The tricuspid valve (TV) is the largest and most apically positioned of the four cardiac valves [1
]: its normal orifice area lies between 7 and 9 cm2
with an average gradient between the right atrium (RA) and right ventricular (RV) being typically <2 mm Hg [2
]. Although TV is also an atrioventricular valve, its anatomy and function have several dissimilarities to the corresponding mitral valve (MV), in part due to the lower pressures in the right heart chambers.
The functional abnormalities resulting from TV disease are classified as primary and secondary, the first being relatively rare, and it is the consequence of a primitive lesion of the TV due to congenital or acquired disease processes that affect the leaflets or chordal structures, or both. Secondary TV disease is more common and is a consequence of other diseases such as left-side heart diseases, pulmonary hypertension, RV dilation, and dysfunction from any cause, without intrinsic lesion of the TV itself [1
]. The most common TV disease in adults is tricuspid regurgitation (TR) and functional tricuspid regurgitation (FTR), with or without tricuspid leaflet tethering, secondary to left heart disease, either myocardial, valvular, or mixed, is responsible for more than 90% of TR in adults [3
]. Irrespective of the specific initial etiology, TR is a progressive disease in the setting of RV and RA remodeling. Tricuspid stenosis (TS) is even more rarely described, accounting for about 2.4% of all cases of organic tricuspid valve disease, and most often coexists with mitral valve pathology, especially in patients with rheumatic heart disease [5
TR is a common finding in most individuals, being found in up to 80–90% of them, and for long it was falsely considered a benign condition with a prolonged clinical latency [6
]. Because of this, it has been relatively neglected both in the literature and clinically as compared to the primary left-sided diseases [3
]. Furthermore, the rarity of TV surgical management, and its high post-operative mortality and morbidity [7
], in addition to the lack of evidence proving the superiority of surgical treatment over medical therapy in severe TR [10
], has led it to be called the “forgotten valve” for a long time [3
Nonetheless, in the last few years, the pathophysiology and impact of TR on the outcome of various heart diseases has been increasingly understood and thus its non-benignity is already established in literature [12
]. Long-term, higher FTR severity is associated with considerably worse survival, independently of other features [13
], and despite TR providing no additive value in advanced congestive heart failure (CHF), it is associated with excess mortality in mild to moderate CHF [15
]. Therefore, severe TR is associated with a poor prognosis, independent of age, biventricular systolic function, RV size, and dilation of the inferior vena cava [12
Hence, a myriad of new research and surgical techniques has been developed aiming to establish the optimal treatment and to ensure perfect surgical timing [16
]. Yet, to this day, TV surgery concomitant to left-sided heart surgery is the only Class I guideline recommended therapy for TR [17
]. The remaining recommendations of the American and European societies lack both stronger evidence and clear benefits, whereas the current recommendation for isolated TV is restricted only to patients with severe TR who are either symptomatic or are developing progressive RV dilatation/dysfunction [17
]. However, such patients with severe TR are often asymptomatic for a long period of time and symptoms may not specific, contributing to surgery’s delay [16
Nonetheless, despite the renewed interest in earlier surgery for patients with severe isolated TR before the onset of severe RV dysfunction or end-organ damage and recent improvement in mid to long-term results [19
], isolated TV surgery remains rare and to this day continues to be associated with the highest surgical risk among all valve procedures and high operative mortality rates, especially in reoperations [7
]. In this framework, catheter-based therapies for patients with severe isolated TR has become an area of rapid evolution and growing interest [22
], furthermore following the trend of valvular heart disease towards less invasive surgical and percutaneous therapies. As a result, multiple transcatheter tricuspid valve interventions (TTVI) have been developed for treating severe TR, at first aiming at TV repair and, more recently, transcatheter tricuspid valve replacement (TTVR) that allowed a new branch of possibilities in the management of TV disease.
