Learning objectives
Impact and pathophysiology of secondary tricuspid regurgitation (TR).
Role of imaging techniques in the assessment and follow-up of TR and of RV function.
Surgical indications, methods and techniques.
Introduction
The tricuspid valve was virtually ignored for a long time in the past. However, the
incidence of tricuspid insufficiency associated with left valvular disease is quite
significant, ranging from 8% to 35% of cases.1
2 This is most common in conjunction with mitral valve disease but association with
aortic valve pathology is not uncommon. It is most frequently related to rheumatic
valve disease and much rarer in association with degenerative mitral valve disease.
In most cases, the tricuspid regurgitation (TR) is so-called ‘functional’, corresponding
to dilatation of the annulus, as a consequence of RV dilatation secondary to pulmonary
hypertension. In 15–20% of cases, however, the injury can be organic, generally of
rheumatic origin, but for the purposes of this work we will restrict our analysis
to secondary (terminology now preferred over functional) TR.
Originally, it was thought that in most patients with secondary TR, surgical treatment
of the mitral valve disease would correct the problems of the right side and, hence,
a conservative (no touch) approach to the tricuspid valve was recommended.3
4
More recently, however, it has become evident that in a significant number of cases
secondary TR does not regress after appropriate correction of the left-side valvulopathy.
Thus, the indications for surgery of the TR have moved towards a progressively more
interventional attitude. Today, it is evident that we must intervene on the tricuspid
valve in cases of obviously severe tricuspid insufficiency and in cases where perioperative
detection of a more significant TR than expected is made, especially when triggered
by increasing load conditions.5
6
In this work, we intend to review the current concepts on the anatomy, physiopathology,
natural history, diagnosis and treatment of secondary TR.
Anatomy
The tricuspid valve is the largest of the heart valves with an anatomical area of
4–6 cm2 and a diameter of 27–29 mm. It lies inferiorly and anteriorly to the mitral
valve, the distance between the mitral and tricuspid annulus being, in normal conditions,
inferior to 8 mm/m2 (displacement index).7 Its anatomical structure is complex and
constituted of the three leaflets, the annulus, the chordae, the papillary muscles
and the adjacent myocardium (atrial and ventricular). The correct function of the
valve depends on the integrity and coordination of all these structures (figure 1).
Figure 1
Anatomy of the tricuspid valve (A) and normal tricuspid annulus (C, left image) with
a non-planar morphology with highest points in the anteroposterior direction and the
lowest in the mediolateral. In patients with functional tricuspid regurgitation, the
annulus becomes more planar (C, right image) and dilated in the anteroposterior diameter
(B). A: anterior, P: posterior; RA, right atrium; TR, tricuspid regurgitation. Adapted
from Shinn and Schaff.11
The septal leaflet is the most medial and is attached directly to the interventricular
septum, the anterior leaflet is usually the largest and extends through the anterior
portion of the annulus, and the posterior leaflet, the smallest, extends through the
inferior and posterior edges of the annulus. The anterior papillary muscle is the
most prominent; it partially originates from the moderator band and provides chordae
to the anterior and posterior leaflets. The septal papillary muscle is less prominent,
even absent in 20% of cases and often rudimentary, providing chordae to the septal
and posterior leaflets. Finally, the posterior papillary muscle is often bifurcated
or trifurcated and provides chordae to the posterior and septal leaflets.8 There are
also multiple accessory chordae attached to the free wall of the RV and to the moderator
band. These are important because they may prevent proper leaflet coaptation in case
of dilatation or dysfunction of the RV, thus causing TR.
The tricuspid annulus has a dynamic and complex 3D structure that differs from the
more symmetrical ‘saddle-shaped’ mitral annulus. A normal tricuspid annulus has a
non-planar, elliptical-shaped morphology, the posteroseptal portion being the lowest
part and the anteroseptal portion the highest.9 In patients with secondary TR, the
annulus becomes dilated (greater increase in the anteroposterior diameter compared
with the mediolateral diameter, consistent with greater dilatation along the RV free
wall), more planar and circular.10
11
Pathophysiology
Secondary TR is the most frequent type and refers to regurgitation not related to
primary organic tricuspid valve disease. The pathophysiology of secondary TR is related
to RV and annular dilatation or tethering (even with little annular dilatation)12
in connection to pulmonary hypertension. In most cases this is secondary to left-side
valvular diseases, but can also occur in primary RV disease or pulmonary hypertension.
