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CardioNerds (Dr. Apoorva Gangavelli, Dr. Cory Sejo, and Dr. Joseph Kassab), discuss tricuspid regurgitation evaluation and management with Dr. Sunil Mankad.

This episode was produced as part of the CardioNerds Academy curriculum by House Einthoven under the guidance of House Chief, Dr. Apoorva Gangavelli and Academy Program Director, Dr. Gurleen Kaur. A matching review article will be published in US Cardiology Review, the official journal of CardioNerds. This discussion was planned in collaboration with the Mayo Clinic Cardiovascular Board Review Course. 

Audio editing by CardioNerds intern Emma Winakur.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Key Points:

1. Tricuspid regurgitation is common and associated with increased mortality at every stage, regardless of etiology. Outcomes are worse with worsening severity, so accurate grading is critical.
2. Etiology is critical to guide treatment decisions. Etiology includes primary vs secondary (atrial or ventricular) vs CIED-related TR. 3D echocardiography can be very helpful in determining TR etiology, especially in CIED-related TR.
3. Diuresis with the goal of euvolemia is step one. Additionally, underlying contributory conditions (eg. pulmonary HTN, HFrEF, atrial fibrillation) should be addressed, if appropriate, and then TR severity reassessed.
4. The choice between T-TEER and TTVR hinges on anatomy, RV function, pulmonary hypertension, and the ability to tolerate anticoagulation. T-TEER is generally first line in atrial functional TR with appropriate anatomy, in patients with poor RV function who cannot tolerate a sudden increase in RV afterload, or in patients who cannot tolerate the necessary anticoagulation with TTVR. TTVR is preferred with wide coaptation gaps and CIED-related TR.
5. This is a team sport. Multidisciplinary discussions utilizing imaging (TTE/TEE, CT), risk scores (TRI-SCORE or TRIO), patient preference, and prior institutional experience are essential for the effective treatment of severe TR.

Notes:

1. What is the clinical importance of tricuspid regurgitation?
   1. TR is very common with approximately 4% of people over 75 having moderate or greater severity.
   2. TR (even mild) is associated with increased mortality. Those outcomes worsen as the TR severity worsens, and this phenomenon is independent of the mechanism of regurgitation.
      
2. What is unique about the tricuspid valve compared to the other cardiac valves?
   1. It is at an anterior location which allows it to be imaged well with transthoracic echocardiography
   2. It is the largest valve and composed generally of 3 leaflets (but very often can have 4+ leaflets).
   3. Importantly, the RV is compliant and changes size and shape readily based on loading conditions. The TV annulus similarly changes size and shape based on hemodynamic conditions such as preload.
      
3. What is a good framework for approaching the causes of tricuspid regurgitation?
   1. Determine the presence and define the severity of TR.
   2. Using TTE, we want to measure the right atrial size, the RV size, and any other concomitant valvular lesions. 
   3. Use TTE (2D and 3D) to characterize leaflet anatomy and characteristics.
   4. Subtypes of TR mechanisms (many times etiology is mixed).
      1. Primary: primary leaflet abnormality, occurs in ~10% of cases. Look for prolapse, flail, endocarditis, etc.
      2. Secondary/functional: leaflets normal but surrounding structures are abnormal.
         1. Atrial: RA and tricuspid annular dilation but normal RV size/shape, and can be related to arrhythmias like atrial fibrillation.
         2. Ventricular: RV dilated and/or dysfunctional with leaflet tethering. Can be related to pulmonary hypertension or primary RV disease.
      3. Cardiac implantable electronic device (CIED): Related to device (usually pacemakers or ICD) interaction with TV leaflets.
         1. Includes perforation, entanglement in subvalvular apparatus, impingement, etc.
         2. 3D TTE particularly helpful to evaluate
            
4. How do we grade TR severity?
   1. It is very important to grade the severity of TR, and this is generally done with echocardiography.
   2. There are both quantitative and qualitative methods which use Doppler and various equations to estimate TR severity.
   3. Current recommendations have expanded TR severity beyond mild/moderate/severe to include “massive” and “torrential” categories.
   4. The most important parameters measured/calculated are vena contracta width, regurgitant volume, regurgitant fraction, and effective regurgitant orifice area. Helpful qualitative metrics include hepatic venous flow reversal.
      
5. When should additional studies beyond transthoracic echocardiography, such as transesophageal echocardiography (TEE), cardiac computed tomography (CT), and cardiac magnetic resonance imaging (MRI) be pursued?
   1. TEE is particularly helpful if TTE views are poor. Since TEE is used during transcatheter intervention, a pre-procedure TEE to define anatomy, determine procedure candidacy, and plan for the procedure is critical. 
   2. CT is also helpful for procedure planning and has particular strengths in defining annulus size and geometry. A CT is required prior to transcatheter tricuspid valve replacement (TTVR).
   3. MRI is helpful for measuring RV volumes and function, but is not generally used to assess TR severity. 
      
