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Fig. 17.4 Red arrow is a deployed TEER clip to the
A2P2 segments of the mitral valve for a ail segment with
resultant two channels during ventricular diastole (green
arrows)
Antithrombotic therapy following TEER is
studied to be aspirin 81 mg indenitely and
Plavix 75 mg for 2 months post procedure. In
patients with atrial brillation or other indications for systemic oral anticoagulation, the regimen is adjusted.
A. Booke et al.
bility, lower rates of thromboembolism, resistance
to endocarditis, and does not require anticoagulation therapy in most patients [2]. Techniques and
concepts regarding MV repair are continually
evolving and range from simple to comprehensive. Simple repairs may only involve placement
of an annular ring to support the valve while
complicated repairs involve both the anterior and
posterior leaet, as well as the chordae. The goal
of the repair is to re-establish the integrity of the
valve, improve coaptation of the leaets, and
decrease annulus size if dilation exists.
In the operating room, MV repairs are immediately assessed by a certied advanced imaging
physician via TEE. If the MV repair is inadequate, immediate MV replacement should be
considered while still in the OR.
Mitral valve replacement is warranted when
the leaets are not salvageable due to presence of
calcication, perforation, infection, or the presence of rheumatic disease. If repair is attempted
in rheumatic disease, the risk of reoperation is
50–60% of patients within 20years [1].
Surgical Management ofMitral
Regurgitation
The timing of surgical intervention for MR
depends on the acuity of the MR (acute vs
chronic) and the cause of the MR (primary vs
secondary). Mortality rates for primary MR
decrease with early surgical intervention before
symptoms and LV systolic dysfunction (LVEF
≤60% or ESD ≥ 40 mm) occur [1]. Once a
patient develops symptoms and LVEF ≤60, the
prognosis is poor [1]. This was conrmed by a
recent data analysis completed by the STS demonstrating reduced survival associated with late
referral for surgical intervention [3]. Close monitoring of MR progression with imaging surveillance, despite presence of symptoms, is vital in
planning surgery before LV dysfunction deteriorates [1].
In MR, surgical correction can be accomplished by either mitral valve repair (MVr) or
mitral valve replacement (MVR). Mitral valve
repair is preferred over mitral valve replacement
and should be attempted if leaets are salvageable. Valve repair is shown to have superior dura-
Surgical Intervention forChronic
Primary MR
The timing of surgery depends on the severity of
the disease and LV function. Unlike surgical treatment of the aortic valve or mitral stenosis, the lack
of symptoms should not delay the timing of intervention for primary MR.In mitral valve prolapse
affecting only half of the posterior leaet, mitral
valve repair is the gold standard of care with outcomes superior to both biological and mechanical
valve replacement [1]. Studies demonstrate that
patients who undergo mitral valve repair for primary MR have a life expectancy equal to that of
the general population after surgery, regardless of
age [4]. When mitral valve repair is successful,
operative mortality rate is <1%, with 95% freedom from reoperation and 80% freedom from
recurrent moderate or severe MR at 15–20years
postoperatively [1]. In accordance with the ACC/
AHA guidelines, if severe primary MR is isolated
to less than half of the posterior leaet and only
simple repair to the posterior leaet is necessary,
MV replacement is considered harmful and
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should not be completed unless MV repair has
been attempted and failed [1].
Surgical Intervention forChronic
Secondary MR
In chronic secondary MR, the role of surgical
intervention is controversial. MR is multifactorial
and restoration of MV competence does not mitigate the underlying cardiac pathology. Although it
has not been shown to directly improve survival,
surgical intervention has been shown to improve
functional outcomes and reduce symptoms [5].
According to the ACC/AHA guidelines, MV
surgery for chronic secondary MR is warranted: [1]
• In the presence of severe symptoms when the
valve is not favorable to TEER.
• When patient is undergoing CABG with
severe MR and LV dysfunction secondary to
CAD.
• When severe MR is isolated from annular
dilation related to atrial brillation, MV sur-
gery with MAZE procedure may be
reasonable.
