2025 ACC专家共识决策路径：临床医生在三尖瓣反流评估和管理中的10个问题

TABLE OF CONTENTS

1. INTRODUCTION 48

2. ASSUMPTIONS AND DEFINITIONS

2.1. General Assumptions 449

2.2. Definitions .................................................... 449

3. SUMMARY GRAPHIC 450

Figure 1. Pathway for TR Evaluation and Management ... 450

448

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|4. DESCRIPTION, RATIONALE, AND IMPLICATION OF PATHWAY|450| |---|---| |4.1. Clinical Recognition of TR|450| |4.2. Classification of TR Etiology and Mechanism|451| |Figure 2. Etiologic Classification of TR|452| |Figure 3. Classification of TR Etiology|453| |4.3. Classification of TR Severity|454| |4.3.1. Echocardiography|454| |Figure 4. Multiparametric Echocardiographic Approach to Grading TR Severity|455| |Figure 5. TEE Assessment of TV Leaflet Morphology|456| |4.3.2. Cardiac Magnetic Resonance and Computed Tomography Assessment of TR Severity|454| |Figure 6. Multiplanar Reconstruction of CMR Imaging to Calculate EF and Quantitate TR Severity|454| |Figure 7. Direct Calculation of TR Regurgitant Volume With 3D Time-Resolved CMR Imaging With Multiplanar Reconstruction|457| |Figure 8. Cardiac CT-Based TV Apparatus Measurements|458| |4.4. Defining Key Adjunctive Features|456| |4.4.1. Right-Side Heart Size and Function|458| |4.4.2. CMR and CT for Assessment of RV Size and Function|458| |4.4.3. Imaging Surveillance|458| |4.5. Natural History of TR|460| |4.5.1. Mortality|460| |Figure 9. Risk Models for A.1-Year and B.3-Year All-Cause Mortality in Patients With TR|461| |4.6.4. Treatment Considerations for HF|462| |4.6.1. Diuretic Therapy|462| |4.6.2. GDMT|462| |4.6.3. Pulmonary Vasodilators|463| |4.6.4. Therapeutic Considerations for RV Failure|463| |4.6.5. Therapeutic Considerations for AF|463| |Figure 10. Conceptual Model of AF Management in the Setting of TR|464| |4.6.6. Therapeutic Considerations for CIED-Related TR|464| |4.6.7. Consequences of Progressive TR and RV Dysfunction|465| |4.6.8. Cardiorenal and Cardiohepatic Syndromes|465| |4.6.9. Referral to Advanced HF Team|466|

|4.7. TV Intervention|4.66| |---|---| |4.7.1. Surgical Treatment of TR|4.66| |4.7.2. Surgery for Isolated TR|4.67| |Figure 11. Risk Score Model to Predict the Outcome of Patients after Isolated TV Surgery|4.68| |4.7.3. TTVI|4.68| |Figure 12. Types of TTVI: Transcatheter TV Repair and TTVR|4.69| |4.7.4. Transcatheter TV Repair|4.69| |4.7.5. TTVR|4.70| |4.7.6. Heterotopic CAVI|4.71| |4.7.7. Choosing Between T-TEER and TTVR|4.71| |Figure 13. TRIVALVE Risk Model for In-Hospital Mortality After TTVI|4.72| |4.8. Management After TV Intervention|4.72| |4.8.1. HF Management|4.73| |Figure 14. Use of Clinical and Laboratory Evaluations in Determining Evolemia at Discharge|4.74| |4.8.2. CIED Considerations Following TV Intervention|4.74| |4.9. Conclusions|4.75| |PRESIDENT AND STAFF|4.76| |PRESIDENT AND STAFF|4.76| |REFERENCES|476| |REFERENCES|482| |Author Relationships with Industry and Other Entities (Relevant)|482| |APPENDIX 2|484| |Peer Reviewer Relationships with Industry and Other Entities (Comprehensive)|484| |APPENDIX 3|486| |Abbreviations|486|

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Transcatheter aortic valve implantation (TAVI) is a mature technology offering a reasonable alternative to surgical valve replacement for the treatment of patients with severe aortic stenosis. Mitral transcatheter edge-to-edge repair (M-TEER) can be successfully applied to select patients with primary or secondary mitral regurgitation (MR). Tricusid regurgitation (TR) has been the subject of more recent and intense clinical investigation. Revised classification schemes for TR etiology and severity have been proposed, clinical prognostic risk scores have been developed, imaging techniques to assess tricuspid valve (TV) structure and function have advanced, and the indications for surgical treatment have been revisited. Importantly, the U.S. Food and Drug Administration approved 2 transcatheter systems for the treatment of patients with symptomatic, severe TR in 2024 specifically to improve health status, including quality of life (QoL).$^{1,2}$ The Centers for Medicare & Medicaid Services announced in March 2025 that it will cover transcatheter TV replacement (TTVR) for the treatment of symptomatic severe TR under coverage with evidence development, although with criteria that differ for those adopted for TAVI and M-TEER. A similar decision for tricuspid transcatheter edge-to-edge repair (T-TEER) is anticipated.$^{3}$ These rapid developments have outpaced the generation of prospective evidence establishing the ability of any TV intervention to reduce the burden of cardiovascular death and heart failure (HF) hospitalizations in these patients for whom earlier recognition, assessment, and prompt referral for treatment are critical. Nevertheless, improving patient-reported QoL in a chronic condition for which there are no medical disease-modifying therapies is a worthy and validated treatment goal. This ECDP is intended to enable the clinician to assimilate the most important developments in this dynamically evolving field to improve the care of patients with severe TR, with emphasis on those with secondary TR, and is focused on the most common clinical areas encountered in practice from evaluation to treatment. Salient points of emphasis are summarized at the end of the document and should serve as a bridge to the future publication of updated ACC/American Heart Association (AHA) guideline recommendations for the management of TR.

In accordance with ACC's relationship with industry (RWI) policy, relevant disclosures for the writing committee and comprehensive disclosures for external peer reviewers can be found in Appendices 1 and 2. To ensure complete transparency, a comprehensive RWI table for the writing committee, including relationships not pertinent to this document, has also been created and is included in the Supplemental Appendix. A list of

abbreviations relevant to this ECDP can be found in Appendix 3. For additional details concerning ECDPs,$^{4}$ please consult the Preface and Methods also included in the Supplemental Appendix.

2. ASSUMPTIONS AND DEFINITIONS

2.1. General Assumptions

1. The focus of this ECDP is the evaluation and management of patients with secondary TR in the chronic setting.

2. The writing committee endorses the evidence-based approach to the evaluation and management of patients with TR recommended in the 2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease.$^{5}$

3. An informed shared decision-making process, incorporating individual patient values and preferences, as well as consensus multidisciplinary team (MDT) recommendations, are essential for patient management.

4. This ECDP is not intended to supplant clinical judgment.

5. This ECDP is based on the highest level of evidence available as of the time when evidence review was closed (November 30, 2024). It is anticipated that updates to the document will be made as new evidence is generated and vetted.

2.2. Definitions

1. Guideline-directed medical therapy (GDMT): treatment options recommended for use by ACC/AHA clinical practice guidelines.

2. Optimal medical therapy (OMT): treatment considered clinically optimal when not specifically defined by clinical practice guidelines.

3. New York Heart Association (NYHA) functional classifications:

$\blacksquare$ Class I: No limitation of physical activity. Ordinary physical activity does not cause symptoms of HF.

$\blacksquare$ Class II: Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in symptoms of HF.

$\blacksquare$ Class III: Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes symptoms of HF.

$\blacksquare$ Class IV: Unable to perform any physical activity without symptoms of HF, or symptoms of HF at rest.

4. Cardiac implantable electronic device (CIED)-related TR: TR that develops via ≥1 of several mechanisms after implantation of a right-sided CIED.

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3. SUMMARY GRAPHIC

Figure 1 provides a summary graphic of the pathway for TR evaluation and management.

![graph TD\n A1[TR symptoms or signs] --> A2[Clinical context]\n A2 --> A3[TTE]\n A3 --> A4[Etiology and Mechanism]\n A4 --> A5[Primary]\n A4 --> A6[Secondary]\n A4 --> A7[CIED]\n A5 --> A8[Determine Severity • Quantitate: RVoL, EROA, RF]\n A6 --> A9[• atrial • ventricular]\n A7 --> A10[• Other testing: TEE, 3-D TEE, CMR, cardiac CT, left/right heart catheterization]\n A8 --> A11[< Mild]\n A8 --> A12[Moderate]\n A8 --> A13[≥Severe]\n A9 --> A8\n A11 --> A14[Optimal Medical Therapy]\n A12 --> A15[Surgery]\n A13 --> A16[TTVI]\n A14 --> A17[• Left-sided heart disease management]\n A14 --> A18[• Diuretics]\n A14 --> A19[• Pulmonary vasodilators]\n A14 --> A20[• OAC and rhythm control for AF]\n A15 --> A21[• Left-sided VHD management]\n A15 --> A22[• Tricuspid valve repair]\n A15 --> A23[• Tricuspid valve replacement]\n A15 --> A24[• CIED management]\n A15 --> A25[• Minimize need for PPM]\n A16 --> A26[• Left-sided VHD management]\n A16 --> A27[• T-TEER]\n A16 --> A28[• TTVR]\n A16 --> A29[• CIED management]\n A16 --> A30[• Minimize need for PPM]\n A31[• Symptoms/exam • Surveillance TTE • OMT, CIED management]\n](1/parseimages/figurec599f62757a74ab39a38d2a419e120a0_0_4.png)

4. DESCRIPTION, RATIONALE, AND IMPLICATION OF PATHWAY

4.1. Clinical Recognition of TR

TR affects 4% of individuals age ≥75 years.$^{6}$ In the Fra- mingham Offspring Study, mild or greater TR was found in 14.8% of men and 18.4% of women.$^{7}$ A recent study

estimated that 1.6 million U.S. residents have moderate or greater TR.$^{8}$ The prevalence of echocardiographically documented TR in the community is approximately 1 in 200 persons and, as observed in other VHDs, increases as a function of age. Increasing severity of TR is associated with excess morbidity and mortality, although even mild TR may be associated with adverse outcomes during

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long-term follow-up.$^{9}$ Recognition of TR is the first step in the pathway for evaluation and management.

Most TR cases clinically encountered are secondary in nature and not related to primary diseases of the valve leaflets or chordae, such as infective endocarditis, rheumatic heart disease, carcinoid, and Ebstein anomaly. The TR that develops after placement of a CIED is best considered separately in view of the mechanisms potentially responsible for its development and its management (Section 4.2).$^{10}$⁻$^{13}$

Mild-to-moderate degrees of TR are usually well tolerated in the short to intermediate term and may be clinically silent. With increasing TR severity, symptoms of systemic venous congestion, such as edema and those reflective of reduced forward cardiac output, including dyspnea and fatigue, may emerge. More advanced manifestations of right-sided congestion, such as abdominal bloating, worsening peripheral edema, weight gain, and anorexia, follow later in the course, and are ominous. Most patients with chronic severe secondary TR are older and have a significant burden of other cardiac and systemic comorbidities. Women outnumber men in most large observational series and atrial fibrillation (AF) is common.

TR on bedside physical examination is more often “seen” than “heard.” Assessment of the jugular venous pulse can be diagnostic. With severe TR, the venous pressure is elevated and a prominent, systolic cv wave with a rapid y descent (in the absence of tricuspid stenosis) can be appreciated. If necessary, the venous pulsations can be timed to the heart sounds, with systolic events confined to the S1-S2 interval. Other signs of chronic, severe TR include hepatomegaly with a pulsatile liver edge, ascites, edema, pleural effusions, and sarcopenia. Scleral icterus or jaundice are very late findings indicative of hepatic failure. A prominent right ventricular (RV) pulsation may impart a parasternal lift. The murmur of chronic TR is holosystolic in timing, high or medium pitched, and best heard at the lower left sternal border. An increase in the intensity of the murmur during inspiration (Carvallo sign) can help distinguish the murmur from others that are holosystolic. When right atrial (RA) pressure is very high, the murmur may not increase in intensity with inspiration, as there is no additional filling of the RV.$^{14}$ In rare patients with severe or greater degrees of TR, a diastolic murmur of functional tricuspid stenosis owing to enhanced diastolic flow can be appreciated.

The physical examination is far less sensitive and specific than transthoracic echocardiography (TTE) for the detection and characterization of TR. Indeed, TR is often first appreciated on a TTE study done for another indication. Findings on TTE can be discordant from those clinically detected. Diuretic therapy may reduce signs of congestion and thus may challenge bedside assessment. Additionally, the severity of TR may wax and wane with

time, necessitating longitudinal follow-up as a component of clinical decision-making.$^{15}$ Referral to a MDT for optimization of medical and rhythm management, and assessment of candidacy for TV intervention should be considered for patients with severe TR in whom advanced treatments would not be considered futile.$^{5}$ There is a premium to be placed on early recognition of progressive TR and prompt referral, given the excess morbidity and mortality associated with late intervention in high-risk patients.

4.2. Classification of TR Etiology and Mechanism

A detailed TR etiology classification system, which has been adopted by European Society of Cardiology/European Association for Cardio-Thoracic Surgery and European Association of Cardiovascular Imaging, as well as the Tricuspid Valve Academic Research Consortium, is shown in Table 1 and Figure 2$^{16}$: 1) primary TR; 2) secondary TR with subclassifications of atrial secondary TR (A-STR) and ventricular secondary TR (V-STR); and 3) CIED-related causative and incidental TR.

V-STR develops because of RV dilation and/or dysfunction that leads to lateral or apical displacement of the papillary muscles, resulting in TV leaflet tethering. Cardiovascular disease processes contributing to V-STR include left-sided valvular or ventricular disease, pulmonary hypertension (PH), and primary RV cardiomyopathies. The morphologic features of A-STR include marked RA and tricuspid annulus (TA) dilation,

|Classification|Subclassification|Etiologies| |---|---|---| |Primary TR||Degenerative (prolapse, flail) Infective endocarditisTrauma to the chest wall or leafletsEbstein anomalyCarcinoid diseaseMediastinal radiationRheumatic disease| |Secondary TR|V-STR|PH due to:LV systolic dysfunction or left-sided valve diseasePulmonary arterial hypertensionChronic lung diseaseChronic pulmonary thromboembolic diseaseIntracardiac shunt| ||A-STR|Atrial arrhythmiaHFpEF| |CIED-related TR|CIED-relatedcausative TR|Direct interaction of the leadwith the TV leaflets or subvalvular apparatus| ||CIED-relatedincidental TR|CIED present but not the direct cause of TR|

Reprinted with permission from Hahn et al.$^{35}$

A-STR = atrial secondary tricuspid regurgitation; CIED = cardiac implantable electronic device; HFpEF = heart failure with preserved ejection fraction; LV = left ventricular; PH = pulmonary hypertension; TR = tricuspid regurgitation; TV = tricuspid valve; V-STR = ventricular secondary tricuspid regurgitation.

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FIGURE 2 Etiologic Classification of TR

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453

 preservation of the conical shape of the RV, normal RV and left ventricular (LV) systolic function, and the absence of leaflet tethering.$^{17,18}$ RA dilation and subsequent TA dilation are most often the result of atrial arrhythmias, although an RA myopathy can develop in the setting of HF with preserved ejection fraction (HFPEF) even in the absence of atrial arrhythmias. AF-related$^{18}$ disruption of TA function can also contribute to A-STR.$^{19}$ In an observational study of patients with newly diagnosed AF in the absence of structural heart disease, 33.6% developed moderate or greater TR during a follow-up period of 13 years. Furthermore, the study demonstrated that older patients, women, and those with persistent or permanent AF were more likely to develop TR.$^{20}$ AF duration is an important contributor to the development of TR. Although a minority of patients develop significant TR early after AF onset, TR incidence and severity increase with time.$^{20,21}$ In patients with AF, TR is associated with a higher risk of HF and increased mortality and prognosis worsens as TR progresses.$^{21-23}$

CIED-related TR can develop if the device interferes with the TV leaflets or subvalvular apparatus (CIED-related causative TR) or if RV pacing leads to RV remodeling (CIED-related incidental TR). CIED-causative TR can occur because of leaflet perforation, lead entanglement in the chordal apparatus, papillary muscle injury, leaflet adherence with the lead, or lead impingement on leaflet motion. Clarifying the type of CIED-related TR is essential to clinical decision making and determination of whether lead extraction may be effective in reducing TR severity.$^{24,25}$ Importantly, worsening of TR may occur within 6 months of CIED implantation, justifying close follow-up of these patients.$^{13}$

Classification of TR is important, as specific TR etiologies may be associated with different outcomes.$^{26}$⁻$^{29}$ Studies have shown that patients with V-STR due to left-sided heart disease have reduced survival compared with that of patients with either primary TR or A-STR$^{27}$,$^{28}$; however, outcomes of patients with V-STR will differ

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based on the cause of RV remodeling or dysfunction.$^{6}$ TR that develops after CIED placement is also associated with reduced survival.$^{24,30-32}$

A recent review summarized the anatomical and physiological parameters that may allow differentiation between A-STR and V-STR (Figure 3) but also suggested that a large proportion of patients present with mixed features in the late stages of disease. Selected patient factors associated with significant A-STR include age >70 years, female sex, persistent AF or flutter, and HFpEF. More recent studies have simplified the definitions to include either the ratio of RA to RV area or the ratio of RA to RV volume at end-systole, together with measures of biventricular function.$^{33,34}$

4.3. Classification of TR Severity

4.3.1. Echocardiography

TTE is the imaging modality of first choice for the evaluation of patients with TR. Using well-defined imaging protocols,$^{36}$ transesophageal echocardiography (TEE) can also be used to quantify the severity of TR. In addition, TEE can aid in the assessment of TV morphology and function when TTE images are suboptimal. TEE image guidance is an essential component of TV intervention. Guidelines recommend assessing TR severity with use of a combination of structural, qualitative, semi-quantitative, and quantitative echocardiographic measures (Figure 4).$^{37,38}$ Structural assessment is the first step and includes an evaluation of RV morphology, RV and RA size, inferior vena cava (IVC) diameter, and respirophasic changes. Characterization of TV leaflet morphology using TEE is essential to predict the response to T-TEER (Figure 5).$^{39}$

Qualitative and semiquantitative measures of TR severity include continuous wave Doppler shape and density, color Doppler jet area, vena contracta diameter, flow convergence zone, and proximal isovelocity surface area (PISA) radius. These parameters are more specific for identifying mild TR. There are several technical limitations to be considered. Because the cutoffs used to describe TR severity are primarily derived from studies of MR severity, the magnitude of TR can be underestimated. The density of the spectral Doppler signal is theoretically proportionate with the number of red blood cells traveling within the regurgitant jet; a weak or faint signal would only indicate mild TR, whereas a very dense signal is consistent with moderate or severe TR. This method depends on TR severity as well as the gain settings and the direction of the jet. The method is unreliable with eccentric jets. Conversely, a narrow regurgitant jet well-aligned with the continuous wave Doppler beam may appear dense and overestimate TR severity.

Hepatic vein flow reversal is a specific sign of clinically significant TR.$^{37}$ It may be affected by the severity of TR as well as RA chamber compliance, the systolic gradient (driving force) between the RV and RA, hepatic remodeling, portal vein microvascular dysfunction, and arrhythmias.

The geometric assumptions behind the calculation of tricuspid effective regurgitant orifice area (EROA) by PISA, namely a hemispheric flow convergence proximal to a circular orifice subtended by a flat surface, are not met in patients with V-STR, and thus PISA may result in systematic underestimation of TR severity.$^{40}$⁻$^{42}$ Using 3-dimensional (3D) volumetric assessment of TR as the comparator, Tomiselli et al$^{43}$ demonstrated that conventional PISA underestimated secondary TR severity in approximately 50% of patients.$^{43}$ EROA by PISA underestimates 3D vena contracta area by approximately 40%, depending upon the regurgitant orifice shape.$^{40}$,$^{41}$ Despite these limitations, EROA by PISA is relatively easy to measure and predictive of worse all-cause mortality and increased cardiovascular events, independent of RV size or function, comorbidities, or pulmonary artery (PA) pressures.$^{44}$⁻$^{46}$ The American Society of Echocardiography guidelines recommend the use of an uncorrected $ERO_{AISA}$ to define TR severity.

TR is commonly graded as mild (1+), moderate (2+), or severe (3+) (Figure 4). Severe (3+) TR is defined by a vena contracta diameter of ≥0.7 cm, EROA of >0.4 cm$^{2}$, and/or TR regurgitant volume (RVol) ≥45 mL/beat.$^{37}$ Trans-catheter TV intervention (TTVI) trials have enrolled pa-tients with TR severity more than double the quantitative criteria for severe$^{47}$ and have highlighted the need for an extended grading scheme to more accurately characterize these patients.$^{48}$ Additional TR grades of massive and torrential have been shown to be prognostically relevant in medically treated patients$^{49}$⁻$^{53}$ and in patients under-going TTVI (Table 2).$^{54}$⁻$^{56}$

Because of complex leaflet morphology and the asymmetric shape of the regurgitant orifice, the use of quantitative Doppler and 3D TEE color Doppler has been recommended to improve the assessment of TR severity.$^{17}$ Underestimation of TR severity by standard guideline-recommended color Doppler methods$^{40,41,43}$ may contribute to the undertreatment of disease.

