scholar
- San Roman JA, Vilacoasta I, Zamarano JL et al (1993) Tranesophageal echocardiography in right sided endocarditis. J Am Coll Cardiol 21:1226–1230View ArticlePubMedGoogle Scholar
- Bruun NE, Habib G, Thuny F et al (2014) Cardiac imaging in infectious endocarditis. Eur Heart 35(10):624–632View ArticleGoogle Scholar
- Durack DT, Lukes AS, Bright DK (1994) New criteria for diagnosis of infective endocarditis: utilization of specific echocardiographic findings. Duke Endocarditis Service. Am J Med 96:200–209View ArticlePubMedGoogle Scholar
- Sparrow PJ et al (2005) MR imaging of cardiac tumors. Radiographics 25(5):1255–1276View ArticlePubMedGoogle Scholar
- O’Donnell DH et al (2009) Cardiac tumors: optimal MR sequences and spectrum of imaging appearances. Am J Roentgenol 193(2):377–387View ArticleGoogle Scholar
- Kim EY et al (2009) Multidetector CT and MR imaging of cardiac tumors. Korean J Radiol 10(2):164–175View ArticlePubMedPubMed CentralGoogle Scholar
- Grebenc ML et al (2002) Cardiac myxoma: imaging features in 83 patients. Radiographics 22(3):673–689View ArticlePubMedGoogle Scholar
- Luna A et al (2005) Evaluation of cardiac tumors with magnetic resonance imaging. Eur Radiol 15(7):1446–1455View ArticlePubMedGoogle Scholar
- Syed ID et al (2008) MR imaging of cardiac masses. Magn Reson Imaging Clin N Am 16(2):137–164View ArticlePubMedGoogle Scholar
- Rajiah P et al (2011) Computed tomography of cardiac and pericardiac masses. J Cardiovasc Comput Tomogr 5(1):16–29View ArticlePubMedGoogle Scholar
- Weinreich DJ, Burke JF, Bharati S et al (1985) Isolated prolapse of the tricuspid valve. J Am Coll Cardiol 6:475–481View ArticlePubMedGoogle Scholar
- Lieppe W, Behar VS, Scallion R et al (1978) Detection of tricuspid regurgitation and two-dimensional echocardiography and peripheral vein injections. Circulation 57:128–132View ArticlePubMedGoogle Scholar