Tricuspid Valve: From Functional TR to Surgical Repair

Tricuspid regurgitation (TR) should be understood not simply as an isolated valvular lesion, but as a disorder of the tricuspid leaflets, annulus, right atrium (RA), right ventricle (RV), and systemic venous circulation. In contemporary practice, secondary TR is far more common than primary TR, particularly in Western populations, and usually reflects annular dilation and leaflet tethering caused by right-heart remodeling. As TR progresses, it promotes further chamber enlargement, worsening annular distortion, venous congestion, and impaired forward flow, thereby creating a self-perpetuating cycle of right-sided failure.[1-4] (PubMed)

1. Etiology of Tricuspid Regurgitation

TR is broadly classified into primary and secondary disease.

1) Primary TR

Primary TR arises from intrinsic abnormalities of the tricuspid valve apparatus itself, including the leaflets, chordae, papillary muscles, or commissural structures. Typical causes include congenital malformations such as Ebstein anomaly and leaflet dysplasia, infective endocarditis with fenestration or chordal rupture, rheumatic or carcinoid involvement, trauma, and myxomatous degeneration. In these patients, the pathology is fundamentally structural, and durable repair often requires direct treatment of the abnormal leaflet or subvalvular lesion in addition to annular remodeling.[2,5] (PubMed)

2) Secondary TR

Secondary TR is the dominant clinical phenotype. Here, the leaflets are often initially normal or near-normal, but coaptation fails because the annulus enlarges and/or the RV remodels. Two major mechanisms are recognized:

• Atrial functional TR: RA enlargement with annular dilation, often associated with atrial fibrillation
• Ventricular functional TR: RV enlargement and geometric distortion with leaflet tethering

This distinction is important because isolated annular dilation may remain amenable to annuloplasty, whereas significant tethering predicts a more complex and less durable repair if annuloplasty alone is used.[1,3,4,6] (PubMed)

3) Additional clinically relevant mechanisms

Other important causes include device- or lead-related TR, TR associated with left-sided valve disease, and mixed lesions in which structural valve disease coexists with annular and RV remodeling. These mixed phenotypes are common in advanced disease and explain why a simple reduction in annular size does not always restore durable competence.[2,5,9] (PubMed)

2. Pathophysiology of TR

The essential hemodynamic lesion in TR is systolic backflow from the RV into the RA. Mild TR may be tolerated for some time, but progressive regurgitation has important structural and systemic consequences.

1) Right-sided volume overload

Regurgitant flow increases the volume burden on both the RA and RV. Over time, this causes:

• RA enlargement
• RV dilation
• progressive annular dilation
• worsening leaflet malcoaptation

As a result, TR often becomes self-reinforcing: regurgitation enlarges the annulus and chambers, and that enlargement in turn worsens regurgitation.[1,4,6] (PubMed)

2) Reduced effective forward flow

In severe TR, part of the RV stroke volume is wasted backward into the RA rather than delivered through the pulmonary circulation. The LV therefore receives less preload, and systemic cardiac output falls. Clinically, this explains why advanced TR can present not only with edema and congestion, but also with fatigue, low-output symptoms, and exercise intolerance. The concept may be summarized simply: the RV cannot effectively fill the LV.[2,5,9] (PubMed)

3) Venous congestion

The backward transmission of pressure into the systemic venous circulation leads to the classic manifestations of right-sided heart failure:

• hepatic congestion
• ascites
• peripheral edema
• pleural effusions
• renal and gastrointestinal congestion in advanced disease

Thus, the clinical burden of TR is not limited to the valve itself; it is largely mediated through chronic venous hypertension and progressive RV dysfunction.[4,6,9] (PubMed)

3. Surgical Principles

The goal of surgical treatment is not simply to “tighten the annulus,” but to restore a stable and anatomically appropriate zone of leaflet coaptation. Repair is generally favored over replacement when feasible, particularly in secondary TR with preserved leaflet tissue. The major principles are:

1. correct annular dilation
2. restore leaflet coaptation
3. preserve the conduction system near the septal annulus
4. avoid distortion of adjacent structures such as the right coronary artery
5. address associated leaflet, commissural, or subvalvular pathology when present

This is especially important because the tricuspid annulus is anatomically heterogeneous: the anterior and posterior annulus are the main targets of reduction, whereas the septal annulus is closely related to the AV node and conduction axis.[2,5,9] (PubMed)

4. De Vega Annuloplasty

De Vega annuloplasty is a suture-based reduction annuloplasty traditionally used for functional TR caused predominantly by annular dilation.

Technique

A double continuous running suture is placed along the anterior and posterior annulus on the RV free-wall side. The septal annulus is generally avoided to reduce the risk of conduction injury. The annulus is then plicated in a controlled manner, often using a sizer to guide the final reduction.

Best indication

De Vega repair is most suitable when:

• TR is predominantly functional
• annular dilation is the main lesion
• leaflet tissue is reasonably preserved
• tethering is limited

Limitation

The major limitation of De Vega annuloplasty is durability. Because the repair depends on suture plication rather than prosthetic stabilization, recurrent annular redilation and recurrent TR are more likely, particularly in patients with advanced RV remodeling or significant tethering.[1,7,10] (PubMed)

5. Ring or Band Annuloplasty

Ring or band annuloplasty is generally considered the more durable reconstructive strategy for secondary TR, particularly when annular distortion is pronounced.

Technique

Interrupted annular sutures are placed mainly along the anterior and posterior annulus, and an incomplete ring or band is implanted. This restores a more stable annular geometry while avoiding excessive manipulation of the septal annulus near the AV node.

