# Tricuspid regurgitation: etiology, prevalence, and prognosis

Marianna Adamo, Mauro Massussi, Gianluigi Savarese, Erwan Donal, Fabien Praz, Francesco Maisano

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Marianna Adamo, Mauro Massussi, Gianluigi Savarese, Erwan Donal, Fabien Praz, et al. Tricuspid regurgitation: etiology, prevalence, and prognosis. European Heart Journal Supplements, 2025, 10.1093/eurheartjsupp/suaf097. hal-05449108

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# Tricuspid regurgitation: etiology, prevalence, and prognosis

Marianna Adamo¹,²*, Mauro Massussi²*, Gianluigi Savarese³, Erwan Donal⁴, Fabien Praz⁵ and
Francesco Maisano⁶

¹ Department of Medical and Surgical Specialties, Radiological Sciences, and Public Health, University of Brescia, Brescia, Italy.

² Cardiac Catheterization Laboratory and Cardiology, ASST Spedali Civili di Brescia, Brescia, Italy

³ Division of Cardiology, Department of Medicine, Karolinska Institute; and Heart and Vascular and Neuro Theme, Karolinska University Hospital, Stockholm, Sweden.

⁴ CHU Rennes, Inserm, LTSI—UMR 1099, University of Rennes, 2 Rue Henri le Guilloux, Rennes F-35000, France

⁵ Inselspital Universitätsspital Bern, Bern, Switzerland

⁶ School of Medicine, Vita-Salute San Raffaele University, Milan, Italy; Department of Cardiac Surgery, IRCCS San Raffaele Hospital, Vita-Salute San Raffaele Scientific Institute, Milan, Italy.

* These authors contributed equally to this paper and are joint first authors

**Correspondence:** Marianna Adamo, MD, PhD

Cardiac Catheterization Laboratory and Cardiology, ASST Spedali Civili di Brescia; Department of Medical and Surgical Specialties, Radiological Sciences, and Public Health, University of Brescia, Brescia, Italy. Piazzale Spedali Civili, 1 – 25123 – Brescia (Italy)

E-mail address: mariannaadamo@hotmail.com

**Disclosures:**

M.A. received speaker honoraria from Abbott Vascular and Edwards Lifesciences. G.S. reported grants and personal fees from CSL Vifor, Boehringer Ingelheim, AstraZeneca, Servier, Novartis, Cytokinetics, Pharmacosmos, Medtronic, Bayer, and personal fees from Roche, Abbott, Edwards Lifescience, TEVA, Menarini, INTAS, GETZ, Laboratori Guidotti, and grants from Boston Scientific, Merck, all outside the submitted work. E.D. reported receiving nonfinancial support
1 from GE Healthcare, receiving grants from Abbott Structural Heart, and receiving personal fees
2 from Pfizer and Alnylam.

3 F.P. received travel expenses from Edwards Lifesciences, Abbott Vascular, Medira, Polares
4 Medical, and Siemens Heathineers. F.M. received grant and/or research institutional support from
5 Abbott, Medtronic, Edwards Lifesciences, Biotronik, Boston Scientific Corporation, NVT, and
6 Terumo; received consulting fees, honoraria personal, and institutional support from Abbott,
7 Medtronic, Edwards Lifesciences, Xeltis, CardioValve, Occlufit, Simulands, and Mtex; and
8 received royalty income/intellectual property rights from Edwards Lifesciences Shareholder
9 (including share options) of CardioGard, CardioValve, Magenta, SwissVortex, Transseptal
10 solutions, 4Tech, and Perifect. No other disclosures were reported.

11

12

13 Abstract

14 Tricuspid regurgitation (TR) is a common yet often overlooked valvular disorder that carries a
15 substantial impact on morbidity and mortality. It is increasingly recognized as a heterogeneous
16 entity with different phenotypes identified (primary, atrial secondary, ventricular secondary, CIED-
17 related). Contemporary population studies and disease-specific registries reveal that secondary TR
18 is highly prevalent in elderly patients, those with heart failure (HF) of any phenotype, and in
19 candidates for transcatheter aortic or mitral interventions. Prognosis varies widely according to
20 etiology, with atrial secondary TR consistently associated with better survival than ventricular
21 secondary TR. Across diverse settings, TR severity is an independent predictor of mortality, and
22 several clinical scores, including the TRI-SCORE, Wang score, and TRIO score, have been
23 developed to refine risk stratification. Recent staging models integrating ventricular function, renal
24 status, and biomarkers suggest that intervention during an intermediate disease phase, before
25 irreversible end-organ damage, may optimize outcomes. Together, these advances underscore the
26 need for accurate phenotyping, structured prognostic assessment, and timely intervention to
27 improve the care of patients with TR.

