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Tricuspid Regurgitation

11 min read

Background #

Tricuspid regurgitation (TR), also known as tricuspid insufficiency, is the backward flow of blood from the right ventricle into the right atrium during systole due to incomplete closure of the tricuspid valve. This leads to right atrial and right ventricular volume overload, progressive chamber dilation, systemic venous congestion, and eventually right-sided heart failure. TR can be functional (secondary to annular dilation or right ventricular pressure overload) or organic (due to structural damage of the valve).

Classification/Types

By Etiology:

Primary (Organic) TR:
  • Rheumatic heart disease
  • Carcinoid syndrome
  • Infective endocarditis
  • Congenital abnormalities (e.g., Ebstein anomaly)
  • Trauma (e.g., pacemaker or ICD lead)
Secondary (Functional) TR:
  • Left-sided heart disease (e.g., mitral stenosis or regurgitation)
  • Pulmonary hypertension
  • Right ventricular dilation or dysfunction
  • Atrial fibrillation (atrial TR due to annular dilation)

By Chronicity:

  • Chronic TR: Gradual development with compensatory right heart dilation; symptoms develop late.
  • Acute TR: Sudden volume overload; rare, often seen in endocarditis or trauma.

Epidemiology

Tricuspid regurgitation is highly prevalent, affecting more than 4% of individuals aged 75 years or older and is as common as aortic stenosis in the general population [1,2]. The prevalence of severe TR has been reported at approximately 1.2% in patients undergoing echocardiography, with significant TR occurring in 0.55% of the general population [3,4]. Prevalence increases significantly with age, with nearly 1 in 25 adults over 75 years presenting with moderate or severe TR [4]. TR is more common in women across all severity grades [1-4]. Secondary (functional) TR is much more common than primary TR, accounting for approximately 91% of cases with identifiable causes, while isolated (idiopathic) TR represents about 8-9% of significant TR cases [3,4]. Functional TR is particularly prevalent in patients with heart failure, atrial fibrillation, pulmonary hypertension, and those with cardiac implantable electronic devices [5-7].

Pathophysiology

The pathophysiology of tricuspid regurgitation is complex and multifactorial, varying by etiology [8,9]. In functional TR, the most common mechanism involves a combination of right ventricular remodeling, annular dilation, and leaflet tethering [10,11]. Left-sided heart disease leads to increased left atrial pressure, resulting in pulmonary hypertension. Because the right ventricle tolerates pressure overload poorly, this leads to RV enlargement and progressive dysfunction, creating the anatomic substrate for TR [11,12]. Right ventricular remodeling, particularly in the mid-segment, causes papillary muscle displacement and leaflet tethering, preventing adequate coaptation [10,13].

Atrial secondary TR represents a distinct phenotype characterized by predominant right atrial and tricuspid annular dilation in the setting of preserved RV function [14]. This phenotype is commonly associated with chronic atrial fibrillation or atrial myopathy in patients with heart failure with preserved ejection fraction. The primary mechanism is annular dilation secondary to right atrial enlargement, with insufficient adaptive leaflet growth to cover the enlarged annular area [14]. In pulmonary hypertension-related TR, leaflet tethering due to lateral and apical papillary muscle displacement is the dominant mechanism, accompanied by mid-ventricular RV dilation and annular dilation [13,15]. The development of TR creates a vicious cycle: regurgitant flow into the right atrium during systole contributes to further RA enlargement, increasing the probability of atrial fibrillation, which in turn exacerbates TR [11]. This progressive nature of TR, particularly when left untreated, leads to worsening right heart failure, systemic venous congestion, and ultimately hepatic and renal dysfunction [16].

