Cardiovascular system Surgical Management of Valvular Heart Diseases.pdf

Cardiovascular system Surgical Management of Valvular Heart Diseases

1. CVS II -Surgical Management
of Valvular Heart Diseases

2. Outline
•Valvular Heart Disease
•General Principles
•Surgical Options
•Mitral Valve Disease
•Mitral Stenosis
•Mitral Regurgitation
•Mitral Valve Operative Techniques
and Results
•Aortic Valve Disease
•Aortic Stenosis
•Aortic Insufficiency
•Aortic Valve Operative Techniques
and Results
•Tricuspid Valve Disease
•Tricuspid Stenosis and
Insufficiency / 829
•Multivalve Disease

3. Objective
•To learn the General Principles of ValvularHeart Diseases
•To know the different ValvularHeart Disease
•To understand its Etiology, Clinical Manifestation, Diagnostic
Procedures and their importance
•To know the different surgical procedures of valvularheart diseases

4. General Principles
•The number of patients undergoing surgical management of valvular
heart disease has increased, aortic or mitral valve procedures
reported in 2006 to 2015.
•Congenital and inherited etiologiesrepresent important clinical
entities, age-associated and acquired conditions still represent the
primary causes of valvularheart disease.

5. •The most common screening method for valvularheart disease is
cardiac auscultation, with murmurs classified based primarily on their
timing in the cardiac cycle, but also on their configuration, location
and radiation, pitch, intensity, and duration. (Table 21-6)
•Although some systolic murmurs are related to normal physiologic
increases in blood flow, some may indicate cardiac disease, such as
valvularaortic stenosis (AS), that are important to diagnose, even
when asymptomatic.

6. Classification of Cardiac Murmur

7. •Diastolic and continuous murmurs, on the other hand, are frequently
pathologic in nature.
•Dynamic cardiac auscultation provides further evidence as to the
significance and origin of many murmurs. (Table 21-7)

8. Hemodynamic alterations in cardiac murmur intensity

9. Auscultation provides initial evidence to the
existence of valvulardisease,
•Signs and symptoms may help narrow the diagnosis.
•Abnormalities in the splitting of the heart sounds and additional heart
sounds should be noted, as should the presence of pulmonary rales.
•Peripheral pulses should be checked for abnormal intensity or timing,
and the presence of a jugular venous wave should be documented.
•Syncope, angina pectoris, heart failure, and peripheral
thromboembolismare important and may help guide diagnosis and
management.

10. Examinations that aid in the Diagnosis and
Classification of various Valvular Disorders
•EKG provides information regarding ventricular hypertrophy, atrial
enlargement, arrhythmias, conduction abnormalities, prior
myocardial infarction, and evidence of active ischemia that would
prompt further workup.

11. •Posteroanterior and lateral chest
X-rays are also easy to obtain
and may yield information
regarding cardiac chamber size,
pulmonary blood flow,
pulmonary and systemic venous
pressure, and cardiac
calcifications.

12. •The gold standard for the
evaluation of valvularheart
disease is transthoracic
echocardiography (TTE), which
is helpful in the noninvasive
evaluation of valve morphology
and function, chamber size, wall
thickness, ventricular function,
pulmonary and hepatic vein
flow, and pulmonary artery
pressures.

13. •Valvular heart disease can produce numerous hemodynamic
derangements.
•If left untreated, it can produce significant pressure and volume
overloadon the affected cardiac chamber.

14. •Heart can initially compensate for alterations in cardiac physiology,
cardiac function eventually deteriorates, leading to decreased patient
functional status, ventricular dysfunction, heart failure, and
eventually death.
•In order to optimize long-term survival, surgery or transcatheter
therapeuticsare recommended in various forms of valvularheart
disease and in an increasing number of elderly and high-risk patients.

15. Structural and functional remodelling following pharmacologic intervention in
volume overload heart failure Kristin Lewis, DVM Pathology Resident/Graduate.