28

29

30

31
## Introduction

Tricuspid regurgitation (TR) is a frequently encountered valvular abnormality, often identified incidentally during routine echocardiographic assessment.(1) Moderate or severe TR affects approximately 4% of individuals over the age of 75—an incidence comparable to that of clinically relevant aortic stenosis or mitral regurgitation.(2)

Despite its prevalence, TR has long been under-recognized and under-treated. Historically, it was regarded as a benign consequence of left-sided heart disease or pulmonary disorders, with the assumption that it would improve following treatment of the primary pathology (2, 3). However, the delay in developing TR-specific diagnostic and therapeutic strategies was mainly driven by technical limitations in echocardiographic quantification and, until recently, the absence of effective interventional options. Furthermore, when TR is not associated with left-sided disease, early symptoms are often mild and unspecific, contributing to under-recognition and lack of timely referral for management (4).

However, several studies have demonstrated that moderate-to-severe TR is independently associated with poor clinical outcomes, including significantly increased mortality—even after adjustment for comorbid conditions (5, 6) Sex-based differences have emerged, with women disproportionately affected by significant TR. Female sex has been identified as an independent predictor of disease severity and progression, possibly related to a higher prevalence of atrial fibrillation (AF) and heart failure with preserved ejection fraction (HFpEF).(7) Additional predictors of TR progression include advancing age and pulmonary hypertension.

In light of growing awareness, mainly due to availability of new strategies for treatment, TR is increasingly being recognized as a disease entity with distinct pathophysiological subtypes, a relevant epidemiological burden, and important prognostic implications. This review addresses three key aspects: etiological classification of TR, current estimates of prevalence, and the evolving understanding of its prognosis and natural history.

## Classification and Etiology of Tricuspid Regurgitation

TR is broadly classified into primary TR (pTR), secondary TR (sTR) and cardiac implantable electronic device (CIED) related, based on the underlying mechanism of valve dysfunction—a distinction with important prognostic and therapeutic implications.(8)
Primary TR, accounting for approximately 5–10% of cases, results from intrinsic abnormalities of the tricuspid valve apparatus, such as leaflet prolapse, congenital malformations, rheumatic disease, infective endocarditis, carcinoid syndrome, or infiltrative disorders.(9, 10) Iatrogenic causes, such as repeated endomyocardial biopsies in heart transplant recipients, also fall into this category.(11) In pTR, valve incompetence is due to structural damage, typically without significant changes in right heart geometry, at least at the initial stages.

By contrast, sTR—which accounts for the vast majority of cases (80%)—is a functional abnormality of structurally normal leaflets, caused by right heart chamber remodeling. Secondary TR arises from annular dilatation and leaflet tethering due to primary or secondary pulmonary hypertension leading to right ventricular (RV) overload (i.e. left-sided heart disease or pulmonary disease), or primary RV (i.e. cardiomyopathy, myocardial infarction), or atrial dysfunction (i.e. long-standing AF).(12)

Contemporary classifications further stratify sTR into two distinct phenotypes with differing pathophysiology and prognostic profiles: ventricular sTR (V-sTR) and atrial sTR (A-sTR).

Ventricular sTR results from RV pressure, leading to RV remodeling, papillary muscle displacement, and leaflet tethering. Common underlying conditions include left-sided HF, pulmonary hypertension, and intrinsic myocardial disease. The CARE-TR registry proposed a refined subclassification of V-sTR into five subgroups:(13) severe left-sided valvular heart disease (LS-VHD); heart failure with reduced ejection fraction (HFrEF) or mildly reduced ejection fraction (HFmrEF) without severe LS-VHD; HFpEF without severe LS-VHD; pre-capillary pulmonary hypertension (PH); isolated RV dysfunction (RVD) without left ventricular disease.

This heterogeneity within V-sTR highlights the need for tailored management strategies.

