Tricuspid regurgitation
Description
- Mostly a secondary (functional) disease of the right ventricle and annulus, not of the leaflets
- Functional ~80-90% | Primary (leaflet) ~10-20%
- Long ignored ("the forgotten valve"), now recognised as an independent predictor of mortality at every level of severity
- Severity grading has been extended beyond "severe"
| Grade | Vena contracta | EROA |
|---|---|---|
| Mild | <3 mm | - |
| Moderate | 3-6.9 mm | 20-39 mm2 |
| Severe | >=7 mm | >=40 mm2 |
| Massive | 14-20 mm | 60-79 mm2 |
| Torrential | >=21 mm | >=80 mm2 |
- The massive/torrential grades exist because outcomes keep worsening above "severe" - and because they identify who fails transcatheter repair
Epidemiology
- Trace-to-mild TR is present in ~65-85% of normal adults - a normal finding, not a diagnosis
- Moderate or severe TR: ~0.5-1% of the population; ~4% over age 75
- F>M for significant TR
- CIED-related TR: significant TR in ~10-30% of patients with a transvalvular RV lead
- Severe TR is profoundly under-treated - historically <1% of patients with severe TR received any intervention
Aetiopathogenesis
A. Secondary (functional) - annular dilatation and leaflet tethering
- Left-sided heart disease - mitral/aortic disease or LV failure -> pulmonary hypertension -> RV dilatation
- Pulmonary hypertension of any group; chronic lung disease; PE
- Atrial functional TR (AFTR) - the fastest-growing category
- Long-standing AF -> RA dilatation -> annular dilatation with NORMAL RV and normal PA pressure
- Distinct entity; responds differently to intervention
- Ventricular functional TR - RV dilatation/dysfunction, RV infarct, RV cardiomyopathy
B. Primary (leaflet/apparatus)
- CIED lead - impingement, adherence, perforation or entanglement of a leaflet
- Infective endocarditis - IVDU, S. aureus; acute severe TR
- Rheumatic - almost always with mitral involvement; leaflet thickening and retraction
- Carcinoid - plaque on the ventricular surface -> fixed, retracted, immobile leaflets -> TR + TS. Right-sided because the lung inactivates serotonin
- Myxomatous prolapse; Ebstein anomaly (apical displacement of the septal leaflet, atrialised RV)
- Trauma (blunt chest, deceleration) - flail chordae or papillary rupture
- Endomyocardial fibrosis; radiation; ergot and fenfluramine/pergolide valvulopathy; RV biopsy (post-transplant)
- Iatrogenic - after mitral surgery, after tricuspid repair
Self-reinforcing loop
- TR -> RV volume overload -> RV dilatation -> annular dilatation -> more TR
- -> RV systolic dysfunction, septal shift, dec LV filling
- -> systemic venous congestion: hepatic, renal, gut
- -> cardiorenal and cardiohepatic syndrome, cardiac cirrhosis, protein-losing enteropathy, cachexia
Diagnosis
Clinical - a right-sided venous story, not a breathless one
- Symptoms are of congestion, not of low output early: fatigue, abdominal fullness/bloating, early satiety, ankle and abdominal swelling, pulsatile discomfort in the neck and right upper quadrant
- JVP: giant CV wave with loss of the x descent, and a rapid y descent
- Elevated JVP is the single most useful bedside finding, and the most often measured badly
- Pansystolic murmur, lower left sternal edge (4th ICS), LOUDER ON INSPIRATION (Carvallo sign)
- Often soft or absent in torrential TR - the pressures equalise. Absence of a murmur does not exclude it
- Pulsatile, tender hepatomegaly (distinguishes TR from other causes of hepatomegaly)
- RV heave (left parasternal), ascites, oedema, jaundice, cachexia
- Signs of the cause: mitral valve disease, loud P2, needle marks, pacemaker box, carcinoid flushing
ECG
- Usually AF; RA enlargement (P pulmonale), RV hypertrophy, RBBB or RSR' in V1
- Delta wave -> think Ebstein anomaly (associated WPW)
Echocardiography - the pivotal test
- Severity - colour jet area (unreliable), vena contracta width, PISA/EROA, hepatic vein systolic flow reversal, dense triangular early-peaking CW Doppler signal
- Mechanism - leaflet morphology, tethering/coaptation gap, annular diameter, lead position
- RV size and function - TAPSE, RV S', fractional area change, RV free wall strain
- TAPSE is load-dependent and overestimates function in severe TR
- RVSP from the TR jet - *unreliable when TR is torrential* (no pressure gradient); do not exclude pulmonary hypertension on this basis
- IVC size and collapse; RA volume
- 3D TOE - essential for planning intervention, and for lead-leaflet relationships
Further
- CMR - gold standard for RV volumes and function, and for regurgitant fraction