Etiology #

Primary Causes:

  • Rheumatic fever
  • Endocarditis (especially with IV drug use or devices)
  • Congenital anomalies (e.g., Ebstein anomaly)
  • Carcinoid heart disease
  • Myxomatous degeneration

Secondary Causes:

  • Left-sided heart failure (e.g., mitral valve disease)
  • Pulmonary hypertension
  • Right ventricular infarction
  • Chronic atrial fibrillation
  • Right ventricular pacing leads

Risk Factors

  • Chronic left-sided heart disease
  • Pulmonary hypertension
  • Atrial fibrillation
  • Intracardiac devices (e.g., pacemaker, ICD)
  • IV drug use
  • Rheumatic heart disease
  • Connective tissue disorders

Clinical Presentation #

I) History (Symptoms)

Chronic TR:
  • Fatigue
  • Lower extremity edema
  • Abdominal fullness and bloating
  • Right upper quadrant discomfort (hepatic congestion)
  • Anorexia and weight loss
  • Ascites
Acute TR:
  • Sudden onset of right heart failure
  • Hypotension (if severe)
  • Dyspnea (if associated with left-sided lesions or pulmonary edema)

II) Physical Exam (Signs)

General Exam:
  • Patients may appear uncomfortable or cachectic in advanced disease
  • May show signs of volume overload (peripheral edema, ascites)
  • May appear dyspneic at rest or with minimal exertion
Vital Signs:
  • Normal or low blood pressure
  • Elevated jugular venous pressure (JVP)
Cardiac Exam:
  • Holosystolic murmur best heard at the left lower sternal border, increases with inspiration (Carvallo’s sign)
  • Right ventricular heave
  • S3 gallop at left lower sternal border
Peripheral Signs:
  • Prominent v-wave in JVP
  • Hepatomegaly (pulsatile)
  • Ascites
  • Peripheral edema
  • Cyanosis (in severe chronic TR with right-to-left shunt)
Pulmonary:
  • Usually clear unless left-sided failure or pulmonary edema coexists

Differential Diagnosis (DDx) #

  • Pulmonary hypertension
  • Constrictive pericarditis
  • Pericardial tamponade
  • Right ventricular failure (non-valvular)
  • Atrial septal defect
  • Mitral stenosis or regurgitation
  • Hepatic cirrhosis (due to similar signs)

Diagnostic Testing #

Initial Tests:

Transthoracic Echocardiogram (TTE):

  • Determines TR severity (jet area, vena contracta, hepatic vein flow reversal)
  • Assesses right atrial and ventricular size and function
  • Evaluates valve morphology

Transesophageal Echocardiogram (TEE):

  • Better visualization of valve leaflets
  • Used in endocarditis, device-related TR

Electrocardiogram (ECG):

  • Right atrial enlargement
  • Right ventricular hypertrophy
  • Atrial fibrillation

Chest X-ray:

  • Cardiomegaly (right heart enlargement)
  • Pleural effusion (occasionally)
  • Clear lungs unless left-sided involvement

BNP/NT-proBNP:

  • May be mildly elevated in isolated TR
  • More elevated if biventricular failure

Cardiac MRI:

  • Accurate quantification of right ventricular size/function and regurgitant volume

Right Heart Catheterization:

  • Confirms pulmonary hypertension
  • Measures right-sided pressures and cardiac output

Treatment #

I) Medical Management

Functional TR:

  • Treat underlying cause (e.g., left-sided heart failure, pulmonary hypertension) [17]
  • Diuretics: mainstay for symptom relief (edema, ascites) [17]
  • Aldosterone antagonists for volume overload [17]
  • Optimize guideline-directed medical therapy for heart failure [17,18]

Primary TR (mild to moderate):

  • Monitor with serial imaging [19]
  • Manage risk factors (e.g., endocarditis prophylaxis if indicated) [20]
Acute TR:
  • Diuresis, vasopressors, treat underlying cause
  • Consider urgent surgical evaluation in endocarditis or trauma

II) Interventional/Surgical

Indications for Tricuspid Valve Surgery [19-21]:

  • Severe TR undergoing left-sided valve surgery (Class I)
  • Severe symptomatic isolated TR with right heart failure refractory to medical therapy, before onset of severe RV dysfunction or end-organ damage (Class IIa)
  • Mild-to-moderate secondary TR undergoing left-sided valve surgery with tricuspid annular dilatation ≥40 mm or ≥21 mm/m² (Class IIa)

Surgical Options:

  • Annuloplasty (preferred in functional TR) [21]
  • Valve replacement (bioprosthetic preferred due to lower thrombosis risk) [21]

Transcatheter Options [22-25]:

Transcatheter Tricuspid Valve Repair (T-TEER):

  • Transcatheter edge-to-edge repair (e.g., TriClip, PASCAL) approved for symptomatic severe TR in patients at high or prohibitive surgical risk [22,23]
  • Provides meaningful reduction in TR severity, improved quality of life, and reduced heart failure hospitalizations [22,23]
  • Residual TR common (mild to moderate in many patients) [23]
  • Class IIb recommendation in ESC/EACTS 2021 guidelines for inoperable patients at experienced centers [20]

Transcatheter Tricuspid Valve Replacement (TTVR):

  • TTVR systems (e.g., EVOQUE, LuX-Valve) now available for patients with complex valve morphology [24,25]
  • Achieves near-complete TR elimination in >95% of patients [24,25]
  • Superior TR reduction compared to T-TEER, associated with greater reverse RV remodeling [26]
  • Demonstrated sustained improvements in functional status, quality of life, and reduction in heart failure hospitalizations at 1 year [24,25]
  • FDA approval of EVOQUE system in 2024 [24]

Consults #

  • Cardiology: Diagnostic evaluation, TR severity grading, and optimization
  • Cardiothoracic Surgery: If surgical correction is needed
  • Infectious Disease: For infective endocarditis management
  • Gastroenterology/Hepatology: If hepatic congestion or ascites dominates
  • Primary Care: Management of comorbidities and routine follow-up

Patient Education, Screening, and Vaccines #

Patient Education:

  • Educate on early signs of right heart failure (leg swelling, fatigue, ascites)
  • Emphasize adherence to diuretics and follow-up
  • Encourage sodium restriction in severe cases
  • Promote good dental hygiene to prevent endocarditis

Screening and Preventive Services (Based on USPSTF Recommendations):

Cardiovascular Risk Assessment [27]:

  • Use Pooled Cohort Equations for CVD risk assessment in appropriate patients
  • Screen for hypertension in all adults aged 18 years or older
  • Screen for prediabetes and type 2 diabetes in adults aged 35-70 years with overweight or obesity

Behavioral Counseling [28]:

  • Offer or refer adults with cardiovascular risk factors to behavioral counseling interventions to promote a healthful diet and physical activity (Grade B recommendation)
  • Individualize the decision to offer behavioral counseling to adults without cardiovascular risk factors (Grade C recommendation)

Statin Therapy [29]:

  • For adults aged 40-75 years with 1 or more CVD risk factors and a calculated 10-year CVD risk of 10% or greater, initiate a statin after informed decision-making (Grade B recommendation)

Aspirin for Primary Prevention [30]:

  • For adults aged 40-59 years with a 10-year CVD risk of 10% or greater, the decision to initiate low-dose aspirin should be individualized (Grade C recommendation)
  • For adults 60 years or older, do not initiate aspirin for primary prevention of CVD (Grade D recommendation)

Vaccinations:

  • Influenza vaccine: Annual vaccination recommended for all adults
  • Pneumococcal vaccine: Recommended for all adults aged 50 years or older with PCV20, PCV21, or PCV15 followed by PPSV23; also recommended for adults 19-49 years with specific risk conditions
  • COVID-19 vaccine: Recommended for all adults according to current CDC guidelines

Follow-Up #

Echocardiography:

  • Mild TR: every 3–5 years
  • Moderate TR: every 1–2 years
  • Severe TR (asymptomatic): every 6–12 months

Monitoring Goals:

  • Right ventricular function and size
  • Progression of TR severity
  • Symptoms and response to diuretic therapy
  • Evaluate candidacy for surgical/interventional therapy

REFERENCES #

[1] Topilsky Y, Maltais S, Medina Inojosa J, et al. Burden of tricuspid regurgitation in patients diagnosed in the community setting. JACC Cardiovasc Imaging. 2019;12(3):433-442.

