Tricuspid Valve Disease¶

Chapter 277 | Part 6: Disorders of the Cardiovascular System

KEY CLINICAL POINTS¶

Tricuspid stenosis (TS) is rare in North America, primarily rheumatic, with 5–10% prevalence in severe mitral stenosis (MS) cases
Tricuspid regurgitation (TR) is predominantly secondary (functional) due to annular dilation or leaflet tethering
Severe TR is managed with surgical repair/ replacement, transcatheter edge-to-edge repair (TEER), or annuloplasty
Anticoagulation for AF uses CHADS-VASc score; TEER reduces TR severity with 1-year mortality <2%
Right heart failure manifestations include hepatomegaly, ascites, and hepatojugular reflux

1. DEFINITION & OVERVIEW¶

Tricuspid valve disease encompasses stenosis (TS) and regurgitation (TR). TS is rare, primarily rheumatic, while TR is predominantly secondary. TS occurs with MS in 5–10% of cases. TR is classified as primary (organic) or secondary (functional) based on etiology.

Table 277-1 Causes of Tricuspid Valve Diseases¶

VALVE LESION	ETIOLOGIES
Tricuspid stenosis	Rheumatic, Congenital
Tricuspid regurgitation	Primary (leaflet/annular)

1.1 Tricuspid Stenosis¶

Defined by diastolic pressure gradient between RA and RV. TS occurs in 5–10% of severe MS cases. Hemodynamically significant TS has valve area ≤ 1 cm² or pressure half-time ≥ 190 ms.

1.2 Tricuspid Regurgitation¶

Primary TR from leaflet/annular abnormalities; secondary TR from RV dilation/pressure overload. Severe TR ( ≥ 4.0 cm RV dilation) is associated with right ventricular dysfunction and systemic venous congestion.

2. EPIDEMIOLOGY¶

TS is rare in North America (rheumatic etiology), more common in women. TR occurs in 85% of cases as secondary (functional) due to annular dilation. Primary TR is rare, often from carcinoid, endocarditis, or Ebstein’s anomaly. TS occurs in 5–10% of severe MS cases.

2.1 Risk Factors¶

Rheumatic fever, congenital heart disease, carcinoid syndrome, endocarditis, radiation, trauma, and CIED leads. PA hypertension accelerates TR progression.

2.2 Demographics¶

TS more common in women; TR prevalence increases with age due to atrial fibrillation and RV remodeling.

3. ETIOLOGY & PATHOPHYSIOLOGY¶

TS: Rheumatic etiology with annular calcification. TR: Secondary (85%) from annular dilation/leaflet tethering; primary (15%) from leaflet damage, Ebstein’s anomaly, or CIED leads. Pathophysiology involves RA/ RV pressure gradients, RV volume overload, and systemic venous congestion.

3.1 TS Pathophysiology¶

Diastolic pressure gradient between RA and RV. TS exacerbates pulmonary congestion, leading to hepatomegaly, ascites, and hepatic dysfunction.

3.2 TR Pathophysiology¶

Backflow from RV to RA increases RA pressure. Severe TR causes RV dilation, systolic dysfunction, and systemic venous congestion. PA hypertension accelerates RV remodeling.

4. CLINICAL FEATURES¶

Symptoms: Fatigue, dyspnea, hepatomegaly, ascites, edema. Physical findings: Distended neck veins with c-v waves, prominent RV pulsation, holosystolic murmur, and hepatojugular reflux. Severe TR may present with right-sided failure after mitral valve surgery.

4.1 Symptoms¶

Fatigue, exertional dyspnea, hepatic congestion, and right-sided failure. Atrial fibrillation may cause functional TR with palpitations.

4.2 Physical Findings¶

Distended neck veins with c-v waves, rapid y descent, hepatomegaly, ascites, and holosystolic murmur. Carvallo’s sign: intensified murmur during inspiration.

5. DIFFERENTIAL DIAGNOSIS¶

Right-sided heart failure, pulmonary hypertension, constrictive pericarditis, and superior vena cava syndrome. Atrial fibrillation may mimic functional TR. TS must be differentiated from MS in patients with right heart failure.

5.1 Secondary TR Mimics¶

Atrial fibrillation, RV dilation, and PA hypertension. Functional TR may be confused with mitral regurgitation.

5.2 TS Differentiation¶

TS presents with hepatic congestion and RA enlargement. MS may have pulmonary vascular congestion without significant TR.

6. INVESTIGATIONS & DIAGNOSIS¶

ECG: RA enlargement, RVH, or inferior MI. Chest X-ray: RA/RV enlargement. TTE: Annular dilation, leaflet prolapse, and RA/IVC size. Doppler: TR velocity profile for PA pressure estimation. Cardiac catheterization: For TS assessment.

6.1 Diagnostic Criteria¶

TS: Valve area ≤ 1 cm² or pressure half-time ≥ 190 ms. TR severity: Annular dilation (>40 mm), RV size, and TR jet area.

6.2 Imaging¶

TTE: Assess annular dilation, leaflet function, and RV size. CMR: Quantify TR severity.TEE: Preoperative evaluation for complex prolapse.

7. MANAGEMENT & TREATMENT¶

Medical management: Diuretics, aldosterone antagonists, and PA pressure reduction. Surgical options: Annuloplasty, valve repair/replacement. TEER (TriClip) for high-risk patients. Perioperative mortality: 8–9% for isolated tricuspid surgery.

7.1 Medical Therapy¶

Diuretics for right heart failure; aldosterone antagonists for hepatic congestion. PA pressure reduction via left-sided valve disease treatment.

7.2 Surgical Options¶

Annuloplasty for annular dilation; valve repair/replacement for severe TR. TEER (TriClip) reduces TR severity with <2% mortality. Mechanical valves have higher thromboembolic risk.

7.3 Algorithms¶

Surgical repair for annular dilation (>40 mm) or RV dysfunction. TEER for high-risk patients with severe TR. Annuloplasty during mitral valve surgery for moderate TR.

8. PROGNOSIS & COMPLICATIONS¶

TS: Mortality from hepatic failure if untreated. TR: Prognosis depends on underlying disease; severe TR with RV dysfunction has poor outcomes. Complications include hepatic cirrhosis, ascites, and right heart failure.

8.1 Complications¶

Hepatic congestion, ascites, anasarca, and hepatic failure. Severe TR may lead to RV systolic dysfunction and systemic venous congestion.

8.2 Prognostic Factors¶

Severity of TR, RV function, PA pressure, and presence of comorbidities. TEER improves quality of life but not mortality in 1-year follow-up.

9. SPECIAL CONSIDERATIONS¶

Pregnancy: Avoid anticoagulants; manage with diuretics. Pediatrics: Congenital TR (Ebstein’s anomaly) requires early intervention. Elderly: Higher risk of complications from surgery. CIED leads: May cause primary TR requiring lead extraction.

9.1 Pregnancy¶

Avoid anticoagulants; manage right heart failure with diuretics. Monitor for hepatic congestion and fetal growth.

9.2 CIED Leads¶

Pacing leads across tricuspid valve cause leaflet entrapment. Lead extraction required for severe TR. Mechanical valves increase thromboembolic risk.

10. KEY POINTS & CLINICAL PEARLS¶

TS is rare; TR is predominantly secondary. 2. TEER (TriClip) reduces TR severity with <2% mortality. 3. Annuloplasty during mitral surgery for moderate TR. 4. CHADS-VASc score guides anticoagulation. 5. Right heart failure manifests as hepatomegaly and hepatojugular reflux.