Atrial sTR, a recently recognized phenotype, is associated with permanent AF and age-related atrial remodeling. It is characterized by isolated annular dilatation due to right atrial enlargement, typically occurring without RV dysfunction, pulmonary hypertension, or significant left-sided heart disease. Although often less symptomatic at onset, A-sTR can progress and is associated with an increased risk of adverse outcomes, particularly in patients with persistent AF and HFpEF.(13)

A recent expert opinion paper defines A-sTR, its risk factors and possible overlap conditions.(14)

A third emerging phenotype is CIED-related TR, which has become increasingly common with the widespread use of pacemakers and defibrillators.(15) CIED-related TR can result from direct mechanical interference of the lead with leaflet motion or from pacing-induced RV dysfunction
1 (dyssynchrony) and annular dilatation; both mechanisms often coexist. This form of TR affects up
2 to 25-45% of device recipients and is associated with rapid progression, higher hospitalization
3 rates, and increased mortality.

4 This nuanced classification—encompassing PTR, V-sTR, A-sTR, and CIED-related TR—provides
5 a foundation for individualized diagnosis, risk stratification, and emerging targeted therapies. (16)

6

## 7 Epidemiology of Tricuspid Regurgitation

8

9 Prevalence of TR in Heart Failure

10 Secondary TR is highly prevalent among patients with HF, affecting individuals across the
11 spectrum of HF phenotypes. Moderate-to-severe TR has been reported in approximately 10-23%
12 of HF patients in previous observational studies. (1, 17, 18) In the European Society of Cardiology
13 – Heart Failure Association (ESC-HFA) Long-Term Registry, moderate-to-severe TR was present
14 in 19.2% of the cohort, with similar rates across HF subtypes (19% in HFrEF, 17.8% in HFmrEF,
15 and 20.3% in HFpEF) (19) and with isolated TR being more frequently observed in HFrEF as
16 compared to TR combined with moderate-to-severe mitral regurgitation. (20) Heitzinger et al.
17 showed a prevalence of severe TR higher in HFrEF as compared to HFmrEF and HFpEF (20% vs.
18 10% and 9%), although the absolute number of patients with severe TR was higher in HFpEF than
19 other HF phenotypes since the latter were less represented. (21)

20

21 Prevalence of TR in Patients with Left-Sided Valvular Disease

22 TR is highly prevalent in patients with left-sided valvular disease, reflecting the close
23 pathophysiological interplay between left-sided lesions and the right heart. In the setting of mitral
24 regurgitation (MR), TR frequently develops as part of the disease continuum.

25 In a cohort of patients with chronic HFrEF and functional MR, moderate-or-greater TR was present
26 in 21% of those with moderate MR and in 52% of those with severe MR, underscoring the
27 progressive right-sided involvement with advancing MR severity. Similarly, in patients with atrial
28 functional MR, moderate-or-greater TR was observed in 43%, highlighting the shared atrial
29 remodeling substrate linking both conditions (22, 23).

30 Population-based and hospital cohorts have consistently shown that significant TR often coexists
31 with mitral or aortic valve disease, particularly in elderly and comorbid patients. Data from large
registries provide further insights: in the transcatheter valve therapy (TVT) registry, which included patients undergoing transcatheter aortic valve implantation (TAVI) or mitral transcatheter edge-to-edge repair (M-TEER), moderate TR was present in 13.1% and severe TR in 2.3% of TAVI patients, while in the M-TEER group, 33.2% had moderate TR and 14.7% had severe TR (24). Similar data were observed in other European studies showing a prevalence of severe TR in 2.8% of TAVI candidates (25) and 27% of M-TEER recipients (26). Collectively, these findings highlight that TR frequently complicates the course of left-sided valvular disease, regardless of whether the latter is managed medically, surgically, or via transcatheter interventions, and its presence may adversely affect outcomes.

## Prevalence of TR Subtypes in Contemporary Registries

Recent registries have provided important insights into the distribution and clinical characteristics of TR subtypes, including A-sTR, and V-sTR.

The CARE-TR registry, a multicenter Italian cohort of 648 patients with severe or greater secondary TR, reported A-sTR in 22.1% and V-sTR in 77.9% of cases.(13) A-sTR was strongly associated with AF and HFpEF, either alone or in combination, and was more frequent among women, who tended to have fewer comorbidities and milder symptoms compared to patients with V-sTR. In contrast, V-sTR was more often linked to left-sided valvular disease, pulmonary hypertension, and myocardial dysfunction, and was characterized by more advanced structural and hemodynamic abnormalities.

