Tricuspid valve: a valve not to be forgotten.

Background

Tricuspid regurgitation is either primary (organic) or secondary (functional) depending on whether there is:

• Pathologic involvement of the leaflets and chordae: Primary (organic) tricuspid regurgitation regards pathologic involvement of the leaflets and chordae, most often related to rheumatic mitral and/or possibly aortic valve pathology, degenerative valve pathology, congenital, infectious, traumatic, or iatrogenic causes - due to pacemaker leads - or to right ventricular endomyocardial biopsy.
• Simple annular dilation: Secondary (functional) tricuspid regurgitation is referred to when simple annular dilation has occurred. It is often associated with pulmonary hypertension, right ventricular dysfunction or atrial fibrillation.

• Impact of tricuspid regurgitation: Persistent moderate to severe secondary tricuspid regurgitation impacts functional capacity and long-term survival (1) hence early surgical correction must be considered. 
• Enduring dysfunction after repair: In cases of severe tricuspid regurgitation, unrepaired TR may still continue to progress, even if left heart valve function is adequately restored. (2) Whether tricuspid regurgitation will recede, remain stable or progress is impossible to predict.

Here we focus on secondary TR in its anatomical, functional, pathological and surgical aspects.

1 - Anatomy and pathophysiology

The tricuspid valve is made up of three leaflets: the anterior leaflet, which is the largest, the posterior leaflet and the septal leaflet.
Each leaflet free edge is connected to the heads of the respective papillary muscle mainly by chordae tendineae.
The leaflets are attached to the tricuspid annulus, which is part of the fibrous skeleton of the heart and has been shown to be complex in structure (i.e. not as symmetrical as that of the mitral valve). The highest point is the anteroseptal segment which is close to the right ventricular outflow tract and aortic valve. The lowest point is located toward the apex and is the posteroseptal segment.
In secondary TR, the tricuspid annulus dilates in the septal-lateral direction. (3) The septal annulus is relatively spared from dilatation as it is part of the septum and of the fibrous skeleton.
The more severe the regurgitation, the more planar and circular the tricuspid annulus becomes. 
The most common form of tricuspid disease is TR secondary to left heart valvular pathology (mostly mitral valve disease). When pulmonary hypertension develops, it can lead to right ventricle and annular dilatation and, eventually, to tricuspid valve tenting. The tricuspid leaflets are morphologically normal but do not coapt adequately. However, not all patients with pulmonary hypertension develop TR, the cause for which seems to be multifactorial and related to other factors such as atrial fibrillation and right heart enlargement. (4)
A phenomenon called “restriction-dilatation syndrome” occurs when right ventricle systolic function “fails”, the diastolic pressure then rises and the interventricular septum moves towards the left ventricle during diastole which in turn will raise left ventricle diastolic pressure, perpetuating the TR (5), a situation that is further aggravated by dilatation of all heart cavities.

2 - Clinical and imaging evaluation

Patients present either as asymptomatic or with varying degrees of right heart failure. Fatigue, weakness, shortness of breath, jugular vein distension, ascites, hepato-splenomegaly, pulsatile liver, pleural effusions and peripheral oedema may be present. In late stages and with hepatic insufficiency, cachexia (loss of weight and fatigue), jaundice and cyanosis may develop. Upon suspicion of tricuspid regurgitation:

1. TTE: 2D transthoracic echocardiography (TTE) is the technique of choice. 
2. Vena contracta: When feasible, measurement of the vena contracta is recommended to quantify TR (VC width = 7 mm defines severe TR); the PISA method is reasonable (EROA = 40 mm² or a R Vol = 45mL indicates severe TR). 
3. Systolic hepatic flow reversal: Systolic hepatic flow reversal is specific to severe TR.
4. In the presence of TR: Right ventricle dimensions, right atrium volume, inferior vena cava diameter and its respiratory kinetics and pulmonary arterial systolic pressure should be evaluated in the presence of TR. 
5. In presence or not of TR: tricuspid annulus dimensions are also important to make a note of; the annulus is considered enlarged if > 40mm or 21mm/m². (6) 
6. Clinical signs of TR and/or right ventricular dysfunction: The degree of TR is highly dependent on loading conditions, so distinct observations can lead to different grades of quantification.
   We believe that clinical signs of TR and/or right ventricular dysfunction, and not only echocardiographic parameters, are an important adjuvant on the global assessment of TR and decision to intervene on the tricuspid valve.  
7. Excursion and velocities: Evaluation of right ventricular function is far more difficult than evaluation of the left ventricle. It is reasonable to use tricuspid annular plane systolic excursion (TAPSE < 15mm) or the systolic myocardial velocities (< 11 cm/s) to identify right ventricular (RV) dysfunction. 
8. CMR: Cardiac magnetic resonance is reserved for patients in whom echocardiographic data are suboptimal or equivocal. This technique is currently the gold standard for the assessment of right ventricle morphology and function. (7)