16. Surgical Options

17. •Valve repair is indicated in patients
with aortic, mitral or tricuspid
insufficiency,
Mitral valve regurgitation -Symptoms and causes -Mayo Clinic

18. •Valve replacement is appropriate in
certain patient populations, it can
be accomplished with either
mechanical or biological
prostheses,
•Choice of valve depends on many
patient-specific factors such as age,
health status, and desire for future
pregnancy indications or
contraindications to
anticoagulation therapy.
Pinterest
Prosthetic heart valves are classified as either mechanical
...

19. Mechanical Valve
•The first bileafletmechanical valve was introduced in 1977.
•Bileafletvalves are comprised of two semicircularleaflets that open
and close, creating one central and two peripheral orifices
•Bileafletmechanical valves have demonstrated excellent flow
characteristics, low risk of late valve-related complications, including
valve failure, and are currently the most commonly implanted type of
mechanical valve prosthesis in the world

20. Mechanical Valve
•Current options for mechanical
valve replacement include either
tilting disc valves or bileaflet
valves.
•Mechanical valves are highly
durable, but require permanent
anticoagulation to mitigate the
risk of valve thrombosis and
thromboembolic sequelae.
https://www.youtube.com/watch?v=hmU7UtzxowU

21. Tissue Valves
•A xenograftvalve is one
implanted from another species,
such as porcine xenograftvalves,
or manufactured from tissue
such as bovine pericardium.
•Stented bovine pericardial valve
is the most mostcommonly
implanted, and the most popular
valve.
https://www.youtube.com/watch?v=ojW7wZRF7Cg

22. Stentless vsStented
•The chief disadvantage of stented tissue valves is a smaller effective
orifice area, which increases the transvalvulargradient referred to as
patient prosthetic mismatch.
•This effect is most pronounced in patients with small prosthetic valve
areas, specifically <0.85 cm2 valve area per square meter body
surface area and may affect survival, symptomatic improvement, and
the hemodynamic response to exercise following surgery.

23. Interactive CardioVascularand Thoracic Surgery, Volume 30, Issue 3, March 2020, Pages 417–423,
https://doi.org/10.1093/icvts/ivz277

25. Homograft
•Homograft valves from human cadavers, also known as allografts,
have been used for aortic valve replacement since the technique was
originally described over 50 years ago.
•Following harvest, these valves are sterilized using an antibiotic
solution and subsequently stored in fixative or cryopreservation
solution.
•Risk of thromboembolic complications with homograft valves is low,
and systemic anticoagulation therapy is not required.

26. •The major shortcoming of homograft valves is their limited long-term
durability due to tissue degeneration.
•Within one year of implantation, these valves undergo substantial
loss of cellular components and subsequent structural compromise,
which may ultimately lead to valve failure.
•Enhanced preservation techniques has improved cellular viability,
which approaches the 15-year viability of xenograftvalves, the limited
availability of these valves and techniques has limited the use of
homograft tissue valves.

27. Autografts.
•1967, Donald Ross described a procedure in which the diseased aortic
valve was replaced using the patient’s native pulmonary valve as an
autograft, which was in turn replaced with a homograft in the
pulmonic position.
•The procedure resulted in minimal transvalvulargradients and
favorable left ventricular mechanics, both at rest and during exercise.
•Known as the Ross procedure, this operation has been shown to be
particularly beneficial in children, as the pulmonary trunk grows with
the child and long-term anticoagulation is not required.

28. Valve Repair.
•Offers a number of advantages over valve replacement, due in large
part to the preservation of the patient’s native valvularand
subvalvularapparatus.
•Avoids the risks of chronic anticoagulation, infection,
thromboembolic complications, and prosthetic valve failure after
surgery.
•In the case of MV repair, freedom from reoperation and valve-related
complications has been excellent in certain patient populations, even
at 20-year follow-up.

29. MITRAL VALVE DISEASE

30. Mitral Stenosis
•Etiology.
•Acquired mitral stenosis (MS) is
most often caused by rheumatic
fever, with approximately 60% of
patients with pure MS
presenting with a clinical history
of rheumatic heart disease.

31. •Acquired causes of MV stenosis include left atrial myxoma, prosthetic
valve thrombosis, mucopolysaccharidosis, previous chest radiation,
and severe annular calcification.