Some authors have demonstrated that loss of contraction of the myocardium surrounding
the annulus is the leading mechanism of TR,13 thus atrial fibrillation can also contribute.
With progressive dilatation of ventricle and annulus, there is a failure of coaptation
and tethering of the leaflets with progression of the TR.
Clinical diagnosis
TR is most often diagnosed at the time of echocardiographic evaluation of left-side
heart disease or evaluation of right heart failure. As indicated above, TR is relatively
well tolerated and patients may remain asymptomatic even with TR of moderate or severe
degree. When symptoms appear, patients may complain of asthenia, fatigue or decreased
exercise tolerance as a result of lower cardiac output. They may also present with
signs of elevated right atrial pressure, such as peripheral oedema and abdominal fullness,
congestive hepatomegaly and ascites. Physical examination findings include jugular
venous distension with a prominent v-wave, hepatomegaly and, rarely, a soft systolic
regurgitant murmur can be heard that increases during inspiration owing to the increased
venous return. Atrial fibrillation as a result of right atrial enlargement is common.
IMAGING OF TRICUSPID REGURGITATION AND RIGHT VENTRICULAR FUNCTION
Evaluation of patients with TR requires the integration of the information from different
cardiac imaging techniques (figure 2). Before left-side valve surgery, careful assessment
of the severity of TR and careful measurement of the tricuspid annulus is mandatory.
Figure 2
Multimodality assessment of the tricuspid valve and RV volumes and function. (A) 3D
echocardiographic assessment of the tricuspid valve. (B) Colour Doppler regurgitant
flow in massive TR. (C) Dense/triangular flow with early systolic peak in a patient
with massive TR. (D) Cine short-axis view showing right and left mass and volumes
assessed by MRI. S, septal leaflet; P, posterior leaflet; A, anterior leaflet; TR,
tricuspid regurgitation.
Transthoracic echocardiography
Transthoracic echocardiography (TTE) is the technique of choice to evaluate the aetiology
of the TR, quantify its severity and determine the annular diameters. Simultaneous
evaluation of the three leaflets is difficult by conventional TTE, requiring the use
of different projections for the correct assessment (long-axis view of RV inflow,
short-axis at the level of the aortic valve, apical four-chamber and subcostal views).
The normal annulus diameter in adults is 28±5 mm and significant dilatation is defined
by a diastolic diameter >40 mm or >21 mm/mm2. Of note, it has been demonstrated that
the annular diameter, as measured from the apical four-chamber view, underestimates
major and minor annular dimensions.10
Quantification of the severity of the TR depends on the combination of different echocardiographic
parameters. Box 1 summarises the main parameters characterising severe TR, according
to the recommendations for the echocardiographic assessment of native valvular regurgitation
from the European Association of Cardiovascular Imaging.14
Box 1
Echocardiographic parameters of severe tricuspid regurgitation (TR)
Doppler derived parameters
▸ Colour Doppler regurgitant flow >30% of the area of the right atrium
▸ Dense/triangular flow with early systolic peak (maximum velocity <2 m/s in massive
TR)
▸ Vena contracta width ≥7 mm
▸ PISA in tricuspid regurgitation
– PISA* radius >9 mm at Nyquist limit of 28 cm/s
– EROA* ≥40 mm2 or regurgitant volume ≥45 mL
▸ Systolic flow reversal in hepatic vein flow
▸ Tricuspid inflow (E-wave) ≥1 m/s
Indirect parameters
▸ Abnormal/flail/large coaptation defect (tenting area >1 cm2)
▸ Inferior vena cava ≥21 mm with <50% collapse
▸ RV enlargement (RV eccentricity index >2)*
*Obtained by dividing the longest right lateral distance by the distance connecting
the ventricular septum and the RV free wall.
▸ PISA, proximal isovelocity surface area; EROA, effective regurgitant orifice area.
