Tricuspid regurgitation

Article written and reviewed by Dr Luca Moretti

Tricuspid regurgitation is systolic backflow from the right ventricle into the right atrium through a tricuspid valve that does not achieve competent coaptation. A physiologic trace is common and allows estimation of pulmonary pressure; disease begins when regurgitation is structurally abnormal or hemodynamically sufficient to remodel the chambers, reduce forward output, and transmit pressure to the systemic veins. Severity must therefore be interpreted together with mechanism and consequences.

The concept of tricuspid regurgitation as a late, passive valvular disorder has been superseded. Significant regurgitation may persist after correction of left-sided disease and progressively drive dilation of the atrium, annulus, and ventricle, eventually causing right-sided heart failure and hepatorenal dysfunction; at the same time, treatment of pulmonary pressure, atrial fibrillation, or volume overload may reduce its dynamic component. It is therefore more useful to define stage and reversibility than to rely on a single snapshot of severity.

This page presents the overall framework, whereas etiology requires a rigorous distinction among primary regurgitation, secondary regurgitation of atrial or ventricular origin, and device-related regurgitation. These categories can coexist: a lead that initially interferes with a leaflet may trigger secondary remodeling, whereas a diseased primary valve may dilate until additional tethering develops.

Classification and mechanisms of regurgitation

In the primary form, the lesion directly involves a leaflet, chord, papillary muscle, or annulus. Endocarditis, carcinoid disease, Ebstein anomaly, trauma, iatrogenic injury, rheumatic disease, degeneration, and connective tissue disorders can produce retraction, perforation, prolapse, flail, or failure of leaflet formation. Identifying the lesion is essential because repair must reconstruct the tissue as well as stabilize the annulus.

Secondary or functional regurgitation occurs when initially normal leaflets can no longer cover a dilated orifice or are pulled into the ventricle. In the ventricular phenotype, pulmonary hypertension, left-sided heart disease, or myocardial disease dilate and sphericalize the ventricle, displace the papillary muscles, and increase tethering. Annular reduction alone may fail when the coaptation gap is dominated by apical traction.

In the atrial phenotype, persistent atrial fibrillation, aging, and heart failure with preserved ejection fraction predominantly dilate the atrium and annulus, whereas the ventricle is initially less deformed and pulmonary pressure may be modest. With progression, volume overload dilates the ventricle and blurs the distinction between categories. The phenotype is a trajectory, not a permanent label.

Transvenous devices can impair coaptation through impingement, adherence, perforation, or entanglement in the chordae. The term CIED-related TR is used when a causal relationship is demonstrated and CIED-associated TR when there is only coexistence, while pacing, dyssynchrony, elevated pressures, and dilation may contribute indirectly; distinguishing these mechanisms is essential because it determines the choice among extraction, a valve procedure, and modification of the pacing strategy.

The Carpentier classification can describe leaflet motion: type I is normal motion with annular dilation or perforation, type II is excessive motion with prolapse or flail, type IIIa is restricted motion in systole and diastole, and type IIIb is restricted motion in systole due to tethering. It is useful for repair but does not replace etiologic classification. Carcinoid disease may show type IIIa, whereas advanced secondary disease typically shows type IIIb.

Regurgitation and tricuspid stenosis can coexist in rheumatic disease, carcinoid disease, or after repair. A high gradient influences the choice of TEER and the number of devices; a small prosthesis can create mismatch. Assessment must always include diastolic flow, even when the systolic jet dominates the image.

Tricuspid regurgitation is dynamic and varies with hemodynamic conditions: inspiration, increased venous return, increased pulmonary pressure, and atrial fibrillation may worsen it, whereas diuresis, vasodilation, and anesthesia may reduce it. Consequently, an intraprocedural examination during positive-pressure ventilation does not necessarily represent ambulatory severity, and the report must be interpreted together with the patient's pressure, rhythm, weight, and current therapy.

Compensatory capacity also depends on the relationship between leaflet surface area and the area they must cover. Some valve growth may accompany dilation, but it becomes insufficient when the annulus and right-sided chamber enlarge more rapidly: the resulting coaptation mismatch may precede a macroscopic gap. In advanced forms, multiple jets, coaptation along a deformed plane, and overlapping etiologic contributions make it reductive to attribute disease to a single segment. The report should therefore describe the entire apparatus and indicate which component is presumed to be correctable.

