Tricuspid Regurgitation: Six Cath-Lab Decision Rules

For most of my working life, severe tricuspid regurgitation was a line near the bottom of the echo report that nobody acted on. We diuresed, we shrugged, and we called it the forgotten valve. That era has ended. We now have three randomised trials, a Class IIa Level A recommendation in the 2025 ESC/EACTS valvular heart disease guideline, and a catalogue that lets me clip or replace.

Here is the part that gets lost between the podium and the cath lab. The randomised evidence is real and it is good evidence, but what it has bought us is symptom improvement and TR grade reduction. It has not bought a demonstrated mortality benefit. TRILUMINATE Pivotal, Tri.Fr and TRISCEND II all point the same way: patients feel better, valves leak less, and none has shown that we make anyone live longer.

That sentence should change who you treat. If the currency is symptoms, then the patient with symptoms attributable to the valve and a right ventricle capable of responding is the patient who profits. The patient dying of an exhausted right heart, precapillary pulmonary hypertension or multi-organ congestion will not be rescued by a technically perfect result. These are the six decision points I apply to tricuspid regurgitation referrals, in order.

Rule one: prove the tricuspid regurgitation is what is making this patient ill

Severity is not the indication. Attribution is. Plenty of patients arrive with torrential tricuspid regurgitation and breathlessness driven by atrial fibrillation burden, deconditioning or unoptimised left-sided disease. Treating the valve in those patients produces a beautiful echo and a disappointed patient.

What I want from the study before I say yes

• Grade beyond severe. Report tricuspid regurgitation on the full scale, including massive and torrential. In bRIGHT (post-approval registry, JACC 2024;84:607–616), 88% of 511 patients at 26 sites were massive or torrential; at one year 81% were moderate or less and KCCQ improved by 19 points.
• Mechanism. Atrial functional, ventricular functional, lead-related or primary. Different diseases wearing the same colour on Doppler.
• Coherence. Ascites, a pulsatile liver, rising bilirubin and escalating loop diuretic in a patient whose left side is quiet is a coherent story. Isolated exertional breathlessness with a normal venous pressure is not.

If attribution is uncertain I do not book the case; I re-review after a fortnight of supervised decongestion.

Rule two: read the right ventricle before you read the valve

The valve is easy. The right ventricle is the whole game. Severe tricuspid regurgitation is also a low-pressure escape route, and when you close it you hand the right ventricle an afterload it has not carried for years.

RV–PA coupling is where I spend my time. TAPSE against estimated PASP, interrogated properly rather than lifted from an automated table, predicts trajectory better than any measure of tricuspid regurgitation severity. I look at basal RV dimension, longitudinal function, septal behaviour, and whether the ventricle has gone from dilated-and-contracting to dilated-and-passive. Two of the eight TRI-SCORE variables — LVEF below 60% and moderate or severe RV dysfunction — are ventricular, not valvular.

When the echo is equivocal, the patient gets a right heart catheter before the Heart Team meeting, not after. For colleagues who want the physiology laid out properly, I keep the relevant material in the cardiology learning center on this site.

Rule three: the tricuspid regurgitation I decline to treat

This is the rule that earns its keep, and the one enthusiastic units skip. The 2025 ESC/EACTS guideline gives transcatheter tricuspid intervention Class IIa, Level A for symptomatic high-risk patients on optimal medical therapy — explicitly conditional on the absence of severe RV dysfunction and precapillary pulmonary hypertension. That clause is not decorative. It is the boundary of the evidence.

1. Severe RV dysfunction. A ventricle already failing under a permissive load will not thank you for removing the pop-off; you convert a chronic problem into an acute one.
2. Precapillary pulmonary hypertension. Here the tricuspid regurgitation is downstream of the real disease. Treat the valve and you have treated the shadow.
3. The TRI-SCORE futility band. The guideline endorses TRI-SCORE for futility assessment, and I use it that way.

How I use TRI-SCORE at the table

TRI-SCORE (Eur Heart J 2022;43:654–662) was derived in 466 patients across 12 French centres. Eight variables, maximum 12 points: age ≥70, NYHA III–IV, right-sided heart failure signs, daily furosemide ≥125 mg, GFR below 30 mL/min, elevated total bilirubin, LVEF below 60%, and moderate or severe RV dysfunction. In-hospital or post-operative mortality runs around 1% in the 0–3 band, 14–18% at 4–5, 25–32% at 6–7, and 33–60% at ≥8. Bias-corrected AUROC was 0.753 against 0.629 for EuroSCORE II.

