Tricuspid-valve repair cut deaths and heart-failure admissions in a new trial

A transcatheter repair of a leaking tricuspid valve reduced a combination of death and heart-failure hospitalisation in older patients with severe tricuspid regurgitation, in a randomised trial published in the New England Journal of Medicine on August 30 [s1]. That is a stronger result than the device field had shown before: the landmark earlier trial of a tricuspid clip improved how patients felt but did not move death or hospitalisation [s2].

TRIC-I-HF matters because it is one of the first tricuspid trials to report a benefit on hard clinical events rather than on symptoms alone — and because its funding was not from the device maker.

The condition and the gap

Severe tricuspid regurgitation — a backward leak through the valve between the right atrium and right ventricle — is common in older people with heart failure and is associated with poor quality of life [s2]. Until recently the only options were open surgery, carrying high risk in this frail group, or medical therapy that treats the consequences rather than the leak.

Transcatheter devices, threaded to the heart through a vein, offered a less invasive route. But the first randomised test of one, TRILUMINATE Pivotal, left the central question open. In that trial of 350 patients, tricuspid edge-to-edge repair met its primary endpoint on a win ratio of 1.48 (95% CI, 1.06 to 2.13; P=0.02), but the components tell the story: the quality-of-life score improved by a mean of 12.3 points against 0.6 in the control group, while the rates of death or tricuspid-valve surgery and of heart-failure hospitalisation did not appear to differ between the groups [s2]. The device made people feel better; whether it kept them alive or out of hospital was unproven.

What TRIC-I-HF did

TRIC-I-HF randomly assigned patients with symptomatic severe tricuspid regurgitation and an increased risk of future heart-failure events, in a 2:1 ratio, to transcatheter tricuspid-valve repair plus medical therapy or to medical therapy alone [s1]. A total of 360 patients underwent randomisation — 237 to the repair group and 123 to medical therapy — with a mean age of 80.3 years, and 56.4% were women [s1].

The first primary endpoint was a hierarchical composite of death from any cause, hospitalisation for heart failure, and quality-of-life improvement at one year, assessed by win ratio [s1]. Only if that was significant would a second primary endpoint be tested: a composite of death from any cause or hospitalisation for heart failure through three years [s1].

The results

The win ratio for the first primary endpoint was 2.42 (95% CI, 1.76 to 3.33; P<0.001), favouring repair [s1]. That cleared the threshold to test the harder endpoint.

Through three years, the Kaplan–Meier estimate for freedom from death or heart-failure hospitalisation was 52.4% (95% CI, 43.2 to 63.6) in the repair group and 21.0% (95% CI, 12.7 to 34.6) in the medical-therapy group, a hazard ratio of 0.40 (95% CI, 0.29 to 0.55; P<0.001) [s1]. Major adverse events within 30 days occurred in 14 patients (5.9%) in the repair group [s1].

On its face, that is a large effect — a more than doubling of the proportion of patients free of death or heart-failure admission at three years, from roughly one in five to one in two.

The caveats that bound it

The win ratio is driven partly by quality of life. The first endpoint is a hierarchical measure in which a symptom improvement counts toward a "win" when death and hospitalisation are tied. The three-year mortality-and-hospitalisation endpoint is the harder test, and it was significant — but it was reached only because the first endpoint was, a sequence built into the design [s1].

It was not a blinded comparison of device versus a sham procedure. The control group received medical therapy, not a placebo intervention, so patient-reported outcomes in particular can be shaped by knowing which group one is in.

The population was specific. These were older patients, mean age 80, selected for symptomatic severe regurgitation and an increased risk of future heart-failure events [s1]. The result should not be read across to milder disease or to younger patients.

Who counts as a "repair" responder is device- and centre-dependent. The trial was conducted across specialised German heart centres, and results at high-volume centres are not guaranteed to transfer.

What is different from before

The honest summary is that TRIC-I-HF reports what TRILUMINATE could not: a reduction in a composite of death and heart-failure hospitalisation, not only in symptoms [s1][s2]. The trial was funded by the German Center for Cardiovascular Research and others, rather than by a device manufacturer [s1]. That does not make the result correct, but it removes one common source of bias from the interpretation.

What to watch

Whether the mortality-and-hospitalisation benefit holds in longer follow-up and in trials outside specialised centres; how it compares with tricuspid-valve replacement rather than repair; and whether guideline bodies move tricuspid intervention earlier in the treatment pathway, as the 2026 ESC heart-failure guidelines continue to be revised. TRIC-I-HF is registered as NCT04634266 [s1].

This article describes trial results for informational purposes only. It is not medical advice and not a recommendation about any procedure or device.

Sources

• [s1] Hausleiter J, Stocker TJ, Geisler T, et al; TRIC-I-HF-DZHK24 Investigators. Tricuspid-Valve Intervention in Heart Failure. New England Journal of Medicine, published online 2026-08-30.
• [s2] Sorajja P, Whisenant B, Hamid N, et al. Transcatheter Repair for Patients with Tricuspid Regurgitation (TRILUMINATE Pivotal). New England Journal of Medicine, 2023-03-04.