Tricuspid Valve Disease¶
Chapter 277 | Part 6: Disorders of the Cardiovascular System · Part 6 – Cardiovascular Disorders · Chapter 277
Key Clinical Points¶
- Tricuspid stenosis (TS) is rare in North America and Western Europe, usually rheumatic in origin, and almost always associated with mitral stenosis (MS).
- Tricuspid regurgitation (TR) is common; >85% of cases are secondary (functional) due to annular dilation and leaflet tethering from RV remodeling.
- Carvallo's sign: A holosystolic murmur of TR that intensifies during inspiration and reduces during expiration or Valsalva maneuver.
- Surgical indications for TR include annular dilation >40 mm on TTE (or >70 mm intraoperatively), history of right heart failure, or PA hypertension.
- Transcatheter edge-to-edge repair (TEER) and transcatheter replacement are options for high/prohibitive surgical risk patients.
- Diuretics and aldosterone antagonists are used to manage systemic venous congestion in severe TR.
- ECG in TS shows RA enlargement (tall P waves in lead II, upright P waves in V) without evidence of RVH.
- Severe TS is characterized by a valve area ≤1 cm² or pressure half-time of ≥190 ms.
- Severe TR leads to RA enlargement, RV volume overload, and eventual systolic dysfunction.
- Perioperative mortality for isolated tricuspid valve surgery is high (~8–9%).
DEFINITION & OVERVIEW¶
• Tricuspid Stenosis (TS): ◦ Rare in North America and Western Europe; generally rheumatic in origin. ◦ More common in women than men. ◦ Does not occur as an isolated lesion; almost always associated with mitral stenosis (MS). ◦ Hemodynamically significant TS occurs in 5–10% of patients with severe MS. • Tricuspid Regurgitation (TR): ◦ Common clinical finding. ◦ Primary (Organic): Resulting from congenital defects, endocarditis, radiation, or trauma. ◦ Secondary (Functional): >85% of cases; caused by annular dilation and leaflet tethering due to RV remodeling (pressure/volume overload), MI, or trauma. ◦ CIED-related: Associated with pacemaker or defibrillator leads causing leaflet entrapment or perforation; also includes functional TR from RV apex pacing.
EPIDEMIOLOGY¶
• Tricuspid Stenosis: ◦ Rare; primarily rheumatic; more common in women. • Tricuspid Regurgitation: ◦ Common; >85% are secondary (functional) in nature.
ETIOLOGY & PATHOPHYSIOLOGY¶
• Tricuspid Stenosis Pathophysiology: ◦ Defined by a diastolic pressure gradient between the RA and RV. ◦ Gradient increases during inspiration and decreases during expiration. ◦ Mean diastolic pressure gradient of 4 mmHg is sufficient to cause systemic venous congestion (hepatomegaly, ascites, edema). ◦ In sinus rhythm: RA a-wave may be very tall; y-descent is prolonged. ◦ Impact on MS: TS can mask hemodynamic/clinical features of associated MS by lowering cardiac output (CO) and preventing rise in CO during exercise. • Tricuspid Regurgitation Pathophysiology: ◦ Backward flow from RV to RA depends on driving pressure (RV systolic pressure) and orifice size. ◦ Severity influenced by: PA systolic pressure, tricuspid valve annulus dimensions, respiratory cycle changes in RV preload, and RA compliance. ◦ Clinical impact: Reduced forward CO; RA enlargement; prominent c-v waves; "ventricularization" of the RA wave form. ◦ Progression: Severe TR → RV dilation (volume overload) → systolic dysfunction (accelerated by PA hypertension or myocardial fibrosis). • Etiologies of Tricuspid Valve Disease: ※ Table 277-1 summarizes causes:
| VALVE LESION | ETIOLOGIES |
|---|---|
| Tricuspid stenosis | Rheumatic, Congenital |
| Tricuspid regurgitation | Rheumatic, Endocarditis, Myxomatous (TVP), Carcinoid, Radiation, Congenital (Ebstein's), Trauma (including that due to RV endomyocardial biopsy), CIED related, Leaflet impingement, adherence, laceration, perforation, avulsion; chordal entrapment |
◦ Secondary TR: Caused by RV/tricuspid annular dilation from pulmonary HTN, post-RV MI, left-sided heart disease, cardiomyopathy, or AF.
CLINICAL FEATURES¶
• General Features: ◦ TS: Marked systemic venous congestion; patients may have little dyspnea despite severe hepatomegaly/ascites. ◦ TR: Often coexists with left-sided disease; symptoms (dyspnea, fatigue) may be dominated by those lesions. ◦ Atrial fibrillation (AF): May cause palpitations and drive functional TR. • Tricuspid Stenosis Specifics: ◦ Severe TS → marked hepatic congestion (cirrhosis, jaundice, malnutrition), anasarca, ascites. ◦ Physical signs: Distended jugular veins; in sinus rhythm, giant a-waves and slow y-descent; prominent presystolic pulsations of enlarged liver. • Tricuspid Regurgitation Specifics: ◦ Neck veins: Distended with prominent c-v waves and rapid y-descents (if no TS). ◦ Physical signs: Hepatomegaly with systolic pulsations, ascites, pleural effusions, positive hepatojugular reflux. ◦ Carvallo's Sign: Holosystolic murmur of TR → intensifies during inspiration → reduces during expiration or Valsalva maneuver. ◦ Differentiation from MR: Distinguished by respiratory variation and extent of RV enlargement.
DIFFERENTIAL DIAGNOSIS¶
• Tricuspid Stenosis: ◦ Often confused with MS due to similar diastolic murmur qualities. ◦ Differentiation: Tricuspid murmur heard best along left lower sternal border/xiphoid; augmented during inspiration; reduced during expiration/Valsalva.