4.3.2. Cardiac Magnetic Resonance and Computed Tomography Assessment of TR Severity

TR quantification by cardiac magnetic resonance (CMR) is performed using a combination of volumetric tracings and phase-contrast imaging (Figure 6). There are currently no specific volumetric cutoffs for TR severity by CMR. In the 2017 American Society of Echocardiography/

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![graph TD\n A1[Chronic Tricuspid Regurgitation by Doppler Echocardiography] --> A2[Does TR meet specific criteria for mild or severe?]\n A2 -->|Probably Mild| A3[SPECIFIC SIGNS OF MILD TR Qualitative • Normal/mild TV abnormality • Thin, small central color jet • No or small convergence zone Incomplete or faint CW jet Semiquantitative • VC width <0.3 cm • PISA radius <0.5 cm at a Nyquist -28 cm/s • Systolic dominant hepatic vein flow Structural: • Normal RV/RA/IVC size]\n A2 -->|Probably Severe| A4[SPECIFIC SIGNS OF SEVERE TR Qualitative • Flail leaflet, large coaptation defect, severe tenting • Large central jet • Large holo systolic convergence zone • Dense triangular CW jet with early peaking Semiquantitative • PISA radius >0.9 at Nyquist -28 cm/s • VC width ≥0.7 cm • Holosystolic reversal of hepatic vein flow Structural • Enlarged RA/RV/IVC]\n A3 --> A5[QUANTITATIVE EVALUATION WHENEVER POSSIBLE]\n A4 --> A6[Indeterminate TR Consider further testing for quantification: TEE or CMR]\n A5 --> A7[EROA <0.2 cm² RVol<30 mL RF≤15%]\n A5 --> A8[EROA 0.2-0.4 cm² RVol 30-44 mL RF 16%-49%]\n A5 --> A9[EROA >0.4 cm² RVol≥45 mL RF≥50%]\n A7 --> A10[Mild TR]\n A8 --> A11[Moderate TR]\n A9 --> A12[Severe TR]\n A10 -->|Poor TTE quality or low confidence in measured Doppler parameters • Discordant quantitation and qualitative parameters and/or clinical data| A6\n A11 -->|Poor TTE quality or low confidence in measured Doppler parameters • Discordant quantitation and qualitative parameters and/or clinical data| A6\n A12 -->|Poor TTE quality or low confidence in measured Doppler parameters • Discordant quantitation and qualitative parameters and/or clinical data| A6\n](1/parseimages/figure4b408596f83b4c9bba6d3ae2215bbc18_0_3.png) Society for Cardiovascular Magnetic Resonance valvular regurgitation guidelines, thresholds for TR severity were adapted from those applied to MR severity. Values for TR regurgitant fraction (RF) were categorized into mild (RF ≤15%), moderate (RF 16%-48%), and severe (RF >48%).$^{37}$ Recent natural history data have shown that CMR-derived RVol ≥45 mL/beat and RF ≥50% associate with the highest risk of 1-year mortality.$^{60}$ This CMR relative RVol cutoffs is concordant with echocardiographic RVol cutoffs for severe TR based on PISA of 45 mL/beat. 3D time-resolved phase-contrast imaging is now commercially available and has the ability to directly measure TV inflow for calculation of RVol (TV inflow

stroke volume [SV] - aortic or pulmonic outflow SV = TV RVol) and directly measure TR volume (Figure 7).$^{61,62}$ Availability of interpretive expertise may limit the routine use of CMR for TR assessment; however, the use of CMR is becoming more widespread.$^{63}$ Cardiac computed Tomography (CT) is currently of limited value in the quantification of TR severity and should not be used for this purpose as part of routine clinical care. CT-based flow models are being developed but are not currently available for routine use. Cardiac CT can allow measurement of the anatomical regurgitant orifice area (Figure 8)$^{64}$; however, correlation of this measurement with echocardiographic EROA or RVol is not well

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 developed. Cardiac CT is a component of preprocedural TTVI planning, particularly for TTVR. There is an emerging role for the use of cardiac CT to assess IVC trajectory offset (a measure of the IVC-TV anatomical relationship) before transcatheter intervention.$^{65}$ The degree of coaxiality of the delivery system to the TV may aid in predicting device trajectory.

4.4. Defining Key Adjunctive Features

4.4.1. Right-Side Heart Size and Function

Echocardiography

A thorough assessment of the RA and RV is critical to the evaluation of severe TR because it helps identify the etiology of TR, determines the impact of TR, assists with procedural planning, and provides prognostic information. TTE is the most common modality for this purpose. Because of the complex shape and contraction pattern of the RV, it is imperative to assess it from multiple acoustic views that use qualitative and quantitative metrics. RV

size should be assessed in a RV-focused apical 4-chamber view to limit foreshortening with measurement of the basal diameter, mid-diameter, and length.$^{67}$ There are age and sex differences in normal RV dimensions.$^{68}$ RV systolic function can be assessed using tricuspid annular plane systolic excursion (TAPSE), 2-dimensional (2D) fractional area change, tricuspid lateral annular systolic velocity (S' velocity), RV global longitudinal strain, RV free wall strain, and 3D RV EF (RVEF). 3D RV size and function measurements more closely approximate CMR RV measurements than 2D measurements. Benchmarks for RV systolic dysfunction include TAPSE <17 mm, 2D fractional area change <35%, and S' velocity <9.5 cm/s.$^{67}$ Acquiring an accurate 3D RVEF is often challenging based on the 2D image quality. A World Alliance Societies of Echocardiography study showed that 3D RVEF may be a better assessment of global RV systolic function than use of 2D parameters such as fractional area change, S' velocity, TAPSE, RV global longitudinal strain, and RV free wall strain. Proposed 3D RVEF lower limits of normal

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|Variable|Mild|Moderate|Severe|Massive|Torrential| |---|---|---|---|---|---| |VC (mm)|<3|3-6.9|7-13.9|14-20.9|≥21| |PISA EROA (mm²)|<20|20-39|40-59|60-79|≥80| |3D VCA (mm²)|||75-94.9|95-114.9|≥115|

Reprinted with permission from Hahn et al.$^{17}$

3D = 3-dimensional; EROA = effective regurgitant orifice area; PISA = proximal isovelocity surface area; TR = tricuspid regurgitation; VC = vena contracta; VCA = vena contracta area.

are 46% for women and 44% for men.$^{69}$ The Tricuspid Valve Academic Research Consortium proposal for grading RV function (Table 3)$^{17}$ requires prospective validation.

The presence of precapillary PH in the setting of severe TR is associated with worse outcomes after T-TEER.$^{70}$ Left-sided heart disease, including LV systolic dysfunction, LV diastolic dysfunction, and left-sided valvular disease, often results in left atrial (LA) and postcapillary PH as a precursor to V-STR. Systolic PA pressure can be estimated by echocardiography, and is assumed to be

equivalent to the RV systolic pressure if there is no significant gradient across the pulmonic valve. The RV systolic pressure can be calculated from the peak TR jet velocity and estimated RA pressure based on IVC dimension using the simplified Bernoulli equation as follows: RV systolic pressure = 4(V)$^{2}$ + RA pressure where V is the peak TR jet velocity.$^{71}$ Recent invasive studies have shown the inaccuracy of the guideline-suggested RA pressure assumptions using IVC size and collapsibility.$^{72}$ In these situations, an invasive assessment with right heart catheterization is advised.$^{17}$ Invasive assessment is also necessary to distinguish precapillary PH from post-capillary PH.

Indexing measures of RV systolic function to afterload, or RV-PA coupling, theoretically describes the efficiency with which RV SV is transferred into the PA. Although the gold standard measure of RV-PA coupling is generated from an invasively derived pressure-volume loop, investigators have used echocardiographic measures of RV function, divided by the echo estimate of systolic PA pressure to estimate this parameter.$^{73}$ TAPSE/systolic PA

 Reprinted with permission from Hahn et al.$^{61}$ CMR = cardiac magnetic resonance; EF = ejection fraction; TR = tricuspid regurgitation.

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 Reprinted with permission from Hahn et al.$^{61}$ A multiplanar reconstruction still frame from a 4-dimensional CMR velocity-encoded acquisition is shown with retrospective valve tracking. In this systolic frame, high-velocity TR flow is represented by a bright green color. The crosshairs can be manipulated in the long-axis images (A and C) to align flow, which can then be measured in the short-axis through-plane of the TR jet (B). Valve tracking (B, polygon) allows semiautomated adjustment of through-plane motion for more accurate assessment of flow. 3D = 3-dimensional; CMR = cardiac magnetic resonance; TR = tricuspid regurgitation.

pressure is associated with outcomes in both medically managed$^{49}$ patients and those following transcatheter device therapy.$^{74}$ A novel 3D echo-based measurements of RV-PA coupling, forward RV SV divided by RV end-systolic volume, has been shown to predict adverse outcomes in patients with TR.$^{75}$

4.4.2. CMR and CT for Assessment of RV Size and Function

CMR is an accurate and reliable tool for quantification of ventricular volumes and ejection fraction (EF). CMR short-axis volume tracings have been shown to be accurate within 2% when compared with ex vivo heart volumes.$^{76,77}$ Several studies have shown an underestimation of cardiac volumes by 2D and 3D echocardiography.$^{78-80}$ CMR can be helpful to assess RV remodeling due to TR as well as reverse remodeling after therapy for TR. There is prognostic value in assessment of baseline RV CMR volumes, although treatment thresholds are not yet established. Several publications have shown reductions in RV volumes by CMR after surgery for TR. Kim et al$^{81}$ showed that RV end-diastolic volume index <164 mL/m$^{2}$ predicted a return to normal postoperative RV function based on effective RVEF (forward SV-RV end-diastolic volume). In a small, single-center

study examining outcomes after TV surgery, preoperative effective RVEF ≤34% combined with RV end-diastolic volume index >100 mL/m$^{2}$ or RF ≥40% was associated with the highest risk of postoperative all-cause and cardiac death.$^{82}$

Normal reference values for RV volumes by CT are similar to those derived by CMR.$^{66}$ Overall, studies have shown excellent agreement between CT and CMR for RV size and function$^{83,84}$; with a recent meta-analysis showing correlation coefficients (r) values between 0.95 and 0.98 for end-diastolic volumes, end-systolic volumes, SVs, and RVEF. The main limitation with CT is its temporary resolution (50-210 ms) compared with that of CMR (15-50 ms). The use of dual- (vs single-) source CT significantly improves temporal resolution but may lead to misregistration artifacts. With the use of appropriate protocols and scanning principles, CT may provide an alternative to CMR for chamber volumetric assessment.

4.4.3. Imaging Surveillance

TTE is the recommended imaging modality for the routine follow-up of patients with TR. It is typically performed at intervals of 6 to 12 months once TR is considered severe, in combination with clinical

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 Adapted from Khalique et al.$^{66}$ A multiplanar reconstruction of the tricuspid apparatus is shown. The cardiac CT angiography was acquired using a tricuspid acquisition protocol with the following parameters: 1) Contrast administration: biphasic contrast bolus of 70/30 contrast saline mixture @ 5 cc/s followed by a saline bolus to allow for smooth contrast bolus without streaking. 2) Contrast triggering: with the bolus tracking method using region of interest in the main pulmonary artery to optimize right sided opacification, 3) Gating: across full cardiac cycle for 20 phases. (A Sagittal view of the right ventricle. (B and C) Measurements of tethering area and height, respectively. (D) Measurement of anatomical regurgitant orifice area that can be obtained by MDCT. 2ch = 2-chamber; 4ch = 4-chamber; ATVL = anterior tricuspid valve leaflet; CT = computed tomography; MDCT = multidetector row computed tomography; PTVL = posterior tricuspid valve leaflet; RA = right atrium; ROA = regurgitant orifice area; RV = right ventricle; TV = tricuspid valve.

assessment of volume status. In 1 population study of patients with at least moderate TR, progression occurred in 19% of patients, and regression occurred in 38% during approximately 2 years of follow-up.$^{15}$ Predictors of progression included older age (HR: 1.03), lower body mass index (HR: 0.95), chronic kidney disease (HR: 1.55), worse NYHA functional class (HR: 1.52), and RV dilation (HR:

||Mild Dysfunction|Moderate Dysfunction|Severe Dysfunction| |---|---|---|---| |TAPSE (mm)|14-17|10-13|<10| |RV s' velocity (cm/s)|9-11|6-8|<6| |RV GLS (%)|18-21|14-17|<14| |RV FWS (%)|20-23|15-19|<15| |FAC (%)|34-37|30-33|<30| |3D RV EF (%)|45-50|35-45|<35|

Reprinted with permission from Hahn et al.$^{17}$

3D = 3-dimensional; EF = ejection fraction; FAC = fractional area change; FWS = free wall strain; GLS = global longitudinal strain; RV = right ventricular; TAPSE = tricuspid annular plane systolic excursion; TVARC = Tricuspid Valve Academic Research Consortium.

1.33). In addition to age, other studies have identified markers of increased left-sided filling pressures (systolic PA pressure and LA enlargement), and AF,$^{85}$ as well as the presence of a pacemaker or defibrillator lead as predictors of TR progression.$^{86}$ Importantly, the overall prevalence of significant TR was 4.3 times greater in females than males by the 8th decade.$^{7}$ These patient risk factors may influence the frequency of surveillance TTE in patients with TR.

Advanced imaging, using TEE, CMR, or cardiac CT, should be considered when the severity of TR or the status of RV function is uncertain after integrated, multiparametric TTE assessment and when planning for TV intervention. TEE is used for preprocedural and intra-procedural guidance under the supervision of an interventional echocardiographer. Reliance on CMR, in preference to TTE, for routine surveillance can also be considered when the technology and interpretive expertise are readily available and TTE images are suboptimal for longitudinal assessment. Access to advanced imaging expertise is essential to help guide the clinician in choosing the right test.

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4.5. Natural History of TR

TR is often present for some time before symptoms and physical examination signs develop and, in some cases, there may be considerable RV enlargement and dysfunction before they are appreciated. Earlier recognition and application of medical interventions, including CIED reprogramming to reduce RV pacing-induced dyssynchrony when appropriate, might impact the rate of TR progression, which may wax and wane with time.

Several large studies and meta-analyses of trials involving patients with chronic HF have confirmed that TR contributes to excess morbidity and mortality, with increasing risk observed for more severe TR grades. Evidence regarding the prognostic implications of secondary TR in acute HF syndromes has varied.$^{87-89}$

The European Society of Cardiology HF Long-Term Registry reported that the prevalence of moderate-to-severe TR is equally distributed across HF phenotypes, ranging from 18% in HF with mildly reduced EF to 20% in HF with reduced EF (HFrEF) and 21% in HFpEF$^{90}$,$^{91}$; however, more recent data from a large Viennese registry suggest that the prevalence of moderate-to-severe TR among HF patients may be higher, 33% in HFpEF and HF with mildly reduced EF, and 50% in HFPrEF.$^{87}$

4.5.1. Mortality

TR has been consistently associated with excess mortality in patients with HF. Indeed, it is best to view TR through this lens. In a large, contemporary, patient-level database of 435,679 U.S. patients with a new HF diagnosis, both prevalent and incident TR were associated with increased mortality risk.$^{92}$ The risk of all cause mortality varied with increasing TR severity (adjusted HR: 1.34 [95% CI: 1.28-1.39]) at 1.5 years for severe vs no TR at baseline; adjusted HR: 2.44 [95% CI: 2.32-2.57] for severe TR developing during follow-up). The detrimental effects of TR were consistent across all HF patient subgroups and were independent of age, gender, rhythm, associated comorbidities, prior cardiac surgery, natriuretic peptide levels, and left ventricular ejection fraction (LVEF). The study did not differentiate between primary and secondary TR, although it is likely that most patients in the registry had secondary TR.$^{88}$

A retrospective French study evaluated intermediate-term survival among 722 patients with moderate-to-severe or greater “isolated” secondary TR defined by a structurally normal TV without pacemaker lead, mild or less left-sided valvular disease, no PH, preserved LVEF (>50%), and no previous cardiac surgery.$^{93}$ The mean age was 75 years, and 62% were women; 81% of patients had AF. All-cause mortality was 24%, approximately twice that expected of a population without TR, at a median follow-up of 22 months. Nearly 50% of the deaths in this study

study were due to a cardiac cause. Secondary TR is present in approximately 21% of patients with HFrEF and was associated with increased mortality.$^{94}$ Anand et al$^{95}$ recently reported the clinical and TTE follow-up of at least moderate TR in 13,611 patients in a registry, populated with individuals with predominantly secondary TR. Using cluster analysis, the investigators identified 5 distinct clinical TR phenotypes. Cluster 1 represented “low-risk TR” with qualitatively less-severe TR, a lower prevalence of RV enlargement, AF, and comorbidities; cluster 2 represented “high-risk TR” with more severe degrees of TR, more AF, larger RVs and more comorbidities; clusters 3, 4, and 5 represented TR associated with lung disease, coronary artery disease, and chronic kidney disease, respectively. Five-year mortality rates in phenotypes 1 to 5 were 38%, 68%, 71%, 67%, and 83%, respectively. As <1% of the cohort underwent TV surgery, these data provide estimates of the untreated natural history of each of the phenotypes among patients with HFrEF. In another series of 212 patients with HFrEF and moderate or less TR, a significant worsening of TR occurred in 22% for 5 years. Progressive TR was associated with larger RA and LA volumes and with higher mortality.$^{94}$

The presence of TR in patients with HFEF is also associated with increased mortality risk.$^{96,97}$ There is also an excess hazard of death when moderate or greater TR coexists with aortic or mitral valve (MV) disease or group 1 PH.$^{98-100}$ The presence of moderate or greater TR at the time of TAVI is associated with a 2-fold increase in mortality risk.$^{98}$

The natural history of A-STR is not well described. As noted, A-STR and V-STR often coexist.$^{101}$ Nonetheless, in studies that separated the etiologies of TR, A-STR has been associated with lower mortality risk compared with that of V-STR.$^{28,29,102}$ The majority of patients in the TRILUMINATE (Trial to Evaluate Cardiovascular Outcomes in Patients Treated With the Tricuspid Valve Repair System Pivotal) randomized study comparing T-TEER plus OMT vs OMT alone, likely had predominantly A-STR. Section 4.7.4 During 1 year of follow-up, the T-TEER plus OMT patients demonstrated an improvement in QoL but no difference in diuretic requirements or 6-minute walk distance (Section 4.7.4). In addition, there were numerically fewer hospitalizations for HF in the OMT group compared with that of the T-TEER plus OMT group.

Paniagua et al.$^{103}$ reported a 25% prevalence of moderate-to-severe TR in patients with transvenous pacemaker leads. Other observational studies have reported a TR development in patients with transvalvular pacemaker or defibrillator leads.$^{104,105}$ In a meta-analysis/ meta-regression analysis, the incidence of CIED-related TR was 24% (95% CI: 20%-28%); TR was associated with increased risks of all-cause mortality (adjusted HR: 1.52;

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A Risk Model for 1-Year All-Cause Mortality in Patients with TR

|Parameter|Score| |---|---| |Age|| |65-74 years|1| |75+ years|2| |Myocardial infarction|1| |Peripheral vascular disease|1| |Chronic lung disease|1| |Chronic kidney disease (creatinine >1.4 mg/dL)|1| |Loop diuretic use|1| |Anemia (Hgb <10 g/dL)|1| |Thrombocytopenia (platelet <15 k/µL)|1| |INR >1.5|1| |Albumin <3.0 g/dL|2| |RV Systolic Fx|| |Mildly impaired|1| |Moderately impaired|2| |Severely impaired|3| |Right ventricular systolic pressure >50 mm Hg|1| |TOTAL|16|

B Risk Model for 3-Year All-Cause Mortality in Patients with TR

|TRIO-RV Score Parameters|Score| |---|---| |Male sex|1| |Age|| |70-79 years|1| |≥80 years|2| |Severe TR|1| |Congestive heart failure|2| |Pulmonary disease|2| |Creatinine of ≥2 ml/dl|2| |Aspartate aminotransferase of ≥40 U/L|1| |Heart rate ≥90 bpm|1| |RVFWS/RVSP <0.43%/mm Hg|3| |Total (max)|15|

 (A) A single site clinical score for patients with at least moderate-to-severe TR assigned points to the 12 variables shown. The score showed a significant association with 1-year all-cause mortality (C statistic = 0.73). (B) Tricuspid Regurgitation Impact on Outcomes, Right Ventricle (TRIO-RV) score was developed from a single-site, retrospective evaluation of patients with moderate-to-severe TR. The score was associated with all-cause mortality (C statistic = 0.67) and was able to separate patients into risk categories. Figure 9A reprinted with permission from Hahn et al.$^{10}$ Figure 9B reprinted with permission from Jamnongraspatorn et al.$^{107}$ bpm = beats per minute; eGFR = estimated glomerular filtration rate; Hgb = hemoglobin; INR = international normalized ratio; RV = right ventricle; RVFWS = right ventricular free wall strain; RVSP = right ventricular systolic pressure; TR = tricuspid regurgitation.