TTE also allows assessment of RV diameters and function in patients with TR. However,
this technique has limitations given the complex morphology of the RV and that most
parameters are influenced by load conditions. Reference values according to the recommendations
for cardiac chamber quantification by the American Society of Echocardiography and
the European Association of Cardiovascular Imaging are displayed in table 1.15
Table 1
Echocardiographic (A) and cardiovascular magnetic resonance (B) reference values of
RV and right atrial size and function in healthy adults
Abnormal
(A) Echocardiography
RV diameter (mm)
Base*
>41
Midventricular level*
>35
Length*
>83
RV wall thickness (subcostal view) (mm)
>5
RA end-systolic area (mm2)
>18
RA volume (mL/m2)
>30
Systolic function
TAPSE (mm)
<17
Pulsed Doppler peak S′ (m/s)
<9.5
RV fractional area change (%)
<35
RV 3D EF (%)
<45
Diastolic function
E/E′ ratio
>6
Tissue Doppler MPI
>0.54
(B) Cardiovascular magnetic resonance
End-diastolic volume/BSA (mL/m2)
>108
End-systolic volume/BSA (mL/m2)
>48
EF (%)
<50
Mass/BSA (g/m2)
>46
BSA, body surface area; MPI, myocardial performance index; RA, right atrium; TAPSE,
tricuspid annular plane systolic excursion.
In addition, TTE also predicts the presence of residual TR post surgery. The severity
of TR, the degree of RV dysfunction, a tenting area >1.63 cm2 and a depth of tethering
>0.76 cm are good indicators of significant residual TR.9
However, the severity of the TR changes within the respiratory cycle. During inspiration,
the tricuspid regurgitant orifice increases (median of 69%) and the peak TR velocity
decreases leading to a smaller change in the regurgitant volume (median of 20%). These
changes of the regurgitant orifice are related to an inspiratory increase in RV size
and morphology resulting in tricuspid annular dilatation, tethering and deficit of
leaflet coaptation.16 Recently, Mutlak et al
17 showed a difference in the peak TR velocity between inspiration and expiration
≥0.6 m/s, with a sensitivity of 66% and specificity of 94% for diagnosis of severe
TR.
Transoesophageal echocardiography
Transoesophageal echocardiography is only indicated when it is not possible to assess
the aetiology of TR by TTE because of poor echocardiographic window.14 Additionally,
transoesophageal echocardiography is indicated in patients with left prosthetic valves
and TR to ensure normal function before surgery of the tricuspid valve. It is also
more useful intraoperatively, especially to assess the final result of repair.
In recent years, real-time 3D TTE has become a basic tool for the assessment of tricuspid
valve pathology, since it permits simultaneous visualisation of the three leaflets,
the commissures and the anatomy of the annulus in a short-axis view.
Cardiovascular magnetic resonance
Cardiovascular magnetic resonance (CMR) permits visualisation of the anatomy and function
of the tricuspid valve. It also permits quantification of the regurgitant volume and
regurgitant fraction.18
However, the most important role of CMR in TR is in the assessment of the LV and RV
volumes and EF, since both parameters have been considered independent predictors
of significant residual TR post surgery.9 CMR has been considered the gold standard
technique to evaluate the ventricular volumes, due to its accuracy and reproducibility.
Reference values for healthy adults (not for severe TR) are displayed in table 1.19
There are no defined cut-off values in terms of RV volumes or EF to indicate surgery
in patients with TR. Kim et al studied 31 patients with CMR previous to tricuspid
valve surgery and suggested that a preoperative RV end-diastolic volume of 164 mL/m2
effectively discriminated patients with normal RV EF from those with depressed EF
at follow-up.20 However, based on the European Society of Cardiology (ESC) guidelines
for the management of grown-up congenital heart disease, significant RV enlargement
exists when the end-diastolic volume is ≥150 mL/m2 and significant RV dysfunction
when the EF is ≤45%.21
Natural history and follow-up
The natural history of severe TR includes a prolonged asymptomatic period with progressive
enlargement of the right atrium and RV due to volume overload. There are limited data
regarding predictors of TR progression. Recently, Shiran et al
22 reported that increased pulmonary artery pressure and permanent atrial fibrillation
were the most powerful risk factors for TR progression. The disease was considered
benign unless associated with pulmonary hypertension or right or left heart failure.
However, Nath et al
23 examined the mortality associated with TR in a retrospective series of 5223 patients
with a follow-up of 4 years. They concluded that moderate and severe TR were associated
with increased mortality and also that increasing TR severity was associated with
worse survival regardless of biventricular systolic pressure and pulmonary hypertension.
Also, it has to be emphasised that uncorrected severe TR is self-perpetuating and
progressive and becomes very incapacitating, with patients needing large amounts of
diuretics and frequently developing liver dysfunction.