32. Clinical Manifestations
•The first clinical signs of MS are those associated with pulmonary
venous congestion, namely exertionaldyspnea, decreased exercise
capacity, orthopnea, and paroxysmal nocturnal dyspnea.
•Hemoptysis and pulmonary edema may develop as the venous
hypertension worsens.
•Advanced MS can also cause pulmonary arterial hypertension and
subsequent right heart failure, manifested as jugular venous
distention, hepatomegaly, ascites, and lower extremity edema.

33. •Atrial fibrillation may develop as left atrial pathology worsens, causing
atrial stasis and subsequent thromboembolism.
•Patients with MS may initially present with signs of arterial
embolization, even rarely with angina from coronary occlusion.

34. Diagnostic Studies.
•EKG -atrial fibrillation, left atrial enlargement, or right axis deviation
•Chest X ray -enlargement of the left atrium and pulmonary artery,
creating a double contour behind the right atrial shadow and
obliterating the normal concavity between the aorta and left
ventricle. Findings consistent with pulmonary congestion may also be
present

35. •The diagnostic tool of choice is TTE, use to calculate the MV area and
to determine the morphology of the MV apparatus, including leaflet
mobility and flexibility, leaflet thickness and calcification, subvalvular
fusion, and the appearance of the commissures.

36. Indications for Operation
•Depending on the severityand the morphology of the diseased MV
(see Table 21-8), balloon commissurotomy, surgical repair, or MV
replacement may be indicated for the treatment of MS (Table 21-9).
http://hridayasamvad.blogspot.com/2014/06/rheumatic-heart-disease.html

37. Severity and the morphology of the diseased
MV

38. Guidelines for MV Surgery

40. Mitral Regurgitation
•Etiology.
•The most important cause of MR is myxomatousdegenerative disease
of the MV, which occurs in 2% to 3% of the population.
•Other important causes of MR include rheumatic heart disease,
infective endocarditis, ischemic heart disease, and dilated
cardiomyopathies.
•Less frequently, MR can be caused by collagen vascular diseases,
trauma, previous chest radiation, hypereosinophilicsyndrome,
carcinoid disease, and exposure to certain drugs.

41. Clinical Manifestations.
•Acute severe MR, patients are often symptomatic and present with
pulmonary congestion and reduced stroke volume.
•In severe cases, patients may present with cardiogenic shock.
•Because the LV has not remodeledin the acute setting, a
hyperdynamicapical impulse may not be present in the precordium.
•The typical systolic murmur of MR may be holosystolicor absent,
with a third heart sound and/or diastolic flow murmur being the only
auscultatoryfindings.

42. •Chronic MR, asymptomatic for long periods of time due to the
compensatory mechanisms of the remodeledLV.
•LV begins to fail, patients become increasingly symptomatic from
exertionaldyspnea, decreased exercise capacity, orthopnea, and
eventually pulmonary hypertension and right heart failure.

43. Physical examination
•Demonstrate displacement of the LV apical impulse due to cardiac
enlargement from chronic volume overload, a third heart sound, or
an early diastolic flow rumble.
•The characteristic auscultatoryfindings also include an apical systolic
murmur, which is variably transmitted to the axilla or the left sternal
border, depending on the location of the pathology.
•Patients may present with AF due to dilatation of the left atrium.
•Findings consistent with pulmonary hypertensionindicate late-stage
disease.

44. Diagnostic Studies
•Chronic MR, ECG and chest X-ray are performed to assess rhythm
status and the degree of pulmonary vascular congestion.
•An initial 2D and Doppler TTE should be performed for a baseline
estimation of LV and left atrial size, LV systolic function, pulmonary
artery pressure, MV morphology, and MR severity.

45. Indications for Operation
•Based on the etiology, morphology, and severity of MR (see Table 21-
8), MV repair, MV replacement with preservation of part or all of the
mitral apparatus may be variably performed for the treatment of MR.
•As the intraoperative findings may dictate MV replacement whenever
a MV repair is planned, current recommendations are for MV surgery
in general (see Table 21-9)

47. Mitral Valve Operative Techniques and Results
•Mitral valve surgery is performed on the arrested heart with the
assistance of cardiopulmonary bypass.
https://www.youtube.com/watch?v=0oZJaeXZO6o

48. Mitral Valve Operative Techniques and Results
•Traditionally, a median sternotomy incision has been used; however,
the left atrium can also be approached via minimally invasive
incisions, such as a right thoracotomy, or a fully endoscopic approach.