Additional observational studies, including patients conservatively managed, have reported A-sTR prevalence ranging between 13% and 26%, depending on the population studied and the criteria used to define A-sTR.(14, 27-29)

The TRIVALVE registry, which included 298 patients undergoing transcatheter tricuspid valve repair (TTVR), similarly reported an A-sTR prevalence of 22%, with the remaining 78% having V-sTR. Patients with V-sTR exhibited more pronounced hemodynamic compromise, higher NT-proBNP levels, and greater symptom burden than those with A-sTR, underscoring the distinct pathophysiological and clinical profiles of these subtypes.(30)

A combined analysis of the Leiden and Leipzig cohorts — including both conservatively managed patients and those undergoing TTVR (29) proposed an echocardiographic definition of A-sTR,
derived using a bioinformatic approach. This definition identifies approximately 15% of patients
with significant TR as having a likely underlying atrial mechanism.

These findings collectively highlight the increasing recognition of A-sTR as a distinct phenotype,
particularly in elderly patients with AF and preserved LV and RV function.

In the EuroTR registry, including patients undergoing transcatheter tricuspid valve edge-to-edge
repair (T-TEER), further illustrated the heterogeneity of TR etiology. In this cohort, TR was
classified as primary in 7.6%, secondary in 84.1%, and mixed primary/secondary in 8.3%. A sub-
analysis showed a prevalence of A-sTR of 31%.(31) Notably, 28.2% of patients had a trans-
tricuspid pacing lead, highlighting the substantial burden of CIED-related TR in contemporary
practice. The majority of patients in this cohort presented with HFpEF (72%), with smaller
proportions having HFmrEF (16.5%) or HFrEF (11.4%).(32)

Together, these findings underscore the heterogeneity of TR in terms of etiology and clinical
presentation and emphasize the importance of distinguishing among its subtypes.

Prognostic Role of Tricuspid Regurgitation

Clinical progression and risk stratification

TR is probably not merely a marker of advanced disease but a possible active contributor to morbidity and mortality, owing to its hemodynamic effects including systemic congestion and decrease in forward stroke volume leading to multi-organ dysfunction. Indeed, TR-related congestion contributes to cardiorenal syndrome (impaired renal function), cardio-hepatic syndrome (liver injury with cholestatic pattern and reduced synthetic function), and gastrointestinal dysfunction (malabsorption, malnutrition, increased intestinal permeability), forming a broader multi-organ syndrome.(33-35)

Importantly, TR may progress insidiously, with mild and nonspecific symptoms such as peripheral
edema and fatigue, underscoring the need for early recognition and intervention.(4)

Identifying patients with worse prognosis who could benefit from closer monitoring and timely
intervention remains a critical unmet need. In this context, several risk stratification tools have
been proposed to predict mortality in patients with significant TR. The TRI-SCORE (36) was
developed to estimate operative mortality in patients undergoing isolated tricuspid valve surgery
and it was validated in different settings (37, 38); the TRIVALVE score was derived to assess
prognosis after TTVI (39); the Wang score was designed to predict 1-year mortality risk in patients
with isolated TR managed medically; (40) and the TRI-O score was introduced to stratify mortality risk in patients with notable TR across broader clinical settings (41). All these scores have demonstrated prognostic value for mortality prediction at follow-up. However, each has limitations: their derivation cohorts were highly selected, only one (TRI-SCORE) has been deeply validated in external cohorts, (42) comparative performance remains unknown, and their ability to predict broader clinical outcomes beyond mortality has yet to be established (Table 1).