Jhawar et al
24 also found that secondary TR is associated with increased mortality and decreased
surgery-free survival. Due to its functional physiology, secondary TR may diminish
or disappear with improvement of the RV function and also after successful correction
of left-side lesions. However, TR can persist or even increase after left-heart surgery,25
26 hence tricuspid valve repair at the time of mitral surgery is nowadays recommended
in cases of severe TR or dilated tricuspid annulus.6
27
The prognostic role of pulmonary hypertension is still controversial. It appears that
patients with moderate pulmonary hypertension preoperatively generally have RV failure
and dilatation, and many of these patients maintain TR after mitral valve surgery,
when not dealt with simultaneous surgery of the tricuspid valve. On the other hand,
patients with severe pulmonary hypertension often show regression of TR and almost
a third of them experience complete resolution following mitral surgery without intervention
on the tricuspid valve.28
Other factors such as age, atrial fibrillation and the presence of a pacemaker lead
are also related to persisting TR and worse outcome.29
In patients with moderate and severe TR, echocardiographic follow-up to monitor RV
function is recommended. Before considering isolated surgery for the tricuspid valve,
in particular redo surgery for severe TR after left-side surgery (see below), information
is needed to rule out any significant residual or recurrent left-side valvular lesions
(or prosthetic dysfunction), and to define the systolic pulmonary pressure and the
volume and function of both ventricles. Based on our clinical experience, we propose
the algorithm for follow-up and surgical indication shown in figure 3.
Figure 3
Proposed algorithm of management and follow-up of patients with isolated TR. CMR,
cardiovascular magnetic resonance; TR, tricuspid regurgitation.
Indications for surgery
Perspectives of the problem
There are various problems in solving the equation of the treatment of secondary tricuspid
valve regurgitation. First is the definition of the indications for surgery; second,
the choice between repair and replacement of the tricuspid valve; and third, the effectiveness
of different methods of repair and/or the type of prosthesis to be used in case of
replacement.
With respect to indications, the decision is difficult because there is no reliable
method of judging the degree of reversibility after correction of the problems on
the left-side valves, the quantification of the TR is difficult as there are no reproducible
methods to measure it, and, finally, there are no satisfactory methods of assessment
of RV function. On the other hand, if there is no argument about the need to intervene
on severe TR, the question of what to do with lesser degrees of TR remains unanswered.
Finally, how to predict which patients will return after successful surgery of the
mitral valve with persistent symptomatic TR?
As discussed above, one good reason for intervening on the tricuspid valve during
left heart valve surgery is that secondary TR accompanied by marked dilatation of
the annulus can produce an irreversible deterioration of RV function, and it is well
known that RV dysfunction affects the postoperative prognosis negatively.30 In addition,
the surgical risk is also increased in cases where there is a significant degree of
clinical and haemodynamic deterioration.
It is also evident that the quality of ‘repair’ of the left-side valvulopathy plays
a key role in the evolution of the disease. Any incomplete or unsatisfactory result
is usually associated with persistence of TR. But even with a perfect and complete
repair of the left heart disease, in many cases progression of the TR can occur and
surgery for isolated TR may be necessary. A much referred work by Dreyfus et al
6 appeared to demonstrate that tricuspid valves with a dilated annulus, even without
or with minimal regurgitation, often evolved to more severe degrees of regurgitation.
The authors measured, intraoperatively, the larger diameter of the tricuspid valve
between the commissures bordering the anterior leaflet and found values above 70 mm
to be predictive of negative outcome. These values correspond to the 40 mm measured
by echocardiography. In practice, the latter is more relevant as the decision to intervene
on the tricuspid valve must be made before the patient goes on the operating table.
Recommendations for TR surgery at the time of left heart valve surgery
Naturally, severe secondary TR requires intervention during surgery of the mitral
or the aortic valve, and this is a class I indication, but current ESC guidelines
(2012) have been modified from previous ones and suggest that ‘surgery should be considered
in patients with mild or moderate secondary TR with dilated annulus (>40 mm or 21 mm/m2)
undergoing left-side valve surgery’ (Class IIa indication, level of evidence C).w31
The American Heart Association/American College of Cardiology (AHA/ACC) guidelines
(2014) give very similar recommendations, in addition indicating that ‘tricuspid valve
repair may be considered for patients with moderate functional TR and pulmonary artery
hypertension at the time of left-side valve surgery’ (Class IIa indication, level
of evidence C).28
For the time being, there is no sufficient scientific evidence for acting in cases
of minimal or absent TR (prophylactic use?), even in the cases of significant dilatation
of the tricuspid annulus.