95% CI: 1.36-1.69; P < 0.001) and HF hospitalizations (adjusted HR: 1.82; 95% CI: 1.19-2.78; P = 0.006).$^{106}$ As recently highlighted in a Heart Valve Collaboratory Workshop, 15% to 37% of patients referred for the initial studies of TTVI had a CIED in place.$^{11}$

Single center-derived risk scores for 1-year and 3-year all-cause mortality in patients with TR have been proposed (Figure 9). Baseline clinical, laboratory, and echo-cardiographic parameters vary across the scores; however, external validation has been lacking.

O'Gara et al 10 Issues for the Clinician in TR Evaluation and Management

4.6. Treatment Considerations for HF

4.6.1. Diuretic Therapy

There are no specific disease-modifying medical therapies (or guideline Class I medical recommendations) for the treatment of TR, although the magnitude of TR can be reduced in many patients with management of left-sided heart disease and AF. Because TR was the strongest multivariable predictor of persistent congestion in patients admitted with acute HF reported from the European Society of Cardiology-EURObservational Research Programme-EORP-Heart Failure Association HF Long-Term Registry,$^{97}$ management of congestion should be a primary treatment goal in this setting.$^{10}$ Despite being a mainstay of treatment for right-sided HF,$^{108}$ diuretics do not appear to alter the course of the underlying disease process, although no randomized data are available to support this.$^{5}$

Loop diuretics are used to manage volume overload in patients with TR; however, their use is often limited by several factors. First, impairment of kidney function in patients with advanced TR can limit the efficacy of diuretic therapy.$^{109}$ In patients with chronic kidney disease, loop diuretic efficacy is impaired by reduced activity of the organic anion transporter and decreased renal blood flow, which may lead to diminished concentrations of the diuretic in the renal tubule.$^{110}$ Second, severe TR leads to renal venous hypertension in peritubular, interstitial, and tubular lumen distributions, which then counteracts intraglomerular perfusion and lowers the glomerular filtration rate. In the presence of tubular dysfunction and increased sodium avidity, diuretic resistance ensues. Third, neurohormonal activation and worsening hemodynamics (lower cardiac output and higher central venous pressure) increase active sodium and water reabsorption, perpetuating congestion and reducing diuretic responsiveness.$^{110}$

There may be additional issues with diuretics. Because of gut congestion and impaired absorption, an oral loop diuretic with higher bioavailability (torsemide, bumetamide) may be considered. The TRANSFORM (Torsemide Comparison with Furosemide for Management of HF) study, however, did not demonstrate a benefit of torsemide over furosemide in patients with chronic HF, but patients were not stratified by TR.$^{111}$ In patients refractory to high-dose oral diuretic therapy, changing administration to an intravenous loop diuretic with a bolus infusion can reduce PA pressures and increase venous capacitance, effects that are postulated to be due to increased prostaglandin release.$^{112}$ Higher doses of loop diuretics may be needed to overcome diuretic resistance; however, this strategy may not be predictably

effective in patients with advanced chronic kidney disease. Last, the addition of a thiazide-like diuretic (oral metolazone or hydrochlorothiazide; intravenous chlorothiazide) can be used for dual nephron blockade.$^{113}$,$^{114}$ More recent data suggest a benefit of adding acetazolamide or sodium-glucose cotransporter-2 (SGLT2) inhibitor to enhance decongestion.$^{115}$,$^{116}$ Aggressive diuretic management may require the input of a pharmacist.$^{10}$

4.6.2. GDMT

The therapeutic approach to secondary TR includes GDMT targeted to the underlying disease, including HF due to left-sided heart disease, AF, and Group 1 (pre-capillary) PH. Proper management of comorbidities, such as hypertension, diabetes, and chronic kidney disease, is essential. Surgical or transcatheter management of significant left-sided valve disease, when indicated, is a priority, as is the appropriate application of pacemaker, cardiac resynchronization device, and/or defibrillator therapy. For patients with HFrEF, in addition to diretics, GDMT consists of a guideline-directed beta-blocker, a mineralocorticoid receptor antagonist, an angiotensin receptor-neprilysin inhibitor if not limited by symptoms or cost (otherwise, an angiotensin receptor blocker or angiotensin-converting enzyme inhibitor), and an SGLT2 inhibitor. Treatment of patients with HF with mildly reduced EF and HFpEF has considerably evolved and should involve the use of SGLT2 inhibitors, and consideration of glucose-dependent insulinotropic polypeptide/glucagon-like peptide-1 receptor agonist in those with obesity, nonsteroidal mineralocorticoid receptor agonists, steroidal mineralocorticoid receptor antagonist, and angiotensin receptor-neprilysin inhibitors.$^{117}$ SGLT2 inhibitors are a Class I recommendation for use for patients with HFpEF and HF with mildly reduced EF in the 2023 European Society of Cardiology Focused Update of the HF Guidelines.$^{118}$ While GDMT across the spectrum of HF has not been specifically studied in patients with severe TR, the efficacy of these therapies would be expected to be similar in patients with and without TR. There is interest in studying the effects of SGLT2 inhibitors and glucagon-like peptide-1 receptor agonist for treatment of isolated TR.

With GDMT, secondary MR due to left-sided heart disease is often reduced$^{108}$ and interventricular septal function improves, resulting in enhanced RV function.$^{119,120}$ Also, the improvement in LV function usually results in lower LV filling pressures and less PH, which also favorably affect RV function and TR severity. It remains uncertain whether there are direct RV benefits of any single component of GDMT. TR can be improved with

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nonpharmacologic interventions targeted to left-sided heart disease. In a study of 852 patients undergoing cardiac resynchronization therapy, 184 (22%) had moderate-to-severe TR at baseline with 75 (41%) showing significant improvement at 6 months.$^{121}$ TR improvement was associated with a greater degree of RV reverse remodeling. In a large Medicare registry of patients undergoing TAVI, 3% had severe TR.$^{122}$ Of those with severe TR, 76.4% improved to moderate or less TR 30 days after transcatheter aortic valve replacement. TR improvement was associated with baseline moderate or greater MR, preserved LVEF, higher aortic valve gradient, and better renal function. Severe residual TR at 30 days predicted a higher 1-year mortality (27.4% severe TR vs 18.7% for moderate TR and 16.8% for mild TR; P < 0.0001).$^{122}$ An analysis from the Society of Thoracic Surgeons/ACC Transcatheter Valve Therapy Registry, using data from 2019 to 2021, suggests that 2.3% of patients undergoing TAVI and 14.7% of those undergoing M-TEER have severe TR at baseline. Patients with severe concomitant TR have a higher burden of comorbidities and lower Kansas City Cardiomyopathy Questionnaire (KCCQ) Overall, summary scores at baseline, 30 days, and 1 year compared with those who do not have significant TR.$^{123}$ They are also less likely to be “alive and well” at 1 year after TAVI or M-TEER. TR severity is expected to improve in approximately 30% to 40% after successful M-TEER; it remains unchanged or worsens in the remainder. Predictors of TR improvement are not fully understood but include female sex, baseline MR and TR grades, MR grade post-M-TEER, and LA dimension.$^{124,125}$ In a report of 213 patients with primary MR undergoing MV surgery, impaired RV function was frequent (30%).$^{126}$ RV recovery was associated more strongly with LV reverse remodeling and septal function than with changes in PA pressures.

4.6.3. Pulmonary Vasodilators

If there is clinical suspicion of precapillary PH, further evaluation, including with right-sided heart catheterization, is mandatory to verify the diagnosis and identify patients who might benefit from pulmonary vasodilator therapy. Approved therapies exist for PA hypertension (Group 1) and chronic thromboembolic PH (Group 4).$^{127}$ Single-agent or initial combination therapy with agents targeting >1 pathogenetic pathway is directed by a PH expert. Typically, therapy is started with a phosphodi-esterase type 5 inhibitor (nitric oxide pathway) and/or an endothelin receptor antagonist. Prostacyclin agonists can

be added. Guanosine monophosphate inducers are another class of agents that work through the nitric oxide pathway. Treatment with high-dose calcium channel blockers is reserved for the small proportion of patients with PH who demonstrate acute vasoresponsiveness in the catheterization laboratory. In the acute setting of severe RV failure with TR, vasopressor and inotrope treatment may be required, as well as mechanical circulatory support. If PH as a cause of the acute RV failure is known, intravenous administration of sildenafil or epo-prostenol may be an option for rapid reduction of RV afterload and circulatory stabilization. Severe and unresponsive precapillary PH is a contraindication to TV intervention.

4.6.4. Therapeutic Considerations for RV Failure

Aside from therapy of the underlying disease, there is no known specific treatment for RV failure. Volume management and decongestion with diuretics are standard.$^{128,129}$ Any therapies that improve LV function and promote reverse remodeling (eg, GDMT, cardiac resynchronization therapy) will likely improve RV function and thus potentially reduce TR.$^{119,126}$ Advanced degrees of nonremediable RV dysfunction are generally considered a contraindication to surgical or transcatheter intervention.

4.6.5. Therapeutic Considerations for AF

Limited data suggest restoration of sinus rhythm is beneficial in select patients with AF and A-STR. In patients who remain in sinus rhythm after direct current cardioversion, RV function and RA volume immediately improve and continue to recover during the next 4 to 6 weeks.$^{130}$ In a study of patients undergoing direct current cardioversion and rhythm control, maintenance of sinus rhythm at 1 year was associated with both anatomical and functional reverse remodeling and a reduction in TR severity.$^{131}$ A regression analysis of clinical and echocardiographic characteristics and OMT showed rhythm control was the only independent factor associated with reverse remodeling.$^{131}$ In an observational study of patients with HF and AF undergoing either rhythm or rate control, rhythm control resulted in reductions in TR and RA size.$^{132}$

Several observational series in patients undergoing catheter ablation of AF similarly support a benefit of rhythm control leading to reverse remodeling. Single-center cohorts of 36-114 patients undergoing ablation have demonstrated a reduction in TR by ≥1 grade in 64%-

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75.5% of patients.$^{133}$⁻$^{135}$ In patients with TR who undergo successful AF ablation, SR has been associated with a reduction in LA volume, RA area, TA diameter, and regurgitant jet area.$^{136}$ Importantly, AF ablation may be less successful in patients with chronic TR. In a series of 294 patients undergoing AF ablation, 12.9% had A-STR and 20% experienced recurrent AF at a mean follow-up of 13.4 months; recurrence was strongly associated with the presence of TR.$^{137}$ Similar findings have been reported following surgical AF ablation. In an observational series, patients with AF who underwent TV surgery and a concomitant maze procedure, compared with those having TV surgery alone, were more likely to be in sinus rhythm at 9 years (56%), and have fewer major cardiovascular and cerebrovascular events at 10 years.$^{138}$ In a propensity-matched cohort of 406 patients undergoing MV repair or replacement with or without a maze procedure for AF, the nonablated group had higher risks of the development of moderate to severe TR, progressive TR, and death.$^{139}$ At 5 years, AF recurrence was associated with progressive TR and deterioration in right-sided heart function.$^{139}$ Another propensity score analysis of 114 patients undergoing surgical AF ablation and TV repair, and a separate cohort of 279 patients with A-STR undergoing catheter AF ablation, identified leaflet tethering height ≥6 mm as a marker of a higher cumulative risks of stroke, recurrent AF, and TR in the catheter ablation group. There were no differences in these risks between the surgical and catheter ablation groups among patients with TV tethering height of <6 mm.$^{140}$

The management of AF in patients with A-STR poses a significant challenge. Observational evidence suggests that AF plays a key role in the development of TR; AF duration and burden are associated with TR progression and severity. Although restoration of sinus rhythm shows promise in select patients to enable reverse remodeling, the efficacy of rhythm control can be difficult to predict because of the complex interplay of coexistent pathologies and dynamic contributors. An individualized approach is necessary.$^{141}$ Figure 10 summarizes the conceptual model of AF management in the setting of TR.$^{132-140}$

4.6.6. Therapeutic Considerations for CIED-Related TR

CIEDs with an RV lead are associated with the development of TR. A systematic review of 29 studies comprising >66,000 individuals, 7,777 of whom underwent CIED implantation, showed a 24% incidence of ≥1 grade worsening of TR in patients who underwent device placement.$^{142}$ An early report of patients with a CIED

 undergoing TV surgery revealed multiple pathologic interactions of the TV and lead (CIED-related causative TR), including leaflet perforation, lead entanglement in chordeae or other structures, papillary muscle perforation, and leaflet adherence or impingement.$^{143}$ TR in this context can also be incidental to the device and related to RV apical pacing.$^{25}$ The exact prevalences of CIED-related causative vs CIED-related incidental TR are not clear, due to limitations in visualization of the mechanism by TTE, varying time periods of assessment, and the use of observational convenience samples.$^{24}$ More recently, 3D TTE has proven useful to delineate the relationship between the RV lead and the TV in >90% of patients.$^{144}$

Management of patients with TR and a CIED system is complex and requires attention to the health status and comorbidities of the patient, the arrhythmia/conduction

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disease diagnosis, and details of the device history. In patients with CIED-related causative TR, consideration should be given to whether lead removal or extraction is likely to ameliorate or worsen TR. Reported numerical probabilities of extraction-related TR improvement or worsening are highly variable. Worsening of TR has been reported in the range of 0% to 15%, with inconsistent definitions and assessment of acute TR and a wide range of lead dwell times before extraction. In a study of 208 patients with mean lead dwell time of 11.8 ± 7.3 years, a >1 grade increase in TR was seen in 11.5% of cases.$^{145}$⁻$^{148}$ Acute TV injury at time of extraction was strongly associated with longer lead dwell times with a graded progression in the rate of acute TV injury from 5.6% in the lowest quartile of lead age to nearly 20% in the highest quartile of lead age (>15-year lead dwell time).$^{145}$ Fibrotic attachments of venous, cardiac, and valvular tissues to endocardial leads progressively develop, supporting the clinical findings of more substantial adhesions, requirement for powered extraction tools, and increased procedural risk in cases with longer lead dwell times.$^{149}$,$^{150}$

The benefit of extraction to improve CIED-related TR is unpredictable and dependent on lead dwell time. In a single-center study of 321 patients (338 leads), there was no significant overall difference in TR severity before and after extraction but use of a laser sheath was associated with a higher risk of worsened TR.$^{148}$ In the overall study cohort, 26.2% developed worsened TR after extraction but an equal percentage had TR improvement; however, when comparing patients with significantly improved TR with patients who had significant worsening, the group with worsened TR had a longer average lead dwell time (7.9 ± 3.3 years vs 3.7 ± 5.7 years).$^{148}$ A study of 119 patients with CIED-related TR undergoing extraction showed improvement in TV function in 35.3%, yet small studies in other high-volume programs have shown no benefit on TR severity with lead extraction.$^{151,152}$ Other factors contributing to TR improvement (or worsening) after lead extraction include the degree of annular dilation, nature of lead-valve interaction, and the degree of lead-related damage to the TV apparatus.$^{152}$ Despite improvements in technique and tools, lead extraction continues to be a challenging procedure with potential for death. Catastrophic complications include exsanguinaation from vascular laceration, TV avulsion, and cardiac perforation with tamponade.$^{150,153}$

The appropriateness of lead extraction should thus be considered in patients referred for CIED-related TR. The MDT should weigh the risks and benefits of lead extraction and potentially reimplantation, especially

considering that most of these patients have multiple comorbidities and frailty. On the other hand, lead extraction has the potential to improve TR. Further, among patients being considered for T-TEER, an indwelling lead can make the leaflets harder to image and the procedure more technically challenging. TTVR in the presence of an RV lead results in lead entrapment.$^{154}$ The published rate of lead entrapment in percutaneous TV intervention studies ranges from 3% to 36%, but few reports include CIED-specific outcomes.$^{155}$ In the Valve-in-Valve International Database registry, 31 patients had an RV lead, 3 of which were extracted before the procedure. Of the 28 entrapped leads, 1 lead was dislodged and 2 failed (10.7%) after 15-month follow-up.$^{156,157}$ Patients who undergo lead extraction before surgical TV replacement and require ventricular pacing may be candidates for pacing all a coronary sinus branch, the use of a leadless device, or an epicardial system. Patients who require defibrillator therapy may be candidates for a subcutaneous or extravascular system. The complexity of decision-making in these circumstances warrants an MDT approach that includes a lead management specialist.

4.6.7. Consequences of Progressive TR and RV Dysfunction

The development of right-sided HF and progressive TR is associated with increased mortality, more HF hospitalizations, and reduced QoL.$^{92,158,159}$ Most patients with severe TR have left-sided heart disease. Over time, with TV annular dilation and worsening TR, the RV dilates further and ultimately fails, leading to increased RV diastolic pressure. In advanced, severe TR with RV failure, the interventricular septum shifts toward the LV, leading to decreased LV cavity size and restricted LV filling, further increasing the already elevated LV diastolic and PA pressures, likely exacerbating RV-PA uncoupling.$^{160}$ The resulting elevated LA and RA pressures can lead to an increased risk of AF, irreversible RV failure, and death. Thus, earlier medical and procedural management of TR is essential to avoid deleterious downstream effects, such as cardiorenal and cardiohepatic syndromes, which can exclude candidacy for advanced therapies.

4.6.8. Cardiorenal and Cardiohepatic Syndromes

Longstanding TR can lead to elevated central venous pressure, chronic volume overload, and many negative downstream effects. Concomitant renal and hepatic dysfunction are frequently encountered in patients with chronic severe TR.$^{161,162}$ Elevated central venous pressure

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is transmitted to the renal vein with resultant elevation of renal venous pressure, decreased renal blood flow, increased interstitial pressure, and worsening renal function.$^{163}$⁻$^{165}$ Elevated central venous pressure is also transmitted to the hepatic veins, leading to a cascade of centrilobular congestion, sinusoidal dilation, and pervenular fibrosis. Centrilobular liver damage can extend to the periphery with connective tissue deposition bridging 1 central vein to the other and sometimes result in cardiac cirrhosis.$^{166}$ Finally, chronic volume overload can lead to systemic congestion that overwhelms the splanchnic microcirculation, leading to intra-abdominal pressure elevation.$^{161}$ Increased intra-abdominal pressure may reduce transmural renal and hepatic perfusion pressures further and lead to worsening end-organ function.$^{161}$

4.6.9. Referral to Advanced HF Team

Finding the “golden moment” for referral for advanced HF therapies, including TV intervention, in patients with HF and significant TR can be challenging, particularly in patients who suffer from RV failure to a greater extent than LV failure.$^{167}$ Patients with significant TR and early signs of cardiorenal disease, cardiohepatic disease, PH, worsening arrhythmias, or >2 hospitalizations in the past year may benefit from a consultation with an advanced HF cardiologist; however, the signs of deteriorating RV function that signal worsening are similar to those with HF in general. The “E” in the acronym I NEED HELP is an excellent starting point for when to consider referral to an HF specialist in the TR patient (Table 4).$^{168}$ A more detailed discussion of criteria that should prompt referral have been outlined by Morris et al.$^{167}$

4.7. TV Intervention

4.7.1. Surgical Treatment of TR

Surgery for Secondary TR at Time of Left-Sided Surgery

Significant TR is frequently encountered among patients who are referred for surgical correction of MR. In low-to-intermediate surgical risk patients with primary MR and severe TR, international practice guidelines recommend TV surgery at the time of MV repair or replacement.$^{5,169}$ If TR is uncorrected, progressive TR may occur despite correction of the MV pathology.$^{170,171}$ Concomitant TV repair during MV surgery is important because late reoperation for residual severe TR is associated with RV failure and high operative mortality.$^{172,173}$ In the majority of cases, TV repair is preferred over TV replacement. Patients with unrepairable intrinsic leaflet disease should undergo TV replacement.$^{174}$ As reported from an analysis

|Letter|Definition|Description| |---|---|---| |I|Inotropes|Previous or ongoing requirement for dobutamine, milrinone, dopamine, or levosimendan| |N|NYHA functional class Natriuretic peptides|Persisting NYHA functional class III or IV and/or persistently high BNP or NT-proBNP| |E|End-organ dysfunction|Worsening renal or hepatic dysfunction in the setting of HF| |E|Ejection fraction|Very low ejection fraction <20%| |D|Defibrillator shocks|Recurrent appropriate defibrillator shocks| |H|Hospitalizations|>1 hospitalization with HF in last 12 months| |E|Edema/escalating diuretics|Persisting fluid overload and/or increasing diuretic requirement| |L|Low blood pressure|Consistently low BP with systolic <90 to 100 mm Hg| |P|Prognostic medication|Inability to up-titrate or need to decrease/cease ACE-I, ARB, ARNI, MRA, or beta-blocker|

Reprinted with permission from Baumwol et al.$^{168}$

ACE-I = angiotensin-converting enzyme inhibitor; ARB = angiotensin receptor blocker; ARNI = angiotensin receptor-neprilysin inhibitor; BNP = B-type natriuretic peptide; BP = blood pressure; HF = heart failure; MRA = mineralocorticoid receptor antagonist; NT-proBNP = N-terminal pro-B-type natriuretic peptide; NYHA = New York Heart Association.

of 88,473 patients from the Society of Thoracic Surgeons database, the addition of concomitant TV repair at the time of MV surgery is not associated with higher operative mortality rates, although it is associated with an increase in risk-adjusted occurrence of any postoperative morbidity (prolonged ventilation, deep sternal wound infection, stroke, renal failure, and reoperation).$^{174}$ An additional important observation from this analysis was a higher risk of permanent pacemaker implantation among patients undergoing concomitant TV repair (14.7%) compared with those without TV repair (5.4%) at the time of MV surgery.$^{174}$ Both preoperative severe RV dysfunction and PH are associated with postoperative RV failure. Patient selection for TV surgery by an MDT is critical. Transcatheter options should be considered for high-risk surgical patients. Hospital admission for preoperative medical optimization (prehabilitation) can be useful for patients with advanced HF and renal or hepatic dysfunction.

