Learning points:
The tricuspid valve is the largest of the heart valves . Its anatomical structure is complex and constituted of the 3 leaflets, the annulus, the chordae, the papillary muscles and the adjacent myocardium.
The correct function of the valve depends on the integrity and coordination of all these structures.These are important because they may prevent proper leaflet coaptation in case of dilatation or dysfunction of the RV, thus causing TR.
In patients with secondary TR, the annulus becomes dilated (greater increase in the anteroposterior diameter compared with the mediolateral diameter, consistent with greater dilatation along the RV free wall), more planar and circular. The most common cause of TR is secondary or functional regurgitation, due to annular dilatation from either right atrial or RV enlargement.
Annular dilation, papillary muscle displacement, or a combination can cause significant TR. This can occur in the setting of RV dysfunction, pulmonary hypertension, or left heart disease. In these conditions, the increased tethering forces result in leaflet malcoaptation and leaflet tethering and tenting. The most common cause of primary TR is myxomatous degeneration.
Although some degree of prolapse is common for the nonplanar TV, actual ‘‘TV prolapse’’ is typically reserved for excessive billowing into the right atrium associated with redundancy of the tricuspid leaflets. Flail leaflets are not typically associated with myxomatous TV disease but rather with closed chest trauma or RV endomyocardial biopsy. Pacemaker leads can result in significant TR by interfering with closure of the TV but rarely cause a flail leaflet or a perforation of the leaflet.