7

8

## Prognostic role of tricuspid regurgitation in Heart Failure

Secondary TR is associated with significantly worse survival in patients with HF, regardless of HF phenotype and setting (chronic, acute, advanced).(18, 20, 21, 43-45) The Vienna HF-TR study provided a comprehensive analysis of sTR's prognostic impact across the full HF spectrum. In this longitudinal cohort of 13,469 HF patients without primary valvular disease, even moderate sTR was associated with substantial excess mortality compared to patients with no or mild sTR, and this risk increased further with severe sTR.(21) During a median follow-up of 44 months, 27.3% of patients died. At four years, the mortality rate for patients with severe sTR was 44%, compared with 24% for those with no/mild sTR and only 2% in the age- and sex-matched general population. At eight years, these rates increased to 61%, 38%, and 15%, respectively. Adjusted HR confirmed that moderate sTR was associated with a 58% increase in mortality risk (HR 1.58, 95% CI 1.48-1.69), while severe sTR conferred more than a twofold increase (HR 2.19, 95% CI 2.01-2.38). These associations remained significant after adjustment for clinical and bootstrap confounder models. Subgroup analyses revealed that the negative impact of sTR was particularly pronounced in younger patients (<70 years: HR 1.97 vs. ≥70 years: HR 1.66, p for interaction = 0.040), as well as in those with hypertension, ischemic heart disease, larger LV dimensions, and preserved RV function. Interestingly, in patients with severely impaired RV function, the association between sTR severity and mortality was attenuated, highlighting the complex interplay between RV failure and TR.(21) Complementary insights from the ESC-HFA long term registry further highlight the prognostic relevance of TR in HF.(20) Among 11,298 HF outpatients with no significant aortic disease and over a median follow-up of 12 months, patients with isolated TR and those with combined MR/TR had markedly higher rates of all-cause mortality (12.8 and 13.3 events/100 patient-years, respectively) compared to patients with isolated MR (9.9/100 patient-years, respectively) or no significant valve disease (5.0/100 patient-years, respectively). After

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adjustment, isolated TR and combined MR/TR were independently associated with worse survival

(HR 1.42 and 1.45, respectively), and similar trends were observed for cardiovascular death and

HF hospitalization. Both isolated TR and combined MR/TR were independently associated with

higher mortality and HF hospitalization compared to isolated MR or no valve disease,

underscoring the particularly adverse prognosis conferred by TR in HF, especially in HFpEF. Data

from Mayo Clinic on 13,026 patients with HFrEF, showed that, as compared to trivial TR, higher

TR grades were independently associated with higher mortality (adjusted hazard ratios 1.09 [1.01-

1.17] for mild TR, 1.21 [1.11-1.33] for moderate TR and 1.57 [1.39-1.78] for severe TR).(18)

Finally, the GALACTIC-HF trial, which enrolled over 8,000 patients with symptomatic HFrEF,

confirmed that moderate-to-severe TR was independently associated with worse outcomes, even

after adjustment for clinical covariates. Patients with moderate/severe TR had a significantly

higher risk of the composite endpoint of HF events or CV death compared to those with no or mild

TR (adjusted HR 1.12–1.14), primarily driven by an increased incidence of HF events and

hospitalizations.(43)

Taken together, these findings emphasize that sTR may not be merely a bystander but a key

contributor to adverse outcomes in HF, across phenotypes and severities, warranting earlier

recognition and targeted intervention.

## Prognostic role of tricuspid regurgitation in left-sided valvular disease undergoing transcatheter treatment

The large analysis from the TVT registry showed that baseline moderate-to-severe TR was

associated with significantly higher mortality and readmission rates at both 30 days and one year

after TAVI and M-TEER. After multivariable adjustment, patients undergoing TAVI with moderate

TR had a 24% increased risk of 1-year mortality (HR 1.24), and those with severe TR had a 65%

increase (HR 1.65) compared with patients with none or mild TR. Similarly, among M-TEER

recipients, moderate TR was associated with a 17% higher 1-year mortality (HR 1.17), and severe

TR with a 49% higher risk (HR 1.49). One-year readmission rates and health status, as measured

by the Kansas City Cardiomyopathy Questionnaire (KCCQ), were also significantly worse in

patients with moderate or severe TR, who achieved smaller improvements in quality of life despite

intervention. (24)
A post hoc analysis of the COAPT trial suggested that M-TEER may mitigate the poor prognosis associated with TR in patients with secondary mitral regurgitation, though these findings are exploratory. (46) Together, these observations underscore the importance of assessing TR severity and considering its management in patients undergoing transcatheter left-sided interventions. Notably, severe TR was an exclusion criterion in the COAPT randomized trial, limiting conclusions about the efficacy of M-TEER in this subgroup. However, a large multicenter European registry specifically examined the evolution of TR after M-TEER and its impact on long-term outcomes (26). Among 503 patients with secondary MR undergoing successful M-TEER, TR improved by at least one grade in ~35%, remained stable in ~46%, and worsened in ~19% at short-term follow-up (median ~3 months). Improvement was more frequent in patients with higher baseline TR (≥2+) and was independently associated with smaller left atrial diameter and optimal MR reduction. Importantly, the degree of TR at short-term follow-up—rather than at baseline—was a strong predictor of long-term mortality: patients with TR ≤2+ had a 42% lower risk of death compared to those with TR ≥3+ (HR 0.58, p=0.011), regardless of baseline TR. These observations reinforce the importance of reassessing TR after M-TEER and considering staged tricuspid intervention if significant TR persists.