Risk stratication for MV repair and MV
replacement can be calculated on the STS website. Refer to Chap. 6 for further discussion and
Table 6.3 for a list of categories assessed with the
risk calculator.
Surgical Approach andValve Selection
As discussed above, MV repair is preferred to
MV replacement in the setting of MR.Surgical
approach begins with visual assessment of the
mitral valve apparatus to determine if repair is
feasible. Figure17.5 depicts visualization of the
mitral valve via the left atrium during surgery.
This mitral valve has a ail posterior leaet
resulting in severe MR.
With surgical intervention of chronic secondary MR, MV replacement should be considered
in cases with ischemic or dilated cardiomyopathy. The durability of a mitral repair depends on
the regression of the underlying dilation, and if
the dilation progresses postoperatively, the repair
will not be durable and survival is limited [1].
Preoperative Assessment
andCalculating Risk
As with other cardiac surgeries, a detailed history,
physical, and a myriad of diagnostic testing is completed to determine patient’s baseline status and
operative risk. A cardiac catheterization should be
completed to assess for any coronary artery disease
that may need to be addressed during the operation.
A thorough dental history should also be obtained
to rule out a disease process which may put patient
at increased risk for developing endocarditis postoperatively. Refer to previous chapters regarding
preoperative assessment for further discussion and
Tables 6.1 and 6.2 in Chap. 6.
Fig. 17.5 Mitral valve with ail posterior leaet. (a)
Anterior leaet. (b) Posterior leaet. (c) Chordae Tendinae
Fig. 17.6 Insertion of valve sutures to implant an annuloplasty ring into mitral position for mitral repair
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Fig. 17.7 Insertion of an annuloplasty ring for mitral
repair utilizing sutures from Fig.17.6
Fig. 17.8 Mitral valve repair of Fig.17.5 with triangular
resection of P2 and placement of ring
With MV repairs, an annuloplasty ring is
always placed to support the annulus and provide
structure, regardless of the type or complexity of
repair. Sutures are rst placed along the annulus
(Fig.17.6) and then the annuloplasty ring is parachuted down into the correct position (Fig.17.7).
Once the repair is complete, the valve is assessed
intra-operatively for residual valvular leak prior
to closure. Successful mitral valve repair with
A. Booke et al.
competent valvular coaptation is demonstrated in
Fig.17.8.
If the mitral valve is unable to be repaired and
replacement is necessary, the type of prosthesis
needs to be addressed. This discussion must be
completed with the patient preoperatively, even if
a MV repair is planned. Refer to the chapters on
valve selection under surgical management of
aortic valve disease for further discussion.
Mitral Stenosis
The etiology of mitral stenosis is most commonly
rheumatic or degenerative (Table 17.3).
Rheumatic fever is the leading cause of mitral
valve disease worldwide and rheumatic MS is
more common in women (80% case) compared
to men [1]. Clinical presentation can vary, and
patients may present earlier in life, even in their
teens. Patients presenting at a younger age, often
have commissural fusion but pliable, noncalcied mitral valve leaets [1]. Patients presenting
later in life more commonly have calcied
brotic mitral leaets in addition to commissural
fusion and subvalvular involvement [1].
Degenerative mitral stenosis is seen in elderly
patients with signicant mitral annular
calcication.
The normal mitral valve orice is 4–6cm2 and
when the mitral orice is <2 cm2 the left atrial
pressure rises to generate blood ow across the
narrowed orice into the LV.To compensate for
increased left atrial pressure, both pulmonary
Table 17.3 Causes of mitral stenosis
Rheumatic fever worldwide
Degenerative from age
Congenital
Chest radiation
Systemic lupus
Rheumatoid arthritis
Carcinoid heart disease
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venous and arterial wedge pressures rise, which
contributes to exertional dyspnea. Untreated,
longstanding MS causes passive backward transmission of the elevated left atrial pressure triggering pulmonary arterial constriction, resulting
in pulmonary changes and subsequent pulmonary
hypertension, RV enlargement with tricuspid
regurgitation, and right heart failure [1]. In
patients with severe MS, cardiac output is near
normal at rest but fails to rise substantially with
exertion.