A more controversial scenario centers on surgical management of mild to moderate TR in patients referred for MV surgery. Guidelines propose that for patients with progressive TR undergoing MV surgery, TV surgery can be beneficial in the context of either TA dilation (TA end-diastolic diameter >4.0 cm (or >21 mm/m$^{2}$, measured on preoperative apical 4-chamber TTE at end-diastole) or prior signs of right-sided HF or PH.$^{5,169}$ In a single-center

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observational study reported by Dreyfus et al,$^{175}$ 311 patients underwent MV repair between 1989 and 2001. Transcatheter TV annuloplasty (TTVA) was performed only if the TA diameter was greater than twice normal size (≥70 mm by intraoperative measurement or 40 mm [21 mm/m$^{2}$] on apical 4- or 2-chamber TTE) regardless of TR grade. TR increased by >2 grades in nearly 50% of the patients with dilated TV annuli who did not undergo TTVA vs 2% of those who did.$^{175}$ This observation suggests that TTVA could be considered when annular dimensions exceed these thresholds, irrespective of the degree of preoperative TR.

Since this initial report 2 decades ago, there has been much debate regarding the need for concomitant TV surgery in those with mild-to-moderate TR during MV surgery. Investigators have shown that postoperative moderate TR is associated with a >50% reduction in 5-year survival and functional status compared with no or mild residual postoperative TR.$^{176}$,$^{177}$ Left uncorrected, moderate or greater TR may progress in approximately 25% of patients and result in worse long-term functional outcomes and survival.$^{178}$ Most recently, Gammie et al$^{179}$ randomized 401 patients undergoing MV surgery for degenerative MR to MV surgery alone or MV surgery plus TV repair in patients with moderate TR or with mild TR and TA dilation. At 2 years, patients who underwent concomitant TV repair experienced a significantly lower incidence of the composite primary endpoint of reoperation for TR, progression of TR by 2 grades, presence of severe TR, or death, compared with those who underwent MV surgery alone (3.9% vs 10.2%; P = 0.02).$^{179}$ The endpoint was driven largely by a reduction in the rate of progression of TR among those with moderate TR at baseline; however, the performance of TV repair was associated with a higher risk of postoperative permanent pacemaker implantation in the combined TV and MV surgery group (14.1% vs 2.5%).$^{179}$ A comparable risk of postoperative permanent pacemaker implantation after TV surgery has been reported from other registries.$^{174,180-182}$

Surgical practice has evolved to the point where concomitant TV repair at the time of MV surgery is performed in most patients with moderate or greater TR, especially in those with a history of right-sided HF, and in some centers for select patients with lesser degrees of TR with annular dilation. When possible, repair should be performed with TTVA using a rigid/semirigid incomplete ring. The long-term implications of permanent pacing require additional study.

4.7.2. Surgery for Isolated TR

The optimal timing of referral for surgical treatment of isolated TR is undefined. Often, surgery is performed too late in the natural history of the disease, due to delayed recognition and patient-related comorbidities. Surgery for isolated TR has commonly been performed when patients present with right-sided HF, deteriorating RV function, or worsening hepatic or renal function. As per the 2020 ACC/AHA Valvular Heart Disease Guideline,$^{5}$ isolated TV surgery can be beneficial to reduce symptoms and recurrent hospitalizations in patients with signs and symptoms of right-sided HF and severe A-STR who are poorly responsive to medical therapy. TV surgery can be considered for select patients who have undergone prior cardiac surgery and who have progressive right-sided HF poorly responsive to medical therapy. The increased risks associated with reoperative surgery in this context require careful MDT assessment and shared decision making. Surgery is not usually offered in the setting of severe PA hypertension or advanced RV dysfunction. A risk score has been developed to predict in-hospital mortality in patients after isolated TV surgery (Figure 11).$^{10}$

Reduction of TR severity can result in improved hepatic congestion and a reduction in diuretic requirements.$^{183,184}$ TV surgery for primary TR is best performed before the development of advanced ventricular dysfunction or severe PH. With successful surgery for primary TR, RA pressure drops, and congestion generally resolves as RV function improves. These favorable changes are associated with improved morbidity and mortality.

Previous studies of outcomes following surgery for isolated TR for primary or secondary TV disease reported early mortality rates of 8%-10%.$^{185-188}$ In these series, patients were referred later in their course and after the development of end-organ damage. Some smaller series have shown improved surgical outcomes with post-operative mortality rates of 3.2% to 5.1%,$^{189,190}$ prompting renewed interest in earlier surgery for patients with severe isolated TR.$^{186,189,191-193}$ Most recently, in an analysis utilizing the national Society of Thoracic Surgeons adult cardiac surgery database of 13,587 patients undergoing isolated TV surgery from 2017 to 2023, Thourani et al$^{194}$ reported an early mortality rate of 5.6% (6%-7% for patients without infective endocarditis as the indication for surgery), a significant improvement compared with historical norms. The investigators observed that outcomes improved with time, including

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 Reprinted with permission from Dreyfus et al.$^{175}$ NYHA = New York Heart Association; LV = left ventricular; RV = right ventricular; TR = tricuspid regurgitation; TV = tricuspid valve.

rates of operative mortality, stroke, renal failure, reoperation, combined morbidity and mortality, prolonged ventilation, and prolonged length of stay.$^{194}$ This analysis has led to a new risk model$^{195}$ for 8 outcomes after isolated TV surgery and can aid as a resource for patient counseling, clinical decision-making, quality improvement, and benchmarking against transcatheter devices applied in comparable patient cohorts. The main limitation of the score relates to the lack of inclusion of any parameter of right-sided heart function or signs of right-sided HF in the model.

The reported improvements following surgery for isolated TR are in part due to better patient selection and careful preoperative assessment of PH and RV function. Prehabilitation, or a period of inpatient medical optimization with diuresis and inotrope administration, has been associated with improved outcomes.$^{189}$ Preoperative variables associated with increased surgical mortality include NYHA functional class III/IV, nonelective surgery and higher Model for End-Stage Liver Disease scores, among others.$^{188}$ Prospective randomized studies comparing isolated TV surgery vs OMT have not been performed; a survival benefit with TV surgery has not been convincingly demonstrated.$^{179,196}$

4.7.3. TTVI

To date, the comparative effectiveness of isolated TV surgery vs TTVI has not been studied. T-TEER has not

been studied against TTVR. Rather, TTVIs have been compared against OMT. Eligibility criteria for randomization in both the Trial to Evaluate Cardiovascular Outcomes in Patients Treated With the Tricuspid Valve Repair System Pivotal$^{56}$ of T-TEER vs OMT and the TRISCEND II (TTVR in Patients with Severe TR II) trial$^{197}$ of TTVR vs OMT included echocardiographic core labadjudicated severe (or greater) TR. Patients in the TRI-LUMINATE study were deemed intermediate or high risk for death or major comorbidity by the cardiac surgeon member of the local MDT. Although surgical risk was not specified as an inclusion criterion in the TRISCEND II study, the median Society of Thoracic Surgeons Predicted Risk of Mortality score was 10%, indicating high surgical risk.$^{198}$

Currently, there are 4 different types of TTVIs: 1) leaflet coaptation devices (T-TEER); 2) annuloplasty; 3) orthotopic TTVR; and 4) heterotopic caval valve implantation (CAVI) (Figure 12).$^{199}$ Another category of “spacers,” which position devices in the regurgitant orifice, may be classified as leaflet coaptation devices, as they form a surface where the leaflets may coapt. Two transcatheter systems received the U.S. Food and Drug Administration’s approval in 2024 for use in patients with symptomatic severe TR despite OMT who are deemed appropriate candidates by a, MDT to improve health outcomes: TriClip (T-TEER, Abbott)$^{3}$ and EVOQUE (TTVR, Edwards Lifesciences).$^{2}$

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469

![graph TD\n A1[Severe Symptomatic TR] --> A2[Transcatheter Valve Repair]\n A1 --> A3[Transcatheter Valve Replacement]\n A2 --> A4[Transcatheter Edge-to-Edge Repair]\n A2 --> A5[Orthotopic Transcatheter Valve Replacement]\n A4 --> A6[PRO: Applies to wide range of anatomies; Less effective for severe leaflet tethering/RV dysfunction; Minimal prosthetic material = lower risk of device thrombosis]\n A4 --> A7[CON: Requires excellent leaflet imaging resolution; Steep learning curve; Modest TR reduction]\n A5 --> A8[PRO: Most effective at reducing TR; Can treat CIED-TR and wide range of pathology]\n A5 --> A9[CON: Available device sizes limits the ability to treat very dilated annuli; Risk of hemodynamic compromise in patients with severe RV dysfunction or pulmonary hypertension; Risk of leaflet thrombosis]\n A10[Transcatheter Annuloplasty] --> A11[PRO: Directly treats annular enlargement, may be favorable for A-STR; Mimics surgical technique]\n A10 --> A12[CON: Long procedural time; High screen fail rate; Cannot use for leaflet pathology]\n A13[Heterotopic Caval Valve Implantation] --> A14[PRO: May be best suited to treat extreme annular dilation, unfavorable anatomy for orthotopic device delivery, and/or severe RV dysfunction; Implantation is more simple and requires less demanding imaging compared to other modalities]\n A13 --> A15[CON: Reduces regurgitant flow but may have less positive effect on forward stroke volume compared to other modalities; Heightened risk of stent thrombosis]\n](1/parseimages/figure8ec55d8884494bc0b56f38d50eba8149_0_4.png)

4.7.4. Transcatheter TV Repair

Repair can be achieved with leaflet approximation devices, “spacers” (which fill the leaflet coaptation gap), annuloplasty procedures, and chordal approximation devices.$^{200}$ T-TEER is based on the surgical Alfieri repair procedure and mimics what has been accomplished for M-TEER. The TriClip system allows for the ability to navigate in septal and lateral directions with a shortened curve, permitting coaxial delivery.$^{199}$ In the pivotal TRI-LUMINATE trial, 350 eligible patients (94% with secondary TR) were randomized 1:1 in an open-label fashion to receive either T-TEER using the TriClip/TriClip G4 system plus OMT (n = 175) or OMT alone (n = 175) at 65 centers in

the United States, Europe, and Canada. The mean age was 78 years, 54.9% were women, 6.6% had undergone prior surgical MV repair, and 11.4% had undergone prior M-TEER. The primary endpoint, a hierarchical composite of all-cause mortality or TV surgery, HF hospitalization, and improvement in QoL scores measured by the KCCQ at 1 year, favored T-TEER (win ratio: 1.48; 95% CI: 1.06-2.13; P = 0.02) driven primarily by an improvement in QoL scores. At 1 year, the KCCQ score increased by a mean of 12.3 points in the T-TEER group vs 0.6 points in the control group (P < 0.001). The other components of all-cause mortality or TV surgery (9.4% vs 10.6%) and HF hospitalization (0.21 vs 0.17 events/patient-year) did not

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differ between the 2 arms at 1 year. The proportion of patients experiencing TR reduction to less than or equal to moderate severity at 30 days was superior with T-TEER (87% vs 4.8%; P < 0.001). The mean increase in the KCCQ score at 1-year follow-up was greater among those who achieved a greater degree of durable TR reduction (15.6 among patients with less than or equal to moderate residual TR at 1 year vs 3.8 among patients with greater than or equal to severe residual TR). Change in 6-minute walk distance from baseline to 1 year was not different between treatment groups. Device safety met the expected thresholds. No device embolization or device thrombosis occurred among patients in the T-TEER group.$^{56}$ The TRI.Fr trial randomized 300 patients with severe symptomatic TR to T-TEER using the TriClip system plus OMT (n = 152) or OMT alone (n = 148) at 24 centers in France and Belgium. The primary outcome, a 3-level ordinal clinical composite score at 12 months, was improved in 74.1% in the T-TEER arm compared with that of 40.6% in the OMT arm (P < 0.001). This benefit was driven primarily by improvements in NYHA functional class and patient global assessment. At 1 year, the KCCQ score increased by a mean of 15.9 points in the T-TEER group vs 0.4 points in the control group (P < 0.001). The proportion of patients with greater than or equal to massive TR at 12 months was 6.8% in T-TEER arm compared with that of 53.5% in the OMT arm (P < 0.001).$^{201}$ Similar results were reported in the single-arm “An Observational Real-world Study Evaluating Severe Tricuspid Regurgitation Patients Treated with the Abbott TriClip™ Device” study.$^{202}$ In a single-arm study of the first generation TriClip system at 3 years, TR was reduced to moderate or less in 79% of subjects. TR reduction achieved at 1 year was sustained through 3 years, along with improved QoL scores and NYHA status. Site-reported HF hospitalization rates also decreased from 0.56 events/patient-year 1 year before device implantation to 0.14 events/patient-year 3 years after device implantation.$^{203}$

The PASCAL system (Edwards Lifesciences) is also designed for T-TEER and has been approved for use in Europe, although not in the United States as of this writing, for treatment of TR. A single-arm early-feasibility study with 29 patients has been completed (Edwards CLASP TR EFS; NCT03745313).$^{204}$ TR reduction appeared durable at 1 year with low complication rates.$^{205}$ The CLASP II TR study (Edwards PASCAL Transcatheter Valve Repair System Pivotal Clinical Trial) of the PASCAL system will randomize 825 patients with symptomatic severe, or greater TR to receive T-TEER plus OMT or OMT alone (NCT04097145).$^{206}$

Although T-TEER can be used to treat a wide range of TV anatomy,$^{207}$ the optimal coaptation gap for successful

T-TEER remains to be defined. In the TRILUMINATE study, patients with coaptation gaps >2 cm were excluded; among included patients, the mean coaptation gap was 5.3 mm. The mean TA diameter among enrolled patients was 4.4 cm. Although TA diameter was not an exclusion criterion, patients with large annuli typically have larger coaptation gaps. The anatomical location of the coaptation gap (ie, which leaflets are most involved), leaflet anatomy (ie, ≥4 leaflets rather than 4), and the degree of leaflet restriction/tethering are also important considerations. Their impact on successful T-TEER needs to be further clarified.$^{57}$ Besler et al$^{208}$ identified a small TR coaptation gap size and a central/anteroseptal TR jet location as independent predictors of procedural success in patients with symptomatic TR undergoing T-TEER. The investigators identified a coaptation gap cutoff value of 7.2 mm as the best discriminator for successful T-TEER, with a success rate of <30% in patients with a gap >10 mm.$^{208}$ Other considerations include the requirement for high-resolution intraprocedural imaging supervised and guided by an interventional echocardiographer, a steep operator learning curve, and modest postprocedural TR reduction.$^{199}$ T-TEER can be successfully performed among patients with indwelling CIED,$^{209}$ but there are frequently additional procedural and imaging challenges for T-TEER in this patient population.

Whereas T-TEER is the most frequently performed TTVI, TTVA replicates the most common surgical repair procedure while preserving the feasibility of future treatment options. The Cardioband system was the first TTVI device approved in Europe.$^{200,210}$ It is not approved for use in the United States. It uses multiple anchoring screws that are implanted using echo guidance to reduce tricuspid annular dimensions. Next-generation devices are expected to simplify the procedure.

4.7.5. TTVR

Orthotopic TTVR is a procedure designed to replace the TV with a bioprosthetic substitute. Given the unique anatomy of the TV, there have been different anchoring and stabilization strategies developed to facilitate positioning. The EVOQUE (Edwards Lifesciences) is currently the only U.S. Food and Drug Administration-approved device for use in the United States as of this writing. In the TRISCEND (TTVR with the EVOQUE System in Patients with Symptomatic Severe TR) single-arm study of 176 patients, cardiovascular mortality was 1.7% and 9.4% at 30 days and 1 year after EVOQUE implantation, respectively. New permanent pacemaker implantation was performed in 13% of patients within 30 days, a rate not significantly different from that reported from surgical series. At 1 year, patients had significant improvement in QoL scores, and functional (NYHA) status.$^{211}$ The

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TRISCEND II randomized clinical trial was an international, multicenter study in which 400 patients with symptomatic severe TR were randomized (2:1) to either TTVR with the EVOQUE device plus OMT or OMT alone.$^{197}$ The mean age was 79 years, 74% were women, 32% had undergone prior valve surgery or intervention, and 95% had AF, CIED-related and primary TR accounted for 14% of patients. Treatment with TTVR plus OMT was superior to OMT alone, as evidenced by a win ratio of 2.02 (95% CI: 1:56-2.62; P < 0.001), an outcome driven primarily by improvements in QoL scores and favorable changes in NYHA functional class. One-year rates of all-cause mortality and hospitalization for HF did not differ between the groups. Echocardiographic core laboratory assessed TR severity was reduced from severe (or greater) to mild or less in 95.3% of patients treated with TTVR. Rates of 30-day all-cause mortality (3.5%), severe bleeding (10.4%), and new permanent pacemaker implantation (24.7%) with TTVR underscore the need for careful patient selection and informed decision-making.

Potential benefits of TTVR include the ability to treat a wider range of TR pathologies compared with that of T-TEER and reduction of TR to mild or less in most patients. Limitations of TTVR include limited available device sizes, leaflet thrombosis, risk of hemodynamic compromise in patients with advanced RV dysfunction or PH, challenges with CIED-lead management (extraction, entrapment), unclear options for future reintervention(s), bleeding, and the risk of permanent pacemaker implantation.

4.7.6. Heterotopic CAVI

Heterotopic transcatheter bioprostheses can be implanted in a bicaval position to reduce symptoms from severe TR in patients who have unfavorable annular dilation (annulus dimension exceeds device size availability), unfavorable anatomy for orthotopic device delivery, or severe RV dysfunction. CAVI is relatively simpler and does not entail the same degree of advanced imaging currently required for orthotopic TTVR. Dedicated prostheses are available with different fixation modalities, such as single bicaval implant or separate valves.$^{199,200,212,213}$ The exact role of CAVI in the field needs to be further developed, considering its simplicity and reproducibility, with the inherent limitation of an intervention that does not address the culprit valve lesion. CAVI does not preclude CIED lead manipulation if needed.