6. What is the approach to the treatment for severe tricuspid regurgitation?
   1. The first step is to try to determine the etiology. For secondary TR, treating the underlying condition is indicated. For example, pulmonary vasodilators for pulmonary HTN or guideline therapy for heart failure with reduced ejection fraction.
   2. Diuretics are the mainstay for treatment, with the goal to obtain euvolemia. This may require inpatient admission to optimize volume status and medication regimen.
   3. Once reversible etiologies are addressed, if the patient is still symptomatic from TR, additional therapies can be considered.
      
7. What is the role of right heart catheterizations (RHC) in patients with severe TR?
   1. RHC is very helpful for many reasons. We use it in TR to help determine volume status, cardiac output, and RV function. Additionally, identifying and characterizing pulmonary hypertension (with pulmonary artery pressures and calculating pulmonary vascular resistance) is an important factor when choosing future therapies. 
      
8. With severe tricuspid regurgitation, when should we refer for intervention (either with surgery or transcatheter repair or replacement)?
   1. Once reversible etiologies are addressed and euvolemia has been achieved, if the patient is still symptomatic from TR despite aggressive medical optimization, additional therapies can be considered.
   2. Once euvolemic, a repeat TTE should be ordered to reassess the severity of the TR.
   3. Use calculators (for example, either the TRI-SCORE or TRIO score) to predict operative mortality for isolated TR surgery.
      
9. What are our transcatheter treatment options in severe tricuspid regurgitation, and how do we choose between them?
   1. The primary approved transcatheter treatment options for severe TR include transcatheter tricuspid edge-to-edge repair (T-TEER) and transcatheter tricuspid valve replacement (TTVR), of which the Edwards EVOQUE valve is the only one currently approved by the FDA. There are other TTVR device under investigation.
   2. These decisions should be made with a multi-disciplinary team including representation from cardiac imaging, interventional cardiology, and cardiothoracic surgery.
   3. Factors that go into the decision between T-TEER and TTVR include anatomy (annulus width, coaptation gap, leaflet length), RV reserve, pulmonary hypertension presence, ability to tolerate anticoagulation, patient preference, and institutional experience. 
   4. T-TEER is generally the first line with atrial functional and suitable anatomy. It is successful at reducing TR but does not generally eliminate it. 
   5. TTVR with EVOQUE is preferred in certain anatomic considerations like a large coaptation gap or when there is CIED-related TR (as this was excluded in T-TEER trials).
      1. Patients must be suitable for anticoagulation to receive TTVR as there is risk of leaflet thrombosis without it.
      2. If moderate/severe pulmonary hypertension is present, or there is poor RV function, TTVR may be avoided as the sudden elimination of TR causes a sudden increase in RV afterload which may not be tolerated.
         
10. What is the role in advanced metrics for evaluating RV function?
    1. Advanced metrics like RV/PA coupling are under investigation but have not made it into the guidelines. The clinical utility is not yet known. 
    2. Assessing the RV function is important as stated above. Dr. Mankad prefers using 3D TTE to calculate an RVEF, or tracking RV longitudinal free wall strain.
       
11. If you do encounter CIED-related TR, how do you treat it?
    1. Evaluate with TTE or TEE. 3D is very helpful to identify relative anatomy and leaflet-device interactions.
    2. There is no clear consensus about treatment if CIED-related TR is the primary mechanism of severe TR. If recently implanted, repositioning may be a valid option, but requires discussions with multiple teams including electrophysiology, advanced cardiac imaging, CT surgery, and interventional cardiology.

References

1. O’Gara PT, Lindenfeld J, Hahn RT, et al. 10 Issues for the Clinician in Tricuspid Regurgitation Evaluation and Management: 2025 ACC Expert Consensus Decision Pathway. J Am Coll Cardiol. 2025;S0735-1097(25)07047-0.
2. O’Gara PT, Little SH, Badhwar V, et al. Operator and Institutional Recommendations and Requirements for Tricuspid Interventions: 2026 ACC/AHA/ASE/HRS/STS Expert Consensus Systems of Care Document. J Am Coll Cardiol. 2026;S0735-1097(26)05481-1.
3. Hahn RT. Tricuspid Regurgitation. N Engl J Med. 2023;388(20):1876-1891.
4. Davidson LJ, Tang GHL, Ho EC, et al. The Tricuspid Valve: A Review of Pathology, Imaging, and Current Treatment Options: A Scientific Statement From the American Heart Association. Circulation. 2024;149(22):e1223-e1238.