49. Mitral Valve Operative Techniques and Results
•The MV is commonly exposed
through a left atrial incision
placed posterior and parallel to
the intra-atrial groove or via a
transseptalapproach through
the right atrium.
https://www.hopkinsmedicine.org/health/treatment-tests-
and-therapies/left-atrial-appendage-closure-procedures

50. Commissurotomy.
•Upon opening the left atrium,
the MV is visualized and the left
atrium is examined for
thrombus.
•A nerve hook or right-angle
clamp is subsequently
introduced beneath the
commissures and used to
evaluate the MV apparatus for
leaflet mobility, commissural
fusion, and subvalvularchordal
abnormalities.
https://www.mitralvalverepair.org/commissures

51. Commissurotomy.
•The commissurotomyis generally stopped 1 to 2 mm from the
annulus where the leaflet tissue thins, indicating the transition to
normal commissural tissue.
•The papillary muscles are subsequently examined and incised as
necessary in order to maximize the mobility of the leaflets.

52. •After the commissurotomyis complete and the associated chordae
tendineaeand papillary muscles are mobilized, leaflet mobility is
assessed.
•The anterior leaflet is grasped with forceps and brought through its
complete range of motion.
•If subvalvularrestriction or leaflet rigidity is identified, further division
or excision of fused chordae and debridement of calcium may be
necessary.
•Occasionally, the leaflets can be debrided carefully to increase
mobility.

53. •In rheumatic patients, the thickened leaflets can be thinned by careful
dissection.
•Valve replacement may be more appropriate if extensive secondary
mobilization is required.
•At the end of the procedure, competence of the valve is assessed
with injection of cold saline into the ventricle.

54. •Open surgical commissurotomyhas an operative risk of <1%, and has
been shown to have good long-term results, with freedom from
reoperation as high as 88.5%, 80.3%, and 78.7% at 10, 20, and 30
years, respectively.
•The incidence of postoperative thromboembolic complications is
generally <1% per patient-year, and the lack of required systemic
anticoagulation precludes the development of hemorrhagic
complications long term.
•In some institutions, balloon valvuloplastyhas replaced
commissurotomy.

55. Mitral Valve Replacement
•If your mitral valve can't be repaired, recommend mitral valve
replacement.
•In this procedure, the diseased mitral valve is remove and replaces it
with a mechanical valve or a tissue valve made from cow, pig or
human heart tissue.
https://www.mayoclinic.org/tests-procedures/mitral-valve-repair-mitral-valve-replacement/about/pac-20384958

56. Mitral Valve Replacement

57. Mitral Valve Repair
•There are many techniques available for
MV repair that are variably used
depending on the preoperative and
intraoperative assessment of valvular
pathology.

58. •On opening the atrium, the endocardium is examined for a jet lesion
(a roughened area caused by a regurgitantjet striking the wall), in
order to better localize the area of valvularinsufficiency.
•The commissures are examined for evidence of prolapse, fusion, and
malformation.
•The subvalvularapparatus and individual leaflets are examined for
areas of prolapse, restriction, fibrosis, and calcifications .

59. •Leaflet perforations are generally repaired primarily, or with a
pericardial patch.
•The degree of annular dilation is also noted.
•The basic components of MV repair based on this assessment may
include resection of the posterior and/or anterior leaflet, chordal
shortening, chordaltransposition, artificial chordalreplacement,
and annuloplasty.
•Recent trends have been toward leaflet preservation.

60. •One of the mainstays of MV repair is triangular resection of the
posterior leaflet.
•Excision of the diseased leaflet tissue extends down towards but
generally not to the mitral annulus.
•After repair has been completed, valvularcompetency is evaluated by
injecting saline into the ventricle with a bulb syringe and assessing
leaflet mobility and apposition.
•If focal insufficiency is identified in other areas, additional procedures
are performed.

