Tricuspid Regurgitation: What You Need to Understand

2. What It Is

Tricuspid regurgitation (TR) is incompetence of the tricuspid valve, allowing backward systolic flow from the right ventricle into the right atrium. The result: volume overload of the right heart, raised RA and central venous pressure, systemic venous congestion, and progressive right heart failure.

TR is extremely common: any degree of TR is present by echocardiography in 65-85% of the adult population 5 / Solid 69208-9). Trace-to-mild TR is a physiological finding. Moderate TR begins to carry prognostic significance. Severe TR is associated with substantially increased mortality, even after adjustment for other comorbidities 5 / Solid .

Grading

TR severity by echocardiography:

• Trace/mild: jet area below 5 cm2, vena contracta below 3 mm, regurgitant fraction below 30%
• Moderate: jet area 5-10 cm2, vena contracta 3-6.9 mm
• Severe: vena contracta above 7 mm, EROA above 0.40 cm2, regurgitant volume above 45 mL
• Massive and torrential TR (now recognized as distinct classes in recent EACVI guidelines)

Functional vs Primary TR

Functional TR (secondary TR): The leaflets are structurally normal but the tricuspid annulus is dilated from RV enlargement, pulling the leaflets apart and preventing coaptation. This is the most common form (approximately 80-90% of severe TR cases). Causes: any condition that dilates the RV or raises RA pressure: AF (the most common, as chronic AF dilates both atria and eventually the RV annulus), pulmonary hypertension, left-sided heart disease (raised left heart pressures transmitted to the right heart), LV systolic dysfunction with pulmonary hypertension.

Primary TR: The leaflets or subvalvular apparatus are intrinsically abnormal:

• Ebstein anomaly (congenital downward displacement of tricuspid leaflets into the RV)
• Rheumatic TR (usually combined with rheumatic mitral and aortic disease)
• Carcinoid syndrome (serotonin-mediated valve leaflet thickening and immobility; right-sided valve predominance)
• Infective endocarditis (particularly in IV drug use: right-sided vegetations on the tricuspid valve; see VALV-006)
• Radiation-induced valve disease
• Iatrogenic TR from pacemaker or ICD leads crossing the tricuspid valve and impairing leaflet coaptation

Lead-related TR: Implanted pacemaker or ICD right ventricular leads can produce TR by mechanical impingement on the tricuspid valve leaflets. Prevalence of significant TR after CIED implant ranges from 10-30% in various series 4 / Promising .

3. The Mechanism

The RV failure cascade

The RV is a thin-walled, crescent-shaped structure adapted for volume work at low pressure. It tolerates volume overload (from TR) better than pressure overload (from pulmonary hypertension). But chronic severe TR creates a volume overload that the RV compensates through dilation. The dilated RV:

1. Further dilates the tricuspid annulus, worsening TR (a self-reinforcing cycle)
2. Pushes the interventricular septum toward the LV (septal shift), impairing LV filling
3. Increases pericardial constraint on the LV
4. Reduces effective forward RV stroke volume, reducing pulmonary blood flow and LV preload

As RV function deteriorates from the combined volume overload and geometric changes, forward output falls. The RA pressure remains chronically raised, maintaining systemic venous congestion. The liver becomes engorged (hepatomegaly, congestive hepatopathy). Ascites develops. Peripheral edema becomes refractory.

Cardiorenal syndrome type 2 from TR: chronically raised central venous pressure reduces renal venous drainage, increasing intrarenal interstitial pressure and impairing glomerular filtration. This “venous congestion-mediated” renal dysfunction is a recognized mechanism of CRS in severe TR. Diuretics improve the renal perfusion but can paradoxically worsen renal function if preload is over-reduced in a preload-dependent RV.

AF as driver and consequence

In functional TR from AF: AF dilates the atria; atrial dilation dilates the tricuspid annulus; annular dilation causes TR; TR further enlarges the RA; more AF. This cycle can progress from mild to severe TR over years of permanent AF. The RV dilates more slowly. The clinical picture arrives gradually: “stable” annual visits where each exam shows a slightly larger liver, slightly worse peripheral edema, and a slightly higher JVP, all attributed to the known diagnosis of “heart failure.”

4. How We Diagnose

The diagnosis of TR should be suspected in any patient with systemic venous congestion (raised JVP, hepatomegaly, ascites, pitting edema) that is disproportionate to the degree of left heart disease.

Auscultation: Holosystolic murmur at the left lower sternal border, increasing with inspiration (Carvallo’s sign: the distinguishing feature from MR, which does not increase with inspiration because inspiration increases right-sided filling, augmenting the RV-to-RA gradient). Severe TR may produce a pulsatile liver and pulsatile jugular veins visible to the eye.