Determinants of Prognosis in Secondary Tricuspid Regurgitation

*Prognosis according to sTR phenotype in observational cohorts:* recent evidence suggests that outcomes in sTR vary substantially according to its underlying phenotype, with A-sTR consistently associated with a more favorable prognosis compared with V-sTR or other non-atrial forms.(28)

The prognostic heterogeneity of sTR phenotypes has been demonstrated in several large cohorts of patients managed both medically and transcatheter. The CARE-TR registry (n=648) provided detailed phenotypic and outcome data in patients with severe sTR, showing that at two years, survival free from the composite of death or HF hospitalization was significantly higher in patients with A-sTR compared with those with V-sTR (73.5% vs. 54.4%, p<0.001), with V-sTR independently associated with a higher risk (adjusted HR 2.00). Within A-sTR, outcomes were worst in patients with both AF and HFpEF compared to AF or HFpEF alone, while within V-sTR, the poorest outcomes were seen in patients with pre-capillary pulmonary hypertension and severe left-sided valvular heart disease. This classification therefore represents a simple tool to identify
high-risk subgroups among V-sTR patients, reinforcing its prognostic relevance and potential value for guiding management strategies (13). These findings were documented also by the Leiden cohort (n=1,037), which applied a structured classification of sTR into atrial and ventricular phenotypes. Over a median follow-up of 78 months, patients with A-sTR had markedly better survival compared to V-sTR (10-year survival: 78% vs. 46%, p<0.001), with V-sTR independently associated with worse outcomes (HR ~2.3). Among V-sTR subtypes, survival was worst in those with pulmonary hypertension and RV dysfunction, whereas A-sTR consistently showed the most favorable prognosis.(27)

Finally, the large Cleveland Clinic series by Wang et al. (n=9,045) further underscored the survival advantage of atrial over ventricular-driven forms of secondary TR. In this cohort, unadjusted 5-year survival was significantly better in atrial functional TR compared to secondary TR from left-sided disease or pulmonary hypertension. In addition, Wang et al. developed and validated a risk prediction model (Wang score) for secondary TR, incorporating clinical, echocardiographic, and laboratory markers of RV dysfunction, pulmonary hypertension, renal and hepatic impairment, and comorbidities. This score demonstrated good discrimination (C-statistic ~0.73) and provides a practical tool to estimate 1-year mortality and guide management decisions.(40)

Consistent findings have also emerged from cohorts of patients undergoing TTVR and T-TEER, reinforcing the prognostic advantage of A-sTR over V-sTR. In the TRIVALVE registry A-sTR was associated with significantly better survival compared with V-sTR at a median follow-up of 10 months (91% vs. 72%, p=0.02). Multivariate analysis identified procedural success as an independent protective factor for mortality (HR 0.41), while V-sTR and high-dose diuretic use showed a trend toward worse outcomes.(30) The EuroTR registry, including 641 patients treated with T-TEER, confirmed these findings. One- and two-year survival rates were significantly higher in patients with A-sTR than in those with non-atrial sTR (1 year: 84.0% vs. 77.6%; 2 years: 79.3% vs. 63.8%; both p<0.001). Similarly, survival free from HF hospitalization at one and two years favored A-sTR over non-atrial sTR. In multivariable Cox regression, A-sTR was independently associated with improved two-year survival free from heart failure hospitalization (HR 0.65, p=0.025).(31)

**Prognosis in trial populations:** consistent findings have also emerged from randomized trials. The pivotal TRILUMINATE trial enrolled 350 highly selected patients, the vast majority with secondary TR, preserved LV function, and a predominance of atrial fibrillation. Severe pulmonary
hypertension (sPAP ≥70 mmHg) and advanced LV dysfunction (LVEF <20%) were exclusion criteria, which resulted in a cohort largely reflecting A-sTR.

At 1 year, TRILUMINATE demonstrated marked symptomatic improvement and quality-of-life benefit but no reduction in mortality or HF hospitalization (47). However, the 2-year follow-up revealed sustained TR reduction and a significant decrease in HF hospitalizations compared with medical therapy, confirming a favorable prognostic signal beyond symptom relief (48).