Pathophysiology, stages, and clinical manifestations

The regurgitant volume enters the atrium and returns to the ventricle during the following diastole. The atrium, annulus, and ventricle dilate to accommodate the overload; the right ventricular wall initially maintains total output, while effective forward output through the pulmonary valve decreases. Annular dilation worsens loss of coaptation and generates a self-perpetuating cycle.

The right ventricle ejects toward a low-impedance pathway, so some functional indices may appear preserved despite already reduced reserve. After correction of regurgitation, however, the entire stroke volume must face the pulmonary circulation and effective afterload increases: a postprocedural reduction in TAPSE or ejection fraction does not necessarily indicate new injury, but severe pre-existing dysfunction may become clinically apparent.

Atrial pressure is transmitted to the venae cavae and liver. The kidney receives lower perfusion and higher venous pressure, reducing filtration and the response to diuretics; intestinal congestion limits absorption and causes enteropathy, while hepatic congestion causes cholestasis, fibrosis, and coagulopathy. Right-sided cardiorenal syndrome is not simply fluid retention and may become poorly reversible.

Symptoms include fatigue, exertional dyspnea, edema, rapid weight gain, abdominal distension, ascites, early satiety, and weakness. Many patients reduce their activity and deny dyspnea. Palpitations reflect atrial fibrillation or flutter; syncope suggests low output, arrhythmia, or pulmonary hypertension and requires broader evaluation.

Examination may show elevated jugular venous pressure with a v wave, hepatojugular reflux, a pulsatile liver, ascites, and edema. The holosystolic murmur at the lower sternal border increases with inspiration but may become softer in torrential regurgitation when pressures equalize rapidly. A dominant v wave without a loud murmur is not contradictory.

Staging integrates the valve, chambers, and organs. Severe regurgitation with a still-adapted ventricle and preserved organs offers greater reversibility; right ventricular dysfunction, low output, precapillary pulmonary hypertension, liver disease, and frailty signal advanced stages. No single threshold defines futility, but accumulating damage reduces the benefit of late correction.

Prognosis worsens as severity increases even after adjustment for comorbidities, but this observational association does not prove that any reduction in the jet automatically improves survival. Transcatheter trials have documented benefits in quality of life, functional class, and remodeling; more recent randomized data have also demonstrated a reduction in the composite of death or hospitalization for heart failure in selected patients, whereas a definite benefit on mortality alone has not yet been demonstrated. Clinical communication must therefore clearly distinguish what has been proven from what is only plausible.

Resting assessment may underestimate limitation. Six-minute walk testing, cardiopulmonary exercise testing, and validated questionnaires such as the KCCQ make reduced reserve, unrecognized adaptation of activities, and response to therapy measurable. During exercise, increased venous return and pulmonary pressure may increase regurgitation and reduce effective forward output; an inadequate blood pressure response or markedly reduced oxygen consumption suggests more advanced disease. These data do not replace imaging, but they prevent the label of “asymptomatic” from depending only on an increasingly sedentary lifestyle.

Quantification and assessment of the right heart

Transthoracic echocardiography is the cornerstone. Dedicated apical, parasternal, and subcostal views define morphology, gap, tethering, annulus, leads, and jets. Color Doppler identifies the origin, but jet area depends on pressure, gain, and the Nyquist limit. A very large low-velocity jet and a small wall-hugging jet can both be severe.

Severity requires a multiparametric approach. Vena contracta, PISA convergence, radius, effective regurgitant orifice area, regurgitant volume, density and contour of the continuous-wave Doppler signal, systolic flow reversal in the hepatic veins, and remodeling should be concordant. Rhythm, respiration, atrial pressure, and technical quality may make individual criteria discordant.

In the conventional grading system, a vena contracta of at least 7 mm, EROA of at least 40 mm², and regurgitant volume of at least 45 mL are compatible with severe regurgitation, but the tricuspid orifice is often elliptical and multiple. Hemispheric PISA tends to underestimate noncircular orifices; multiple jets cannot be summarized by measuring only the largest one. Values are guides, not substitutes for integrated judgment.

