Introduction
The tricuspid valve apparatus is a complex and dynamic structure that interacts intricately with surrounding anatomy. The vast majority of patients with tricuspid valve disease have tricuspid valve regurgitation (TR), whereas a minority present with tricuspid stenosis (TS). TR represents a significant epidemiologic burden, with an estimated 1.6 million Americans affected by this condition and only 8000 tricuspid valve surgeries performed nationwide on a yearly basis. , Untreated severe TR is associated with poor outcomes from long-standing volume overload on the right ventricle (RV), with up to 36% 1-year mortality rate. In patients undergoing tricuspid valve surgery, 60% of patients received tricuspid valve replacement, while 40% underwent tricuspid valve repair. Despite the increase in surgical volumes, mortality remains high and unchanged, at 8% to 9%. The high mortality associated with tricuspid valve surgery is thought to be attributed to delayed referral for intervention, whereby irreversible RV dysfunction and end-organ damage have already ensued, increasing surgical risk. In patients who undergo tricuspid bioprosthetic valve replacement, over half require reintervention at 15 years due to prosthetic valve degeneration. Recently, percutaneous transcatheter tricuspid valve interventions have evolved as an option for patients who are at high risk for surgery and are the focus of this chapter.
Tricuspid valve anatomy and pathophysiology
The tricuspid valve is composed of an annulus, three leaflets, and supporting structures (chordae and papillary muscles). The tricuspid valve annulus is a saddle-shaped structure angled inferiorly toward the RV apex posteromedially and superiorly toward the right atrium anteroseptally. At the septum, the tricuspid annulus is a thin fibrous structure, whereas anteriorly and posteriorly it becomes more muscular, underpinning the mechanism of annular dilatation in the anteroposterior direction that is frequently observed in functional TR. Surrounding the annulus, important structures pertinent to any tricuspid intervention include the bundle of His and the right coronary artery. The tricuspid valve typically has three leaflets: anterior, which is the largest; posterior; and septal. The anterior and posterior leaflets are characterized by multiple scallops and are thinner than the mitral valve leaflets. The three leaflets are anchored by two main papillary muscles, the anterior and posterior, and sometimes a third rudimentary muscle on the interventricular septum. The anterior papillary muscle is fused with the moderator band and has chordal attachments to the anterior and posterior leaflets, whereas the posterior papillary muscle is attached to the inferior RV free wall and sends chordae to the septal and anterior leaflets. The septal leaflet has unique direct chordal attachments to the interventricular septum without a papillary muscle.
TR may occur as a result of primary leaflet abnormalities (e.g., pacemaker lead–induced injury, prolapse/flail leaflet, congenital abnormalities (such as Ebstein anomaly), rheumatic disease, and carcinoid disease) but more frequently occurs secondarily due to tricuspid annular dilatation and/or RV enlargement. In pulmonary hypertension or untreated left-sided valvular heart disease, progressive RV pressure overload eventually results in RV failure and secondary TR due to tethering of tricuspid leaflets and annular dilatation. More commonly, severe TR is observed as a consequence of chronic atrial fibrillation, where progressive atrial enlargement causes tricuspid annular dilatation, and severe TR that occurs in isolation from other valvular heart disease. The degree of annular dilatation and severity of TR can vary widely. Recent recommendations have included an expansion of TR grading beyond severe to also include massive and torrential grades, to more accurately reflect severity of disease.
Transcatheter therapies in the native tricuspid valve remain challenging because of the following anatomic features:
- 1.
The tricuspid valve (average 10 cm 2 ) is larger than the mitral valve (average 7 cm 2 ) and is subject to a very wide range of dilatation in severe TR.
- 2.
The tricuspid valve annulus is not a rigid structure.
- 3.
The tricuspid valve leaflets and chordae are thin, risking injury during interventions.
- 4.
The angulation from the inferior vena cava (IVC) to the tricuspid valve is variable and can pose a challenge to device delivery from the femoral route.
- 5.
The lack of chord-free zones on the leaflets, the presence of muscle bands, and the presence of pacemaker leads, as well as the thin RV wall, especially at the apex, can add complexity and risk to tricuspid procedures.
Currently clinical percutaneous interventions in the tricuspid valve are limited to off-label use of aortic balloon-expandable valves in failed bioprosthetic valves, as described in the previous chapter, and off-label use of the MitraClip device in the tricuspid position. However, there are several novel dedicated tricuspid transcatheter devices under active investigation, a few of which will be described briefly in this chapter.
Percutaneous repair for native tricuspid regurgitation (spacer therapy, edge-to-edge plication, percutaneous annuloplasty)
Several percutaneous repair devices are currently being investigated for use in secondary TR due to annular dilatation and work by different mechanisms ( Fig. 25.1 ). Current evidence for these investigational devices is limited to early feasibility trials and case series. Spacer therapy, mainly the Forma device (Edwards LifeSciences, Irvine, CA), is a foam-filled balloon that is delivered via a left subclavian approach and positioned across the tricuspid valve and secured to the interventricular group right ventricle with a fixation anchor. This device occupies the space created by tricuspid valve malcoaptation and serves as a surface of contact for leaflet coaptation ( Fig. 25.2 ).