https://doi.org/10.1016/j.jcmg.2018.06.014

[2] Hahn RT. Tricuspid Regurgitation. N Engl J Med. 2023;388(20):1876-1891.

https://doi.org/10.1056/NEJMra2216709

[3] Nath J, Foster E, Heidenreich PA. Impact of tricuspid regurgitation on long-term survival. J Am Coll Cardiol. 2004;43(3):405-409.

https://doi.org/10.1016/j.jacc.2003.09.036

[4] Topilsky Y, Nkomo VT, Vatury O, et al. Clinical outcome of isolated tricuspid regurgitation. JACC Cardiovasc Imaging. 2014;7(12):1185-1194.

https://doi.org/10.1016/j.jcmg.2014.07.018

[5] 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(6):857-867.

https://doi.org/10.1002/ejhf.2869

[6] Adamo M, Chioncel O, Benson L, et al. Prevalence, clinical characteristics and outcomes of heart failure patients with or without isolated or combined mitral and tricuspid regurgitation: An analysis from the ESC-HFA Heart Failure Long-Term Registry. Eur J Heart Fail. 2023;25(7):1061-1071.

https://doi.org/10.1002/ejhf.2854

[7] Offen S, Strange G, Playford D, et al. Prevalence and prognostic impact of tricuspid regurgitation in patients with cardiac implantable electronic devices: From the national echocardiography database of Australia. Int J Cardiol. 2023;370:338-344.

https://doi.org/10.1016/j.ijcard.2022.10.160

[8] Topilsky Y, Khanna A, Le Tohic A, et al. Tricuspid valve regurgitation: epidemiology and pathophysiology. Curr Cardiol Rep. 2018;20(11):103.

https://doi.org/10.1007/s11886-018-1039-4

[9] Hahn RT, Badano LP, Bartko PE, et al. Tricuspid regurgitation: recent advances in understanding pathophysiology, severity grading and outcome. Eur Heart J Cardiovasc Imaging. 2022;23(7):913-929.

https://doi.org/10.1093/ehjci/jeac009

[10] Dreyfus J, Galloo X, Taramasso M, et al. Comparison of 2 echocardiographic phenotypes of functional tricuspid regurgitation. JACC Cardiovasc Imaging. 2023;16(11):1403-1417.

https://doi.org/10.1016/j.jcmg.2023.05.007

[11] Mangieri A, Montalto C, Pagnesi M, et al. Mechanism and implications of the tricuspid regurgitation: from the pathophysiology to the current and future therapeutic options. Circ Cardiovasc Interv. 2017;10(7):e005043.

https://doi.org/10.1161/CIRCINTERVENTIONS.117.005043

[12] Prihadi 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(39):3574-3581.

https://doi.org/10.1093/eurheartj/ehy352

[13] Dietz MF, Prihadi EA, van der Bijl P, et al. Prognostic implications of right ventricular remodeling and function in patients with significant secondary tricuspid regurgitation. Circulation. 2019;140(10):836-845.

https://doi.org/10.1161/CIRCULATIONAHA.119.039630

[14] Muraru D, Guta AC, Miglioranza MH, et al. Atrial secondary tricuspid regurgitation: pathophysiology, definition, diagnosis, and treatment. Eur Heart J Cardiovasc Imaging. 2024;25(9):1211-1227.

https://doi.org/10.1093/ehjci/jeae048

[15] Spinner EM, Shannon P, Buice D, et al. In vitro characterization of the mechanisms responsible for functional tricuspid regurgitation. Circulation. 2011;124(8):920-929.

https://doi.org/10.1161/CIRCULATIONAHA.110.003897

[16] 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;40(5):476-484.

https://doi.org/10.1093/eurheartj/ehy641

[17] Adamo M, Chioncel O, Pagnesi M, et al. Epidemiology, pathophysiology, diagnosis and management of chronic right-sided heart failure and tricuspid regurgitation. A clinical consensus statement of the Heart Failure Association (HFA) and the European Association of Percutaneous Cardiovascular Interventions (EAPCI) of the ESC. Eur J Heart Fail. 2024;26(1):18-33.

