Echo Reference — Valve Regurgitation
Tricuspid & Pulmonary Regurgitation
TR qualitative and quantitative severity grading with the expanded 5-grade system (including massive and torrential). PR qualitative and quantitative grading including PR index and pressure half-time. Integration algorithms for both valves.
Tricuspid Regurgitation — Qualitative Parameters
TR is present in the majority of adults and is usually trivial or mild. Significant TR is most commonly secondary (functional) — caused by RV and/or tricuspid annular dilatation from pulmonary hypertension, left heart disease, or atrial fibrillation. Primary (organic) TR from leaflet disease is less common. The expanded 5-grade severity system now includes "massive" and "torrential" categories to better characterise patients being considered for transcatheter intervention.
| Parameter | Mild | Moderate | Severe |
|---|---|---|---|
| Colour jet area | Small, central, thin | Intermediate | Very large central or wall-hugging jet |
| Vena contracta width (mm) | < 3 | 3 – 6.9 | ≥ 7 |
| CW Doppler signal | Faint, parabolic | Dense, parabolic | Dense, triangular (early peaking) with or without CW signal cutoff |
| Hepatic vein flow | S-dominant (normal) | S-blunted | Systolic reversal |
| Tricuspid inflow | Normal | Variable | E-dominant (> 1.0 m/s), diastolic-dominant forward flow |
CW signal in severe TR: In very severe (massive/torrential) TR, the CW signal may become triangular with a low peak velocity and early systolic cutoff. This occurs because rapid RV–RA pressure equalisation reduces the driving gradient. A low TR velocity does not exclude severe TR — in fact, it may indicate it. Always correlate with colour flow, vena contracta, and hepatic vein Doppler.
TR Quantitative Parameters — Expanded 5-Grade System
The traditional 3-grade system (mild/moderate/severe) has been expanded to 5 grades to better stratify patients with advanced TR who may be candidates for transcatheter tricuspid intervention. The "massive" and "torrential" categories identify patients with extreme volume loading who have the worst prognosis.
| Parameter | Mild | Moderate | Severe | Massive | Torrential |
|---|---|---|---|---|---|
| EROA (cm²) | < 0.20 | 0.20 – 0.39 | 0.40 – 0.59 | 0.60 – 0.79 | ≥ 0.80 |
| RVol (mL/beat) | < 30 | 30 – 44 | 45 – 59 | 60 – 74 | ≥ 75 |
| VC width (mm) | < 3 | 3 – 6.9 | 7 – 13 | 14 – 20 | ≥ 21 |
| 3D VC area (cm²) | — | — | 0.40 – 0.59 | 0.60 – 0.79 | ≥ 0.80 |
PISA limitations in TR: The PISA method is frequently used for TR quantification but has important limitations. The TR orifice is often non-circular (crescent-shaped in functional TR), the regurgitant orifice is dynamic throughout systole, and the aliasing hemisphere may be difficult to optimise. 3D vena contracta area is increasingly preferred as a more direct measure of orifice size, particularly for massive and torrential TR where the 2D vena contracta underestimates severity due to the non-circular geometry.
TR Integration Algorithm
| Step | Action |
|---|---|
| 1. Screen | Colour jet area and CW signal. Small thin jet with faint CW → mild, no further quantification needed. |
| 2. Semi-quantify | Vena contracta width in the apical 4-chamber or RV-focused view. VC < 3 mm → mild. VC ≥ 7 mm → at least severe. Consider 3D VC area if available. |
| 3. Supportive signs | Hepatic vein Doppler: systolic reversal → at least severe. CW signal morphology: triangular/early-peaking with low velocity → massive or torrential. Tricuspid inflow E > 1.0 m/s → volume-loaded. |
| 4. Quantify | PISA for EROA and RVol (apply angle correction for non-hemispheric convergence). 3D VC area where available. Apply 5-grade thresholds. |
| 5. Consequences | RV size and function (dilatation, reduced TAPSE/FAC/strain). RA dilatation. IVC dilatation. Septal flattening. These indicate haemodynamic impact and support the severity assessment. |
TR Clinical Context
Primary vs Secondary TR
| Feature | Primary (Organic) TR | Secondary (Functional) TR |
|---|---|---|
| Mechanism | Intrinsic leaflet or chordal pathology | Normal leaflets with annular dilatation and/or leaflet tethering from RV remodelling |
| Common causes | Endocarditis, carcinoid, rheumatic, radiation, Ebstein anomaly, flail leaflet, pacemaker/ICD lead impingement | Pulmonary hypertension (any cause), left heart disease, AF-related annular dilatation, RV infarction, dilated cardiomyopathy |
| Leaflet morphology | Abnormal — thickened, retracted, prolapsing, flail, or perforated | Structurally normal — coaptation failure from annular dilatation or apical tethering |
| Annulus | May be normal or dilated | Typically dilated (> 40 mm or > 21 mm/m²) |
| Management implication | Surgical repair or replacement targeting the valve itself | Treat the underlying cause (PH, left heart disease). Annuloplasty at the time of left-sided surgery. Transcatheter intervention for isolated secondary TR. |
Annular Dilatation
Tricuspid annular diameter ≥ 40 mm (or ≥ 21 mm/m² indexed) in the apical 4-chamber view at end-diastole indicates significant annular dilatation and is an independent risk factor for TR progression. Annular dilatation is the primary mechanism of AF-related TR, which has emerged as an increasingly recognised entity — TR occurring in patients with long-standing AF even without pulmonary hypertension or significant left heart disease.