4.7.7. Choosing Between T-TEER and TTVR

The choice between T-TEER and TTVR is relegated to the MDT (Table 5). Considerations include TV anatomy and function, RV function, PA pressures, patient-related comorbidities (hepatic/renal dysfunction, frailty, ability

|May Favor T-TEER|May Favor TTVR| |---|---| |Septal-lateral coaptation gap ≤7 mm|Septal-lateral coaptation gap >7 mm| |Anterior-septal jet location|Anterior-posterior jet location| |≤3 TV leaflets|>3 TV leaflets or scallops| |Focal primary disease of TV (eg), prospise); mild leaflet tethering|Significant TV leaflet tethering or thickening| |Absence of CIED leads, or CIED leads located in commissure or away from TR jet location|CIED-related TR*| |Good intraprocedural imaging windows for lateral visualization|Poor leaflet visualization| |Advanced renal dysfunction (CT with contrast is necessary for TTV planning)|| |Intolerance or inability to take anticoagulation|| |*Although TTVR can more often be performed than T-TEER in CIED-related TR, intervention in this context careful consideration by the MDT. For instance, jailing or entrapment of leads by the TTVR frame may create significant challenges. Lead extraction for infection may not be feasible. Entrapment of ICD leads may pose unique challenges, such as potentially impacting the ability to deliver effective ATP. Other factors to consider when comparing T-TEER and TTVR include MDT experience and expertise, patient comorbidities, RV function, and PA pressures.|| |ATP = antichutarcia pacing; CIED = cardiac implantable electronic device; CT = computed tomography; ICD = implantable cardioverter-defibrillator; MDT = multi-disciplinary team; PA = pulmonary artery; RV = right ventricular; T-TEER = tricuspid transcatheter edge-to-edge repair; TR = tricuspid regurgitation; TTVI = transcatheter tricuspid valve intervention; TTVR = transcatheter tricuspid valve replacement; TV = tricuspid valve.||

to tolerate anticoagulation), and the MDT's experience and expertise.$^{200}$ Head-to-head trials have not been performed, and it is unlikely they will be. Whereas TR reduction is generally less robust with T-TEER compared with that of TTVR, it is a comparatively safer procedure with fewer complications, including rhythm disturbances, bleeding, CIED ramifications, and RV dysfunction, and is generally considered first-line therapy for most patients with appropriate anatomy. Favorable anatomical features for T-TEER include small septolateral coaptation gap (≤7 mm), anteroseptal jet location, focal primary disease, ≤3 leaflets, absence of CIED leads, or CIED lead present that are located in the commissure or away from the jet location, and good intraprocedural imaging windows for leaflet visualization.$^{214}$ Operator experience and comfort may enable the successful pursuit of T-TEER in more complex anatomies.$^{207}$ Conversely, TTVR is preferred in cases of larger septolateral coaptation gap, anteroposterior jet location, >3 leaflets or scallops, significant leaflet thickening or tethering, CIED-related TR, and poor leaflet visualization. As TTVR requires performance of a preprocedural contrast CT, it may be less suitable for patients with advanced renal dysfunction. Further, the need for routine anticoagulation may be challenging for many patients with TR, especially those with frailty or

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 Cut-off of 2.5 to determine High vs Low Risk

Reprinted with permission from Russo et al.$^{219}$ GFR = glomerular filtration rate; GGT = gamma-glutamyl transferase; LVEF = left ventricular ejection fraction; TTVI = transcatheter tricuspid valve intervention.

significant liver disease, although it should be considered as these patients often have high CHA₂DS₂-VASc (Congestive heart failure, Hypertension, Age [>65 = 1 point, >75 = 2 points], Diabetes, previous Stroke/transient ischemic attack [2 points], Vascular disease [peripheral arterial disease, previous myocardial infarction, aortic atheroma]) scores.

A small percentage of patients with primary TR were included in the randomized trials of TTVI vs OMT. U.S. Food and Drug Administration approval of the devices was not contingent upon the etiology of severe TR, although the experience to date chiefly pertains to patients with secondary TR. Ongoing studies in the TTVI space that may impact future recommendations for referral include CLASP II TR (Edwards PASCAL Transcatheter Valve Repair System Pivotal Clinical Trial; NCT04097145),$^{206}$ TRICI-HF (TRICuspid Intervention in Heart Failure Trial) (T-TEER, TTVA; NCT04634266),$^{215}$ TRINITY (TRIal to Evaluate TraNsvenous TrICuspid Valve ReplacementenT With LuX-Valve Plus System in Patients With Severe or Greater Tricuspid Regurgitation) (LuX-Valve Plus TTVR; NCT05436028),$^{216}$ TRICAV (A Prospective, Multicenter Clinical Trial of the TricValve® Transcatheter Bicaval Valve System in Subjects With Severe Tricuspid Regurgitation - TRICAV trial) (CAVI TricValve; NCT06137807),$^{217}$ and TRACE-NL (Evaluation of the Safety, Efficacy and Cost-Effectiveness of Transcatheter Tricuspid Valve Repair in Patients with Severe Tricuspid Regurgitation in the Netherlands) (T-TEER TriClip or PASCAL vs OMT; NL-OMON53966).$^{218}$

The Tricuspid Valve Intervention Risk Score to predict 1-year mortality or HF hospitalization after TTVI was derived from an international registry of 483 patients

who had undergone transcatheter treatment of severe TR between 2016 and 2022 (84% T-TEER, 8% TTVR) with a variety of devices (Figure 13).$^{219}$ One-third of the patients in the cohort underwent concomitant MV intervention. The score utilized 5 easily measured variables: 1) AF at baseline; 2) estimated glomerular filtration rate <30 mL/min; 3) elevated gamma-glutamyl transferase or bilirubin; 4) signs of right-sided HF; and 5) LVEF <50% and demonstrated modest discrimination (C statistic = 0.68), sensitivity and specificity in the heterogenous population analyzed. Incorporation of both surgical and transcatheter TV intervention risk scores into MDT deliberations and patient shared decision making can be considered as appropriate, but refinements in these scores will be needed as experience accumulates. It is anticipated that the next iteration of the ACC/AHA Guidelines for the Management of Patients With VHD will include updated recommendations for surgical and transcatheter TV intervention for patients with severe native valve TR. The current 2021 European Society of Cardiology Guideline contains a Class IIb recommendation for transcatheter treatment of severe secondary TR in inoperable patients at a Heart Valve Center with expertise in the treatment of TV disease.$^{169}$

4.8. Management After TV Intervention

Common characteristics of patients presenting for TV intervention include older age, HF, longstanding persistent AF, prior cardiac (valve, coronary, rhythm) procedures, and impaired renal and hepatic function. Management considerations in patients after surgical or transcatheter TV intervention are linked closely with

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their comorbidity profile. Continued provision of GDMT for HF, decongestion, and anticoagulation, with attention to drug pharmacokinetics, is foundational. Management of newly implanted or existing CIEDs is supervised by device experts. Surgical patients may receive epicardial lead systems. Other patients may receive leadless pacemakers, coronary sinus leads, or subcutaneous or extravascular implantable cardioverter-defibrillators. Nutrition, diet, physical activity, and cardiac rehabilitation should be addressed. Multidisciplinary care is most often coordinated by advanced HF teams but can be transitioned to other clinicians as health status improves. In general, the treatment of the underlying disease process in patients with secondary TR may significantly improve the degree of RV dysfunction after intervention; however, not all patients improve because of irremediable RV dysfunction, residual LV dysfunction, altered interventricular septal mechanics, persistent PH, AF, and/or their combination.

Following TR intervention, the RV encounters an abrupt increase in afterload, a physiological response that is more frequently observed after surgical valve replacement and TTVR than T-TEER due to the more effective reduction in TR with the former approaches. Pressure-volume analyses predict that afterload will increase as the RV ejects a greater proportion of its SV into the PA rather than the low impedance RA. Although ejection phase indices of RV function (ie, TAPSE) decline after TTVR, there is an observable decrease (or favorable change) in RV-PA uncoupling, as measured by the ratio of TAPSE-to-PA systolic pressure, a change that associates with better 1-year survival, and implies sufficient contractile reserve to overcome the abrupt increase in RV afterload.$^{74}$ Pre-TV intervention assessment and optimization of RV function are critical.

RV function is typically reduced$^{220}$ after TTVI because of intrinsic structural myocardial abnormalities and in response to the increased in effective after load after TR reduction. Whereas baseline RV dysfunction is associated with reduced event-free survival, a reduction in echo- cardiographic measures of RV function following TTVI has not been associated with adverse outcomes.$^{221}$ In fact, these measures may be associated with greater RV reserve and improved outcomes. Following TTVI, there is an expectation of reverse RV remodeling. In the single- arm TRILUMINATE study, patients showed early 30-day RV reverse remodeling after successful T-TEER with re- ductions in RV end-diastolic dimension, RA volume, and TA diameter, as well as an increase in TAPSE.$^{222,223}$ Whereas TR reduction was sustained, and RV end- diastolic dimension remained stable during 2 years of follow-up, RA volume and TA diameter-factors that favor TR progression-increased, despite continued favorable effects on TAPSE. The magnitude of RV reverse

remodeling may be limited by pre-existent RV contractile dysfunction, the degree of residual or recurrent TR, pulmonary vascular resistance, and the severity of coexistent left-sided heart disease. LV filling, SV, and cardiac index may improve after TV intervention for isolated TR due to favorable effects on ventricular interdependence and septal shift toward the right-sided heart following a reduction in RV size.$^{224}$ Although the increase in LV preload post-TV intervention could potentially increase LV diastolic pressure and exacerbate left-sided HF, this phenomenon was not observed in a small study (n = 20) of patients with HFpEF after T-TEER.$^{225}$ T-TEER increased LV SV and LV end-diastolic volume without increasing LV end-diastolic pressure. Consequently, LV diastolic function improved. The increase in LV end-diastolic volume correlated with a decrease in RV end-diastolic volume. Secondary to a decrease in early RV filling, improvements in early LV filling were observed. Whether increased LV preload post-TV intervention is detrimental in patients with pre-existent left-sided disease is difficult to predict on an individual basis, although it should be considered.

4.8.1. HF Management

Continuation of a multipronged HF treatment regimen is required postintervention. It is important to determine effective decongestion and maintain euvolemia with direutics following hospital discharge. Determining euvolemia in an individual patient may be challenging. Both relief of dyspnea and attaining preadmission body weight are poor markers of decongestion. Patients with severe TR and right-sided HF may not display the typical physical examination findings associated with left-sided HF, such as those indicative of pulmonary congestion. Although many noninvasive parameters to detect congestion have been used as surrogates for the presence of increased filling pressures (RA pressure >7 mm Hg or pulmonary capillary wedge pressure >18 mm Hg), their value in detecting the optimal euvolemic point without residual hemodynamic congestion is unclear. Over-emphasis on serial biomarker levels as surrogates for changes in volume status might lead to inappropriate dose escalation of loop diuretics among patients without significant residual congestion and potentially increase the aggregate risks of hypotension, renal dysfunction, and other adverse events. With these limitations in mind, a combination of clinical, bedside appraisal, and biomarker/imaging assessment is reasonable when assessing adequate diuresis (Figure 14).

Other postintervention considerations include: 1) maintenance or addition of spironolactone, not only as a K$^{+}$ (potassium ion)-sparing; diuretic, but also as an agent to counter any degree of secondary hyperaldosteronism related to residual hepatic congestion; 2) continued

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|||EUVOLEMIA|EUVOLEMIA|EUVOLEMIA|EUVOLEMIA|EUVOLEMIA| |---|---|---|---|---|---|---| |Clinical evaluation|Orthopnea|None|None|Mild|Moderate|Severe/worst| |Clinical evaluation|JVP (cm)|<8 and no HJR|<8|8-10 or HJR+|11-15|>16| |Clinical evaluation|Hepato megaly||Absent|Liver edge|Moderate pulsatile enlargement|Massive enlargement and tender| |Clinical evaluation|Edema||None|+1|+2|+3/+4| |Clinical evaluation|6 MWT|>400 m|300-400 m|200-300 m|100-200 m|<100 m| |Technical evaluation|NP (one of both): -BNP -NT-proBNP||<100 <400°|100-299 400-1500|300-500 1500-3000|>500 >3000| |Technical evaluation|Chest X-ray|clear|clear|cardiomegaly|- pulmonary venous congestion* - small pleural effusions*|- Interstitial or alveolar edema| |Technical evaluation|Vena Cava imaging|None of two: - Max diameter >2.2 cm -collapsibility <50%|One of two: - Max diameter >2.2 cm -collapsibility <50%|Both: - Max diameter >2.2 cm -collapsibility <50%||| |Technical evaluation|Lung Ultrasound|<15 B-lines when scanning 28-sites|15-30 B-lines when scanning 28-sites|>30 B-lines when scanning 28-sites|||

Reprinted with permission from Mullens et al.$^{113}$ *Chest X-ray can be clear, but presence of abnormalities suggests higher degree of congestion. 6MWT = 6-minute walk test; BNP = B-type natriuretic peptide; HJR = hepatojugular reflux; HR = heart rate; JVP = jugular venous pulsation; NP = natriuretic peptide; NT-proBNP = N-terminal pro-B-type natriuretic peptide.

management of left-sided heart disease; 3) directed treatment of precapillary PH when indicated; 4) management of AF, which in most patients comprises continuation of rate control and anticoagulation; 5) CIED management; and 6) nutrition, salt restriction, and a dedicated program of cardiac rehabilitation.

4.8.2. CIED Considerations Following TV Intervention

Patients who undergo percutaneous or surgical TV intervention often require permanent pacemaker implantation. In a study of Medicare beneficiaries who underwent surgical TV repair or replacement, 18.9% underwent subsequent permanent pacemaker implantation.$^{181}$ In a randomized controlled trial examining the

efficacy and safety of TTVA during MV surgery for severe degenerative MR in patients with moderate TR or mild TR with annular dilation, permanent pacemaker implantation was required in 14.1% of patients in the MV surgery plus TTVA group compared with that of 2.5% of patients in the MV surgery alone group (interrater reliability 5.75; 95% CI: 2.27-14.60).$^{179}$ In a subsequent analysis of this trial, performance of TTVA, older age, and lower LVEF were independent risk factors for permanent pacemaker implantation.$^{226}$ Rates of CIED implantation are higher for surgical TV replacement (between 15% and 34%).$^{197}$

Although data are limited for TTVI, a new permanent pacing system was implanted within 30 days of the

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postprocedure in 24.7% of patients enrolled in the TRISCEND II study of TTVR.$^{197}$ In the TRILUMINATE trial, 2.9% of patients in both the T-TEER and control groups received permanent pacemakers by 1 year.$^{56}$

The most common indications for permanent pacemaker implantation after TV surgery are AF with symptomatic bradycardia, complete heart block, and sinus node dysfunction.$^{227}$ Options for pacing include transvenous RV pacing, coronary sinus branch pacing, leadless RV pacing, and epicardial pacing. Despite limited data, RV pacing using a lead across a newly implanted surgical TV bioprostthesis is generally avoided due to concerns for increased risk of structural valve degeneration.$^{228}$ In a series of 791 patients who underwent surgical TV repair, a transvenous pacemaker was found to be an independent transvenous pacemaker for late TR of 2+ or 3+ severity.$^{229}$ Conversely, other series have not reported an increased incidence of significant prosthetic TR after RV lead placement.$^{230}$ Coronary sinus branch pacing circumvents crossing the TV and is a standard technique in the era of biventricular pacing systems. A retrospective review of 23 patients with TV disease who underwent pacing using a coronary sinus approach showed excellent and stable lead parameters with normal function during 5.3 years of follow-up.$^{231}$ Of note, the lead position was chosen based on lead parameters and stability rather than a need for cardiac resynchronization therapy. Leadless pacing systems are an appealing choice in this scenario, although a basal position may not avoid valve-pacemaker interaction. A small series of 14 patients who received a leadless pacemaker after TV surgery showed stable lead parameters and no interference with the TV.$^{232}$ The high rate of pacemaker placement after TV surgery warrants consideration of placing epicardial pacing leads at the time of surgery that can be tunneled and connected with a generator as indicated. A consecutive series of 80 patients who underwent epicardial pacemaker placement after TV surgery or combined valve procedures showed a 6.3% rate of revision for lead dysfunction, 1 pocket infection, 1 cardiac arrest due to pacing-induced ventricular tachycardia, revision to biventricular pacing in 7%, and reliable lead parameters during 32 months of follow-up.$^{233}$

For patients with pre-existing RV transvenous leads who undergo TV surgery, the leads are either repositioned to reduce the risk of interference with the operated valve or removed with implantation of a nontransvalvular system. Depending on the findings from pre- and intraprocedural imaging, transvenous leads can be maintained in selected patients undergoing T-TEER. For patients undergoing TTVR, however, the

||Factor|Risk| |---|---|---| |Preprocedural factors|Age|Increases with age| |Preprocedural factors|Lower LVEF|Higher| |Preprocedural factors|Conduction disease|Higher| |Procedural factors|TEER|Low| |Procedural factors|TTVR|Moderate| |Procedural factors|Surgery|Moderate| |Procedural factors|Multiple surgical valve|Highest| |Pacemaker options|Conventional RV lead|May worsen TV function| |Pacemaker options|Coronary sinus lead|Avoids TV interaction| |Pacemaker options|Leadless device|May avoid TV interaction| |Pacemaker options|Epicardial device|Avoids TV interaction|

LVEF = left ventricular ejection fraction; RV = right ventricle; TEER = transcatheter edge-to-edge repair; TTVR = transcatheter tricuspid valve replacement; TV = transcatheter valve.

lead can be “jailed” against the prosthetic device and native tissue. The risks related to “jailing” include: 1) inability to extract the lead (ie, in the setting of infection); and 2) lead malfunction. A risk-benefit analysis of these possible adverse consequences should be carefully weighed against the ability to extract the lead before intervention, the pacemaker dependence status of the patient, and the risk of pacemaker infection. The need for preprocedural electrophysiology input in these instances is critical, preferably with access to an expert in lead extraction especially for patients who are pacemaker dependent (Table 6).

4.9. Conclusions

The availability of transcatheter interventions to treat severe TR has energized the cardiovascular community to improve evaluation and management strategies targeted at this valve lesion. Most patients encountered in practice have secondary TR, which develops in the context of other cardiopulmonary diseases. Figure 1 highlights the important messages embedded in this document and the key knowledge and practice objectives for the clinician:

1. Screen for TR early by: 1) anticipating its development in context of left-sided heart disease, AF, PH, or following CIED placement; 2) assessing the venous wave form on physical examination; and 3) incorporating the findings from TTE that may have been performed for another indication.

2. Define the etiology, mechanism, and severity of TR with TTE as the preferred initial imaging modality.

3. Apply indications for advanced imaging with TEE, cardiac CT, and CMR, and selectively use cardiac catheterization to augment characterization of TR

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severity, improve anatomical assessment when indicated, and aid in planning for TV intervention.

4. Manage left-sided heart disease with GDMT and intervention when indicated for HF, VHD, AF, and PH.

5. Incorporate understanding of the natural history of TR and consider referral to an advanced heart disease specialist for patients with moderate or greater TR, especially when HF symptoms are progressing and/or diuretic therapy has been escalated.

6. Recognize indications for referral to MDT for consideration of surgical or transcatheter TV intervention.

7. Anticipate CIED management issues before and after TV intervention, in collaboration with other members of the MDT and a device expert. Recognize the potential hazards with CIED lead extraction.

8. Counsel patients on expected benefits and risks with TV surgery and currently available TTVIs, utilizing MDT consensus and shared decision making. Refer to ACC CardioSmart TR module for tips on shared decision-making.$^{234}$

9. Design appropriate evaluation and treatment strategies for postsurgical or transcatheter intervention

with attention to medical, rhythm, device, and anti-coagulant management.

10. Establish goals of care and treatment expectations for patients in whom TV intervention is considered by the MDT to be inappropriate or not feasible.

The tricuspid space continues to rapidly evolve. Updated recommendations for the management of TR are anticipated in the next iteration of the ACC/AHA VHD Guidelines.

PRESIDENT AND STAFF

Christopher M. Kramer, MD, FACC, President Cathleen C. Gates, Chief Executive Officer Richard J. Kovacs, MD, MACC, Chief Medical Officer Brendan Mullen, Senior Executive Vice President Joseph M. Allen, MA, Team Leader, Science & Quality Amy Dearborn, Team Leader, Decision Science Ashleigh M. Covington, MA, Team Leader, Decision Science Dahsina S. Bhatia, MPH, Project Manager, Decision Science Delivery Grace D. Ronan, Senior Production and Operations Manager, Clinical Policy Publication

REFERENCES

1. US Food and Drug Administration. Edwards EVO-QUE tricuspid valve replacement system. Accessed March 28, 2025. https://www.accessdata.fda.gov/cdrh/docs/pdf23/P230013A.pdf

2. U.S. Food and Drug Administration. TriCip4 system. Accessed March 28, 2025. https://www.accessdata.fda.gov/cdrh/docs/pdf23/P230007A.pdf

3. Centers for Medicare & Medicaid. Transcatheter tricuspid valve replacement (TTVR). Accessed March 27, 2025. https://www.cms.gov/medicare-coverage-database/view/naccal-decision-memo.aspx?proposed-N&ncaid=3148fromTracking=Y8__YJZ1OmFjYz61ZpvOmYwNDZhYTEONTKOMZ1zlNDhNDZhNmM30Tg4ZT1LTQyOjc6YWVMOZT1oY3E2ZDM3DZQWy7dkYWU1OTYO ODZIMWMXyZj1MDVLMNTjYAyTNjYyEjNyMONMDN1KYZE9ZnQzYy3Mml4NZQ0OQ6VDpG

4. Januzzi Jr J, Jr, Ahmad T, Binder LG, et al. 2019 Methodology for creating expert consensus decision pathways: a report of the American College of Cardi-ology. J Am Coll Cardiol. 2019;74:1138-1150.

5. Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA guideline for the management of patients with valvular heart disease: a report of the American College of CardiACC/AHA guideline for the management of patients with valvular heart disease: a report of the American College of CardiACC/AHA tional Committee on Clinical Practice Guidelines. J Am Coll Cardiol. 2021;77:e25-e197.

6. Topilsky Y, Maltais S, Medina inojosa J, et al. Burden of tricuspid regurgitation in patients diagnosed in the community setting. JACC Cardovasc: Imaging. 19;22:433-442.

7. Singh JP, Evans JC, Levy D, et al. Prevalence and clinical determinants of mitral, tricusid, and

regurgitation (the Framingham Heart Study). Am J Cardiol. 1999;83:897-902.

8. Enriquez-Sarano M, Messika-Zeitoun D, Topilsky Y, et al. Tricuspid regurgitation is a public health crisis. Prog Cardiovasc Dis. 2019;62:447-451.

9. Offen S, Playford D, Strange G, et al. Adverse prognostic impact of even mild or moderate tricuspid regurgitation: insights from the National Echocardiography Database of Australia. J Am Soc Echocardiogr. 2022;35:810-817.

10. Hahn RT, Bremer MI, Cox ZL, et al. Tricuspid regurgitation management for heart failure. JACC Heart Fail. 2023;11:1084-1102.

11. Hahn RT, Wilkoff BL, Kodali S, et al. Managing implanted cardiac electronic devices in patients with severe tricuspid regurgitation: JACC state-of-the-art review. J AM Coll Cardiol. 2024;83:2002-2014.

12. Andreas M, Burri H, Praz F, et al. Tricuspid valve and cardiac implantable electronic devices. Eur Heart J. 2024;45:346-365.

13. Leong DP, Dokainish H, Mondesert B, et al. Effects of implantable cardioverter-defibrillator leads on the tricuspid valve and right ventricle a randomized trial. JACC Clin Electrophysiol. 2024;10:2088-2096.

14. Ambrosino M, Sangoi M, Monzer N, et al. Tricuspid regurigation in a current interventional management. J Am Heart Assoc. 2024;13:03 e032999.

15. Arteagoltia Bolumburu A, Monteagudo Ruiz JM, Maha P, et al. Determinants of tricuspid regurgitation progression and its implications for adequate management. JACC Cardiovasim. Imaging 2024;17:579-591.

16. Praz F, Muraru D, Kreidel F, et al. Transcatheter treatment for tricuspid valve disease. EurolIntervention. 2021;17:91-808.

17. Hahn RT, Lawlor MK, Davidson CJ, et al. Tricuspid valve academic research consortium definitions for tricuspid regurgitation and trial endpoints. J Am Coll Cardiol. 2023;82:1711-1735.

18. Muraru D, Badano LP, Hahn RT, et al. Atrial secondary tricusid regurgitation: pathophysiology, definition, diagnosis, and treatment. Eur Heart J. 2024;45:895-911.

19. Muraru D, Guta AC, Ochoa-Jimenez RC, et al. Functional regurgitation of atrioventricular valves and atrial fibrillation: an elusive pathophysiological link deserving further attention. J Am Soc Echocardiogr. 2020;33:42-53.

20. Patlolla SH, Schaff HV, Nishimura RA, et al. Inci- dence and burden of tricuspid regurgitation in patients with atrial fibrillation. J Am Coll Cardiol. 2022;80: 2289-2298.

21. Abe Y, Akamatsu K, Ito K, et al. Prevalence and prognostic significance of functional mitral and tricuspid regurgitation despite preserved left ventricular ejection fraction in atrial fibrillation patients. Circ J. 2018;82:1451-1458.

22. Dietz MF, Goedemans L, Vo NM, et al. Prognostic implications of significant isolated tricuspid regurgitation in patients with atrial fibrillation without left-sided heart disease or pulmonary hypertension. Am J Cardiol. 2020;135:84-90.

23. Fujisawa T, Kimura T, Ikemura N, et al. Effect of tricuspid regurgitation on the reported quality of life

JACC VOL. 87, NO. 4, 2026 FEBRUARY 3, 2026:447-486

O'Gara et al 10 Issues for the Clinician in TR Evaluation and Management

and subsequent outcomes in patients with atrial fibrillation. J Am Heart Assoc. 2022;11:e022713.

24. Addetia K, Harb SC, Hahn RT, et al. Cardiac implantable electronic device lead-induced tricuspid regurgitation. JACC Cardiovasc Imaging. 2019;12:622-636.

25. Vaturi M, Kusniec J, Shapira Y, et al. Right ventricular pacing increases tricuspid regurgitation grade regardless of the mechanical interference to the valve by the electrode. Eur J Echocardiogr. 2010;11:550-553.

26. Prihadi EA, delgado V, Leon MB, et al. Morphologic types of tricuspid regurgitation: characteristics and prognostic implications. JACC Cardiovasc Imaging. 2019;12:491-499.

27. Dietz MF, Prihadi EA, van der Bijl P, et al. Sex-specific differences in etiology and prognostic in patients with significant tricuspid regurgitation. Am J Cardiol. 2021;147:109-115.

28. Gavazzoni M, Heibron F, Badano LP, et al. The atrial secondary tricuspid regurgitation is associated to more favorable outcome than the ventricular phenotype. Front Cardiovasc Med. 2022;9:1022755.

29. Schlotter F, Dietz MF, Stolz L, et al. Atrial functional tricusid regurgitation: novel definition and impact on prognosis. Circ Cardiovasc Interv. 2022;15: e01958.

30. Delling FN, Hassan ZK, Platkowski G, et al. Tricusid regurgitation and mortality in patients with transvenous permanent pacemaker leads. Am I. Car- diol. 2016;117:988-992.

31. Hoke U, Auger D, Thijsen J, et al. Significant leaduced tricuspid regurgitation is associated with poor prognosis at long-term follow-up. Heart 24;100; 960-968.

32. Al-Bawardy R, Krishnaswamy A, Rajeswaran J, et al. Tricuspid regurgitation and implantable devices. Pacing Clin Electrophysiol. 2015;38:259-266.

33. Stolz L, Kresoja KP, von Stein J, et al. Atrial secondary tricuspid regurgitation: insights into the EuroTR registry. JACC Cardiovasc Interv, 2024;17:2781-2791,

34. Clement A, Muraru D, Fiscaro S, et al. Utility of the ratio between the size of the right atrium and the right ventricle at end-systole to diagnose atrial secondary tricuspid regurgitation. J Am Soc Echocardiogr. 2025;38(3):212-223.

35. Hahn RT, Badano LP, Barto PE, Pei at. Trucissid regurgitation: recent advances in understanding pathophysiology, severity grading and outcome. Eur Heart J Cardiovasc Imaging. 2022;23:913-929.

66. Hahn RT, Saric M, Falestra FF, et al. Recommended standards for the performance of transesophageal echocardiographic screening for structural heart intervention: from the American Society of Echocardiogr. J Am Soc Echocardiogr. 2022;35:1-76.

37. Zoghbi WA, Adams D, Bonow RO, et al. Recommendations for noninvasive evaluation of native valvular regurgitation. a report from the American Society of Echocardiography developed in collaboration with the Society for Cardiovascular and for Cardiovascular. Negorreson. J Am Soc Echocardiogr. 2027;303:371.

38. Lancellotti P. Pibarot P, Chambers J. et al. Multi-modality imaging assessment of native valvular regurgitation: an EACVI and ESC council of valvular

heart disease position paper. Eur Heart J Cardiovasc Imaging. 2022;23:e171-e232.

39. Sugiura A, Tanaka T, Kasur R, et al. Leaflet configuration and residual tricuspid regurgitation after transcatheter edge-to-edge tricuspid repair. JACC Cardiovasc Interv. 2021;14:2260-2270.

40. Dahou A, Ong G, Hamid N, et al. Quantifying tricuspid regurgitation severity: a comparison of proximal isovelocity surface area and novel quantita-tive doppler methods. JACC Cardiovasc Imaging. 2019;12:560-562.

41. Utsunomiya H, Harada Y, Susawa H, et al. Comprehensive evaluation of tricuspid regurgitation location and severity using vena contracta analysis: a color Doppler three-dimensional transeasophageal echocardiographic study. J Am Soc Echocardiogr. 2019;32:1526-1537.

42. Ozturk C, Schueler R, Weber M, et al. Comparison of different imaging modalities for the quantification of tricuspid valve geometry and regurgitation: a retrospective, single-center study. Health Sci Rep. 2020;3:e159.

43. Tomaselli M, Badano LP, Mene R, et al. Impact of correcting the 2D PISA method on the quantification of functional tricuspid regurgitation severity. Eur Heart J Cardiovasc Imaging. 2022;13:459-1470.

44. Topilsky Y, Nkomo VT, Vatur O, et al. Clinical outcome of isolated tricuspid regurgitation. JACC Cardiovasc Imaging. 2014;7:1185-1194.

45. Benfari G, Antoine C, Essayagh B, et al. Functional mitral regurgitation outcome and grading in heart failure with reduced ejection fraction. JACC Cardiovasc Imaging. 2021;14:2033-2315.

46. Chorin E, Rozenbaum Z, Topilsky Y, et al. Tricuspid regurgitation and long-term clinical outcomes. Eur Heart J Cardiovasc Imaging. 2020;21:157-165.

47. Hahn RT, Meduri CU, Davidson CJ, et al. Early feasibility study of a transcatheter tricuspid valve annuloplasty: SCOUT trial 30-day results. J Am Coll Cardiol. 2017;619:1795-186.

48. Hahn RT, Zamorano JL. The need for a new tricuspid regurgitation grading scheme. Eur Heart J Cardiovasc Imaging. 2017;18:1342-1343.

49. Fortuni F, Dietz MF, Prihadi EA, et al. Prognostic implications of a novel algorithm to grade secondary tricuspid regurgitation. JACC Cardiovasc Imaging. JACC Cardiovasc Imaging. JACC Cardiovasc Imaging. JACC 2021;14:1085-1095.

50. Santero P, Marc Delastlo, Gonzee Gane, A, et al. Mid-term outcome of severe tricuspid regurgitation: are there any differences according to mechanism and severity? Eur Heart J Cardiovasc Imaging. 2020;23:103-1929.

51. Some KBY, Daletid, Køn Hry, M et al. Refining severe tricuspid regurgitation definition by echocardiography with a new outcomes-based "massive" grade. J Am Soc Echocardiogr. 2020;33:1087-1094.

5. Peri Y, Sadeh B, Sherez C, et al. Quantitative assessment of effective regurgitant orifice: impact on risk stratification, and cut-off for severe and torrental tricusid regurgitation grade. Eur Heart J Cardiovasc Imaging. 2020;21:768-776.

53. Omori T, Uno, Shimada S, et al. Impact of new grading system and new hemodynamic classification on long-term outcome in patients with severe tricusid regurgitation. Circ Cardiovasc Imaging. Circ 2021;14:e011805.

54. Miura M, Alessandrini H, Alkhodair A, et al. Impact of massive or torrential tricuspid regurgitation in patients undergoing transcatheter tricuspid valve intervention. JACC Cardiovasc Interv. 2020;13:1999-2009.

55. Nickenig G, Weber M, Lurz P, et al. Transedge-to-edge repair for reduction of tricuspid regurigation: 6-month outcomes of the TRILUMINATE single-arm study. Lancet. 2019;394:2002-2011.

56. Sorajia P, Whisenant B, Hamid N, et al. Trans-catheter repair for patients with tricuspid regurgita-tion. N Engl J Med. 2023;388:1833-1842.

57. Hahn RT, Weckbach LT, Noack T, et al. Proposal for a standard echocardiographic tricuspid valve nomenclature. JACC Cardiovasc Imaging. 2021;14: 1299–1305.

58. Holda MK, Zhingre Sanchez JD, Bateman MG, laiza P.A. Right atrioventricular valve leaflet morphology redefined: implications for transcatheter repair procedures. JACC Cardiovasc Interv. 2019;12:169-178.

59. Wafae N, Hayashi H, Gerola LR, Vieira MC. Anatomical study of the human tricuspid valve. Surg Radiol Anet. 1990;12:37-41.

60. Zhan Y, Debs D, Khan MA, et al. Natural history of functional tricusid regurgitation quantified by car- diovascular magnetic resonance. J Am Coll Cardiol. 2020;76:1291-1301.

61. Hahn RT, Thomas JD, Khalique OK, et al. Imaging assessment of tricuspid regurgitation severity. JACC Cardiovasc Imaging. 2019;12:469-490.

62. Feneis JF, Kyubwa E, Atianzar K, et al. 4D Flow MRI quantification of mitral and tricuspid regurgitation: reproducibility and consistency relative to conventional MRI. J Magn Reson Imaging. 2018;48:1147-1158.

63. Villines TC, Rodriguez-Lozano P, Mallawarachchi I, et al. Discarpes in noninvasive traditional and advanced testing for coronary artery disease: findings from the INCAPS-COVID 2 study. Am J Cardiol. 2024;24:85-93.

64. Lopes BBC, Sorajja P, Hashimoto G, et al. Tricuspid anatomic regurgitant orifice area by functional DSCT: a novel parameter of tricuspid regurgitation severity. JACC Cardicovasc Imaging. 2021;14:1669-1672.

65. Hanard LS, Vahl TP, Chung CJ, et al. Impact of inferior vena cava entry characteristics on tricuspid annular access during transcatheter interventions. Catheter Cardiovasc Interv. 2022;99:1268-1276.

66. Khalique OK, Cavalcante JL, Shah D, et al. Multi-modality imaging of the tricuspid valve and right heart anatomy. J ACZ Cardiovasc Imaging. 2019;12:516-531.

67. Lung RM, Badano LP, Mor-Avi V, et al. Recom-mendations for cardiac chamber quantification by echocardiography in adults: an update from the American Society of Echocardiography and the Euro-pean Association of Cardiovascular Imaging. J Am Soc Echocardiogr. 2015;28:1-39.

68. Addetia K, Miyoshi T, Citro R, et al. Two-dimensional echocardiographic right ventricular size and systolic function measurements stratified by sex, age, and ethnicity: results of the world alliance of societies of echocardiography study. J Am Soc Echocardiogr. 2021;34:11-48-1157.

69. Addita K, Miyoshi T, Amuthan V, et al. Normal values of three-dimensional right ventricular size and function measurements: results of the World Alliance

O'Gara et al 10 Issues for the Clinician in TR Evaluation and Management

JACC VOL. 87, NO. 4, 2026 FEBRUARY 3, 2026:447-486

Societies of Echocardiography study. J Am Soc Echocardiogr.

Societies of Echocardiography study. J Am Soc Echocardiogr. 2023;36:858-866.

70. Stocker TJ, Hertell H, Orban M, et al. Cardiopulmonary hemodynamic profile predicts mortality after transcatheter tricuspid valve repair in chronic heart failure. JACC Cardiovasc Interv. 2021;14:29-38.

71. Rudski LG, Lai WW, Afiloal J, et al. Guidelines for the echocardiographic assessment of the right heart in adults: a report from the American Society of Echocardiography endorsed by the European Association of Echocardiography, a registered branch of the European Society of Cardiology, and the Canadian Society of Echocardiography. J Am Soc Echocardiogr. 2010;23: 685-713.

71. Rudski LG, Lai WW, Afiloal J, et al. Guidelines for the echocardiographic assessment of the right heart in adults: a report from the American Society of Echocardiography endorsed by the European Association of Echocardiography, a registered branch of the European Society of Cardiology, and the Canadian Society of Echocardiography. J Am Soc Echocardiogr. 2010;23: 685-713.

72. Sugiura A, Tanaka T, Kavsur R, et al. Refining accuracy of RV-PA coupling in patients undergoing transcatheter tricuspid valve treatment. Clin Res Cardiol. 2024;113:177-186.

73. Hahn RT, Lerakis S, Delgado V, et al. Multimodality imaging of right heart function: JACC scientific state-ment. J Am Coll Cardiol. 2023;81:954-1973.

74. Brener Mi, Lurz P, Hausleiter J, et al. Right ventricular-pulmonary arterial coupling and afterload reserve in patients undergoing transcatheter tricuspid valve repair. J Am Coll Cardiol. 2022;79:448-461.

75. Gavazzoni M, Badano LP, Cascella A, et al. Clinical value of a novel three-dimensional echocardiography-derived index of right ventricle-pulmonary artery coupling in tricuspid regurgitation. J Am Soc Echocardogr. 2023;36:1544-1166.

76. Jauhiainen T, Jarvinen VM, Hekali PE, et al. MR gradient echo volumetric analysis of human cardiac casts: focus on the right ventricle. J Comput Assist Tomogr. 1998;22:899-903.

77. Koch JA, Poll LW, Godehardt E, et al. Right and left ventricular volume measurements in an animal heart model in vitro first experiences with cardiac MRI at 1.0 T. Eur Radiol. 2000;10:455-458.

78. Caiani EG, Corsi C, Zamorano J, et al. Improved semiautomated quantification of left ventricular volumes and ejection fraction using 3-dimensional echocardiography with a full matrix array transducer: comparison with magnetic resonance imaging. J Am Soc Echocardiogr. 2005;18:779-788.

79. Mor-Avi V, Jenkins C, Kuhl HP, et al. Real-time 3-dimensional echocardiographic quantification of left ventricular volumes: multicenter study for validation with magnetic resonance imaging and investigation of sources of error. JACC Cardiovasc Imaging. 2008;1:413-423.

80. Tamborini G, Piazzese C, Lang RM, et al. Feasibility and accuracy of automated software for transorathic three-dimensional left ventricular volume and function analysis: comparisons with two-dimensional echocardiography, three-dimensional transthoracic manual method, and cardiac magnetic resonance imaging. J Am Gastro. Echocardiogr. 2017;30:1049-1058.

81. Kim HK, Kim YJ, Park EA, et al. Assessment of haemodynamic effects of surgical correction for severe functional tricusid regurigation; cardiac magnetic resonance imaging study. Eur Heart J. 2010;31:1520-1528.

82. Park JB, Kim HK, Jung JH, et al. Prognostic value of cardiac MR imaging for preoperative assessment of patients with severe functional tricusid regurgitation. Radiology. 2016;280:723-734.

83. Plumhans C, Muhlenbruch G, Rapaee A, et al. Assessment of global right ventricular function on 64-MOCT compared with MRI. Aur J Am J Roentgenol. 2008;190:1358-1361.

84. Maffei E, Messalli G, Martini C, et al. Left and right ventricle assessment with cardiac CT: validation study vs. cardiac MR. Eur Radiol. 2012;22:1041-1049.

85. Muttal D, Khalil J, Lessick J, et al. Risk factors for the development of functional tricusid regurgitation and their population-attributable fractions. JACC Cardiovasc Imaging. 2020;13:1643-1651.

86. Prihad EA, van der Bijl P, Gursoy E, et al. Development of significant tricuspid regurgitation over time and prognostic implications: new insights into natural history. Eur Heart J. 2018;39:3574:3581.

87. Heitzinger G, Pavo N, Koschatko S, et al. Contemporary insights into the epidemiology, impact and treatment of secondary tricuspid regurgitation across the heart failure spectrum. Eur J Heart Fail. 2023;25:857-867.

88. Wang N, Fulcher J, Abeysuriya N, et al. Tricuspid regurgitation is associated with increased mortality independent of pulmonary pressures and right heart failure: a systematic review and meta-analysis. Eur Heart J. 2019; J.40:476-484.

89. Mutlak D, Lessick J, Khalil S, et al. Tricuspid regurgitation in acute heart failure: is there any incremental risk? Eur Heart J Cardiovasc Imaging. 2018;19:993-1001.

90. Bartko PE, Huismann Mi, Hung J, et al. Secondary valve regurgitation in patients with heart failure with preserved ejection fraction, heart failure with mid-range ejection fraction, and heart failure with reduced ejection fraction. Eur Heart J. 2020;41:2799-2810.

91. Chioncel O, Lainscak M, Seferovic PM, et al. Epidemiology and one-year outcomes in patients with chronic heart failure and preserved, mid-range and reduced ejection fraction: an analysis of the ESC Heart Failure Long-Term Registry. Eur J Heart Fail. 2017;19: 1574-1585.

92. Messika-Zeitoun D, Verta P, Gregson J, et al. Impact of tricuspid regurgitation on survival in patients with heart failure: a large electronic health record patient-level database analysis. Eur J Heart Fail. 2020;22:1830-1813.

93. Tribuollay C, Vanhaecke P, Dreyfus J, et. al. Natural history of isolated functional tricuspid regurgitation. J Am Heart Assoc. 2024;13:e033933.

94. Spinta G, Bartko PE, Heitzinger G, et al. Natural course of nonsevere secondary tricusid regurgitation. J Am Soc Echocardiogr. 2021;34:13-19.

9. Anand V, Scott CG, Hyun MC, et al. The 5 phenotypes of tricupid regurgitation: insight from cluster analysis of clinical and Hochecardiographic variables. JACC Cardiovasc Inter. 2023;16:156-165.