https://doi.org/10.1002/ejhf.3106

[18] Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. J Am Coll Cardiol. 2022;79(17):e263-e421.

https://doi.org/10.1016/j.jacc.2021.12.012

[19] 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 Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2021;143(5):e72-e227.

https://doi.org/10.1161/CIR.0000000000000923

[20] Vahanian A, Beyersdorf F, Praz F, et al. 2021 ESC/EACTS Guidelines for the management of valvular heart disease. Eur Heart J. 2022;43(7):561-632.

https://doi.org/10.1093/eurheartj/ehab395

[21] Brescia AA, Watt TMF, Rosenbloom LM, et al. Tricuspid valve surgery: contemporary use, outcomes, and implications for future trials. Ann Thorac Surg. 2022;113(6):1842-1849.

https://doi.org/10.1016/j.athoracsur.2021.06.046

[22] Sorajja P, Whisenant B, Hamid N, et al. Transcatheter repair for patients with tricuspid regurgitation. N Engl J Med. 2023;388(20):1833-1842.

https://doi.org/10.1056/NEJMoa2300525

[23] Lurz P, Stephan von Bardeleben R, Weber M, et al. Transcatheter edge-to-edge repair for treatment of tricuspid regurgitation. J Am Coll Cardiol. 2021;77(3):229-239.

https://doi.org/10.1016/j.jacc.2020.11.038

[24] Gray WA, Abramson SV, Lim S, et al. 1-Year Outcomes of Cardioband Tricuspid System From a Multicenter Study. JACC Cardiovasc Interv. 2022;15(17):1768-1776.

https://doi.org/10.1016/j.jcin.2022.07.006

[25] Hausleiter J, Stolz L, Lurz P, et al. Transcatheter tricuspid valve replacement. J Am Coll Cardiol. 2025;85(3):265-291.

https://doi.org/10.1016/j.jacc.2024.10.071

[26] Davidson CJ, Lim DS, Smith RL, et al. Early Feasibility Study of Cardioband Tricuspid System for Functional Tricuspid Regurgitation: 30-Day Outcomes. JACC Cardiovasc Interv. 2021;14(1):41-50.

https://doi.org/10.1016/j.jcin.2020.10.017

[27] US Preventive Services Task Force, Curry SJ, Krist AH, et al. Risk Assessment for Cardiovascular Disease With Nontraditional Risk Factors: US Preventive Services Task Force Recommendation Statement. JAMA. 2018;320(3):272-280.

https://doi.org/10.1001/jama.2018.8359

[28] US Preventive Services Task Force, Krist AH, Davidson KW, et al. Behavioral Counseling Interventions to Promote a Healthy Diet and Physical Activity for Cardiovascular Disease Prevention in Adults Without Cardiovascular Risk Factors: US Preventive Services Task Force Recommendation Statement. JAMA. 2022;328(4):367-374.

https://doi.org/10.1001/jama.2022.10951

[29] US Preventive Services Task Force, Davidson KW, Barry MJ, et al. Statin Use for the Primary Prevention of Cardiovascular Disease in Adults: US Preventive Services Task Force Recommendation Statement. JAMA. 2022;328(8):746-753. https://doi.org/10.1001/jama.2022.13044

[30] US Preventive Services Task Force, Davidson KW, Barry MJ, et al. Aspirin Use to Prevent Cardiovascular Disease: US Preventive Services Task Force Recommendation Statement. JAMA. 2022;327(16):1577-1584. https://doi.org/10.1001/jama.2022.4983

[31] US Preventive Services Task Force. Immunizations for Adults. Referred to CDC Advisory Committee on Immunization Practices.

https://www.uspreventiveservicestaskforce.org/uspstf/recommendation/immunizations-for-adults

Updated on November 25, 2025

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Table of Contents
  • Background
  • Etiology
  • Clinical Presentation
  • Differential Diagnosis (DDx)
  • Diagnostic Testing
  • Treatment
  • Consults
  • Patient Education, Screening, and Vaccines
  • Follow-Up
  • REFERENCES

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