Patients with mitral stenosis are at increased
risk of developing atrial brillation and
thrombi in the left atrium (valvular atrial
brillation).
Symptoms
The most common presenting symptom is exertional dyspnea or cough, followed by exercise
intolerance. Patients may also present with symptoms of right heart failure. Symptoms from MS
are exacerbated by physical exertion, tachycardia, volume shifts, fever, severe anemia, pregnancy, and thyrotoxicosis.
Physical Exam/Cardiac Studies
The mitral stenosis murmur is best heard at the
apex and described as an opening snap with a low
pitched, rumbling, diastolic murmur. It is very
difcult to appreciate.
ECG. If there is left atrial enlargement, it may
be reected by the p wave. In patients with pulmonary hypertensions, the ECG may show right
axis deviation and RV hypertrophy [6].
Echocardiogram. TTE is used to evaluate
mitral leaets along with extent of valvular calcication into the mitral apparatus, the transvalvular gradient, degree of chamber enlargement and
function, concomitant tricuspid valve disease,
and pulmonary pressures. TEE may be used to
obtain superior images of the mitral valve for
planning of intervention (see Fig.17.9).
Fig. 17.9 Echo showing mitral stenosis. Heavily calcied and reduced mobility of the mitral leaets in the left
panel with restricted diastolic mitral ow in the right
panel suggestive of severe mitral stenosis. Note the tricuspid valve is open conrming diastole
174
Adapted from (6)
Stage
Definition Symptoms
Valve AnatomyValve Hemodynamics
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Table 17.4 Stages of mitral stenosis
A. Booke et al.
A At risk of MS
Progressive MS
B
Asymptomatic severe MS
C
Symptomatic severe MS
D
None
None
None
Decreased exercise
tolerance
Extertional dyspnea
Mild valve doming during diastole
Rheumatic valve changes with
commissural fusion and diastolic
doming of the mitral valve leaflets
Planimetered mitral valve area
>1.5 cm
Rheumatic valve changes with
commissural fusion and diastolic
doming of the mitral valve leaflets
Planimetered mitral valve area
£1.5 cm
Rheumatic valve changes with
commissural fusion and diastolic
doming of the mitral valve leaflets
Planimetered mitral valve area
£1.5 cm
Cardiac Catheterization. Left and right heart
catheterization is helpful for hemodynamic
assessment and to assess concomitant disease.
Staging of MS requires the combination of
patient symptomatology, valve anatomy and
hemodynamics, along with assessment of cardiac
consequences from MS, as seen in Table17.4.
Normal transmitral flow velocity
Increased transmitral flow velocities
Mitral valve area >1.5 cm
2
2
2
Diastolic pressure half-time <150 ms
Mitral valve area £1.5 cm
Diastolic pressure half-time ³150 ms
Mitral valve area £1.5 cm
Diastolic pressure half-time ³150 ms
2
2
2
Mitral Stenosis Management
Patients with rheumatic mitral stenosis and valvular atrial brillation, prior embolic event, or LAA
thrombus should be initiated on warfarin (INR goal
2–3). There is no evidence to support DOACs in
atrial brillation secondary to MS. Control or lowering of heart rate with beta blockers or calcium
channel blockers are useful as it lengthens the diastolic lling period, lowers the LA pressure, and
decreases symptoms. Cardioversion may be performed but does not durably restore sinus rhythm.
Amiodarone is most effective in maintaining sinus
rhythm post cardioversion [7]. Diuretics, digoxin,
and ivabradine may also help improve symptoms.
Patients with clinically signicant rheumatic
MS (mitral valve area ≤ 1.5 cm2 and diastolic
mitral gradient ≥5–10 mmHg) should be followed annually with TTE.TTE helps determine
the severity of stenosis and when severe MS is
present will help determine the suitability for
Percutaneous Mitral Balloon Commissurotomy
Fig. 17.10 Yellow arrow shows a markedly enlarged left
atrial appendage (LAA) with the organized thrombus on
CT imaging. DOACs are contraindicated for treatment of
thrombus associated with mitral stenosis
(PMBC) versus surgery. TEE will further evaluate the mitral valve anatomy, presence of MR,
and left atrial appendage thrombus (Fig.17.10).
