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Tricuspid regurgitation (TR) is insufficiency of the tricuspid valve causing blood flow from the right ventricle to the right atrium during systole.
The most common cause is dilation of the right ventricle.
Most commonly diagnosed in patients with coexistent conditions, and has been previously considered an innocent bystander to more consequential diseases of the left heart and pulmonary vasculature.
TR is present in approximately 80% of the population when evaluated by screening echocardiography.
Its prevalence, as with the other valve diseases, increases with age.
It is more often diagnosed in men than women, but the overall prevalence of clinically significant tricuspid regurgitation may be able to four times as high among women.
Unless accompanied by clinical signs and symptoms of edema, fatigue, and exercise tolerance, TR is often mistaken for signs and symptoms of aging, leading to delay in diagnosis and management.
Untreated severe tricuspid regurgitation is associated with substantial morbidity and poor quality of life.
Severe TR medical management is associated with a one year mortality rate of 36-42%.
Patients with moderate or severe regurgitation have a long-term risk of death from any cause that is increased by a factor of 2–3.2 after adjustment for age and sex.
Even mild TR is associated with nearly 30% increase at all-cause, long-term mortality.
A study of outcomes for aortic, mitral, and tricuspid valve disease showed that all-cause mortality was higher for tricuspid regurgitation, than for aortic valve disease or mitral valve disease.
Patients with tricuspid regurgitation often have congestive right heart failure, and impaired cardiac output, which leads to symptoms of excessive fatigue and peripheral edema.
Progressive TR is common particularly in patients undergoing mitral valve surgery.
An estimated 1.6 million Americans have moderate or severe TR.
Tricuspid regurgitation usually occurs in a normal valve affected by RV dilation; less often there is an intrinsic valve disorder such as due to infective endocarditis, carcinoid syndrome, certain drugs.
The tricuspid valve is the largest valve in the heart, and typically has three leaflets of unequal size.
The number of valve leaflets may vary, with the most common variant consisting of two posterior leaflets.
Tricuspid valve leaflets, are thinner than mitral valve, leaflets, and are supported by chordae attached to major anterior papillary muscle along the lateral wall of the mid right ventricle, as well as smaller posterior papillary muscles.
Posterior papillary muscles supply chordae to the posterior leaflet, and the posterior segment of the septal leaflet.
The complex chordal arcades and attachments make the tricuspid valve sensitive to changes in the position and function of the free wall of the right ventricle and of the interventricular septum.
It is primarily functional, that is, it develops secondary to right ventricular and tricuspid annular remodeling in response to chronic left-sided heart disease or pulmonary hypertension.
Primary tricuspid regurgitation occurs due to an intrinsic valve disease and is attributable to congenital abnormalities (Ebstein’s anomaly) infective endocarditis, rheumatic heart disease, carcinoid heart disease, toxic effects of chemicals, tumors, blunt trauma, or myxomatous degeneration.
In patients with secondary tricuspid regurgitation, the intrinsic structure of the leaflets appear normal, but abnormalities of the right atrium or right ventricle that result in leaflet malcoaptation occur.
TR is commonly seen with rheumatic or carcinoid tricuspid valve disease.
Atrial abnormalities are seen in 10 to 25% of patients with secondary TR, and is seen in association with the presence of atrial fibrillation.
Primary disease of the tricuspid valve leaflets is less common and is related to infection, trauma, or a congenital abnormality.
Primary tricuspid regurgitation can occur from traumatic rupture of the tricuspid valve from blunt trauma.
Tricuspid regurgitation after heart transplantation occurs in approximately 20% of patients.
The incident of tricuspid valve endocarditis in the US is increasing with increases in intravenous drug use, antibiotic resistance, and the use of cardiac implantable electronic devices.
A growing population of patients who have isolated TR, occurs in the absence of primary tricuspid valve leaflet disease, left heart disease or pulmonary hypertension.
Isolated TR is associated with atrial fibrillation and intracardiac devices.
Approximately 25 to 29% of patients with permanent pacemakers have tricuspid regurgitation, and the cardiac implantable electronic device is thought to be the cause of TR in 7 to 45% of patients.
Atrial fibrillation is associated with left and right atrial dilatation, annular dilatation, and atrioventricular valve regurgitation,
Symptoms and signs are usually absent.
Some patients with isolated TR are symptomatic, and well compensated where others progress to end stage right ventricular failure with intractable volume overload and organ dysfunction.
The majority of patients with isolated TR women and patients with atrial fibrillation and hypertension, and these patients are frequent hospitalized for heart failure.
Severe TR decreases survival and quality of life to the right ventricular dysfunction, congestive hepatopathy and renal failure.
Isolated TR is associated with excess mortality, and renal dysfunction, and severely elevated right atrial pressures.
In severe TR can cause neck pulsations, a holosystolic murmur, and right ventricular–induced heart failure or atrial fibrillation can occur.
Jugular venous distention may occur.
Severe TR may cause abdominal distension, hepatic enlargement, and peripheral edema.
Diagnosis is by physical examination and echocardiography.