Surgical techniques
It is generally believed that the long-term results of tricuspid annuloplasty are
more favourable than those obtained after valve replacement, whether by mechanical
or bioprosthetic implants.
Survival after tricuspid valve replacement has been reported as low as 35% and up
to 75% after 10 years,27
w32
w33 naturally depending on the population and pathology, but these numbers are clearly
lower than those that are observed after tricuspid annuloplasty, as well as those
observed in the general population,w34 although some found no significant differences.w35
And the choice of prosthesis—mechanical or biological—is still controversial, each
type having advantages and disadvantages,w36 but, again with not much scientific evidence
of differences in survival.
Therefore, we believe that only exceptionally should the tricuspid valve be replaced.
Evidently, annuloplasty is the surgery of choice in these conditions, also because
the valve tolerates very well a less than perfect result, with regards to mild degrees
of residual regurgitation.
The most used operation on the tricuspid valve was the De Vega annuloplasty, first
described in 1972,w37 which is based on the fact that the dilatation of the tricuspid
annulus occurs mainly in its anterior and posterior segments, while remaining generally
unchanged in the septal portion, a concept developed by Carpentier et al
w38 (figure 1). Other methods of suture annuloplasty, including several forms of bicuspidisation,w39
have been used by several authors but, in our experience (MJA), a modified De Vega
technique, by interposition of Teflon felt pledgets for each annular bite of the suture,
thus minimising the risk of tearing, which we have described more than three decades
ago, has consistently produced excellent results (figure 4).w40
Figure 4
Suture annuloplasty: De Vega (A) and modified De Vega annuloplasty (B).
On the other hand, an increasing number of authors consider it important to use a
prosthetic ring. Rigid rings or bands of various types have been used to remodel the
posterior and anterior segments of the annulus (figure 5). The annular remodelling
concept, by contrast with simple narrowing, is appealing and several studies appeared
to prove greater freedom from recurrent TR in the long-term follow-up, although this
has generally not translated into better patient survival.w41
w42 The use of a ring is specifically indicated when there is organic involvement
of the tricuspid valve, usually associated with stenosis, generally of rheumatic origin,
in which case a commissurotomy is usually also required.
Figure 5
Ring annuloplasty (Left—in diastole; Right—during systole).
Results of TV surgery
In a recent report, Kim et al, concluded that long-term survival after TV surgery
for severe TR was ‘affected by several preoperative factors including advanced heart
failure symptoms, comorbidity, end-organ dysfunction and laboratory abnormalities,
but not by the type of surgery or causes of TR’.w43
w44
As discussed above, although currently most people claim better results with rings
than with suture annuloplasties, there is no evidence that this impacts on survival.
Similar considerations may be made for valve replacement versus repair, although here
we have to recognise the adverse impact of prosthetic-related complications, which
tend to appear late in the follow-up.
In fact, the results of annuloplasty alone are not always consistent. Among other
factors, this may be related to the degree of narrowing of the tricuspid orifice,
hence it has been suggested that the size of the tricuspid annulus should be reduced
appropriately considering patients’ body size to prevent recurrent TR.w45
On the other hand, tenting of the tricuspid valve in cases of significant dilatation
of the RV is known to be a factor for persisting or recurrent regurgitation. In these
cases, some authors have suggested pericardial patch enlargement of the tricuspid
leaflets.w46 The edge-to-edge ‘clover’ technique has also been suggested in these
circumstances.w47
Finally, there appears to be little difference between replacement with bioprostheses
and mechanical valves. Mechanical valves in the tricuspid position in multivalvular
procedures are generally associated with higher mortality and also with increased
incidence of thromboembolic complications and valvular dysfunction by pannus; although
thrombolysis appears to lead to more favourable results here. On the other hand, bioprostheses
appear to degenerate faster in the tricuspid position, especially in younger patients.
However, with the advent of percutaneous valve-in-valve implantation, this may be
less of a problem in the future.