As the TV is being treated more often, also by surgical replacement, prostheses malfunctioning should be expected. Solutions as valve-in-valve and valve-in-ring with transcatheter aortic valve (TAVI) devices are in some way applicable to the tricuspid position. Some case reports have already been published and the most frequently used devices are the Melody™ (Medtronic, Minneapolis, MN, USA) transcatheter pulmonary valve (TPV) from Medtronic and the TAVI XT®
and SAPIEN 3®
(Edwards Lifesciences, Irvine, CA, USA) [23
]. The first one has a major limitation as the maximum diameter size is 22 mm, and for the TV, it is too small. The procedures of valve-in-valve and valve-in-ring have been shown to be safe and feasible.
3. Transcatheter Tricuspid Anatomic Challenges
Many lessons have been learned in the past decades about transcatheter valve replacement and although many of the concepts of TAVR and TMVR can be transposed to the TV [22
], a better comprehension of the anatomical and functional peculiarities of the tricuspid valve and right heart chambers is essential to develop new techniques and to improve those already available, thereby overcoming the specific challenges related to TTVI.
First, surrounding the TV are four four key anatomic structures: the conduction system (atrioventricular node and right bundle of His), the right coronary artery, the noncoronary sinus of valsalva, and the coronary sinus ostium [1
]. Therefore, the possible injury risks during transcatheter tricuspid interventions are elevated and with potential severe complications. Moreover, due to the trabeculated and thin RV wall, other approaches, such as the transapical, become hindering [22
Compared with the MV, the tricuspid annulus is larger, with regurgitant orifice areas often twice those in the mitral position (up to 9 cm2
area in normal condition, much larger in the presence of functional TR); in addition, its leaflets are thinner and more fragile [22
]. Hence, the major interventional issue related to the TV compared to the MV lies in its larger orifice. As such, a complete occlusion of the regurgitant area can be very troublesome with the current repair devices that were originally intended for smaller gaps. For the same reason, a replacement device would also have to be extremely large to cover and seal the entire TV area, especially in the absence of any type of annular calcification or leaflet—which is almost never seen in native tricuspid valves—to aid its anchoring [27
The TA is a saddle-shaped ellipsoid that becomes planar and circular as it dilates [1
]. Peculiarly, TA dilation does not occur symmetrically, occurring primarily in the anterolateral free wall in patients with left-sided heart disease with sinus rhythm, expanding mostly along the posterior border with less prominent leaflet tethering in patients with functional TR secondary to chronic atrial fibrillation (AF). Therefore, its preferential dilation of the anterior and posterior leaflets allows malcoaptation between the anteroposterior and posteroseptal commissures, rather than the anteroseptal commissure. This organic pattern has important therapeutic implications for TV repair, especially for leaflet-based approaches [22
Similarly to the MV, the TV has a common antegrade approach. While the most used site is currently the transfemoral access, through the inferior vena cava (IVC), there are some devices that are delivered through a transjugular approach [22
]. However, the absence of transseptal support and the short distance between the IVC orifice and the TV annulus, combined with the loss of anatomical landmarks under pathologic conditions (RA and RV dilation), makes catheter navigation even more cumbersome than in the setting of a mitral valve intervention, resulting in a complete lack of stabilization and difficult coaxiality, which can lead ultimately into an improper positioning of the repair/replacement device [22
]. Besides the anatomical disadvantages, as tendency of cardiac implantable electrical devices (CIEDs) spreads, so will increase the difficulty of future TTVI. The presence of pacemakers, implantable cardioverter defibrillators (ICDs) or cardiac resynchronization therapy (CRT) devices will make navigating the catheter and fixing it in an optimal position even more problematic.
In addition to its anatomical peculiarities, the tricuspid valve also presents its own unique challenges on the imaging side. Since the TV is located more anteriorly compared to the MV, intraprocedural TEE guidance is particularly difficult in tricuspid procedures. In some circumstances, a combination of TEE, TTE, and intracardiac echocardiography (ICE) is needed to obtain adequate imaging quality [22
Despite differences and challenges, in contrast to the mitral and aortic valves, the right heart valves are open-angulated and widely separated by the crista supraventricularis, making the risk of obstruction of the right ventricular outflow tract almost insignificant [22
], thereby decreasing one of the most feared complications of percutaneous procedures.