INVESTIGATIONS & DIAGNOSIS¶
- Electrocardiography (ECG): ◦ Look for RA enlargement: Tall, peaked P waves in lead II; prominent, upright P waves in lead V. ◦ Clinical Clue: Absence of RVH in a patient with right-sided heart failure and suspected MS → suggests associated tricuspid valve disease.
- Chest Radiography: ◦ Combined TS/MS: Prominent RA and superior vena cava; azygos vein engorgement; less pulmonary vascular congestion than isolated MS.
- Echocardiography (TTE): ◦ Tricuspid Stenosis: → Identify thickened valve, diastolic dome → measure transvalvular gradient. → Severe TS criteria: Valve area ≤ 1 cm² OR pressure half-time ≥ 190 ms. ◦ Tricuspid Regurgitation: → Assess RA dilation, RV volume overload, and tricuspid leaflet status (prolapsing, flail, scarred, or displaced/tethered). → Identify hepatic vein systolic flow reversal (sign of severe TR). → Use color flow Doppler to assess severity.
- Cardiac Catheterization: ◦ Not routinely necessary for assessment of TS.
MANAGEMENT & TREATMENT¶
- Preoperative Preparation (TS): → Salt restriction, bed rest, and diuretic therapy → reduces hepatic congestion/bleeding risk.
- Medical Management: → Diuretics: Useful for severe TR with systemic venous congestion. → Aldosterone antagonists: Used to manage systemic venous congestion in severe TR.
- Surgical Intervention (Tricuspid Stenosis): → Recommended for moderate or severe TS. → Timing: Preferably at time of surgical mitral commissurotomy or MVR.
- Surgical Intervention (Tricuspid Regurgitation): → Recommended for severe TR undergoing left-sided surgery. → Also performed for moderate/mild TR if: → Annular dilation >40 mm (TTE) or >70 mm (intraoperative) → OR history of right heart failure → OR PA hypertension.
- Transcatheter Options: → Transcatheter edge-to-edge repair (TEER): Option for high/prohibitive surgical risk patients. → Transcatheter replacement: Option for high/prohibitive surgical risk patients.
PROGNOSIS & COMPLICATIONS¶
• Survival and Mortality: ◦ Isolated tricuspid valve surgery: High perioperative mortality (~8–9%). ◦ Risk factors for mortality: Reoperation hazards, reduced RV function. • Complications of Severe TR: ◦ RV volume overload → systolic dysfunction. ◦ Progression accelerated by PA hypertension or myocardial fibrosis.
SPECIAL CONSIDERATIONS¶
• Infective Endocarditis: → Prophylaxis indicated for patients with prior history of endocarditis. • Atrial Fibrillation (AF): → Can be the driver of TR or emerge later due to remodeling.
KEY PEARLS & CLINICAL TRAPS¶
• Diagnostic Clues: ◦ Carvallo's sign is a hallmark of TR. ◦ Tricuspid murmur is best heard at the left lower sternal border; its respiratory variation distinguishes it from MR. ◦ Absence of RVH in patients with right-sided failure and MS suggests TS. • Exclusion Criteria: ◦ TS rarely occurs as an isolated lesion; if suspected, always look for associated MS.
FLOWCHARTS¶
Management of Tricuspid Regurgitation (Figure 277-2)¶
The following pathways determine the management of Tricuspid Regurgitation (TR) based on severity, etiology, and clinical context:
Pathway A (Severe, Primary): 1. Tricuspid regurgitation → Severe TR (Stages C and D) → At time of left-sided valve surgery → Primary TR → TV surgery (1).
Pathway B (Severe, Secondary - Medical Failure): 1. Tricuspid regurgitation → Severe TR (Stage C or D) → Right heart failure Stage D → Secondary TR → Poorly responsive to GDMT → Annular dilation without \uparrowPAP or left-sided disease → Absence of severe \uparrowPR or RV systolic dysfunction → TV surgery (2b).
Pathway C (Severe, Secondary - Anatomical/Hemodynamic): 1. Tricuspid regurgitation → Severe TR (Stage C or D) → Right heart failure Stage D → Secondary TR → Poorly responsive to GDMT → Annular dilation without \uparrowPAP or left-sided disease → [Presence of severe \uparrowPR or RV systolic dysfunction] → TV surgery (2a).
Pathway D (Severe, Primary - Specific Conditions): 1. Tricuspid regurgitation → Severe TR (Stage C and D) → At time of left-sided valve surgery → Primary TR → [Annular dilation or systolic dysfunction] → TV surgery (2a).
Pathway E (Progressive, Surgical Timing): 1. Tricuspid regurgitation → Progressive TR (Stage B) → At time of left-sided valve surgery → Annular dilation >0.4 cm or prior right HF → TV surgery (2a).
Pathway F (Progressive, Non-Surgical Timing): 1. Tricuspid regurgitation → Progressive TR (Stage B) → [No left-sided surgery mentioned/implied] → Annular dilation >0.4 cm or prior right HF → TV surgery (2b).
Key Thresholds & Definitions: • Severity Stages: Stage C and D (Severe), Stage B (Progressive). • Annular Dilatation: >0.4 cm (used to define significant dilation in the Progressive TR branch). • Clinical Status: "Poorly responsive to GDMT" (Guideline-Directed Medical Therapy). • Hemodynamics: \uparrowPAP (Pulmonary Artery Pressure), \uparrowPR (Pulmonary Resistance), and RV systolic dysfunction.
Reference Tables¶
TABLE 277-1 Causes of Tricuspid Valve Diseases¶
Harrison's 22e, p.2059
| VALVE LESION | ETIOLOGIES |
|---|---|
| Tricuspid stenosis |
Rheumatic Congenital |