Echocardiography: The primary diagnostic and grading tool. Requires dedicated TR views (RV-focused views, hepatic vein Doppler for systolic reversal, IVC dilation above 2.1 cm). Hepatic vein systolic flow reversal is a specific sign of severe TR (the raised RA pressure is transmitted back to the hepatic veins during RV systole). IVC dilation above 2.1 cm with less than 50% inspiratory collapse indicates raised RA pressure. Severe TR with dilated IVC, hepatic vein reversal, and massive RA and RV dilation is a picture of established right heart failure.

Right heart catheterization: Provides definitive hemodynamic assessment: RA pressure, RV pressure, PA pressure, cardiac output, PCWP (to assess left-sided contribution to the right heart problem). High RA pressure with low PA pressure (normal or low pulmonary vascular resistance) indicates volume-driven RV failure. High RA pressure with high PA pressure indicates pulmonary hypertension-driven RV failure.

5. The Evidence

TR’s prognostic significance: Topilsky series (2021)

Topilsky Y, et al., JACC 2021 (10.1016/j.jacc.2021.01.057): In a series of 5,215 echocardiographic patients with functional TR, moderate-to-severe TR was associated with significantly higher 5-year mortality compared to trace-mild TR, independent of age, sex, LV function, and other comorbidities. The hazard ratio for death was 1.64 (95% CI 1.47-1.83) for moderate TR and 2.66 (95% CI 2.29-3.09) for severe TR 5 / Solid . This quantified what was clinically suspected but historically ignored.

TRILUMINATE Pivotal: TriClip for severe TR (2023)

The TRILUMINATE Pivotal trial enrolled 350 patients with severe or greater TR who were not suitable for surgery and randomized them to transcatheter tricuspid edge-to-edge repair (TEER) with TriClip (Abbott) versus medical therapy 5 / Solid .

Results at one year: TriClip reduced TR to moderate or less in 87% of patients at 30 days (persistent at 1 year), significantly improved quality of life (KCCQ +12.3 points vs +0.6 for control, p < 0.001), and improved functional capacity. The primary endpoint (hierarchical composite of death, tricuspid valve surgery, hospitalization, KCCQ improvement, and NYHA improvement) strongly favored TriClip over medical therapy.

What TriClip did NOT definitively show in TRILUMINATE Pivotal: a mortality benefit. The trial was not powered for mortality. Survival curves at one year were not significantly different. The benefit was in quality of life, symptoms, and functional class.

The FDA approved the TriClip for symptomatic TR in August 2023 as the first transcatheter tricuspid repair device approved in the United States. This was a landmark moment: for decades, tricuspid intervention in the United States was limited to surgical repair at the time of other heart surgery. Now there is a minimally invasive catheter option.

The TRISCEND II trial (transcatheter tricuspid valve replacement with the EVOQUE device) showed that tricuspid valve replacement via catheter produced more complete TR elimination than edge-to-edge repair 4 / Promising . Approval of EVOQUE pending regulatory review at time of writing.

Dreyfus principle: concomitant tricuspid annuloplasty

Dreyfus GI, et al., JACC 2005 (10.1016/j.jacc.2004.09.054): In patients undergoing mitral valve surgery, prophylactic tricuspid annuloplasty in patients with annular dilation (above 40 mm) regardless of TR severity significantly reduced post-operative late TR development 5 / Solid . This established the principle that the tricuspid annulus, once dilated, does not shrink back even if the mitral disease driving it is corrected. Concomitant tricuspid repair at the time of left heart surgery is now recommended when annular dilation is present.

The 2021 ACC/AHA valve guidelines recommend tricuspid repair at the time of left heart surgery when tricuspid annulus diameter is above 40 mm (or above 21 mm/m2 BSA) 5 / Solid .

6. The Patient Experience

The patient with isolated severe functional TR is one of the most under-served patients in structural heart disease. For years, the absence of effective catheter-based therapy meant TR was treated with diuretics and described as “managed.” The diuretics removed some of the fluid but never addressed the mechanism. The liver continued to congest. The ascites returned. The RV continued to enlarge. Repeated hospitalizations for “refractory heart failure” consumed healthcare resources without addressing the structural problem.

The newly approved TriClip changes this. A patient like the retired firefighter from Rockford, with severe functional TR and RV dilation, now has a catheter-based option available at structural heart programs. The procedure: femoral vein access, transseptal to the RA (or direct IVC approach to the RA), navigation to the tricuspid valve, and deployment of one or two TriClip devices to the central coaptation zone of the tricuspid valve. Hospital stay 1-2 days.

The TRILUMINATE QOL data showed that the symptom improvement was rapid and clinically meaningful. A 12-point improvement in KCCQ at one year is larger than seen with most heart failure drug trials.

The failure cascade that the firefighter was on: progressive RV dilation, increasing diuretic requirement, progressive hepatic congestion, and potential RV failure within 3-5 years. TriClip interrupts that cascade. Whether it also improves survival (which TRILUMINATE was not powered to show) is being tested in larger ongoing trials.

For patients with lead-related TR who still have RA or RV indications for a device, lead revision or addition of a separate device with leadless pacing (Micra, Medtronic, or ENABLE, Boston Scientific) can remove the offending lead from the tricuspid zone. This is a complex decision requiring electrophysiology and structural heart collaboration.