Three-dimensional vena contracta area visualizes the orifice without assuming its shape, but it depends on resolution and frame rate. The massive and torrential categories extend the scale beyond severe to describe populations with extreme EROA and vena contracta values. They are useful for measuring reductions after a procedure: moving from torrential to severe may represent a substantial change while remaining within the highest traditional category.

Hepatic vein Doppler shows systolic flow reversal in severe forms, but atrial fibrillation, pacemakers, sampling, and atrial compliance alter the pattern. Jet velocity estimates pulmonary systolic pressure, but in massive regurgitation it may be low because pressures equalize; an apparently normal pressure does not exclude pulmonary vascular disease or a failing ventricle.

Right ventricular function is assessed with TAPSE, S’, fractional area change, free-wall strain, 3D ejection fraction, dimensions, and pressure signs. TAPSE and S’ measure one region and are load-dependent; after sternotomy they may decrease without an equivalent global loss of function. Strain and 3D measurements add sensitivity, but there is no single universally accepted threshold for withholding intervention.

Cardiac magnetic resonance is the reference for right ventricular volumes and ejection fraction when image quality and rhythm permit. It quantifies regurgitation from the difference between right ventricular stroke volume and pulmonary flow, accounting for shunts and other regurgitant lesions. CT is central for assessing annular anatomy, the right coronary artery, venae cavae, leads, and planning replacement. Transesophageal echocardiography guides procedures, but the anteriorly located tricuspid valve can be difficult to visualize.

Right-heart catheterization measures pressures, output, and vascular resistance and is part of the work-up of every candidate for tricuspid intervention, as well as cases with inconclusive echocardiography. Severe TR may make Doppler estimation of pulmonary pressure unreliable and conceal a precapillary component. Thermodilution may be less accurate, and the Fick method requires reliable oxygen consumption; mean atrial pressure and v waves provide information on congestion, but sedation and diuresis alter the picture.

Complete staging includes a complete blood count, sodium, creatinine and eGFR, bilirubin, transaminases, alkaline phosphatase, albumin, coagulation tests, and natriuretic peptides. No value is specific, but a trajectory of cholestasis, hypoalbuminemia, and renal failure documents the systemic cost of congestion. Abdominal ultrasonography and elastography may show hepatomegaly, ascites, and increased stiffness, which in the congested liver does not necessarily equal cirrhosis. Before attributing organ damage to the valve, independent liver disease, kidney disease, and malnutrition should be excluded because they affect both risk and reversibility.

Medical, surgical, and transcatheter treatment

Medical therapy treats the cause and congestion. Loop diuretics, mineralocorticoid receptor antagonists, and sequential nephron blockade are tailored to renal function, sodium, and blood pressure; treatment of left-sided heart failure, control of atrial fibrillation, and specific therapy for pulmonary hypertension when indicated may reduce secondary regurgitation. No drug can recreate coaptation in a structural lesion.

Surgery is recommended for severe primary or secondary regurgitation during left-sided valve surgery. Concomitant annuloplasty is also considered at lower grades when the annulus is dilated or risk factors for progression are present. This strategy prevents late disease that is difficult to reoperate on, but it must balance the risk of pacemaker implantation and randomized evidence of reduced regurgitation against procedural events.

In isolated disease, symptoms, progressive dilation, right ventricular function, pulmonary pressures, and organ status determine timing. Repair with a prosthetic ring is preferred when tissue quality and tethering permit; neochordae, patch repair, or augmentation address specific lesions. Replacement is chosen for destruction, retraction, or an irreparable gap, generally with a bioprosthesis and pacing planning.

Tricuspid TEER grasps the leaflets and reduces the coaptation gap. Randomized trials in older symptomatic patients have demonstrated high safety, reduced regurgitation, and improved quality of life compared with medical therapy alone; at two years, TRILUMINATE also observed fewer recurrent heart-failure hospitalizations, while mortality remained similar and crossover limits some late comparisons. Gap, jet location, number of leaflets, leads, gradient, and imaging determine feasibility.

