**2. Anatomy and physiology**

The heart has four functional valves and TV is the largest one, with a normal orifice area between 7–9 cm2 (**Figure 1**) [6], apically located. Due to the low pressure differences between the RA and the RV, the large size of the TV can function at low gradient (<2 mm Hg) and low peak transtricuspid diastolic velocities [6]. The leaflets, the papillary muscles, the chordal attachments, and the annulus (with attached atrium and ventricle) are the components of the TV [7]. The integrity and harmony of these components result successful valve function.

## **2.1 The leaflets**

TV closure during systole needs the normal function of the leaflets and their relationship with chordae and papillary muscle, although they are also closely related to the size and function of RV. RV pressure overload and remodeling was associated with up to 49% increase in TV leaflet size compared to controls in recent screenings, and when this increase in size was insufficient to cover the tricuspid valve closure area, there was a gradual increase in TR severity. observed [8]. The TV typically consists of 3 leaflets of unequal size. Healthy subjects may have anatomical

**Figure 1.**

*A) Tricuspid valve and rhe relations with the other valves. B) The weak sies of the tricuspid aparatus with tendency for dilation.*

### *Tricuspid Valve Repair DOI: http://dx.doi.org/10.5772/intechopen.108821*

variants consisting of 2 (bicuspid) leaflets or more than 3 leaflets [9]. Definition according to their anatomical positions in the body, these 3 leaflets would be septal, anterior-superior, and inferior: called septal, anterior, and posterior leaflets [10]. The anterior leaflet is the largest, whereas the posterior leaflet is notable for the presence of multiple scallops. The septal leaflet is the smallest and arises medially, directly from the tricuspid annulus above the interventricular septum. It is attached to the tricuspid annulus directly above the interventricular septum [11]. The anatomical markings for each leaflet vary considerably based on the size and shape of the annulus; still, the commissure between the septal and posterior leaflets is often prominent, located near coronary sinus entrance into the right atrium (**Figure 2**).

When we examine the integrity of the four heart valves the noncoronary sinus of valsalva of aortic root is typically adjacent to commissure between the septal and anterior leaflets: the anteroseptal commissure. This is the longest commissure, as the anterior and septal leaflets are often the longest circumferentially. The coaptation of the TV is typically at or just below the level of the annulus with a coaptation length of 5–10 mm [12]. This coaptation length is the potential reserve for keeping the function of the TV when right side of the heart is affected as dilation.

### **2.2 Chordae and papillary muscles**

Tensor apparatus of TV are the papillary muscles and chordae. The posterior and septal leaflets supported by medial papillary muscle group cordae and anterior and posterior leaflets supported by anterior papillary muscle group cordae [6].

The accessory chordae may protrude from the right ventricular free wall or the moderator band. Hence, the septal and anterior leaflets of the TV are attached to the interventricular septum, and the anterior and posterior leaflets are attached to a

### **Figure 2.**

*The schematic seen of the Tricuspid Valve and the relation of heart conduction system (AVN: AN node, SVC: Superior Vena Cava, FO: Fossa Ovalis (Also this is the key anatomic tissue for trans septal mitral valve intervention), RV: Right Ventricle).*

large anterior papillary muscle along the anterolateral right ventricular wall. Due to the fixed length of the chordae, the displacement of septal or lateral wall positions of the RV would affect tricuspid leaflet coaptation. Therefore, tricuspid annular sizing algorithms have been based on the dimension of the base of the septal leaflet [13]. The number of chordae varied from 17 to 36 with an average of 25 chordae [7]. Since the septal leaflets that is fixed to the septal wall is quite immobile, there is little space for the free wall of the right ventricle/tricuspid annulus to expand (**Figure 1**) [14].

Transcatheter interventions of the heart, the chordae can interact with catheters and interventional devices, causing additional difficulty during transcatheter approaches for TV. Besides, the mechanical properties and superstructure of the TV chordae tendineae in normal humans are composed of somewhat flat collagen bundles made of collagen fibrin matrices, with less extensibility than normal mitral valve chordae of comparable size [15].

### **2.3 Tricuspid valve annulus**

The TV is situated within an elliptical, nonplanar annulus. The normal tricuspid ring is D-shaped, non-planar with two distinct segments: a larger C-shaped segment corresponding to the free wall of the RA and RV, and a shorter, relatively straighter segment corresponding to the septal leaflet and the ventricular septum [7]. Flexible fibroadipose tissue is the composition the annular ring. During the cardiac cycle composition of the annulus allows geometrical changes, it is rounder during diastole, and during systole it becomes more elliptical by the interventricular septum bulges into the RV [16]. The tricuspid annulus has a complex, three-dimensional structure that differs from the more symmetrical "saddle-shaped" mitral ring. This shape has implications for the design and implementation of new annuloplasty rings, rather than the existing planar annuloplasty rings in the tricuspid position [11]. Fukuda et al. conducted a real-time, three-dimensional transthoracic echocardiographic research and examined 15 healthy subjects and 16 patients with functional TR (12/16 had moderate to severe TR). They mapped the tricuspid annulus throughout the cardiac cycle and reconstructed it using a computer workstation. The healthy subjects had a non-planar, elliptical tricuspid annulus, with the posteroseptal segment being the lowest relative to the right ventricular apex and the anteroseptal segment being the highest. Patients with functional TR often had rather planar annulus compared to the elliptical shape in healthy subjects; the latter mainly expanded in the septallateral direction (F resulting in a more circular shape. The authors concluded that novel approaches or rings tailored to the unique shape of the tricuspid ring could improve ventricular function and reduce leaflet stress [17].

