Tricuspid StenosisEdit
Tricuspid stenosis (TS) is a relatively uncommon valvular heart disease in which narrowing of the tricuspid valve orifice impedes diastolic flow from the right atrium into the right ventricle. This obstruction is most often part of a broader spectrum of right-sided heart conditions, and TS can be primary (due to disease of the valve itself) or secondary (functional) when processes such as dilation of the tricuspid annulus or concurrent cardiac disease contribute to the narrowing. The primary consequence is elevated right atrial pressure with systemic venous congestion and reduced pulmonary perfusion, yielding a clinical picture dominated by signs of right-sided heart failure.
Historically, rheumatic involvement of the tricuspid valve was the classic cause of TS, but contemporary etiologies include carcinoid syndrome, congenital malformations, infectious endocarditis with scarring, prosthetic valve dysfunction, and less commonly radiation-induced valvular disease. In many patients, TS is not an isolated problem but occurs in the setting of other valvular or intracardiac abnormalities, such as mitral disease or pulmonary hypertension, which can drive secondary changes to the tricuspid apparatus. Management and prognosis therefore hinge on understanding the underlying cause as well as the extent of valvular obstruction.
Pathophysiology
The tricuspid valve lies between the right atrium and right ventricle and normally opens wide in diastole to allow filling of the right ventricle. When TS is present, the orifice area is reduced, creating a diastolic pressure gradient across the valve. This forces the right atrium to generate higher pressures to drive flow, leading to venous congestion in the systemic circulation. Over time, the right atrium enlarges, which can predispose to atrial arrhythmias such as atrial fibrillation. The resulting hemodynamic profile includes hepatomegaly, ascites, peripheral edema, and, in advanced cases, impaired liver and renal function due to chronic congestion.
Etiology and epidemiology
- Primary tricuspid stenosis: Diseases that directly affect the valve leaflets and supporting structures, including rheumatic heart disease and carcinoid syndrome. Carcinoid-related TS is driven by fibrous deposits on the leaflets and subvalvular apparatus, often sparing the left-sided valves.
- Secondary (functional) TS: Right atrial enlargement or right ventricular dilation from other cardiac processes, particularly severe pulmonary hypertension or left-sided heart disease, can cause annular dilation and leaflet malcoaptation, producing stenosis in the absence of intrinsic valve disease.
- Other causes: Congenital tricuspid anomalies, prosthetic valve dysfunction, infective endocarditis–related scarring, radiation-induced valvulopathy, and certain connective tissue disorders.
See also: rheumatic heart disease, carcinoid syndrome, pulmonary hypertension.
Clinical presentation
Symptoms are often related to the degree of obstruction and the level of systemic venous congestion. Common findings include: - Fatigue and exercise intolerance due to reduced forward flow - Signs of right-sided heart failure: jugular venous distension, hepatomegaly, ascites, peripheral edema - Dyspnea that may reflect concurrent pulmonary or left-sided heart disease - A diastolic murmur best heard along the left lower sternal border, sometimes accentuated with inspiration
Atrial arrhythmias can occur, particularly in patients with marked right atrial enlargement. The presentation may be subtle in milder cases.
Diagnosis
- Echocardiography is the cornerstone, providing assessment of valve anatomy, leaflet mobility, and the transvalvular gradient. Key measurements include the tricuspid valve area and Doppler-derived pressure gradients across the valve.
- Electrocardiography and chest imaging may reveal right atrial enlargement, signs of pulmonary hypertension, or comorbid cardiac disease.
- Cardiac catheterization can quantify right atrial pressure, the diastolic gradient across the tricuspid valve, and the overall hemodynamic impact, particularly when noninvasive testing is inconclusive or when planning intervention.
- Additional testing may evaluate for underlying etiologies such as carcinoid syndrome (including biochemical testing) or rheumatic disease history.
See also: echocardiography, cardiac catheterization.
Management
Management of TS focuses on symptom relief, treatment of underlying causes, and, when appropriate, restoration of valve function.
- Medical therapy: Diuretics and other measures to manage systemic congestion are commonly used to relieve edema and ascites. Treatment of associated conditions (e.g., control of carcinoid syndrome or management of pulmonary hypertension) is essential.
- Addressing underlying etiologies: In carcinoid-related TS, treatment targets the carcinoid process; in rheumatic cases, immunologic and antithrombotic considerations may apply; left-sided heart disease or pulmonary hypertension should be treated to reduce secondary tricuspid involvement.
- Interventions on the valve:
- Tricuspid valve repair (valvuloplasty) or replacement can be considered for severe, symptomatic TS or when there is significant obstruction despite optimal medical therapy.
- Percutaneous approaches, such as balloon valvotomy, may be appropriate in selected patients, especially when surgical risk is high or candidacy for open surgery is limited.
- Choice of repair versus replacement depends on valve anatomy, comorbidities, and patient-specific risk-benefit considerations.
- Postoperative and long-term care: Anticoagulation considerations after valve surgery, surveillance for prosthetic valve function, and management of recurrent or residual symptoms.
See also: tricuspid valve repair, tricuspid valve replacement, balloon valvotomy.
Prognosis
Prognosis in TS depends largely on the severity of obstruction, the presence of concomitant cardiac disease, and the response to treatment of the underlying cause. Isolated mild TS carries a favorable outlook, while severe TS with comorbid conditions carries higher risk and may necessitate timely intervention to improve quality of life and survival. When combined with untreated pulmonary hypertension or significant left-sided heart disease, outcomes worsen, although modern diagnostic and therapeutic options have improved longevity for many patients.