Transcatheter annuloplasty reduces annular size in annulus-dominant phenotypes. Orthotopic transcatheter valve replacement more completely abolishes regurgitation and can treat large gaps, but it carries risks of bleeding, need for pacemaker implantation, thrombosis, and right-sided failure from increased afterload. The randomized TRISCEND II trial showed substantial benefit in symptoms and quality of life without demonstrating a significant reduction in mortality or hospitalization at one year; patient selection remains decisive.

Heterotopic caval valve prostheses reduce systemic backflow without correcting the valve and have a more limited role. Valve-in-valve and valve-in-ring procedures treat failed bioprostheses or repairs with a defined anchoring structure. No technology is universally superior: morphology and ventricular reserve guide the choice among repair, replacement, or conservative therapy.

The 2025 European guidelines support structured assessment and have elevated transcatheter interventions to an option that should be considered in symptomatic high-risk patients without severe right ventricular dysfunction or precapillary pulmonary hypertension. The class of recommendation does not eliminate judgment: trials excluded many end-stage patients, and technical success may be futile when multiorgan damage is irreversible.

Technology selection balances the potential for reduction against hemodynamic tolerance. TEER is favored by mobile leaflets, a well-visualized grasping zone, an accessible jet, and a limited gap; an already elevated diastolic gradient or reduced valve area limits the number of implants. A markedly dilated annulus with modest tethering may provide a rationale for annuloplasty. Large gaps and marked tethering may favor replacement, provided access, dimensions, right ventricular function, and thrombotic risk are acceptable. The absence of direct randomized comparisons prevents a universal ranking of these strategies.

Follow-up, prognosis, and Heart Team

Follow-up records symptoms, functional class, weight, diuretic dose, rhythm, jugular venous pressure, edema, ascites, and renal and hepatic status. Echocardiography compares severity, annular size, volumes, right ventricular function, and pulmonary pressure under known loading conditions. A single improvement after diuresis does not prove resolution, just as a worse measurement during volume overload does not define anatomical progression.

Early assessment at a Heart Valve Centre allows treatment before the end-stage phase. Clinical cardiology, imaging, heart failure, interventional cardiology, surgery, electrophysiology, anesthesia, and hepatorenal expertise estimate risk and reversibility. The goal is not to find a device for every anatomy, but to choose the timing and intervention that can provide measurable benefit for that patient.

After repair or replacement, a baseline examination is obtained. Residual regurgitation, gradient, right ventricular function, pulmonary pressure, device stability, leads, and access sites are assessed. An increase in gradient requires comparison with heart rate and flow; new regurgitation may result from dehiscence, detachment, progression of tethering, or endocarditis.

A favorable response includes less congestion, lower diuretic requirements, improved KCCQ and exercise capacity, reverse remodeling, and fewer hospitalizations. The ventricle may decrease in size without normalization of function; the liver and kidneys may recover only partially. Measuring only the TR grade misses outcomes that matter to the patient and may overestimate a reduction that provides no clinical benefit.

Prevention includes timely treatment of left-sided heart disease, control of pressure and rhythm, careful lead selection, and concomitant correction when indicated. After a device or prosthesis, antithrombotic therapy and endocarditis prophylaxis depend on the technology and risk profile. CIED infection requires a specific pathway, not chronic antibiotic therapy without source control.

Tricuspid regurgitation is therefore a disease of the entire right-sided cardiovascular system. The jet is the central sign, but outcome depends on cause, pulmonary pressure, ventriculoarterial coupling, organ reserve, and time. Accurate quantification followed by passive observation until advanced ascites develops is not good care; the purpose of diagnosis is to identify a window in which disease is still reversible.

Shared decision-making must make clear what is expected: relief of congestion, greater independence, fewer hospitalizations, or longer survival are not interchangeable endpoints. In frail patients, a documented symptomatic improvement may be a reasonable goal even without evidence of a survival benefit; in the presence of severe pulmonary vascular disease, end-stage right ventricular dysfunction, or life expectancy limited by other illnesses, a technically feasible procedure may offer no net benefit. Palliative care and competent symptom control are part of the same pathway and do not represent abandonment of treatment.