7. Decisions and Trade-Offs

Who is a TriClip candidate?

The TRILUMINATE Pivotal eligibility requirements inform current practice:

• Severe or greater TR (EROA above 0.40 cm2 or vena contracta above 7 mm)
• Symptomatic (NYHA Class II or above)
• Not suitable for tricuspid surgery or not amenable to concomitant surgery
• TR anatomy amenable to clip deployment (adequate coaptation gap, sufficient leaflet tissue to grasp)
• Absence of RV failure that is too advanced for benefit (EF below 20%, RA pressure above 30 mmHg without ability to improve with TR reduction)

The challenge: patients with very advanced RV failure (RVEF below 20%) are unlikely to recover even with TR reduction. TRILUMINATE enrolled patients earlier in the disease process. Waiting too long (until the firefighter has a palpable liver at 4 cm and ascites) reduces the likelihood of meaningful benefit.

Surgery vs transcatheter approach

Tricuspid surgery (annuloplasty, repair, or replacement) carries higher operative risk than left-sided surgery because right heart failure surgery in a compromised RV carries high perioperative mortality. Isolated tricuspid surgery is associated with 5-10% in-hospital mortality at most centers 4 / Promising . High-volume tricuspid surgery centers have reported better outcomes.

For the patient who needs isolated tricuspid intervention (not at the time of other surgery), the options are:

1. TriClip: lower procedural risk, partial TR reduction, established QOL benefit
2. Surgery: more complete TR correction but higher risk, particularly in RV-compromised patients
3. Tricuspid valve replacement via catheter (EVOQUE or TRISCEND-type devices): pending broader approval

The selection between TriClip and surgery requires a multidisciplinary structural heart team assessment, an experienced cardiac surgeon’s opinion on operative risk, and shared decision-making with the patient.

Diuretics and the preload paradox

Severe TR patients are preload-dependent: the dilated, volume-overloaded RV needs adequate filling to generate sufficient forward flow. Aggressive diuresis that removes too much volume can reduce RV preload below the minimum required for adequate pulmonary blood flow, causing low output. The clinical target: eliminate obvious congestion signs (JVP normalization, hepatomegaly regression, resolution of ascites) while maintaining adequate cardiac output. Daily weight, creatinine monitoring, and clinical reassessment guide the titration.

Atrial fibrillation in severe TR

AF and TR are frequent companions. AF causes loss of the atrial contribution to RV filling, worsens functional TR by increasing RA pressure, and accelerates annular dilation. The clinical sequence often runs: paroxysmal AF → LA and RA pressure elevation → progressive tricuspid annular dilation → moderate TR → AF becomes persistent → TR worsens to severe.

Rate control in AF with severe TR: target resting heart rate below 80 bpm. Aggressive rate control reduces TR duration per beat and limits RV volume loading. Rhythm control in AF with severe TR: cardioversion may temporarily reduce TR by lowering RA pressure. Durability of sinus rhythm without addressing the TR or RA dilation is low. For patients undergoing TriClip, concurrent AF ablation is sometimes performed in the same sitting at experienced centers; outcomes data are emerging 4 / Promising .

Anticoagulation in TR with AF follows standard AF stroke risk guidelines. The presence of severe TR does not alter the anticoagulation indication.

8. The SDE Synthesis

Tricuspid regurgitation is the clearest example of a condition where “stable” is a clinical illusion. The firefighter from Rockford was “stable” on paper for years while his tricuspid annulus dilated, his RV enlarged, and his right heart failure progressed to the point where his liver was palpable and his legs had not been normal in two years.

The SDE Audit and Cohort approach to TR is to take it seriously from the first detection of moderate or greater severity. A patient with moderate-to-severe TR and any degree of RV dilation or raised RA pressure on echocardiography should be tracked with annual imaging, not put in the “stable heart failure” monitoring category and seen annually.

For patients with severe TR who are TRILUMINATE-eligible, the SDE Executive tier facilitates structural heart program referral. In Illinois, TriClip is available at Northwestern Memorial Hospital (Chicago), University of Chicago Medical Center, Rush University Medical Center (Chicago), and NorthShore University HealthSystem (Evanston). Carle Foundation Hospital (Urbana) provides regional coordination for downstate Illinois patients.

The TRISCEND II data on transcatheter valve replacement is promising for patients whose anatomy is not suitable for clip repair. The rapidly evolving tricuspid intervention landscape means that a patient who was told “nothing can be done about your tricuspid valve” two years ago may now have options. The SDE platform stays current with this landscape.

The firefighter from Rockford has an appointment at Rush University’s Structural Heart Program next month. He is a TriClip candidate. The liver may stop growing. The legs may normalize. His quality of life may return to what it was four years ago, before the TR became severe.

That appointment was delayed three years because the disease was called “stable” by providers who were not looking at the trend.