Degenerative, Nonrheumatic
CalcicMS
Calcic MS is the result of calcication of the mitral
annulus that extends into the leaets bases resulting
in narrowing of the annulus and progressive leaet
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rigidity [1, 8]. There is usually no commissural
fusion and typically the leaet tips are unaffected
[1, 8]. Degenerative MS is usually observed in the
elderly population and progression of MS is variable and may range from 1 to 9 mmHg annually
(Fig.17.9). The prognosis for patients with this type
of MS is extremely poor with a 50% mortality
within 5 years [1]. These patients are typically at
high risk for any intervention given the extent of
calcication, advanced age, and comorbidities.
Medical management is the same as for rheumatic MS.Degenerative MS is not amenable to
PMBC and severe mitral annular calcication
(MAC) limits surgical options given the difculty
in attaching a prosthetic mitral valve and risk of
narrowing the mitral orice. MV repair is usually
not feasible and MV replacement is the treatment
of choice. Due to the risk, current guidelines recommend surgical intervention only once the MS
becomes severe, patient become extremely symptomatic, and medical therapy is no longer effective [1]. The evaluation of transcatheter therapies
(TMVR) in the mitral position is ongoing. A multidisciplinary team approach is essential in these
complex patients.
Rheumatic Mitral Stenosis Intervention
The optimal treatment of patients with rheumatic
MS is either percutaneously mitral balloon commissurotomy (PMBC) or surgery (Fig.7in 2020
AHA/ACC Valve Guidelines [1]). PMBC is performed by advancing balloon catheters across the
mitral valve and expanding them to split the
mitral commissures. Long-term follow-up demonstrated that at 10 years 70–80% of patients
with a good initial PMBC result were free of
symptoms, and 30–40% remained free of symp-
Table 17.5 Contraindications for percutaneous mitral
balloon commissurotomy in rheumatic MS
• Mitral valve area>1.5cm
• Left atrial thrombus
• More than mild MR
• Severe or bicommissural calcication
• Absence of commissural fusion
• Concomitant CAD requiring surgery
• Severe concomitant aortic or tricuspid valve disease
requiring surgery
2
toms out to 20years [9]. In symptomatic patients
with severe rheumatic MS (valve area≤1.5cm2),
< 2+ moderate MR, and absence of LA thrombus,
PMBC is recommended [9]. Contraindications to
PMBC are listed in Table17.5.
An anatomic mitral morphology score can be
used to determine the suitability of PMBC and to
evaluate the appearance of the commissures and
degree of calcication. Clinical factors such as age,
NHYA class, presence/absence of atrial brillation,
and Wilkins score assist in predicting outcome.
The Wilkins score uses echocardiographic param-
eters to grade rheumatic MS for possible PMBV
using characteristics of (1) leaet mobility, (2) leaet
thickening, (3) leaet calcication, and (4) sub valvular thickening. Each characteristic can have four
points if the disease is more severe for a maximum
of 16. A score of <8–9 are considered candidates for
PMBV depending on degree of mitral insufciency
and a score of >9–10, especially with moderate MR
should be considered for surgery.
Mitral valve repair or replacement are both
utilized in the surgical treatment of MS.The surgical approach to MS depends on the pathology
of the disease, the involvement of the valve leaflets, and the extent of calcication present. As
stated above, PMBC is the rst-line therapy for
Rheumatic MS unless contraindicated. According
to the ACC/AHA, MV surgery for rheumatic MS
is warranted in the following patients [1]:
• Severe MS (mitral valve area≤1.8cm2),
• MS with severe limiting symptoms,
• Who are not a candidate for PMBC given
unfavorable valve morphology or presence of
left atrial thrombus,
• Previous failure of PMBC, and
• Already undergoing cardiac surgery for
another reason.