The tricuspid annulus is a dynamic structure that can produce significant changes (up to ∼30%) in the area it creates during the cardiac cycle. It is greater in end-systolic/early diastole and during atrial systole, as well as under loading conditions [6]. When measured in healthy subjects using 3D echocardiography, the normal tricuspid annulus has a circumference of 12 ± 1 cm and an area of 11 ± 2 cm<sup>2</sup> [17]. During surgery it is more difficult to identify the TV annulus when it compared with the mitral valve annulus. The posteroseptal tricuspid annulus is more ventricular, but anteroseptal portion is more atrial [18].

### **3. Cause, diagnosis, and natural history**

Two forms of TR are primary and secondary. Primary TR is seen less and can be the congenital or acquired disease processes that affect the leaflets or chordal structures, or both. Secondary or functional TR (STR or FTR) is more common and *Tricuspid Valve Repair DOI: http://dx.doi.org/10.5772/intechopen.108821*

secondary to other diseases like left-side heart diseases, pulmonary hypertension, RV dilation, and dysfunction from any cause, without intrinsic lesion of the TV itself. Enlargement of the valve annulus and the right ventricle is the main reason of the STR, any cause of left heart dysfunction or disease of myocardial or valvular causes, RV volume and pressure overload, and dilation of cardiac chambers can be the reason. Less common causes of tricuspid valve pathology include rheumatic, congenital, or other causes (endocarditis, leaflet tear/prolapse, chordal rupture, papillary muscle rupture, or myxomatous degeneration of the tricuspid valve) [19].

## **3.1 Classification of tricuspid regurgitation**

## See **Table 1**.

### *3.1.1 Primary tricuspid regurgitation*

Primary TR is seen less than the secondary form may be congenital (Ebstein's anomaly) or acquired diseases of the TV (myxomatous degeneration of the tricuspid valve, leading to TV prolapse, endocarditis, carcinoid syndrome, rheumatic disease, radiation, or trauma). The latter is crucial for patient selection and clinical decision-making, so the two must be differentiated. One of the only causes of TR is that the leads of a pacemaker or defibrillator that pass from the RA to the RV can directly affect the leaflet coaptation. This has been reported in case reports and small series, but might be more important and common than currently detected. In a 2008 publication, by Kim et al. researched the effect of a transtricuspid permanent pacemaker or implantable cardiac defibrillator in 248 subjects using echocardiograms before and after device implantation. The authors found grade 1 or greater worsening of TR after implant in 24.2% of the subjects, and TR worsening was more common in implantable cardiac defibrillators than in permanent pacemakers with mild or lower TR at baseline [20]. The current guidelines do not recommended removal in patients with TR and transtricuspid pacing leads due to the potential to damage the valve and result in serious conditions [21].

### *3.1.2 Secondary (functional) tricuspid regurgitation*

The most common cause of TR is secondary or "functional" insufficiency. STR can be categorized based on the underlying cause or the morphological abnormality of the tricuspid apparatus; some morphologies are clearly associated with specific underlying diseases:



### **Table 1.**

*Tricuspid regurgitation classification table.*

pulmonary artery pressure estimated by Doppler >50 mm Hg with no identifiable clinical cause),

3.STR due to any RV dysfunction (myocardial disease or RV ischemia/infarction),

4. STR with no detectable cause of TR (idiopathic STR).

Some morphological abnormalities associated with STR may co-occur, including:

1.tricuspid leaflet attachment or tenting,

2.displacement of papillary muscles,

3.RV dysfunction,

4. enlargement of the annulus and/or RA.

Several studies have concluded that atrial fibrillation (AF), ischemic heart disease associated with mitral regurgitation, rheumatic heart disease, and a large left atrium are associated risk factors of TR [22].

Many factors as preload, afterload, myocardial wall thickness and contractility which can limited by the intact pericardium are determining the right ventricle ejection fraction and the stroke volume. The RV Wall thickness is about 3–4 mm and the mass is approximately six times less than the LV. The RV is adapted to eject blood against a lower pulmonary vascular resistance. RV is low pressure highly compliant cardiac chamber because of low afterload results in reduced wall tension and characterises RV physiology. Before progressive RV dilatation, dysfunction and


*and TR, tricuspid regurgitation [23].*

### **Table 2.**

*Stages of tricuspid regurgitation (AHA Guidelines).*

failure progression RV can tolerate this high volume state for prolonged periods. This may occur with or without the development of pulmonary vasculopathy (from chronic high flow). Cresent shape of the RV changes with chronic volume overload to spherical form till limitation of the pericardial capacity. Ventricular interdependence shifts the ventricular septum leftward. LV filling is impaired further compounding a fall in cardiac output (**Table 2**) [8].