Importantly, a real-world analysis showed that only ~50% of patients would have been TRILUMINATE-eligible, with excluded patients having more comorbidities and worse survival, underscoring the trial's limited generalizability.(49)

The recently published TRI.fr trial provided complementary evidence in a broader European population.(50) In this study, 300 patients with severe symptomatic sTR were randomized to T-TEER plus guideline-directed medical therapy (GDMT) versus GDMT alone. Exclusion criteria were similar to TRILUMINATE (LVEF<35% and precapillary pulmonary hypertension with sPAP ≥60 mmHg), again selecting patients with preserved LV function and advanced annular or leaflet remodeling. At 1 year, T-TEER significantly reduced TR severity (severe TR in 6.8% vs. 53.5% in GDMT) and improved patient-reported outcomes, with a 14.5-point gain in Kansas City Cardiomyopathy Questionnaire (KCCQ) scores compared with GDMT (p<0.001). These results mirror those of TRILUMINATE, where an 18-point KCCQ improvement was observed. Notably, the TRI.fr population had a higher prevalence of massive/torrential TR at baseline (≈99% vs. 72% in TRILUMINATE), yet still achieved substantial TR reduction and quality-of-life gains.

Together, TRILUMINATE and TRI.fr provide robust evidence that T-TEER improves symptoms and quality of life in carefully selected patients with secondary TR, predominantly of atrial phenotype, while also suggesting a potential prognostic benefit in reducing HF hospitalizations with longer follow-up.

Beyond T-TEER, transcatheter tricuspid valve replacement (TTVR) has recently emerged as a complementary strategy for patients unsuitable for edge-to-edge repair. The TRISCEND II trial randomized 400 patients with at least severe, symptomatic TR (pTR or sTR) to receive the EVOQUE TTVR system or optimal medical therapy in a 2:1 ratio. The trial population was markedly symptomatic (79% NYHA III/IV; mean KCCQ 49) and included 38% with pacing leads. At 1 year, EVOQUE achieved near-universal TR elimination and a twofold clinical benefit over
1 medical therapy (win ratio 2.02; P<0.001), driven by improved symptoms and quality of life, with
2 numerically lower all-cause mortality and HF hospitalization (51).

3 **Prognosis according to disease stage and comorbidity burden**: several markers of advanced HF
4 (i.e. recurrent HF hospitalizations, malnutrition, RV dysfunction, pulmonary hypertension, clinical
5 signs of right HF) have been reported as associated with poor outcome in patients with TR,
6 especially in the setting of TTVI. (52-56) A large multicenter analysis of 1,885 patients with severe
7 symptomatic TR by Schlotter et al. proposed a disease stage classification based on a
8 multiparameter score integrating biventricular function, renal dysfunction, and neurohormonal
9 activation (BNP/NT-proBNP) derived from patients undergoing T-TEER, (57) Patients were
10 categorized into early, intermediate, and advanced stages, which correlated with progressively
11 higher 1-year mortality (6%, 15%, and 31%, respectively; p<0.01). When comparing T-TEER to
12 conservative therapy across stages, T-TEER was associated with significantly lower 1-year
13 mortality in the intermediate stage (13% vs. 21%; HR 0.73; p=0.03), but no benefit was observed
14 in early or advanced stages. These findings suggest that intervention at the intermediate stage—
15 before irreversible end-organ damage and hemodynamic collapse—may optimize outcomes.
16
17 A sub-analysis of the TRIVALVE cohort specifically examined patients with RVD and PH. Among
18 300 patients meeting these criteria, RVD was present in 81%, PH in 42%, and both in 24%.
19 Prognosis in this high-risk group was strongly influenced by end-organ damage and procedural
20 success. Patients with significant renal dysfunction (eGFR <45 mL/min) and/or hepatic congestion
21 had markedly higher estimated 1-year mortality rates (44%), rising to 58% when procedural failure
22 was also present. Notably, patients with neither renal/hepatic dysfunction nor procedural failure
23 demonstrated survival comparable to those with procedural success despite some end-organ
24 impairment. These findings underscore the critical impact of right-sided end-organ dysfunction
25 and procedural success on outcomes in patients with advanced TR undergoing transcatheter
26 therapy. (58)

## Conclusion

27 TR is a prevalent and clinically significant valvular disorder, most commonly sTR in nature, with
28 distinct phenotypes including ventricular and atrial forms. TR is reported as a possible independent
29 driver of morbidity and mortality, since it may contribute to a multi-organ syndrome.
30 Contemporary registries have highlighted its high prevalence, particularly in elderly patients, those
1 with HF, as well as those undergoing transcatheter interventions for left-sided valve disease or
2 CIED.