Like PMBC, the preferred approach to surgical
management is mitral valve repair with commissurotomy. During surgical commissurotomy, a
sternotomy is completed, the heart is placed on cardiopulmonary bypass, and under direct visualization the ssure between the mitral leaets is
separated. This technique is not routinely performed by surgeons in the United States and should
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A. Booke et al.
only be completed at experienced centers [1]. If
neither a PMBC repair nor open commissurotomy
can be completed, then a mitral valve replacement
may be considered in rheumatic stenosis.
As with other cardiac surgeries, a detailed history, physical, and a myriad of diagnostic testing
are completed to determine patient’s baseline status and operative risk. As with any valve surgery,
a thorough dental history should be obtained to
rule out a disease process which may put patient
at risk for endocarditis postoperatively. Risk
stratication for MV repair and MV replacement
can be calculated on the STS website. Refer to
Chap. 6, Table 6.3 for a list of categories assessed
with the risk calculator.
Mitral Valve Selection
Provider and patient must jointly decide between a
bioprosthetic and mechanical valve conduit in case
a valve replacement is warranted. This decision is
multifactorial and is based on patient age, life
expectancy, medical compliance, and ability to tolerate long-term systemic anticoagulation. Refer to
the section on valve selection under surgical management of aortic stenosis for further discussion.
The ACC/AHA guidelines for mitral valve
replacement recommend mechanical valves in
patients <65 years old and tissue valves in
patients ≥65years old [1]. A mechanical valve in
the mitral position for mitral stenosis has the
highest long-term embolic risk and requires strict
therapeutic INR levels postoperatively. Refer to
Figs. 11 and 12 for the 2020 AHA/ACC Valve
Fig. 17.11 Mitral valve replacement with a bioprosthetic
valve
Guidelines [1]. Figure 17.11 demonstrates a
mitral valve replacement with a bioprosthetic
valved conduit viewed from the left atrium. The
mitral bioprosthetic conduits are manufactured as
a trileaet valve for structural support.
References
1. Otto CM, Nishimura RA, Bonow RO, Carabello BA,
Erwin JP III, Gentile F. 2020 ACC/AHA Guideline for
the management of patients with valvular heart disease: a report of the American College of Cardiology/
American Heart Association Joint Committee on
clinical practice guidelines. J Am Coll Cardiol.
2021;77(4):e25–e197.
2. Fedak PWM, McCarthy PM, Bonow RO. Evolving
concepts and technologies in mitral valve repair.
Circulation. 2008;117(7):963–74.
3. Gammie JS, Chikwe J, Badhwar V, Thibauld DP,
Vemulapalli S, Thourani VH. Isolated mitral valve
surgery: The Society of Thoracic Surgeons adult
cardiac surgery database analysis. Ann Thorac Surg.
2018;106(3):716–27.
4. Watts TMF, Brescia AA, Murray SL, Burn DA,
Wisniewski A, Romano MA, Bolling SF, Michigan
Mitral Research Group (MMRG). Degenerative mitral
valve repair restores life expectancy. Ann Thorac Surg.
2020;109(3):494–801.
5. Bonow RO, O’Gara PT, Adams DH, Badhwar V,
Bavaria JE, Elmariah S, et al. 2019 AATS/ACC/
SCAI/STS expert consensus systems of care document: operator and institutional recommendations and
requirements for transcatheter mitral valve intervention. J Am Coll Cardiol. 2020;76(1):96–117.
6. Hein M, Schoechlin S, Schulz U, Minners J, Breitbart
P, Lehane C, Neumann F-J, Ruile P.Long-term follow up of hypoattenuated leaet thickening after transcatheter aortic valve replacement. JACC Cardiovasc
Interv. 2022;15(11):1113–22.
7. O'Brien SM, Feng L, He X, Xian Y, Jacobs JP, Badhwar
V, etal. The Society of Thoracic Surgeons 2018 adult
cardiac surgery risk models: part 2- statistical methods and results. Ann Thorac Surg. 2018;105:1419–28.