Late-onset TR
New-onset or worsening TR late after mitral valve surgery, resulting from an earlier
conservative policy, is an increasingly common phenomenon.w48 Reoperation on the tricuspid
valve has a high mortality that some initial reports showed to be up to 50%. For these
reasons, many authors recommended medical treatment and postponement of surgery until
right heart failure became refractory to medication. However, factors for risk at
reoperation are high functional class, severe RV failure and large dimensions of the
RV, especially in the presence of a low EF, and high pulmonary artery pressure and
elevated pulmonary arterial resistance, all of which are progressive, thus calling
for surgery at an earlier stage. More recently, the reported mortality of the surgical
reintervention has been much lower, in the order of 10%, and even lower in others’
and our own experience.w49
w50
Hence, the recent ESC guidelines suggest that ‘surgery should be considered in patients
with severe TR who are asymptomatic or have severe progressive RV dilatation/dysfunction,
in the absence of left-side valve dysfunction, severe right or LV dysfunction, and
severe pulmonary vascular disease’ (class IIa).w31 Slightly differently, the ACC/AHA
guidelines classify it as a Class IIb indication.28 Therefore, there is a need for
close follow-up of patients in this situation and surgery should be recommended before
severe RV dysfunction occurs (see algorithm in figure 3). However, overwhelming comorbidities
and limited life expectancy may be contraindications to perform surgery.
When surgery is undertaken, there are various types of access to the tricuspid valve,
with the choice usually residing between repeat sternotomy and a right thoracotomy.
In the former, reopening of the sternum is sometimes done only after institution of
cardiopulmonary bypass, especially if the pericardium had not been closed during the
previous operation and the RV is bulging against the sternum, as seen on the X-ray
or CT scan. On the other hand, the right thoracotomy is becoming increasingly preferred
because it allows a more direct approach to the valve, after incision of the fused
pericardium and right atrial wall. Minimally invasive techniques have also been suggested
in these cases.w51
w52
Future, non-surgical options
All percutaneous techniques currently used for treatment of mitral regurgitation may
be adapted to percutaneous repair or replacement of the TV.w53 These may be based
on the tricuspid leaflets or annulus.
Percutaneous edge-to-edge repair, a replication of the clover technique developed
by Alfieri et al for correction of TR in congenitally corrected transposition of the
great arteries, has been described and can be used similarly in functional TR, using
the Evalve MitraClip system.w54
The Millipede system, which involves the placement of a ring with an attachment system,
via either minimally invasive surgical or percutaneous methods, has been tested to
restore the native tricuspid annular shape and diameter. The Mitralign concept of
percutaneous mitral repair has been used for bicuspidisation of the tricuspid valve,
aimed at converting a regurgitating trileaflet valve into a functioning bileaflet
valve, with some degree of success.w55
Finally, implantation of a valved stent in the tricuspid position has been described,
either as a primary replacement of the tricuspid valve or to treat a degenerated bioprosthesis.
This can be done via femoral approach or through direct transatrial access. Recently,
valves in the superior vena cava and/or inferior vena cava have been implanted to
prevent damage to the liver and other organs, a concept previously tested in failing
Fontan circulation.w56
Although the tricuspid valve is more difficult to access because of its 3D geometry
and because of the large size of the right atrium in these patients, current 2D and
3D echo imaging technologies allow easy and accurate placement of all types of implants
in the correct location.
Conclusions
The most important recent advance in our knowledge in this field is that secondary
TR is not a truly functional entity, because it entails intrinsic anatomical abnormalities
of the TV apparatus, such as annular dilatation and deformation.25
Secondary dilatation of the tricuspid annulus is present in a significant number of
patients with left heart valve disease, even in the absence of TR. This is a progressive
disease that does not always resolve with the correction of the left-side lesion.
Tricuspid intervention at the time of the surgery to the left-side valve usually helps
to improve the functional capacity without significant increase in perioperative mortality
and morbidity.
Patients with late appearing severe TR after correction of left-side lesions need
careful follow-up in order to indicate redo surgery before the development of severe
RV dysfunction.
Additionally, patients should be maintained on anticongestive therapy (diuretics and
vasodilators), probably for life, even after successful correction of TR.
Key messages
Secondary TR is a serious and progressive condition.
Tricuspid repair should be considered at the time of surgery for left-valve disease
in cases of more than trivial TR and dilated annulus.
Close follow-up of the RV function is needed in patients with previous surgery in
order to improve the results of redo surgery.
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