96. Bartko PE, Arfsten H, Heitzinger G, et al. Natural history of bivalvular functional regurgitation. Eur Heart J Cardiovasc Imaging. 2019;20:565-573.

97. Chioncel O, Mebazaa A, Maggianti AP, et al. Acute heart failure congestion and perfusion status - impact of the clinical classification on in-hospital and long-term outcomes; insights from the ESC-EORP-HFA Heart Failure Long-Term Registry. Eur J Heart Fail. 2019;21:1338-1352.

98. Takagi H, Hari Y, Kawai N, et al. Impact of concurrent tricuspid regurgitation on mortality after transcatheter aortic-valve implantation. Catheter Cardiovasc Interv. 2019;93:946-953.

99. Hahn RT, Asch F, Weissman NJ, et al. Impact of tricuspid regurgitation on clinical outcomes: the COAP T trial. J Am Coll Cardiol. 2020;76:1305-1314.

100. Yoshida K, van Wezenbeek J, Wessels JN, et al. Tricuspid regurgitation in pulmonary arterial hypertension: a right ventricular volumetric and functional analysis. Eur Respir J. 2024;63:2301696.

101. Stone GW, Lindenfeld J, Abraham WT, et al. Transcatheter mitral-valve repair in patients with heart failure. N Engl J Med. 2018;379:2307-2318.

102. Galloo X, Dietz MF, Fortuni F, et al. Prognostic implications of atrial vs. ventricular functional tricusid regurgitation. Eur Heart J Cardiovasc Imaging. 2023;24:733-741.

103. Paniagua D, Aldrich HR, Lieberman EH, et al. Increased prevalence of significant tricuspid regurgitation in patients with transvenous pacemakers leads. Am J Cardiol. 1998;82:1130-1132.

104. Kim JB, Spevack DM, Tunick PA, et al. The effect of transvenous pacemaker and implantable cardioverter defibrillator lead placement on tricuspid valve function: an observational study. J Am Soc Echocardiogr. 2008;21:284-287.

105. de Cock CC, Vinkers M, Van Campe LC, et al. Long-term outcome of patients with multiple (> or = 3) noninfected transvenous leads: a clinical and echocardiographic study. Pacing Clin Electrophysiol. 200;23;423-426.

106. Safriyu I, Mehta A, Adefuye M, et al. Incidence and prognostic implications of cardiac-implantable device-associated tricuspid regurgitation: a meta-analysis and meta-regression analysis. Am J Cardiol. 2023;209:203-211.

107. Jamnongprasatporn S, Lara-Breitinger KM, Pislaru SV, et al. Incremental prognostic value of right ventricular-pulmonary artery coupling to a clinical risk score in tricuspid regurgitation: the TRIO-RV score. J Am Soc Echocardiogr. 2025;38:239-246.

108. Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA guideline for the management of heart failure: executive summary: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guide lines. J Am Coll Cardiol. 2022;79:1757-1780.

109. Butcher SC, Fortuni F, Dietz MF, et al. Renal function in patients with significant tricuspid regurgitation: pathophysiological mechanisms and prognostic implications. J Intern Med. 2021;290:715-727.

110. Palmer LG, Schnermann J. Integrated control of Na transport along the nephron. Clin J Am Soc Nephrol. 2015;10:676-687.

111. Mentz RJ, Anstrom KJ, Eisenstein EL, et al. Effect of torsemide vs furosemide after discharge on all cause mortality in patients hospitalized with heart failure: the TRANSFORM-HF randomized clinical trial. JAMA. 2023;329:214-223.

112. Liguori A, Casini A, Di Loreto M, et al. Loop di-cretics et the secretion of prostacyclin in vitro, in healthy persons, and in patients with chronic heart failure. Eur J Clin Pharmacol. 1999;55:117-124.

113. Mullens W, Damman K, Harjola VP, et al. The use of diuretics in heart failure with congestion - a position

JACC VOL. 87, NO. 4, 2026 FEBRUARY 3, 2026:447-486

O'Gara et al 10 Issues for the Clinician in TR Evaluation and Management

statement from the Heart Failure Association of the European Society of Cardiology. Eur J Heart Fail. 2019;21:137-155. 114. Felker GM, Ellison DH, Mullens W, et al. Diuretic therapy for patients with heart failure. JACC state-of-the-art review. J Am Coll Cardiol. 2020;7:115-178. 115. Mullens W, Dauw J, Martens P, et al. Acetazamide in acute decompensated heart failure with volume overload. N Engl J Med. 2022;387:1185-1195. 116. Cox ZL, Collins SP, Hernandez GA, et al. Efficacy and safety of dapaglifozin in patients with acute heart failure. J Am Coll Cardiol. 2024;8:135-1306. 117. Bartkowiak J, Agarwal V, Otero D, et al. Management of patient with tricuspid regurgitation and heart failure with preserved rejection function. JACC Case Rep. 2025;30:103287. 118. McDonagh TA, Metra M, Adamo M, et al. 2023 Focused update of the 2021 ESC guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur Heart J. 2023;44:3627-3639. 119. Buckberg G, Hoffman Jl. Right ventricular architecture responsible for mechanical performance. Uinfying or ventricular septum. J Thorac Cardiovasc Surg. 2014;148:3166-3717. 120. Houston BA, Brittain EL, Tedford RJ. Right ventricular failure. N Engl J Med. 2023;388:1111-1215. 121. Stassen J, Galloo X, Hirasawa K, et al. Tricuspid regurgitation and cardiac resynchronization therapy: Event Vessels. 2020;35:842-851. 122. Zahr F, Elmariah S, Vemulapalli S, et al. Impact of tricuspid regurgitation on outcomes of transcatherate aortic valve replacement with balloon-expandable valves. JACC Cardosciv Interv. 2024;17:1916-1931. 123. Sammour YM, Cohen DJ, Arnold S, et al. Association of baseline tricuspid regurgitation with health status and clinical outcomes after TAVR and mitral TEER. JACC Cardiovasc Interv. 2024;17:1905-1915. 124. Groger M, Hirsch K, Belf, ed. D at. Predictors of improvement in concomitant tricuspid regurgitation following transcatheter edge-to-mitral valve repair. J Clin Med. 2023;12:6191. 125. Adamo M, Pagnesmi M, Ghizhi Gz, et al. Evolution of tricuspid regurgitation after transcatheter edge-to-edge mitral valve repair for secondary mitral regurgitation and its impact on mortality. Eur J Heart Fail. 2022;24:2175-2184. 126. Le Tourneau T, Deswarte G, Lamblin N, et al. Right ventricular systolic function in organic mitral regurgitation: impact of biventricular impairment. Circulation. 2013;12:1597-1608. 127. Maron BA. Revised definition of pulmonary hypertension and approach to management: a clinical primer. J Am Heart Assoc. 2023;12:e029024.

130. Yan X, Meyre PB, Aeschbacher S, et al. Right heart structure and function after electrical cardio- version for atrial fibrillation. Cardology. 2023;148: 402-408. 131. Soulat-Dufour L, Lang S, Addetia K, et al. Restoring sinus rhythm reverses cardiac remodeling and reduces valvular regurgitation in patients with atrial fibrillation. J Am Coll Cardiol. 2022;79-951-661. 132. Si J, Ding Z, Chen X, et al. Effects of rhythm control for atrial fibrillation on cardiac remodeling and valvular regurgitation in patients with heart failure. Cardiovasc Drugs Ther. 2025;39:85-96. 134. Markman TM, Plappet T, De feria Alsina A, et al. Improvement in tricuspid regurgitation following catheter ablation of atrial fibrillation. J Cardovasc Electrophysiol. 2020;31:2883-2888. 134. Ukita K, Egami Y, Nohara H, et al. Predictors and outcomes of tricuspid regurgitation improvement after radiofrequency catheter ablation for persistent atrial fibrillation. J Cardiovasc Electrophysiol. 2023;34: 1360-1366. 135. Cha MJ, Lee SA, Cho MS, et al. Reduction of moderate to severe tricuspid regurgitation after catheter ablation for atrial fibrillation. Heart. 2024;110:523-530. 136. Itakura K, Hidaka T, Nakano Y, et al. Successful catheter ablation of persistent atrial fibrillation is associated with improvement in functional tricuspid regurgitation and right heart reverse remodeling. Heart Vessels. 2020;35:842-851. 137. Nakamura K, Takagi T, Kogame N, et al. Impact of atrial mitral and tricuspid regurgitation on atrial fibrillation recurrence after ablation. J Electrocardiol. 2021;66:114-121. 138. Park L, Jeong DS, Park SJ, et al. Impact of made procedure in patients with severe tricuspid regurgitation and persistent atrial fibrillation. J Thorac Cardiovasc Surg. 2023;166:478-488;475. 139. Wang J, Han J, Li Y, et al. Impact of surgical ablation of atrial fibrillation on the progression of tricuspid regurgitation and right-sided heart redomeling after mitral-valve surgery: a propensity-score matching analysis. J Am Heart Assoc. 2016;5:004-8231. 140. Wang J, Li S, Ye Q, et al. Catheter ablation or surgical therapy in moderate-severe tricuspid regurgitation caused by long-standing persistent atrial fibrillation. Propensity score analysis. J Cardiovasc Surg. 2020;15:277. 141. Lebehn M, Hahn RT. Rhythm control of atrial fibrillation positively affects tricuspid regurgitation. JACC Case Rep. 2025;30:103311. 142. Alinamat S, Doyle M, Krishnan K, Biederman RWW. Worsening tricuspid regurgitation associated with permanent pacemaker and implantable cardioverte-defibrillator implantation: a systematic review and meta-analysis of more than 66, 000 subjects. Heart Rhythm. 2023;20:1491-1501. 143. Lin G, Nishimura RA, Connolly HM, et al. Severe symptomatic tricuspid valve regurgitation due to permanent pacemaker or implantable cardioverte defibrillator leads. J Am Coll Cardiol. 2005;45:1672-1675. 144. Mediratta A, Addetia K, Yamat M, et al. 3D Echocardiographic location of implantable device leads and mechanism of associated tricuspid regurgitation. JACC Cardiovasc Imaging. 2014;7:337-347.

145. Park SJ, Gentry JL 3rd, Varma N, et al. Transvenous extraction of pacemaker and defibrillator leads and the risk of tricuspid valve regurgitation. JACC Clin Electrophysiol. 2018;4:1421-1428. 146. Franceschi F, Thuny F, Giorgi R, et al. Incidence, risk factors, and outcome of traumatic tricuspid regurgitation after percutaneous ventricular lead removal. J Am Coll Cardiol. 2009;53:2168-2174. 147. Pecha S, Castro L, Gosau N, et al. Evaluation of tricuspid valve regurgitation following laser lead extraction. Eur J Cardiothorac Surg. 2017;51:1108-1111. 148. Shanafelt C, Middour TG, Ibrahim R, et al. Outcomes of tricuspid regurgitation after lead extraction. J Cardiosc Electrophysiol. 2024;35:929-938. 149. Novak M, Dvorak P, Kamaryt P, et al. Autopsy and clinical context in deceased patients with implanted pacemakers and defibrillators: intracardiac findings near their leads and electrodes. Europace. 2009;11: 1510-1516. 150. Kancharla K, Acker NG, Li Z, et al. Efficacy and safety of transvenous lead extraction in the device laboratory and operating room guided by a novel risk stratification scheme. JACC Clin Electrophysiol. 2019;5: 174-182. 151. Polewczyk A, Jacheć W, Nowosielecka D, et al. Lead dependent tricuspid valve dysfunction-risk factors, improvement after transvenous lead extraction and long-term prognosis. J Clin Med. 2022;11:89. 152. Nazmul MN, Cha YM, Lin G, et al. Percutaneous pacemaker or implantable cardioverter-defibrillator lead removal in an attempt to improve symptomatic tricuspid regurgitation. Europace. 2013;15:409-413. 153. Bongiorni MG, Kennergren C, Butter C, et al. The European Lead Extraction ConTRolled (ELECTRA) study: a European European Heart Rhythm Association (EHRA) Registry of Transvenous Lead Extraction Outcomes. Eur Heart J. 2017;38:2995-3005. 154. Taramasso M, Gavazzoni M, Pozzoli A, et al. Outcomes of TTVI in patients with pacemaker or defibrillators leads: data from the TriValve registry. JACC Cardovasc Interv. 2020;13:554-564. 155. Cabriels JK, Schaller RD, Koss E, et al. Lead management in patients undergoing percutaneous tricuspid valve replacement or repair: a'heart team' approach. Europace. 2023;25:euad300. 156. Anderson JH, McElhinney DB, Aboulhosn J, et al. Management and outcomes of transvenous pacing leads in patients undergoing transcatheter tricuspid valve replacement. JACC Cardiovasc Interv. 2020;13: 2012-2020. 157. Paz Rios LH, Alsaad AA, Guerrero M, Metzl MD. Tricuspid valve-in-valve jailing right ventricular lead is not free of risk. Catheter Cardiovasc Interv. 2020;96: E758-E760. 158. Meyer P, Filippatos GS, Ahmed MI, et al. Effects of right ventricular ejection fraction on outcomes in chronic systolic heart failure. Circulation. 2010;121: 252-258. 159. Adamo M, Metra M, Claggett BL, et al. Tricuspid regurgitation and clinical outcomes in heart failure with reduced ejection fraction. JACC Heart Fail. 2024;12-552-563. 160. Lanceellotti P, Moura L, Pierard LA, et al. European Association of Echocardiography recommendations for the assessment of valvular regurgitation. Part

12. Konstam MA, Kiernan MS, Bernstein D, et al. Evaluation and management of right-sided heart failure: a scientific statement from the American Heart Association. Circulation. 2018;137e578-e622. 129. Maddox TM, Januzzi JL Jr, Allen LA, et al. 2024 ACC expert consensus decision pathway for treatment of heart failure with reduced ejection fraction: a report of the American College of Cardiology Solution Set Oversight Committee. J Am Collol. 2024;83: 1444-1488.

O'Gara et al 10 Issues for the Clinician in TR Evaluation and Management

JACC VOL. 87, NO. 4, 2026 FEBRUARY 3, 2026:447-486

2: mitral and tricuspid regurgitation (native valve

2. mitral and tricuspid regurgitation (native valve disease). Eur J Echocardiogr. 2010;11:307-332.

161. Verbrugge FH, Dupont M, Steels P, et al. Abdominal contributions to cardiorenal dysfunction in congestive heart failure. J Am Coll Cardiol. 2013;62: 485-495.

162. Poelzl G, Ess M, Von der Heidt A, et al. Concomitant renal and hepatic dysfunctions in chronic heart failure: clinical implications and prognostic significance. Eur J Intern Med. 2013;24:177-182.

163. Testani JM, Khera AV, St John Sutton MG, et al. Effect of right ventricular function and venous congestion on cardiorenal interactions during the treatment of decompensated heart failure. Am J Cardiol. 2010;105:511-56.

164. Guglin M, Rivero A, Matar F, Garcia M. Renal dysfunction in heart failure is due to congestion but not low output. Clin Cardiol. 2011;34:113-116.

65. Nohria A, Hasselblad V, Stebbins A, et al. Cardiromal interactions: insights from the ESCAPE trial. J Am Coll Cardiol. 2008;51:1268-1274.

166. Koehne de González A, Leffowitch JH. Heart disease and the liver: pathologic evaluation. Gastro-enterol Clin North Am. 2017;46:421-435.

167. Morris AA, Khazanie P, Drazner MH, et al. Guidance for timely and appropriate referral of patients with advanced heart failure: a scientific statement from the American Heart Association. Circulation. 2021;144:e238-e250.

168. Baumwol J. "I Need Help"-A mnemonic to aid timely referral in advanced heart failure. J Heart Lung Transplant. 2017;36:593-594.

169. Vahanian A, Beyersdorf F, Praz F, et al. 2021 ESC/EACTS guidelines for the management of valvular heart disease. Eur Heart J. 2022;43:561-632.

170. Shiran A, Sagie A. Tricuspid regurgitation in mitral valve disease incidence, prognostic implications, mechanism, and management. J Am Coll Cardiol. 2009;53:401-408.

171. Goldstone AB, Howard JL, Cohen JE, et al. Natural history of coexistent tricusid regurgitation in patients with degenerative mitral valve disease: implications for future guidelines. J Thorac Cardiovasc Surg. 2014;148:2802-2809.

172. Jeganathan R, Armstrong S, Al-Alao B, David T. The risk and outcomes of cooperative tricuspid valve surgery. Ann Thorac Surg. 2013;95:119-124.

173. Pflanmuiller Rz M, Misfeld M, et al. Isolated tricuspid valve surgery in patients with previous cardiac surgery. J Thorac Cardiovasc Surg. 2013;46:841-847.

147. Badhwar V, Rankin JS, He M, et al. Performing concomitant tricuspid valve repair at the time of mitral valve operations is not associated with increased operative mortality. Ann Thorac Surg. 2017;103:587-593.

157. Dreyfus J, Audureau E, Bohbot Y, et al. TRI-SCORE: a new risk score for in-hospital mortality prediction after isolated tricuspid valve surgery. Eur Heart J. 2022;43:654-662.

176. Di Mauro M, Bivona A, la OAL, et al. Mitral valve surgery for functional mitral regurgitation: prognostic role of tricuspid regurgitation. Eur J Cardhorαurg, 2009;35:635-639.

177. Calafrio AM, Gallina S, laco AL, et al. Mitral valve surgery for functional mitral regurgitation: should moderate-or-more tricuspid regurgitation be treated? of breypensity score analysis. Ann Thorac Surg. 2009;87: 698-703.

178. Kwak JJ, Kim YJ, Kim MK, et al. Development of tricuspid regurgitation late after left-sided valve surgery: a single-center experience with long-term echocardiographic examinations. Am Heart J. 2008;155:732-737.

179.�gamme JS, Chu MWA, Falk V, et al. Concomitant tricuspid repair in patients with degenerative mitral regurgitation. N Engl J Med. 2022;386:327-339.

180. Zaheer S, Holmes SD, Rodriguez E, et al. Factors associated with permanent pacemaker placement after tricuspid valve operations. Ann Thorac Surg. 2025;119:377-387.

181. Kassab J, Har SC, Desai MY, et al. Incidence, risk factors, and outcomes associated with permanent pacemaker implantation following tricuspid valve surgery. J Am Heart Assoc. 2024;13:023726.

182. Alqahtani F, Berzingi CO, Aljohani S, et al. Contemporary trends in the use and outcomes of surgical treatment of tricusid regurgitation. J Am Heart Assoc. 2017;6:e007599.

183. Maeder MT, Holst DP, Kaye DM. Tricusid regurgitation contributes to renal dysfunction in patients with heart failure. J Card Fail. 2008;14:824-830.

184. Lau GT, Tan HC, Krithardes L. Type of liver dysfunction in heart failure and its relation to the severity of tricuspid regurgitation. Am J Cardiol. 2002;90:1405-1409.

185. Dreyfus GD, Corbi PJ, Chan KM, Bahrami T. Secondary tricuspid regurgitation or dilatation. which should be the criteria for surgical repair? Ann Thorac Surg. 2005;79:127-132.

186. Vassileva CM, Shabosky J, Boley T, et al. Tricuspid valve surgery: the past 10 years from the nationwide impatent sample (NIS) database. J Thoroc Cardiovasc Surg. 2012;143:1043-1049.

187. Zack CJ, Ender FA, Chandraskelar P, et al. National trends and outcomes in isolated tricuspid valve surgery. J Am Coll Cardiol. 2017;70:2953-2960.

188. Chen Q, Bowdish ME, Malas J, et al. Isolated tricuspid operations: the Society of Thoracic Surgeons adult cardiac surgery database analysis. Ann Thorac Surg. 2023;115:1162-1170.

189. Hamandi M, Smith RL, Ryan WH, et al. Outcomes of isolated tricuspid valve surgery have improved in the modern era. Ann Thorac Surg. 2019;108:11-15.

190. Wang TKM, Akuyz K, Xu B, et al. Early surgery is associated with improved long-term survival compared to class i indication for isolated selevatic prugidreguration. J Thorac Cardiovasc Surg. 2023;16:91-100.

191 Kim Y, KJwon DA, Kim HK, et al. Determinants of surgical outcome in patients with isolated tricuspid regurgitation. Circulation. 2009;12:1672–1678.

192. Kim JB, Jung Sh, Choo SJ, et al. Clinical and echocardiographic outcomes after surgery for severe isolated tricuspid regurgitation. J Thor Cardicovasc Surg. 2013;146:278-284.

193. Topilsky Y, Khanna AD, Oh JK, et al. Preoperative factors associated with adverse outcome after

tricuspid valve replacement. Circulation. 2011;123: 1929-1939.

194. Thourani VH, Bonnell L, Wyler von Ballmoos MC, et al. Outcomes of isolated tricuspid valve surgery: a Society of Thoracic Surgeons analysis and risk model. Ann Thorac Surg. 2024;118:873-881.

