Fig. 18.1
Anatomy of the tricuspid valve and surrounding structures (Adapted from Carpentier et al. [28])
Fig. 18.2
Papillary muscles supporting the tricuspid valve leaflets (Adapted from Carpentier et al. [28])
Pathophysiology of Functional Tricuspid Regurgitation
Functional tricuspid regurgitation (FTR) occurs due to loss of leaflet coaptation as a result of two pathologies: dilatation of the tricuspid annulus and/or leaflet tethering, both of which occur due to right ventricular remodeling and dilatation as a result of raised pulmonary artery pressures from left sided heart valve disease [6, 7]. These two pathologies may co-exist, with one pathology leading to the other, or they may be distinct. Tricuspid annular dilatation can also be caused by long standing atrial fibrillation [8]. It is referred to as functional as the leaflets are normal in morphology but their function is impaired due to dilatation of the tricuspid annulus which pulls them apart, or right ventricular dilatation, elongation and altered geometry which displaces the papillary muscles laterally and apically, tethering the leaflets and preventing adequate leaflet coaptation [9]. Raised pulmonary artery pressures due to left sided heart valve disease contribute to these pathologies and exacerbates the severity of FTR [9, 10]. The severity of TR is greatest when both tricuspid annular dilatation and leaflet tethering are present.
Due to the high compliance of the right ventricular chamber, changes in preload, afterload and right ventricular contractility can affect the severity of TR and tricuspid annular dimensions significantly. Assessment of these parameters should therefore be done preoperatively in the awake patient and not during general anesthesia as this can induce vasodilatation and venodilatation with reductions in afterload and preload and hence TR severity.
Tricuspid Annular Dilatation
Early morphological changes in the heart secondary to left sided heart valve disease and atrial fibrillation which eventually leads to TR include an enlargement of the left and right atrium, the right ventricle and the tricuspid annulus [6, 11]. As the tricuspid annulus starts to dilate, it also assumes a more circular configuration, losing its 3-dimensional geometry [6, 11, 12]. In addition, the normal tricuspid annulus decreases in size during systole; this dynamic motion of the tricuspid annulus is lost in functional TR and may be another mechanism contributing to it [12].
In the early stages, right ventricular and annular remodeling occur without significant TR [6]. The anterior tricuspid annulus can dilate up to 40 % while the posterior annulus can dilate up to 80 %; the septal annulus is relatively fixed due to its anatomical relationship to the fibrous skeleton of the heart. [13] Right ventricular dilatation also occurs and can be significant [14, 15]. Dilatation of the tricuspid annulus is the most common cause of FTR [10]. The severity of TR increases with increasing tricuspid annular diameter size [4, 16]. Pulmonary hypertension secondary to left sided valvular heart disease is an important contributing factor [9, 11, 17].
Tricuspid annular dilatation pulls the tricuspid valve leaflets apart, particularly the anterior and posterior leaflets, decreasing leaflet coaptation (Fig. 18.3). Functional TR ensues once the annulus is dilated by more than 40 % its normal size [4, 5]. Increasing annular size results in increasing TR [11]. The degree of annular dilatation and hence the severity of TR can vary depending on the preload and afterload conditions, and also right ventricular (RV) contractility. Once the tricuspid annulus is dilated, it is unlikely to be reversible.
Fig. 18.3
Tricuspid valve seen from the right atrium showing the direction of tricuspid annular dilatation which mainly involves the anterior and posterior annulus (From Ton-Nu et al. [27])
Tricuspid Leaflet Tethering
Tethering of the tricuspid leaflet is another cause of FTR [10]. As the right ventricle dilates due to raised pulmonary artery pressures, it can assume a more elongated or eccentric geometry, thereby pulling the anterior papillary muscle apically and laterally, and tethering the tricuspid valve leaflets as a result, preventing adequate leaflet coaptation [9, 18]. Right ventricular eccentricity has been shown to be independently associated with TR severity [4]. This pathology is distinct from tricuspid annular dilatation although the two can co-exist, with tricuspid annular dilatation progressing to leaflet tethering with progressive RV dilatation and eccentricity [6]. The reverse is also true and leaflet tethering can progress to annular dilatation. Increased right ventricular sphericity can also result; here the septal papillary muscles are also displaced laterally, i.e., towards the left ventricle [9].
Tricuspid Leaflet Adaptation
It has recently been demonstrated that right ventricular pressure overload and remodeling was associated with an increase in tricuspid valve leaflet size by as much as 49 % compared to controls, and when this increase in size was inadequate to cover the tricuspid valve closure area, a graded increase in TR severity was observed [19]. Inadequate leaflet enlargement in response to annular dilatation may be another mechanism of functional tricuspid regurgitation, although further studies are needed to confirm this hypothesis. Similar observations were previously made in functional mitral regurgitation [20]. The biological mechanism for increased leaflet area was previously demonstrated in a sheep model in which mechanical leaflet tethering or stress caused by papillary muscle retraction reactivated embryonic pathways for leaflet growth [19, 21].
Stages of Functional Tricuspid Regurgitation
Three stages of FTR can be recognized depending on the degree of tricuspid annular dilatation and the presence or absence of leaflet tethering: [22, 23]
Stage 1: The tricuspid annulus is not dilated, the leaflets coapt normally from body to body, there is no leaflet tethering.
There is usually no TR or the TR is usually mild.
Stage 2: The tricuspid annulus is dilated to more than 40 mm, the leaflets coapt abnormally from edge to edge only, there is no leaflet tethering or leaflet tethering is mild (less than 8 mm)
TR is usually mild or moderate but may increase in severity depending on right ventricular preload, afterload and contractility.
Stage 3: The tricuspid annulus is dilated to more than 40 mm, there is no leaflet coaptation, leaflet tethering is significant (greater than 8 mm)
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