3 The heterogeneous pathophysiology of TR and its substantial prognostic role underscore the need
4 for improved awareness, early diagnosis, and timely intervention before irreversible right heart
5 and end-organ dysfunction develop.

6

7 **Figure Legends**

8 **Figure 1. Prevalence of TR based on etiology and prognostic aspects.**

9 pTR – primary tricuspid regurgitation; sTR – secondary tricuspid regurgitation; CIED-TR –
10 cardiac implantable electronic device-related tricuspid regurgitation; A-sTR – atrial secondary
11 tricuspid regurgitation; V-sTR – ventricular secondary tricuspid regurgitation; AF – atrial
12 fibrillation; HFpEF – heart failure with preserved ejection fraction; HFrEF – heart failure with
13 reduced ejection fraction; LS-VHD – left-sided valvular heart disease; PH – pulmonary
14 hypertension; RVD – right ventricular dysfunction; T-TEER – transcatheter tricuspid edge-to-edge
15 repair.

16 **References**

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28 29
<table><thead><tr><th></th><th>TRI-SCORE</th><th>TRIO Score</th><th>Wang Score</th><th>TRIVALVE Score</th></tr></thead><tbody><tr><th>PARAMETERS</th><td><ul><li>Age ≥70 years (+1)</li><li>NYHA functional Class III-IV(+1)</li><li>Right-sided heart failure signs (+2)</li><li>Daily furosemide ≥125 mg (+2)</li><li>Glomerular filtration rate &lt;30 mL/min (+2)</li><li>Elevated total bilirubin (+2)</li><li>Left ventricular ejection fraction &lt;60% (+1)</li><li>TAPSE &lt;17 mm or S'DTI &lt;9.5 cm/s, or visual RV dysfunction (+1)</li></ul></td><td><ul><li>Age 70-79 years (+1); ≥80 years (+2)</li><li>Male (+1)</li><li>Chronic lung disease (+1)</li><li>Congestive HF (+1)</li><li>Creatinine ≥2 mg/dL (+2)</li><li>AST ≥40 U/L (+1)</li><li>HR ≥90 beats/min (+1)</li><li>Severe TR (+1)</li></ul></td><td><ul><li>Age 65-74 years (+1); ≥75 years (+2)</li><li>Myocardial Infarction (+1)</li><li>Chronic lung disease (+1)</li><li>Loop diuretic use (+1)</li><li>PAD (+1)</li><li>Hb &lt;10 g/dL (+1)</li><li>INR &gt;1.5 (+1)</li><li>Creatinine ≥1.4 mg/dL (+1)</li><li>Albumin &lt;3.0 g/dL (+2)</li><li>Platelets &lt;15000/ml (+1)</li><li>RV SP &gt;50 mmHg (+1)</li><li>RV dysfunction (mild +1, moderate +2, severe +3)</li></ul></td><td><ul><li>Atrial Fibrillation (+1)</li><li>Glomerular filtration rate &lt;30 mL/min (+1)</li><li>Elevated GGT or Bilirubin (+1)</li><li>Signs of right HF (+1)</li><li>Left ventricular ejection fraction &lt;50% (+0.5)</li></ul></td></tr><tr><th>MAXIMUM SCORE</th><td>Total: 12 points<br>High severity score: ≥ 10 points</td><td>Total: 12 points<br>High severity score: ≥ 7 points</td><td>Total 16 points<br>High severity score: ≥ 12 points</td><td>Total: 4.5 points<br>High severity score: ≥ 2.5 points</td></tr><tr><th>PURPOSE</th><td>Mortality risk in isolated TV surgery</td><td>Long term mortality risk in patients with significant TR</td><td>1-year mortality in patients with isolated TR</td><td>Mortality/HF hospitalization in patients undergoing transcatheter tricuspid valve intervention</td></tr><tr><th>VALIDATION</th><td>Widely externally validated (multiple independent cohorts across Europe and internationally)</td><td>Externally validated (geographically distinct cohort, and tested in independent cohorts)</td><td>Partially validated externally (tested in independent cohorts in comparative studies, but no dedicated external validation paper)</td><td>Not externally validated (only internally/derivation validation so far)</td></tr></tbody></table>
<figure><img src="image_2.png" /><figcaption>Figure 1
165x93 mm (DPI)</figcaption></figure>

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