Echocardiography is the primary imaging technique for identifying the cause, morphologic features, and severity of TR, with the recognition of cardiac MRI and cardiac CT have increasing roles.
In most cases it is benign and does not require treatment.
Rarely patients require annuloplasty or valve repair or replacement.
Tricuspid regurgitation may be
Primary
Secondary
Primary tricuspid regurgitation is less common,and can be due to valvular abnormalities caused by infective endocarditis in users of illicit IV drugs, carcinoid syndrome, blunt chest trauma, rheumatic fever, idiopathic myxomatous degeneration, congenital defects, Ebstein anomaly, Marfan syndrome, and use of certain drugs such as ergotamine, fenfluramine, phentermine, Iatrogenic causes include pacemaker leads that cross the tricuspid valve and valve damage sustained during RV endomyocardial biopsy.
Secondary tricuspid regurgitation is more common.
It is most commonly caused by dilation of the right ventricle (RV) with malfunction of a normal valve, as occurs in pulmonary hypertension, RV dysfunction–induced heart failure (HF), and pulmonary outflow tract obstruction.
Long-standing severe TR may lead to RV dysfunction–induced HF and atrial fibrillation.
While tricuspid regurgitation usually causes no symptoms, but some patients experience neck pulsations due to elevated jugular pressures.
Patients may have symptoms of severe TR including fatigue, abdominal bloating, and anorexia.
With tricuspid regurgitation patients may also develop symptoms of AF or atrial flutter.
Moderate to severe tricuspid regurgitation signs include: jugular venous distention, with a prominent merged c-v wave and a steep y descent, and sometimes enlarged liver and peripheral edema.
In severe TR, a right jugular venous thrill may be palpable.
In severe TR a systolic hepatic pulsation and an RV impulse at the left lower sternal border may be present as well.
On auscultation a holosystolic murmur at the left middle or lower sternal border may be heard, the 1st heart sound (S1) may be normal or barely audible if a tricuspid regurgitation murmur is present; the 2nd heart sound (S2) may be split with a loud pulmonic component [P2] in pulmonary hypertension, or single because of prompt pulmonic valve closing with merger of P2and the aortic component.
A 3rd heart sound (S3) may be audible near the sternum with RV dysfunction induced heart failure.
The murmur of tricuspid regurgitation is frequently not audible, but when appreciated, it is a holosystolic murmur heard best at the left middle or lower sternal border or at the epigastrium with the patient is sitting upright or standing.
A high-pitched TR murmur may be heard if TR is trivial and due to pulmonary hypertension, or it may be medium-pitched if TR is severe and has other causes.
In the absence of a murmur, the diagnosis is best made by the appearance of the jugular venous wave pattern and the presence of hepatic systolic pulsations.
The murmur of TR varies with respiration, becoming louder with inspiration (Carvallo sign).
Mild tricuspid regurgitation is most often detected on echocardiography coincidentally
Moderate or severe TR may be suggested by history and physical examination, and confirmed by echocardiography.
Severe TR presents with signs and symptoms of chronic right heart failure, systemic fluid retention, leading to elevated jugular venous, pressure, peripheral edema, and ascites, reduced intestinal absorption, anasarca, decreased cardiac reserve, exercise intolerance, dyspnea, poor functional capacity, decreased cardiac output, progressive end-organ damage caused by venous, congestion, and under perfusion.
End stage TR is associated with cachexia with poor absorption of nutrients and a systemic proinflammatory state.
Continued reduce cardiac output, and other neurohormonal changes may result in liver and kidney disease.
The development of a cardiohepatic syndrome is associated with increased risk of bleeding in TR and is an independent predictor of death or hospitalization for heart failure.
Severe TR is characterized echocardiographically by ≥ 1 of the following:
2-Dimensional failure of coaptation or flail
Large regurgitant jet on color Doppler
Large flow convergence zone proximal to the valve
Vena contracta width > 7 mm
Systolic flow reversal in the hepatic veins (specific for severe TR)
Transtricuspid E wave dominant > 1 cm/sec
Dense, triangular, early peaking, continuous wave Doppler of TR jet.
Two-dimensional echocardiography detects the structural abnormalities present in primary TR.
Cardiac MRI is now the pref2242ed method for evaluating RV size and function, which typically should be done when echocardiographic image quality is inadequate.
An ECG and chest x-ray are often done as part of evaluation.
In advanced cases, may show tall peaked P waves caused by right atrial enlargement, a tall R or QR wave in V1 characteristic of RV hypertrophy, or AF.
While a chest x-ray is usually normal, in advanced cases with RV hypertrophy or RV dysfunction, it may show an enlarged superior vena cava, an enlarged right atrial or RV silhouette, or pleural effusion.
Hepatic dysfunction may be seen in patients with severe TR.
Cardiac catheterization provides accurate measurement of pulmonary pressure when TR is severe.
Severe tricuspid regurgitation has a poor prognosis, even if it is initially well-tolerated.
As with left-sided valvular regurgitation, the volume-overloaded ventricle eventually decompensates irreversibly.
Very mild tricuspid regurgitation is a normal finding and requires no action.