- Right heart catheterisation - confirm pulmonary pressures and PVR when the echo is equivocal or when TR is torrential
- Bloods - LFTs (congestive hepatopathy, high bilirubin, low albumin), UEC, INR (nutritional/hepatic), BNP, iron studies
- Liver assessment (elastography, MELD-XI) before intervention - hepatic dysfunction predicts a poor result
- 5-HIAA if carcinoid suspected
Management
- *The central error is referring too late. Once the RV has failed and the liver and kidney are congested, no intervention improves outcome*
A. Treat the cause and the left side first
- Correct left-sided valve disease - much functional TR improves
- Pulmonary hypertension - treat the mechanism (group-specific therapy)
- Rhythm control / ablation for AF - halts atrial functional TR progression
- CIED-related TR: consider lead revision, extraction, or a leadless/CS-placed lead
- Optimal HF therapy for the underlying ventricle
B. Medical - decongestion, no mortality benefit
- Loop diuretic, often at high dose and often needing IV in decompensation
- Add an MRA - aldosterone escape and hepatic congestion both favour it
- Acetazolamide or a thiazide for diuretic resistance (ADVOR)
- Salt and fluid restriction, daily weights
- Aggressive diuresis reduces preload -> reduces annular dilatation -> reduces TR. Under-diuresis makes the echo look worse than the valve is
- Anticoagulate for AF; iron replacement if deficient
C. Surgery
- Class I: severe TR in a patient undergoing left-sided valve surgery - the highest-yield decision, and the most frequently missed
- Class IIa: moderate TR with annular dilatation >=40 mm (or >21 mm/m2) at the time of left-sided surgery - prevents late TR
- Isolated severe TR: symptomatic despite medical therapy, or progressive RV dilatation/dysfunction, before end-organ damage
- Repair (annuloplasty ring) is preferred over replacement; bioprosthesis if replacement required
- *Isolated redo tricuspid surgery after previous left-sided surgery carries very high mortality (~10-20%)* - which is exactly why it is done at the index operation
D. Transcatheter tricuspid intervention - the change in this field
| Device | Type | Evidence |
|---|---|---|
| TriClip / PASCAL | T-TEER (edge-to-edge, Alfieri-like) | TRILUMINATE Pivotal, Tri.Fr - large reduction in TR, better KCCQ and NYHA |
| EVOQUE | Transcatheter valve replacement | TRISCEND II - more complete TR elimination; higher pacemaker rate |
- Indication: symptomatic severe TR despite optimal medical therapy, at intermediate or greater surgical risk, with suitable anatomy, decided by a Heart Team
- *Both improve symptoms and quality of life. NEITHER has demonstrated a mortality benefit* - state this plainly when consenting
- Poor candidates: severe RV dysfunction, severe pulmonary hypertension, advanced hepatic or renal dysfunction, torrential TR with a large coaptation gap (T-TEER fails), limited life expectancy
- Availability in Australia is limited to selected structural heart centres
Associations
- Atrial fibrillation - both cause (atrial functional TR) and consequence
- Left-sided valve disease - especially mitral
- Pulmonary hypertension of any group; COPD, OSA, chronic thromboembolic disease
- CIED - pacemaker or ICD leads
- Ebstein anomaly (+ WPW, ASD/PFO), congenitally corrected TGA
- Carcinoid syndrome (+ pulmonary valve disease, flushing, diarrhoea)
- Rheumatic heart disease, injecting drug use, infective endocarditis
- Congestive hepatopathy, cardiac cirrhosis, cardiorenal syndrome, cachexia, protein-losing enteropathy
Natural history & complications
- Severe TR carries excess mortality independent of RV function, pulmonary pressure and left-sided disease
- ~1-year mortality of untreated symptomatic severe TR is high; ~35-40% 1-year mortality in torrential disease
- Progression is the rule once the annulus dilates - the loop is self-perpetuating
- Atrial functional TR progresses with AF duration - a reason to pursue rhythm control early
Poor prognostic markers
- RV dysfunction (low RV free wall strain, FAC)
- Hepatic and renal dysfunction - MELD-XI, bilirubin, ascites
- Massive/torrential grade, large coaptation gap
- Cachexia, low albumin, recurrent admissions, NYHA III-IV
- Pacemaker dependency, severe pulmonary hypertension
Complications
- Right heart failure, ascites, congestive cirrhosis
- Cardiorenal syndrome and diuretic resistance
- Atrial arrhythmias, thromboembolism
- Malnutrition/protein-losing enteropathy
- Follow serially with echo and RV function; refer to a structural heart team before RV or liver failure supervenes, not after**
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