Tethering Height & Area
In secondary TR, the coaptation point is displaced apically. Tethering height (distance from the annular plane to the coaptation point) > 8 mm and tethering area > 1.6 cm² predict persistence or recurrence of TR after annuloplasty. Severe tethering may favour replacement over repair, or indicate a need for transcatheter intervention if surgical risk is prohibitive.
Pulmonary Regurgitation — Qualitative Parameters
Physiological PR is present in the majority of normal individuals and is usually trivial. Significant PR is most commonly seen after repair of tetralogy of Fallot (absent or dysplastic pulmonary valve), pulmonary valvotomy, or with pulmonary hypertension. In the context of repaired tetralogy of Fallot, PR severity is a key determinant of the timing of pulmonary valve replacement.
| Parameter | Mild | Moderate | Severe |
|---|---|---|---|
| Colour jet width / RVOT width (%) | Narrow (< 25%) | Intermediate (25–50%) | Wide (> 50%), filling RVOT in diastole |
| CW Doppler signal | Faint, slow deceleration | Dense, variable deceleration | Dense with steep deceleration and early termination of diastolic flow |
| PR pressure half-time (ms) | > 100 | — | < 100 |
| PR duration | Throughout diastole | Throughout diastole | May be abbreviated (early diastolic termination due to rapid PA–RV equalisation) |
PHT in PR: A short PR pressure half-time (< 100 ms) indicates rapid equalisation of PA and RV diastolic pressures — consistent with severe PR (large regurgitant orifice) or elevated RV diastolic pressure (restrictive RV physiology). In severe "free" PR (e.g. absent pulmonary valve after TOF repair), the CW signal may terminate before end-diastole entirely, with laminar to-and-fro flow in the RVOT on colour Doppler.
PR Quantitative Parameters
| Parameter | Interpretation |
|---|---|
| PR index (PR duration ÷ total diastolic duration) | < 0.77 suggests severe PR. Indicates early termination of the PR signal due to rapid PA–RV pressure equalisation. This cutoff identifies a CMR-derived PR fraction > 25%. |
| Vena contracta width (mm) | Limited data for PR. VC ≥ 7 mm suggests severe (extrapolated from left-sided regurgitation data). |
| Diastolic flow reversal in main PA | Holodiastolic reversal in the main PA → at least moderate PR. Analogous to descending aorta reversal in AR. |
| RV volumes (CMR) | CMR is the reference standard for PR quantification. RV EDVi > 150 mL/m² or RV ESVi > 80 mL/m² are thresholds for PVR consideration in repaired TOF. |
CMR vs echo for PR: Echo-derived PR severity is semi-quantitative at best. For repaired tetralogy of Fallot and other conditions where PR drives intervention timing, CMR is the reference standard for RV volumes and PR regurgitant fraction. Echo remains essential for serial monitoring and anatomical assessment but should be complemented by CMR when intervention is being considered.
PR Integration Algorithm
| Step | Action |
|---|---|
| 1. Screen | Colour jet width relative to RVOT. Narrow jet → mild. Wide jet filling RVOT → likely severe. |
| 2. CW Doppler | Signal density, deceleration slope, and PR duration. Dense signal with steep deceleration and early termination → severe. PHT < 100 ms → severe. |
| 3. PR index | PR duration ÷ total diastolic duration. < 0.77 → severe (early termination of diastolic flow). Useful as a semi-quantitative cross-check. |
| 4. Consequences | RV dilatation (RVD1 > 42 mm or indexed values) and RV dysfunction (reduced TAPSE, S', FAC, strain) indicate haemodynamic impact. RV dilatation out of proportion to the apparent PR severity should prompt re-evaluation of PR quantification or CMR. |
| 5. CMR | Refer for CMR if PR severity is uncertain, intervention is being considered, or serial RV volume tracking is needed (especially repaired TOF). |
PR Clinical Context — Repaired Tetralogy of Fallot
Chronic severe PR after TOF repair leads to progressive RV dilatation and eventual RV dysfunction. The timing of pulmonary valve replacement (PVR) balances the risk of RV remodelling against the finite lifespan of bioprosthetic valves. Current consensus favours PVR before irreversible RV dysfunction develops.
| Parameter (CMR-derived) | PVR Considered |
|---|---|
| RV EDVi | ≥ 150 mL/m² (or ≥ 160 mL/m² in some centres) |
| RV ESVi | ≥ 80 mL/m² |
| RV EF | < 47% (declining) |
| PR regurgitant fraction | ≥ 40% |
Restrictive RV physiology: In some repaired TOF patients, the RV is non-compliant (restrictive), producing antegrade diastolic flow in the PA coinciding with atrial contraction. This can paradoxically limit the degree of PR (shorter diastolic regurgitation time) while indicating RV diastolic dysfunction. Restrictive physiology is generally associated with a better exercise capacity but may mask the true severity of the volume load.
References
- Zoghbi WA, et al. Recommendations for Noninvasive Evaluation of Native Valvular Regurgitation: A Report from the American Society of Echocardiography. J Am Soc Echocardiogr. 2017;30(4):303–371.
- Hahn RT, et al. Tricuspid Regurgitation Grading: A Proposal from the ASE, EACVI, and STS. J Am Soc Echocardiogr. 2023;36(9):893–919.
- Vahanian A, et al. 2021 ESC/EACTS Guidelines for the Management of Valvular Heart Disease. Eur Heart J. 2022;43(7):561–632.
- Stout KK, et al. 2018 AHA/ACC Guideline for the Management of Adults With Congenital Heart Disease. Circulation. 2019;139(14):e698–e800.