Medical treatment of HF is largely limited to diuretic agents, which can improve symptoms in some patients.
Loop diuretics can reduce volume load and reduce pulmonary pressures and mineralcorticoid antagonists added can reduce the congestion in patients with advanced disease.
Sometimes annuloplasty or valve repair or replacement is indicated.
The tricuspid valve can easily be repaired during mitral valve surgery and concomitant repair is recommended for mild or moderate tricuspid regurgitation with annular dilatation of 4.0 cm or more.
Patients with severe tricuspid regurgitation should undergo operation as soon as symptoms are present, or when there is moderate, progressive RV enlargement or dysfunction.
Surgical treatment of isolated tricuspid regurgitation is associated with increased risk of surgery, because of right ventricular dysfunction, hepatorenal dysfunction due to chronic chronic venous hypertension and patients often have had previous cardiac surgery.
Surgical options include:
Annuloplasty
Valve repair
Valve replacement
Annuloplasty refers to the suturing of the tricuspid valve annulus to a prosthetic ring or a tailored reduction in annulus circumferential size when TR is due to annular dilation.
Tricuspid valve repair or replacement is indicated when TR is due to primary valve abnormalities or when annuloplasty is not technically feasible, and if due to carcinoid syndrome or Ebstein anomaly.
Patients with severe symptomatic TR have a 10 to 12% hospital mortality associated with isolated surgical tricuspid replacement.
A bioprosthetic valve is used to reduce the risk of thromboembolism associated with the low pressures of the right heart.
Bioprosthetic valves last longer than 10 yr.
A bioprosthetic valve requires temporary anticoagulation.
A holosystolic murmur is heard best at the left middle or lower sternal border or at the epigastrium when the patient is sitting upright or standing.
The murmur of tricuspid regurgitation becomes louder with inspiration.
It is usually well tolerated, but severe cases may require annuloplasty, valve repair, or valve replacement.
For patients with severe symptomatic TR, diuretic therapy is recommended to manage systemic congestion.
Loop diuretics are typically used, and aldosterone antagonists may be added, especially in cases of hepatic congestion.
In secondary TR, addressing the underlying cause, such as reducing pulmonary artery pressures and pulmonary vascular resistance, can be beneficial.
Medical therapy is effective for secondary TR due to heart failure with reduced left ventricular ejection fraction (HFrEF).
Additionally, restoring normal sinus rhythm can be effective for secondary TR associated with atrial fibrillation.
For severe TR, surgical intervention is considered when medical therapy is insufficient.
Tricuspid valve repair is generally preferred over replacement due to lower operative risks.
Tricuspid valve replacement may be necessary in cases of significant annular dilation or intrinsic leaflet disease.
Surgery is indicated in symptomatic severe primary TR to alleviate systemic venous and hepatic congestion and to prevent irreversible liver damage.
Intervention before the onset of significant right ventricular dysfunction or end-organ damage is encouraged.
Transcatheter tricuspid valve interventions (TTVI) are viable alternatives, particularly for high-risk surgical candidates.
These procedures include transcatheter edge-to-edge repair (TEER), annuloplasty devices, and valve replacement technologies.
The TRILUMINATE trial demonstrated transcatheter edge-to-edge repair (TEER) significantly reduces TR severity and improves quality of life in patients with severe symptomatic TR, with 87% of patients achieving TR reduction to moderate or less at 30 days.in one study.
Transcatheter annuloplasty devices, such as the Cardioband and Trialign systems, aim to reduce annular dilation and improve leaflet coaptation., with significant reductions in TR severity and improvements in functional status.
Severe TR is managed medically with diuretic agents.
Surgery is limited since patients have a variety of conditions that increase surgical risk.
Surgical guidelines recommend that tricuspid valve surgery be done in conjunction with left heart surgery or in symptomatic patients with severe TR and right ventricular dilation who do not have severe right ventricular dysfunction.
Operative mortality from isolated tricuspid valve surgery ranges from 8 to 10%, although more favorable outcomes are reported in specialized valve centers.
Tricuspid percutaneous transcatheter edge to edge repair (TEER) is safe in patients with severe tricuspid regurgitation, and reduces the severity of tricuspid regurgitation and is associated with improvement in quality of life.
TEER involves a transvenous approach, and approximates the tricuspid valve leaflets by deploying a clip to hold the leaflet together and reduce tricuspid regurgitation without the need for cardiopulmonary bypass or cardiac surgery.
TEER reduces, tricuspid, regurgitation, alleviate symptoms, reduces, neurohormonal activation, and induces reverse modeling of the right heart, compared with medical therapy alone:but this trial did not show difference in the incident of death or hospitalization for heart failure at one year, suggesting that coexisting conditions are primary determinants of outcome.
TEER is the most common trans catheter therapy worldwide.
TEER compared to medically treated patients is associated with the lower incidence of the composite end point of death and rehospitalization.
Metaanalysis showed mortality rate of 5% for the TEER procedure at 30 days, and an overall mortality of 25% at one year.
TEER devices can reduce tricuspid regurgitation to moderate or less than 80 to 85% of patients and two mild or less and only 30 to 50% of patients.