Key takeaways 

  • Severe tricuspid regurgitation is a heart valve disorder associated with debilitating symptoms and increased risk of death.  
  • The TRIC-I-HF trial studied transcatheter valve repair plus medical therapy vs. medical therapy alone in patients with severe tricuspid regurgitation at high risk of heart failure events. 
  • Transcatheter tricuspid valve repair resulted in improvement in heart failure hospitalisation and all-cause mortality. 
  • These results may be used to inform future guidelines. 

Munich, Germany – 30 August 2026: Transcatheter tricuspid valve repair significantly improved clinical outcomes in high-risk patients with severe tricuspid regurgitation, according to results presented in a Hot Line session today at ESC Congress 2026[1] and published simultaneously in the New England Journal of Medicine. 

Tricuspid regurgitation is a heart valve disorder where the tricuspid valve leaks, leading to enlargement of the right side of the heart. Severe tricuspid regurgitation is associated with symptoms of heart failure including fatigue, shortness of breath and fluid overload, and is linked to increased mortality. Medical options for treating severe tricuspid regurgitation are limited. Transcatheter tricuspid interventions have evolved as important treatment strategies and alternatives to surgery. 

The TRIC-I-HF trial, led by Principal Investigators, Professor Jörg Hausleiter and Professor Thomas Stocker of Ludwig-Maximilians-University, Munich, Germany, was designed to investigate whether a strategy of transcatheter tricuspid valve repair in addition to medical therapy improves clinical outcomes in patients with symptomatic and severe tricuspid regurgitation when compared with medical therapy alone. 

"Previous studies have shown that transcatheter tricuspid valve interventions can effectively reduce tricuspid regurgitation and improve patient-reported outcomes, including quality of life," said Professor Thomas Stocker. “However, their effect on heart failure hospitalisations and mortality remained unclear. In TRIC-I-HF, we enrolled patients in the advanced stages of the disease with higher risk for future heart failure events compared with previous randomised controlled trials.” 

The TRIC-I-HF trial was conducted in 29 high-volume heart valve centres in Germany. Increased risk for future heart failure events was defined by heart failure hospitalisation in the prior year, the presence of cardiorenal syndrome or evidence of cardiohepatic syndrome. A total of 360 patients were randomised: 237 to transcatheter tricuspid valve repair plus medical therapy and 123 to medical therapy alone. Their mean age was 80.3 years and 56.4% were women. Of the patients undergoing intervention, 98% were treated with tricuspid transcatheter edge-to-edge repair (T-TEER). 

The researchers demonstrated that both primary endpoints were met with tricuspid valve repair.  

The first primary endpoint of all-cause mortality, heart failure hospitalisation and failure to achieve quality-of-life improvement at one year significantly favoured tricuspid valve repair over medical therapy alone (win ratio 2.42; 95% confidence interval [CI] 1.76 to 3.33; p<0.001). 

Tricuspid repair also resulted in significantly greater freedom from the co-primary endpoint of all-cause mortality or heart failure hospitalisation at three years than medical therapy alone (52.4% vs. 21.0%; hazard ratio 0.40; 95% CI 0.29 to 0.55; p<0.001). This benefit was driven by reductions in both all-cause mortality and heart failure hospitalisation. 

“Among these high-risk patients, transcatheter tricuspid valve repair on top of medical therapy resulted not only in quality-of-life improvements but also in meaningful and sustained reductions in hard clinical outcomes, which has not been demonstrated before with the intervention. Early and pronounced separation of the event curves in these patients with advanced heart failure underscores the immediate benefit of tricuspid valve repair when added to optimised medical therapy, establishing the intervention as an effective disease-modifying therapy,” concluded Professor Jörg Hausleiter. 

ENDS 

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