I do not use it as a surgical calculator. I use the top band as a warning light. A patient at ≥8 — high furosemide, bad kidneys, rising bilirubin, poor right ventricle — usually has organ failure that has outrun the valve. That patient needs palliative-intent decongestion and an honest conversation, not a device.

Rule four: match the device to the anatomy and to the pacemaker you will accept

Once I have committed to treating the tricuspid regurgitation, the choice between edge-to-edge repair and replacement is largely anatomical: coaptation gap, leaflet tethering, lead position, annular dimensions. But there is a second axis operators under-weight, which is conduction cost. T-TEER in TRILUMINATE Pivotal carried a new permanent pacemaker rate of 5.5%. TTVR in TRISCEND II carried a new pacemaker or CIED rate of 24.7%, with severe bleeding 10.4% and cardiovascular death 3.1% at 30 days. Replacement buys a far more complete result — mild-or-less tricuspid regurgitation in 95.3% versus 2.3% at 30 days — and you pay for it in conduction and bleeding.

Rule five: optimise first, and let the Heart Team own the decision

The 2025 ESC/EACTS guideline puts Heart Team evaluation at Class I, Level C. I treat that literally: nobody goes forward on one operator’s enthusiasm, and the surgical voice matters even when the answer is transcatheter.

Remember how young this field is. The 2020 ACC/AHA guideline still frames tricuspid regurgitation surgically: its only Class I surgical recommendation is tricuspid surgery at the time of left-sided valve surgery in severe disease, with Class IIa for severe primary disease with right heart failure. It predates the randomised transcatheter era entirely. If you are teaching this, the summaries in the Cardiology Books learning center and the case-based modules on structural and interventional courses are where I send trainees.

Optimal medical therapy is a precondition, not a formality. Untitrated loop diuretic, missing mineralocorticoid antagonist, uncontrolled atrial fibrillation — that is not a candidate, that is an unfinished referral.

Rule six: name the benefit you are actually buying

TRILUMINATE Pivotal randomised 572 patients, mean age 78.1, 58.9% female. The one-year hierarchical composite was positive but carried by KCCQ improvement alone, +12.3 points, not by death and not by heart-failure hospitalisation. Stroke was 1.9% versus 2.5%. Two-year data (Circulation 2025, ACC.25) are more encouraging on events: heart-failure hospitalisation 0.19 versus 0.26 per patient-year, joint frailty model HR 0.72, p=0.02. Moderate-or-less tricuspid regurgitation at two years was 84% with device against 21% of controls who remained on medical therapy. You will see 63% quoted for that control arm; that figure includes the 142 of 241 eligible controls who crossed over after year one, and is not a fair comparator.

TRISCEND II gave a win ratio of 2.02 and near-total elimination of the tricuspid regurgitation, and at two years TR control and symptom benefit held — with no all-cause mortality difference in the primary comparison. The three-year figures everyone quotes (79% moderate or less, NYHA III/IV falling from 76% to 19%, heart-failure hospitalisation 0.56 to 0.14 per patient-year, mortality 27%) come from the 98-patient single-arm TRILUMINATE study in JACC Cardiovascular Interventions 2024, not from the randomised trial. Single-arm data with 27% mortality and no control tell you about trajectory, not attribution.

What I tell the patient

Roughly these words. Your tricuspid valve leaks badly, and that leak is why your legs swell, your abdomen fills and you cannot walk to the gate. I can put a device in through a vein in your groin and make the tricuspid regurgitation much smaller. In the trials most people felt better and needed hospital less often. What the trials have not shown is that this makes people live longer, and I will not tell you it does. If your right heart is too weak, or your lung pressures are the real problem, the procedure would put you through something without the benefit — and I will say so.

Patients handle that conversation well. Colleagues handle it worse, because it removes the comfort of feeling heroic.

None of this argues against treating tricuspid regurgitation. It argues for treating it deliberately. The randomised era has given us devices that work, deployment success above 97%, and thirty-day event rates unthinkable a decade ago. What it has not given us is a survival signal, and until it does the honest framing of transcatheter tricuspid regurgitation therapy is superb symptom surgery performed through a vein. Select for a right ventricle that can respond, decline where TRI-SCORE and precapillary physiology say the disease has won, and be candid at consent about what tricuspid regurgitation treatment is proven to deliver today. The mortality question is answerable — it needs longer follow-up, trials without crossover contamination, and probably earlier intervention before the right ventricle is spent — and I expect the next five years of tricuspid regurgitation data to tell us whether treating sooner finally moves that endpoint.

Written and clinically reviewed by Dr A M Thirugnanam, MD, MSICP, FSCAI, Ph.D., Senior Interventional Cardiologist. Last reviewed 6 August 2026. This article is for medical education and does not replace individual clinical judgement or local protocols.

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