8. Vahanian A, Beyersdorf F, Praz F, Milojevic M, Baldus
S, Bauersachs J, Capodanno D, Conradi L, De Bonis
M, De Paulis R, Delgado V, Freemantle N, Gilard M,
Haugaa KH, Jeppsson A, Jüni P, Pierard L, Prendergast
BD, Sádaba JR, Tribouilloy C, Wojakowski W, ESC/
EACTS Scientic Document Group, ESC National
Cardiac Societies. 2021 ESC/EACTS Guidelines for
the management of valvular heart disease: developed
by the task force for the management of valvular heart
disease of the European Society of Cardiology (ESC)
and the European Association for Cardio-Thoracic
Surgery (EACTS). Eur Heart J. 2022;43(7):561–632.
9. The Society of Thoracic Surgeons. 2022. https://www.
sts.org/resources/risk- calculator.
Tricuspid Valve Disease
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AnneBooke, MichaelRinaldi, ElisabethA.Powell,
LarryWatts, andRichardMusialowski
18
Tricuspid Insuciency/
Regurgitation (TI/TR)
Etiology
TR is categorized as primary or secondary.
Secondary is more common, occurring in >90%
of patients with TR (Table18.1). At least 70% of
adults have some degree of TR [1]. Most primary
TR is related to implantable devices. Functional
TR is secondary to dilation of the RA/RV annulus with leaet tethering and is associated with
pulmonary hypertension, atrial brillation, cardiomyopathy, and mitral disease. Functional TR
is associated with pulmonary hypertension, RV
dilation, RV infarction, or cardiomyopathy.
Importantly, TR is an independent predictor of
mortality.
In early TR, right atrial dilation occurs, resulting in annular dilatation. This process causes
reduction in leaet coaptation and with progression of TR, adaptive RV dilation occurs with RV
A. Booke · M. Rinaldi · L. Watts · R. Musialowski
Sanger Heart and Vascular Institute, Atrium Health,
Charlotte, NC, USA
e-mail: Anne.Booke@atriumhealth.org;
Michael.Rinaldi@atriumhealth.org;
Larry.Watts@atriumhealth.org;
Richard.musialowski@atriumhealth.org
E. A. Powell (*)
Banner University Medical Center, Tucson, AZ, USA
e-mail: elisabeth.powell@bannerhealth.com
remodeling to maintain cardiac output [2]. This
cycle progresses until clinical signs of right heart
failure develop (see Chap. 22). Severe, refractory
TR is associated with hepatic and renal failure
due to venous hypertension.
Symptoms
Symptoms of TR are due to two pathologic
mechanisms: pulmonary congestion and central
venous congestion. Patients develop fatigue,
exertional dyspnea, and also symptoms associated with right heart failure including orthopnea,
abdominal bloating or right upper abdominal discomfort, PND, and peripheral edema.
Physical exam findings with TR include
systolic murmur that increases in intensity
Table 18.1 Etiology of tricuspid regurgitation
Secondary (normal
Primary (abnormal leaets)
Rheumatic disease LV dysfunction
Congenital heart disease-
Ebstein’s anomaly
Myxomatous changes Pulmonary
Carcinoid heart disease Inltrative disease of
Iatrogenic- device entrapment,
biopsy injury
Radiation Left sided valve
leaets)
RV infarction
hypertension
the RV
Atrial annular dilation
disease
Chronic RV pacing
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
R. Musialowski, K. Allshouse (eds.), Cardiovascular Manual for the Advanced Practice Provider,
https://doi.org/10.1007/978-3-031-35819-7_18
177
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A. Booke et al.
with inspiration, prominent JVD, peripheral
edema, hepatomegaly, ascites, and a third
heart sound that also increases with inspiration (RV S3).
Evaluation
ECG. Usually non-diagnostic, although may see
signs of RA or RV enlargement, bizarre RBBB
pattern, evidence of prior inferior MI, or atrial
brillation [3].
Imaging. The etiology and severity of TR are
assessed by TTE (Fig. 18.1). When indicated,
TEE, MRI, or CT scan may be used to provide
additional information about the tricuspid valve
and RV function. Particular attention should be
paid to TR grade/regurgitant jet, valve morphology (annular dimension, leaet coaptation/tethering), enlargement of RA/RV/IVC to properly
stage TR, pulmonary systolic pressure, and
degree of hepatic vein reversal [4].