195. The Society of Thoracic Surgeons. Risk calculator - isolated tricuspid valve surgery. STS - Adult Cardiac Surgery Database. Accessed February 2025. https://isolatedtvsurgcal.research.sts.org/

196. Axtell AL, Bhamhani V, Moonsamy P, et al. Surgery does not improve survival in patients with isolated severe tricuspid regurgitation. J Am Coll Cardiol. 2019;74:715-725.

197. Hahn RT, Makkar R, Thourani VH, et al. Transcatheter valve replacement in severe tricuspid regurgitation. N Engl J Med. 2025;392:115-126.

198. Grayburn PA, Kodali SK, Hahn RT, et al. TRIS-CEND II: novel randomized trial design for transcatheter tricuspid valve replacement. Am J Cardiol. 2024;225:171-177.

199. Welle GA, Hahn RT, Lindenfeld J, et al. New approaches to assessment and management of tricuspid regurgitation before intervention. JACC Cardiovasc Interv. 2024;17:837-858.

200. Maisano F, Hahn R, Sorajja P, et al. Transcatheter treatment of the tricuspid valve: current status and perspectives. Eur Heart J. 2024;45:876-894.

201. Donal E, Dreyfus J, Leurent G, et al. Transcatheter edge-to-edge repair for severe isolated tricuspid regurgitation: the Tri.Fr randomized clinical trial. JAMA. 2025;333:124-132.

202. Lurz P, Besler C, Schmitz T, et al. Short-term outcomes of tricuspid edge-to-edge repair in clinical practice. J Am Coll Cardiol. 2023;82:281-291.

203. Nickenig G, Lurz P, Sorajia p, et al. Percutaneous edge-to-edge repair for tricuspid regurgitation: 3-year outcomes from the TRILUMINATE study. JACC Cardiovasc Interv. 2024;17:2133-2122.

204. ClinicalTrials.gov. Edwards CLASP TR EFS (CLASP TR EFS). Accessed March 26, 2025. https://clinicaltrials.gov/study/NCT03745313

205. Kodali SK, Hahn RT, Davidson CJ, et al. 1-Year outcomes of transcatheter tricuspid valve repair. J Am Coll Cardiol. 2023;81:1766-1776.

206. Edwards PASCAL transcatheter valve repair system pivotal clinical trial (CLASP II TR). Accessed March 24, 2025. https://clinicaltrials.gov/study/NCT04097145

207. Adams DH, Tang GHL, Whensenant BK, et al. Transcatheter edge-to-edge repair in patients with complex tricuspid valve anatomy. JACC Cardiovasc Interv. 2024;17:2749-2760.

208. Besler C, Orban M, Rommel KP, et al. Predictors of procedural and clinical outcomes in patients with symptomatic tricusid regurgitation undergoing transcatheter edge-to-edge repair. JACC Cardiovasc Interv. 2018;11:1119-1128.

209. Naik H, Price MJ, Kapadia S, et al. Tricuspid transcatheter edge-to-edge repair in patients with transvalvular CIED leads: the TRILUMINATE pivotal trial. JACC Clin Electrophysiol. 2025;11(5):1012-1020. https://doi.org/10.1016/j.jacep.2025.01.001

210. Kuwata S, Taramasso M, Nietlispach F, Maisano F. Transcatheter tricuspid valve repair toward a surgical

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standard: first-in-man report of direct annuloplasty

standard: first-in-man report of direct annuloplasty with a Cardiaband device to treat severe functional tricuspid regurgitation. Eur Heart J. 2017;38:1261.

211. Kodali S, Hahn RT, Makkar R, et al. Transfemoral tricuspid valve replacement and one-year outcomes: the TRISCEND study. Eur Heart J. 2023;44:4862-4873.

212. Wild MG, Lubos E, Cruz-Gonzalez I, et al. Early clinical experience with the TRICENTO bicaval valved stent for treatment of symptomatic severe tricuspid regurgitation: a multicenter registry. Circ Cardiovasc Interv. 2022;15:e011302.

213. Figulla HR, Kiss K, Lauten A. Transcatheter interventions for tricuspid regurgitation - heterotic technology. TricValve. Eurolintervention. 2016;12: Y16-Y118.

24. Bartkowiak J, Hahn RT. The essential role of ongoing reassessment of patients with secondary tricuspid regurgitation. JACC Case Rep. 2024;29:102659.

215. TRICuspid intervention in heart failure trial (TRIC-HF). Accessed March 24, 2025. https://clinicaltrials.gov/study/NCT04634266

216. A study to evaluate the safety and performance of Lux-Valve plus system for tricuspid replacement. Accessed March 24, 2025. https://clinicaltrials.gov/study/NCT0463260

217. TRIvalcive biCAlva valve system for severe tricuspid regurgitation (TRICAV-L). Accessed March 24, 2025. https://clinicaltrials.gov/study/NCT06137807

218. Mensen OM. Evaluation of the safety, efficacy and cost-effectiveness of transcatheter tricuspid valve repair in patients with severe tricuspid regurgitation: study protocol for a randomized controlled trial. Accessed March 20, 2025. https://onderzoekmetmensen.nl/en/node/53966/pdf

219. Russo G, Pedicino D, Pires Marafon D, et al. TRI-VALVE score: a risk score for mortality/hospitalization

prediction in patients undergoing transcatheter tricuspid valve intervention. JACC Cardiovasc Interv. 2024;17:270-279.

220. Sannino A, llardi F, Hahn RT, et al. Clinical and echocardiographic outcomes of transcatheter tricuspid valve interventions: a systematic review and meta-analysis. Front Cardiovasc Med. 2022;9: 919395.

221. Vogelhuber J, Tanaka T, Kavsur R, et al. Outcomes of transcatheter tricuspid edge-to-edge repair in patients with right ventricular dysfunction. Circ Cardiovasc Interv. 2024;17:013156.

222. Zur L P, von Bardeleben RS, Weber M, et al. Transcatheter edge-to-edge repair for treatment of tricuspid regurgitation. J Am Coll Cardiol. 2021;77:2029.33:2293. https://doi.org/10.1016/j.jacc.2020.11.038

233. von Bardeleben RS, Lurz P, Sorajja P, et al. Two-year outcomes for tricuspid repair with a transcatheter edge-to-edge valve repair from the transattantic TRULUMINATE trial. Circ Cardiovasc Interv. 2023;16: e012888.

224. Kresoja K, Rommel KP, Rosch S, et al. Hemodynamic implications of transcatheter tricuspid valve repair in HFpEF Patients - HERACLES-HFpEF. Eur Heart J. 2023;44(Suppl 2):ehad655.1763. https://doi.org/10.1093/eurheart/ehad655.1763

225. Kresoja KP, Rosch S, Schober AR, et al. Implications of tricuspid regurgitation and right ventricular volume overload in patients with heart failure with preserved ejection fraction. Eur J Heart Fail. 2024;26: 1025-1035.

226. Ailawadi G, Voisine P, Raymond S, et al. Pace- maker implantation associated with tricuspid repair in the setting of mitral valve surgery: insights from a cardiothoracic surgical trials network randomized trial. J Thorac Cardiovasc Surg. 2024;167:2104-2116. e2105.

227. Jokinen JJ, Turpeinen AK, Pitkanen O, et al. Pacemaker therapy after tricuspid valve operations: implications on mortality, morbidity, and quality of life. Ann Thorac Surg. 2009;87:1806-1814.

228. Martins RP, Galand V, Leclercq C, Daubert JC, Cardiac electronic implantable devices after tricuspid valve surgery. Heart Rhythm. 2018;15:1081-1088.

229. Mazine A, Bouchard D, Moss E, et al. Transvalvular pacemaker leads increase the recurrence of regurgitation after tricuspid valve repair. Ann Thorac Surg. 2013;96:816-822.

230. Eleid MF, Blauwet LA, Cha YM, et al. Bio-prosthetic tricuspid valve regurgitation associated with pacemaker or defibrillator lead implantation. J Am Coll Cardiol. 2012;59:813-818.

231. Hoheria A, van Zyl M, Scott LR, et al. Single-site ventricular pacing via the coronary sinus in patients with tricuspid valve disease. Europace. 2018;20:636-642.

232. Theis C, Huber C, Kaesemann P, et al. Implantation of leadless pacing systems in patients early after tricuspid valve surgery: a feasible option. Pacing Clin Electrophysiol. 2020;43:1486-1490.

233. Bazire B, Para M, Raffoul R, et al. Prophylactic epordial pacemaker implantation in tricuspid valve replacement. Eur J Cardiothorac Surg. 2023;64(6): ezad344. https://doi.org/10.1093/ejcts/ezad344

234. CardioSmart I. have tricuspid regurgitation, now what? Accessed February 25, 2025. https://www.cardiosmart.org/assets/decision-aid/i-have-tricuspid-regurgitation-now-what

KEY WORDS ACC Expert Consensus Decision Pathway, cardiac implantable electronic device, heart failure, transcatheter edge-to-edge repair, transcatheter tricuspid valve replacement, transcatheter valve, tricuspid regurgitation

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APPENDIX 1. AUTHOR RELATIONSHIPS WITH INDUSTRY AND OTHER ENTITIES (RELEVANT)– 10 ISSUES FOR THE CLINICIAN IN TRICUSPID REGURGITATION EVALUATION AND MANAGEMENT: 2025 ACC EXPERT CONSENSUS DECISION PATHWAY

|Committee Member|Employment|Consultant|Speakers Bureau|Personal Research|Institutional, Organizational, or Other Financial Benefit|Expert Witness| |---|---|---|---|---|---|---| |Patrick T. O'Gara (Chair)|Brigham and Women's Hospital-Watkins Family Distinguished Chair in Cardiology/Sr. Physician, Professor of Medicine|None|None|None|None|None| |JoAnn Lindenfeld (Vice Chair)|Vanderbilt University Medical Center-Professor of Medicine; Director, Advanced Heart Failure and Transplant Section|AbbottAlleviantAstraZenecaBoehringerIngelheimBostonScientificCordio MedicalCVRxEdwardsLifesciencesImpulseDynamicsMerckNovartisV-WAVE†|None|AstraZenecaSensibleMedicalVoluMetrix|AstraZenecaDICTATE-AHFVoluMetrix|None| |Rebecca T. Hahn|Columbia University-Professor of Medicine; Director of Interventional Echocardiology|None|AbbottBaylisMedicalEdwardsLifesciencesPhilips|None|AbbottBostonScientificEcho Core LabEdwardsLifesciencesMedtronicNovartis|None| |Megan Joseph|University of Michigan-Assistant Professor, CardiovascularMedicine|None|None|None|None|None| |Omar K. Khalique|St. Francis Hospital and Catholic Health|AbbottCroiValveEdwardsLifesciencesPhilipsRestoreMedical†Siemens|None|None|None|2018, stroke afterEP procedure†| |Prateeti Khazanie|University of Colorado-AssociateProfessor, Medicine-Cardiology|None|None|None|None|None| |Dharam J. Kumbhani|UT Southwestern, Dallas-Professor of Medicine; SectionChief, Interventional Cardiology|None|None|None|None|None| |Robert Page II|University of Colorado-Professor, Departments of Clinical Pharmacy and Physical Medicine|None|None|None|None|None| |Kristen K. Patton|University of Washington-Professor of Medicine|None|None|None|American HeartAssociationJAMACardiology|None|

Continued on the next page

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APPENDIX 1. CONTINUED

|Committee Member|Employment|Consultant|Speakers Bureau|Personal Research|Institutional, Organizational, or Other Financial Benefit|Expert Witness| |---|---|---|---|---|---|---| |Vinod H. Thourani|Piedmont-Professor of Cardiac Surgery|Artivion Boston Scientific Edwards LifesciencesGore MedicalJenaValveShockwave Medical|None|Abbott Medtronic|None|None|

This table represents the relationships of committee members with industry and other entities that were determined to be relevant to this document. These relationships were reviewed and updated in conjunction with all meetings and/or conference calls of the writing committee during the document development process. The table does not necessarily reflect relationships with industry at the time of publication. A person is deemed to have a significant interest in a business if the interest represents ownership of ≥5% of the voting stock or share of the business entity, or ownership of >$5,000 of the fair market value of the business entity; or if funds received by the person from the business entity exceed 5% of the person's gross income for the previous year. Relationships that exist with no financial benefit are also included for the purpose of transparency. Relationships in this table are modest unless otherwise noted. According to the ACC, a person has a relevant relationship IF: a) the relationship or interest relates to the same or similar subject matter, intellectual property or asset, topic, or issue addressed in the document; b) the company/entity (with whom the relationship exists) makes a drug, drug class, or device addressed in the document or makes a competing drug or device addressed in the document; or c) the person or a member of the person's household, has a reasonable potential for financial, professional, or other personal gain or loss as a result of the issues/content addressed in the document.

*This disclosure was entered under the Clinical Trial Enroller category in the ACC's disclosure system. To appear in this category, the author acknowledges that there is no direct or institutional relationship with the trial sponsor as defined in the ACC Disclosure Policy for Writing Committees.

†Significant relationship.

ACC = American College of Cardiology; DICTATE-AHF = Dapaglifozin in Acute Heart Failure; EP = electrophysiology; JAMA = Journal of the American Medical Association.

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APPENDIX 2. PEER REVIEWER RELATIONSHIPS WITH INDUSTRY AND OTHER ENTITIES (COMPREHENSIVE)— 10 ISSUES FOR THE CLINICIAN IN TRICUSPID REGURGITATION EVALUATION AND MANAGEMENT: 2025 ACC EXPERT CONSENSUS DECISION PATHWAY

|Reviewer|Representation|Employment|Consultant|Speakers Bureau|Ownership Interest/Partnership/Principal|Personal Research|Institutional, Organizational, or Other Financial Benefit|Expert Witness| |---|---|---|---|---|---|---|---|---| |Vinay Badhwar|Content Reviewer-ACC Expert|West Virginia University-Gordon F. Murray Professor and Executive Chair|None|None|None|None|Abbott*PRIMARY,NHLBI*SUMMIT+Tendyne*|None| |Jamieson M. Bourque|Official Reviewer-ACC Imaging Section Council|University of Virginia-Associate Professor of Medicine and Radiology|GE HealthCare|None|None|None|None|None| |Megan Coylewright|Official Reviewer-Solution Set Oversight Committee|University of Tennessee Health Science Center College of Medicine-Chattanooga; Interventional Cardiologist and Editor, ACC CardioSmart|■ Alleviant† ■ American College of Cardiology CardioSmart-Editor† ■ Boston Scientific† ■ Edwards Lifesciences†Medtronic†|None|None|■ Abbott‡ ■ MTRAL study (DSMB)|■ ACCCTR: Up-ping Your Game‡Cardiovascular Research Foundation‡Heart Valve Collaboratory‡MDEpiNet PASSION‡Society for Cardiovascular Angiography &Interventions‡|None| |Laura Davidson|Official Reviewer-ACC Interventional Section Council|Northwestern University-Assistant Professor of Medicine|None|None|None|■ Edwards Lifesciences|■ Cardiaband TR, Edwards Lifesciences*CLASP II TR, Edwards Lifesciences*EMPOWER, Shockwave Medical*FLASH Registration, REDUCE, Gore Medical*STORM-PE, Penumbra*TANDEM II, CroiValve*TRILUMINATE, Abbott*TRISCEND, Edwards Lifesciences*|None| |Ersilia M. DeFilippis|Official Reviewer-ACC Heart Failure Section Council|Columbia University Irving Medical Center-Assistant Professor of Medicine|None|■ AstraZeneca|None|None|■ Abiomed†|None| |Michael E. Halkos|Official Reviewer-ACC Surgery Section Council|Emory Healthcare-Chief and Professor of Surgery|■ Medtronic†|None|None|None|None|■ 2018, CABG complications ■ 2020, adverse events after CABG ■ 2022, complications after CABG| |Purvi Parwani|Official Reviewer-ACC Imaging Section Council|Loma Linda University Health-Associate Professor of Medicine|■ Medtronic|■ AstraZeneca Bristol Myers Squibb†|None|None|None|None|

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APPENDIX 2. CONTINUED

|Reviewer|Representation|Employment|Consultant|Speakers Bureau|Ownership Interest/ Partnership/ Principal|Personal Research|Institutional, Organizational, or Other Financial Benefit|Expert Witness| |---|---|---|---|---|---|---|---|---| |Megan Pelter|Official Reviewer-ACC Heart Failure Section Council|University of California, Los Angeles-Advanced Heart Failure and Transplant Attending|None|None|None|None|None|None|

This table represents all relationships of reviewers with industry and other entities as disclosed by the reviewers, including those not deemed to be relevant to this document, at the time it was being reviewed. The table does not necessarily reflect relationships with industry at the time of publication. A person is deemed to have a significant interest in a business if the interest represents ownership of ≥5% of the voting stock or share of the business entity, or ownership of ≥$5,000 of the fair market value of the business entity; or if funds received by the person from the business entity exceed 5% of the person's gross income for the previous year. Relationships that exist with no financial benefit are also included for the purpose of transparency. Relationships in this table are modest unless otherwise noted. Please refer to https://www.acg.org/Guidelines/About-Guidelines-and-Clinical-Documents/Relationships-with-Industry-Policy for definitions of disclosure categories or additional information about the ACC Disclosure Policy for Writing Committees.

*Relationship with this company is limited to enrolling patients in clinical trials. This disclosure was entered under the Clinical Trial Enroller category in the ACC's disclosure system. To appear in this category, the reviewer acknowledges that there is no direct or institutional relationship with the trial sponsor as defined in the ACC Disclosure Policy for Writing Committees.

No financial benefit.

ACC = American College of Cardiology; ACCCTR = American College of Cardiology Clinical Trials Research; CABG = coronary artery bypass graft; CLASP = Edwards PASCAL TrAnScatheter Valve RePair System Pivotal Clinical Trial; DSMB = Data Safety Monitoring Board; EMPOWER = Equity in Modifying Plaque Of WomEn With UndeRtreated Calcified Coronary Artery Disease; FLASH = FlowTriever All-Comer Registry for Patient Safety and Hemodynamics; MDEPiNet PASSION = Medical Device Epidemiological Network Initiative for Predictable and SuStainable Implementation of National Cardiovascular Registries; MITRAL = Mitral Implantation of Transcatheter Valves trial; NHLBI = National Heart, Lung, and Blood Institute; REDUCE = Septal Occluder Device for Patent Foramen Ovale Closure in Stroke Patients; STORM-PE = Study Treating Oacute Reversible Myocardial Injury in Pulmonary Embolism; SUMMIT = Clinical Trial to Evaluate the Safety and Effectiveness of Using the Tendyne Transcatheter Mitral Valve System for the Treatment of Symptomatic Mitral Regurgitation; TANDEM = Early Feasibility Study of the DUO System for Tricuspid Regurgitation; TR = tricuspid regurgitation; TRISCEND = Transcatheter Tricuspid Valve Replacement in Patients with Severe Tricuspid Regurgitation.

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APPENDIX 3. ABBREVIATIONS

2D = 2-dimensional 3D = 3-dimensional A-STR = atrial secondary tricuspid regurgitation ACC = American College of Cardiology AF = atrial fibrillation AHA = American Heart Association CAVI = caval valve implantation CIED = cardiac implantable electronic device CMR = cardiac magnetic resonance CT = computed tomography ECDP = expert consensus decision pathway EF = ejection fraction EROA = effective regurgitant orifice area GDMT = guideline-directed medical therapy HF = heart failure HFpEF = heart failure with preserved ejection fraction HFREF = heart failure with reduced ejection fraction HR = hazard ratio IVC = inferior vena cava KCCQ = Kansas City Cardiomyopathy Questionnaire LA = left atrial LV = left ventricular LVEF = left ventricular ejection fraction M-TEER = mitral transcatheter edge-to-edge repair MDT = multidisciplinary team MR = mitral regurgitation MV = mitral valve

NYHA = New York Heart Association OMT = optimal medical therapy PA = pulmonary artery PH = pulmonary hypertension PISA = proximal isovelocity surface area QoL = quality of life RA = right atrial RF = regurgitant fraction RV = right ventricular RVEF = right ventricular ejection fraction RVol = regurgitant volume RWI = relationship with industry SGLT2 = sodium-glucose cotransporter-2 SV = stroke volume TA = tricuspid annulus TAPSE = tricuspid annular plane systolic excursion TAVI = transcatheter aortic valve implantation TEE = transesophageal echocardiography T-TEER = tricuspid transcatheter edge-to-edge repair TR = tricuspid regurgitation TTE = transthoracic echocardiography TTVA = transcatheter tricuspid valve annuloplasty TTVI = transcatheter tricuspid valve intervention TTVR = transcatheter tricuspid valve replacement TV = tricuspid valve VHD = valvular heart disease V-STR = ventricular secondary tricuspid regurgitation

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