Advantages

Compared with suture-only repair, ring annuloplasty offers:

• better annular remodeling
• better resistance to redilation
• more reproducible geometry
• improved long-term durability

Current evidence supports ring annuloplasty as the preferred technique for isolated annular dilation, whereas De Vega repair is better regarded as a selective option rather than the default approach.[1,7,10] (PubMed)

6. Annuloplasty Alone Is Not Always Enough

A key limitation of standard annuloplasty is that it primarily addresses annular size, not leaflet tethering. When significant tethering accompanies annular dilation, annuloplasty alone is often insufficient. In such cases, a durable repair may require additional leaflet or subvalvular procedures, or in some patients consideration of replacement. This concept is central to modern surgical decision-making, because recurrent TR is strongly linked to uncorrected tethering and advanced RV remodeling.[1,4,7,10] (PubMed)

7. Timing of Intervention

One of the most important contemporary lessons is that TR should not be treated too late. Severe TR is an accepted indication for surgery, and moderate TR with significant annular dilation also deserves serious consideration, especially when left-sided valve surgery is already planned. Position statements and reviews have emphasized annular dilation thresholds such as ≥40 mm or ≥21 mm/m² as markers of clinically relevant remodeling. Concomitant repair at the time of left-sided surgery can prevent late progression of TR and may reduce the need for high-risk reoperation.[5,8,9] (PubMed)

8. Practical Surgical Perspective

A pragmatic surgical framework is as follows:

Consider De Vega annuloplasty when:

• the lesion is predominantly annular
• tethering is limited
• tissue quality is acceptable
• a simpler repair is appropriate

Favor ring/band annuloplasty when:

• annular dilation is substantial
• annular geometry is distorted
• RV remodeling is more advanced
• long-term durability is a major priority

Consider additional repair maneuvers when:

• leaflet restriction or tethering is significant
• commissural fusion or stenosis is present
• leaflet/subvalvular pathology contributes importantly to malcoaptation

In other words, the surgical plan should be mechanism-based rather than formulaic.[1,3,5,7,9] (PubMed)

9. Key Takeaways

• Secondary TR is much more common than primary TR and is usually driven by annular dilation and leaflet tethering from right-heart remodeling.
• Progressive TR worsens venous congestion, RV dysfunction, and systemic output.
• De Vega annuloplasty remains a recognized option, but ring annuloplasty is generally more durable.
• Annuloplasty alone is insufficient when major tethering is present.
• Repair should be performed before irreversible RV failure and severe systemic venous congestion become established.
• Concomitant treatment during left-sided valve surgery is often crucial in preventing late TR progression.[1,4,5,7-10] (PubMed)

References

[1] De Bonis M, Taramasso M, Lapenna E, Alfieri O. Management of tricuspid regurgitation. F1000Prime Rep. 2014;6:58.

[2] Rogers JH, Bolling SF. The Tricuspid Valve: Current Perspective and Evolving Management of Tricuspid Regurgitation. Circulation. 2009;119(20):2718-2725.

[3] Taramasso M, Vanermen H, Maisano F, Guidotti A, La Canna G, Alfieri O. The growing clinical importance of secondary tricuspid regurgitation. J Am Coll Cardiol. 2012;59(8):703-710.

[4] Prihadi EA, Delgado V, Leon MB, Enriquez-Sarano M, Topilsky Y, Bax JJ. Morphologic Types of Tricuspid Regurgitation: Characteristics and Prognostic Implications. JACC Cardiovasc Imaging. 2019;12(3):491-499.

[5] Rodés-Cabau J, Taramasso M, O'Gara PT. Diagnosis and treatment of tricuspid valve disease: current and future perspectives. Lancet. 2016;388(10058):2431-2442.

[6] Mangieri A, Montalto C, Pagnesi M, Jabbour R, Rodés-Cabau J, Moat N, Colombo A, Latib A. Mechanism and Implications of the Tricuspid Regurgitation: From the Pathophysiology to the Current and Future Therapeutic Options. Circ Cardiovasc Interv. 2017;10(7):e005043.

[7] Pozzoli A, Buzzatti N, Vicentini L, De Bonis M, Alfieri O. Results of tricuspid valve surgery for functional tricuspid regurgitation: acute and long-term outcomes and predictors of failure. Minerva Cardioangiol. 2017;65(5):491-499.

[8] Antunes MJ, Rodríguez-Palomares J, Prendergast B, De Bonis M, Rosenhek R, Al-Attar N, Barili F, Casselman F, Folliguet T, Iung B, Lancellotti P, Muneretto C, Obadia J, Pierard L, Suwalski P, Zamorano P. Management of tricuspid valve regurgitation: Position statement of the European Society of Cardiology Working Groups of Cardiovascular Surgery and Valvular Heart Disease. Eur J Cardiothorac Surg. 2017;52(6):1022-1030.

[9] Gatti G, Dell’Angela L, Fiore A, Avtaar Singh SA, Couetil JP, Folliguet T, Sinagra G, Mazzaro E, Nappi F. Basic pathophysiology and options of treatment for surgical management of functional tricuspid regurgitation: a systematic review. J Thorac Dis. 2022;14(12):5208-5224.

[10] Pozzoli A, Buzzatti N, Vicentini L, De Bonis M, Alfieri O. Results of tricuspid valve surgery for functional tricuspid regurgitation: acute and long-term outcomes and predictors of failure. Minerva Cardioangiol. 2017;65(5):491-499.