3 - Management, surgical indications and techniques

There is no reliable method to predict how much of the TR will reverse after correction of left heart valve dysfunction and experience indicates that a significant and varying percentage of patients will have recurrence of TR during follow-up, even with a perfectly-functioning left-sided valve. (2)
This is particularly true in rheumatic mitral valve disease as opposed to degenerative disease.
Ischemic mitral regurgitation is also prone to late recurrent or de novo TR. (8) On the other hand, reoperation for severe isolated TR carries a significant surgical risk. (9) Hence the dilemma of when and what to do to the tricuspid valve when performing mitral (or aortic) valve surgery. A recent trend, however, has developed towards a more aggressive approach to intervention.
Current guidelines (ESC/EACTS and ACC/AHA) recommendations are based on expert experience and opinion and still hold minor differences (Table 1).
Table 1 – European and American Guidelines on Secondary Tricuspid Regurgitation.

Nevertheless there is a consensus to operate when faced with severe TR in a patient undergoing left-sided valve surgery (class I). (10) We, as well as an increasing number of surgeons are being more aggressive towards concomitant secondary TR and are operating even when mild to moderate TR is present with a tricuspid dilated annulus (≥40mm or ≥21mm², class IIa).(11) In rheumatic mitral valves, particularly after mitral repair, especially if the result is short of optimal, the probability of persistent TR after surgery is greater than in degenerative mitral pathology.
Furthermore, the seminal work of Dreyfus et al. (12) has shown that TR may occur late after left side valve surgery in patients with dilated annuli, even in the absence of significant TR, which has led some experts to advocate prophylactic tricuspid annuloplasty in these patients, but this is still far from consensual.
Recently Kim et al. (13) reported predictors of mortality and adverse events as being correlated to preoperative factors such as advanced heart failure symptoms, comorbidities and end-organ dysfunction and laboratorial abnormalities moreso than to the type of surgery or the causes of TR. They conclude that earlier referral for surgical correction should be recommended to avoid these risk factors.
The primary goal of surgery should be 1) to eliminate TR and 2) to restore the size and shape of the tricuspid annulus. This can be generally achieved with annuloplasty procedures (suture or ring) which aim to reduce the size of the anterior and posterior portions of the annulus, preserving the septal portion. Although some reports (14,15) have favoured the use of a ring, we have been using a modified De Vega technique (5,16) for more than three decades, with good results. Mild degrees of residual regurgitation are usually well tolerated and tend to decrease over time as the right ventricle re-remodels. We usually reserve the implantation of a rigid ring for when there is organic involvement of the tricuspid valve or a severe enlargement of the tricuspid annulus and significant RV dysfunction.
Other authors have recommended alternative or complementary repair techniques such as leaflet patch augmentation and neo-chordal implantation. 
Tricuspid valve replacement should be reserved for the rare case of a late failed repair or for cases of significant distortion or destruction of the leaflets. In such circumstances, bioprostheses are recommended in patients older than 65 years, whereas mechanical valves are preferred in younger patients, unless contra-indicated.

4 - Medical Therapy 

As for medical therapy, diuretics are used to reduce venous congestion. Beta-blockers, and vasodilating agents (e.g., angiotensin-converting enzyme inhibitors and angiotensin receptor blockers) may be associated. This therapy should be started before surgery and continued afterwards to give the chance to the right ventricle to re-remodel and to reduce the diameter of the tricuspid annulus, further decreasing the grade of regurgitation. Additional measures include restriction of fluid and dietary sodium intake. Adapted therapy of the underlying disease is to be sought.

Conclusions

Significant TR often accompanies left side heart valve pathology and does not always reverse with its correction. As suggested by the recent changes to the European (ESC/EACTS) guidelines, today we not only intervene in severe TR, but act “prophylactically” in apparently less severe disease.