Tricuspid valve

Anatomy

The tricuspid valve ensures that there is no backflow from the right ventricle to the right atrium during systole. The tricuspid valve, as its Latin name suggests, consists of three leaflets: the septal (S), the anterior (A) and posterior (P) leaflets, of which the anterior leaflet is the largest. The tricuspid valve is distinguished not only by the number of valve leaflets as compared to mitral valve, but also by its method of attachment. The mitral valve chordae attach to only two papillary muscle heads where the chordae of tricuspid attach to much more muscle heads and also directly into the interventricular septum. The valve is located slightly more towards the apex as compared to the mitral valve.

Cross section of heart valves

Regurgitation

Quantification of tricuspid regurgitation

Grading the severity of TR
TR severity classesMildModerateSevere
Qualitative parameters
Valve morphologyNormal or mild abnormal leafletsModerately abnormal leafletsSevere valve leasions/flail/large coaptation defect/ severe tenting
Colour flow TR jet 𝛼Small, narrow, centralModerate centralLarge central or eccentric wall impinging jet of variable size
Flow convergence zoneNot visible, transient or smallIntermediate in size and durationLarge throughout systole
CW signal Faint/partial/parabolicDense/parabolic or triangularDense/often triangular with early peaking (peak <2m/s in massive TR)
Semi-quantitative parameters
Hepatic vein flow 𝛽Systolic dominanceSystolic bluntingSystolic flow reversal
Tricuspid inflowA-wave dominantVariableE-wave dominant (≥ 1m/s) 𝜀
PISA radius (mm) 𝛾≤56-9>9
VC width (mm) 𝛼,𝛿<33-6,9>7
3D VC area or EROA (mm²)75-94
Quantitative parameters
EROA (mm²)<2020-39≧40
R Vol (mL)<3030-44≧45
RF (%)≦1516-49≧50
Structural parameters
RV, RA, IVC size 𝜁Usually normalNormal or mild dilationUsually dilated
CW, continuous wave; EROA, effective regurgitant orifice area; RA, right atrium; RV right ventricle; TR, tricuspid regurgitation; RF, regurgitant fraction; R Vol regurgitant volume; VC, vena contracta.
𝛼 At Nyquist limit of 50-60 cm/s.
𝛽 Unless other reasons, of systolic blunting (Atrial fibrillation, elevated RA pressure).
𝛾 Baseline Nyquist liit shift of 28cm/s.
𝛿 When VC width is assessed as an average ofmeasurements performed biplane the treshold value for severe TR is >9mm.
𝜀 In the absence of other causes of elevated LA pressure and of mitral stenosis.
𝜁 Unless for other reasons, the RA and RV size and VCI are usually normal in patients with mild TR, An end-systolic RV eccentricity index >2 is in favour of severe TR. In acute severe TR, the RV size is often normal. In chronic severe TR, the RV is classically dilated. Accepted cut-off values for non-significant right-sided chambers enlagement (measurements obtained from the apical four-chamber view): mid RV dimension ≤33mm, RV end-diastolic area ≤28cm², RV end-systolic area ≤16cm², RV fractional area change >32%, maximal 2D RA volume ≤33mL/m². An IVC diameter <21mm in considered normal. The IVC is dilated when the diameter is >25mm.

Echocardiographic criteria for the definition of severe tricuspid valve regurgitation: an integrative approuch.

ParameterCriteria
Qualitative
Valve morphologyAbnormal/flail/large coaptation defect
Colour flow regurgitant jetVery large central jet or eccentric wall impinging jet *
CW signal of regurgitant jetDense/triangular with early peaking (peak <2 m/s in massive TR)
Semiquantitative
Vena contracta width (mm)≥ 7 *
Upstream vein flowSystolic hepatic vein flow reversal
InflowE-wave dominant ≥ 1 m/s **
PISA radius (mm)> 9 ***
Quantative
EROA (mm²)≥ 40
Regugitant volume (mL/beat)≥ 45
Enlargement of cardiac chamber/vesselsRV, RA, IVC
* At Nyquist limit of 50-60 cm/s.
** In the absence of other causes of elevated LA pressure
*** Baseline Nyquist limit shift of 28 cm/s.

Outcome-based cut-off values for the quantitative parameters used to grade tricuspid regurgitation severity by Dopplerechocardiography.  
VariableLow riskIntermediate riskHigh risk
VC (mm)<33 - 6>6
EROA (cm²)<0.150.15 - 0.30>0.30
RegVol (ml)<1515 - 30>30
RegFR (%)<2525 - 45>45
EROA, effective regurgitant orifice area; RegFr, regurgitant fraction; RegVol, regurgitant volume; VCavg, vena contracta width.
Eur Heart J Cardiovasc Imaging (2021) 22, 155-165
Proposed expansion of the ‘Severe’ grade
VariableMildModerateSevereMassiveTorrential
VC (mm)<33 - 6.97 - 1314 - 20≥21
EROA (cm²)<0.200.20 - 0.390.40 - 0.590.60 - 0.79≥80
3D VCA or quantitative EROAa (cm²)*0.75 - 0.940.95 - 1.14≥1.15
VC, vena contracta; EROA, effective regurgitant orifice area; 3D VCA, three-dimensional vena contracta area.
*3D VCA and quantitative Doppler EROA cut-offs may be larger than PISA EROA.
Eur Heart J Cardiovasc Imaging (2017) 18, 1342–1343

TR vena contracta

Causes of tricuspid regurgitation

Functional TRSecundary TR
Disorders of the right ventricle: RV infarction, dilated cardiomyopathyEbstein anomaly
Secondary to pulmonary hypertension, for example: cor pulmonale, pulmonary embolism, or primary.Infective Endocarditis
Mitral stenosis or mitral regurgitationTrauma
Left-right shunt, such as an atrial septal defect or a ventricular septal defectRheumatic fever
Eisenmenger syndrome (rare)Carcinoid
Pulmonary stenosisPapillary muscle disorders
HyperthyroidismConnective tissue diseases such as Marfan Syndrome.
Non-infectious endocarditis, such as SLE or rheumatoid arthritis
Damage from the electrode of a pacemaker or ICD

Stenosis

Tricuspid valve stenosis is usually caused by rheumatic fever which mostly occurs during childhood. The rarely reported second causes of tricuspid valve stenosis include tumour obstruction, carcinoid disease and obstructed tricuspid valve prosthesis.

Quantification of tricuspid stenosis

ParameterMildModerateSevere
TVA (cm²)< 1
PHT (ms)> 190
PGmean (mmHg)> 5
VTI (cm)> 60

References

European Heart Journal - Cardiovascular Imaging (2022) 23, e171–e232
Eur J Echocardiogr. 2009 Jan;10(1):1-25
Eur J Echocardiogr. 2010 May;11(4):307-32
European Heart Journal (2017) 00, 1?53
European Heart Journal - Cardiovascular Imaging (2017) 18, 1342–1343
European Heart Journal - Cardiovascular Imaging (2021) 22, 155–165