Tricuspid Valve Disorders
Daniel H. Cooper
Thomas K. Kurian
High-Yield Findings
Severe tricuspid regurgitation
Vena contracta width >0.7 cm
RA area occupied by tricuspid regurgitation (TR) jet ≥40%
Gross leaflet malcoaptation
TV annulus dilatation >4 cm
Dense, early peaking TR CW Doppler envelope
Hepatic vein systolic flow reversal
RA/RV enlargement
Evidence of RV volume overload
Severe tricuspid stenosis
Leaflets thickened, calcified, fused, immobile
Diastolic leaflet doming
RA enlargement
Elevated TV peak inflow velocity >1 m/s
Mean TV gradient >7 mmHg
Pressure half time >190 ms
Key Views
Parasternal RV inflow tract (RVIT)
Parasternal short-axis RV inflow/outflow
Apical four chamber
Subcostal four chamber
Tricuspid Regurgitation
General Principles
TR is common. Some degree of TR is found in nearly 80% to 90% of the population.
Primary valvular causes of TR include Ebstein’s anomaly (see Chapter 17), carcinoid (see Chapter 19), endocarditis (see Chapter 14), myxomatous degeneration, and rheumatic disease. Secondary causes include any process that leads to tricuspid annulus dilatation due to right ventricular and/or right atrial enlargement (e.g.,
Pulmonary hypertension, left ventricular dysfunction, left-to-right shunts, right ventricular infarction).
Mild TR in general is benign. Moderate to severe TR is associated with reduced long-term survival, even in the absence of comorbid pulmonary hypertension or ventricular dysfunction.
Assessment of TR by Transthoracic Echocardiography (TTE)
General Principles
The tricuspid valve (TV) consists of three, anatomically distinct leaflets (anterior, posterior, septal).
These leaflets are thinner and have an annulus that is larger than the mitral valve. The valve is more apically displaced in location compared to the mitral valve and is not in direct continuity with the pulmonic valve.
The TV sits anterior and rightward of the mitral valve. It is separated from the pulmonic valve by the infundibulum.
Key Point:
The atrio-ventricular (AV) valves are always associated with their respective ventricle. The relative position of the AV valves has important ramifications. In patients with congenital heart disease where the ventricular position may be altered the RV may be recognized by the more apically displaced TV. An AV canal defect is recognized by the AV valves being on the same plane. Ebstein’s anomaly is recognized by the septal tricuspid leaflet being markedly apically displaced.
Key Point:
This is in contrast to the left heart where there is no infundibulum and the mitral and aortic valves are separated only by a fibrous continuum. This has ramifications for the effects of mitral and aortic valvular pathology such as endocarditis, which can spread to either valve causing annular or aortic root abscess.
2D Echocardiogram
In general, tricuspid leaflet location, thickness, mobility, and coaptation should be assessed in all available views.
The RVIT is the one view where the posterior leaflet is seen along with the anterior leaflet, otherwise in the parasternal short-axis and apical four-chamber view the anterior and septal leaflets are seen (see Fig. 12-1A).
With Ebstein’s anomaly there is (a) apical displacement (>0.8 cm/m2) of the septal leaflet, (b) a large, “sail-like” anterior leaflet with a variable number of tethering attachments to the anterior RV free wall, and (c) atrialization of the RV secondary to apically displaced TV coaptation (see Fig. 12-1B). The size of the RV that remains unaffected is a major determinant of prognosis.
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