Trace to mild degrees of TR are commonly
detected on TTE in patients with normal valves
and are of no physiological consequence [3].
Management
Medical therapy is limited and attention should
be focused on reversing any underlying causes of
TR. Management of heart failure is the rst
approach to management of TR, with the use of
diuretics to treat volume overload and medical
therapy for patients who have pulmonary arterial
hypertension (PAH), particularly WHO type II
(see Chap. 22). Patient with volume overload and
hepatic congestion are more responsive to torsemide over furosemide. Use of loop diuretics can
be limited as RV function worsens or in those
with low output syndrome. Patients with reduced
LVEF contributing to TR should be initiated on
GDMT to ofoad the LV.In patients with TR secondary to annular dilation from atrial brillation
Fig. 18.1 The left panel shows a closed tricuspid valve with defect and annular dilatation. The right panel shows a
green arrow indicating severe secondary tricuspid regurgitation
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it is benecial to restore sinus rhythm. There are
limited options for patients who have advanced
TR with end-stage heart failure and low cardiac
output [3, 4].
Timing of intervention upon the tricuspid
valve is tricky as the disease can progress quickly,
is often associated with concomitant pulmonary
hypertension or permanent atrial brillation, and
also a poor prognosis.
Surgical treatment is performed for select
patients with valvular disease. Surgical intervention should be completed with the presence of
moderate to severe TR at the time of a left-sided
valve operation. Once the left-sided valve lesion
is corrected and there is reduction of the right
ventricular afterload, TR may not improve. If the
TV is not intervened upon at the time of the leftsided valve surgery, there is a 25% chance that
there is progression of the TR if certain risk factors are present [3]. These risk factors include
dilated annulus >4.0 cm, history of right-sided
HF, and atrial brillation [3]. If the TR is not corrected at the time of the initial operation, and
does not improve postoperatively, reoperation for
severe isolated TR is associated with a perioperative mortality of 10–25% [3]. Even in cases
where only mild to moderate secondary TR
exists, tricuspid valve (TV) intervention should
still be considered.
Transcatheter tricuspid valve interventions are
emerging as an alternative for highly symptomatic patients who are felt to be too high risk for
conventional open-heart surgery and research is
ongoing in determining effectiveness. There are
currently no guidelines addressing transcatheter
tricuspid valve therapies. Novel transcatheter
therapies are evolving and include “leaetplasty”
with clip therapy, valve replacement, percutaneous repair, and annuloplasty.
the primary cause for TR stems from left-sided
heart disease, the number one indication for surgical intervention is the presence of severe TR at
the time of a left- sided valve operation [3]. When
possible, a repair should be attempted prior to
replacement. Repairs are preferred to replacement in TR as they do not require long-term anticoagulation, have greater durability, and are
resistant to endocarditis. Repair of the tricuspid
valve usually only requires an annuloplasty ring
or band to decrease annular dilation, create support, and improve coaptation of the leaets. A
TVr with an annuloplasty ring is demonstrated in
Fig.18.2.
Replacement of the tricuspid valve is reasonable when the valve is unrepairable or in select
secondary forms of TR.Valves should undergo
replacement when the TR is a primary defect in
the valve leaet such as with injury from device
leads, endocardial biopsy, trauma, or in infectious endocarditis. TV replacement should also
be completed if a TV repair has failed. A TVR
with a bioprosthetic valve is demonstrated in
Fig.18.3 Guidelines for surgical intervention of
TR are outlined in Fig.10in the 2020 AHA/ACC
Valve Guidelines [3].
Isolated TR intervention is rare and perioperative mortality risk is considered high. Intervention
is more dependent on the presence of right-sided
heart failure, progressive RV dilation, and dysfunction. According to the ACC/AHA guidelines,
isolated TV surgery is considered reasonable in
Surgical Management ofTricuspid
Regurgitation
Surgical treatment of moderate to severe TR can
be accomplished by either tricuspid valve repair
(TVr) or tricuspid valve replacement (TVR). As
Fig. 18.2 Tricuspid valve repair with placement of an
annuloplasty ring
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