61. •The anterior leaflet may be repaired via chordalshortening, chordal
transposition, artificial chordalreplacement, and triangular resection
of the anterior leaflet.
•Chordalshortening has generally been abandoned in favor of chordal
replacement.

62. •Annular dilation is generally corrected using a MV annuloplasty
device, such as a ring or partial band.
•Annuloplastyis known to improve the durability of all types of MV
repair

63. TranscatheterMitral Valve Repair and
Replacement.
•Transcathetermitral valve repair is now in clinical use in patients with
chronic severe primary MR in whom surgery would be too great a
risk, as judged by a heart team approach including a cardiologist
skilled in structural heart intervention and an experienced mitral
valve surgeon.

64. AORTIC VALVE DISEASE

65. Aortic Stenosis
•Etiology.
•The most common cause of adult aortic stenosis (AS) is calcification of
a normal trileafletor congenital bicuspid aortic valve, particularly in
patients >70 years of age, and rheumatic heart disease.

67. Clinical Manifestations
•The characteristic auscultatoryfindings of AS include a harsh,
crescendo-decrescendo systolic murmurat the right second or third
intercostal space, often with radiation to the carotid arteries.
•As the disease progresses, aortic valve closure may follow pulmonic
valve closure, causing paradoxical splitting of the second heart sound.
•Other physical findings associated with AS include an apical impulse
commonly described as a “prolonged heave,” and the presence of a
narrow and sustained peripheral pulse, known as pulsusparvuset
tardus.
•The classic symptoms of AS are exertionaldyspnea, angina, and
syncope

68. Diagnostic Studies
•EKG –evidence of LV hypertrophy is found in 85% of patients with AS,
the correlation between the absolute electrocardiographic voltages in
precordial leads and the severity of AS is poor.
•Signs of left atrial enlargement and various forms and degrees of
atrioventricularor intraventricularblock due to calcific infiltration of
the conduction system.

69. •Routine chest X-ray usually demonstrates a normal heart size, with
rounding of the left ventricular border and apex.
•A late finding on chest X-ray is cardiac enlargement, or cardiomegaly,
a sign of LV failure.

70. •Transthoracic echocardiography is indicated in all patients with a
systolic murmur graded ≥2/6, a single second heart sound, or
symptoms characteristic of AS.
•Initial TTE examinations are often diagnostic and provide an
assessment of left ventricular size and function, the degree of left
ventricular hypertrophy, the degree of valvularcalcification, and the
presence of other associated valvulardisease.
•Doppler evaluation should be performed to define the maximum jet
velocity, which is a useful measure for following disease severity and
predicting clinical outcome

71. Indications for Operation.
•Based on the severity of AS (Table 21-10) and the predicted risk with
surgical aortic valve replacement (SAVR) determined using the STS
risk calculator, SAVR or transcatheteraortic valve replacement (TAVR)
may be recommended for the treatment of AS (Table 21-11).

73. Aortic Insufficiency
•Etiology.
•The most common cause of isolated aortic insufficiency (AI) in
patients undergoing AVR is aortic root disease, and it represents over
50% of such patients in some studies.

74. •Other common causes of AI include congenital abnormalities of the
aortic valve such as bicuspid aortic valve, calcific degeneration,
rheumatic disease, infective endocarditis, systemic hypertension,
myxomatousdegeneration, dissection of the ascending aorta, and
Marfansyndrome.
•Less common causes of AI include traumatic injuries to the aortic
valve, ankylosingspondylitis, syphilitic aortitis, rheumatoid arthritis,
osteogenesisimperfecta, giant cell aortitis, Ehlers-Danlossyndrome,
Reiter’s syndrome, discrete subaorticstenosis, and ventricular septal
defects with prolapse of an aortic cusp

75. Clinical Manifestations
•In cases of acute severe AI, patients are symptomatic and invariably
present with compensatory tachycardia, often associated with acute
pulmonary congestion and cardiogenic shock.

76. •Patients with chronic AI, symptoms of heart failure and myocardial
ischemia develop after the compensatory phase.
•Patients gradually begin to complain of exertionaldyspnea fatigue,
orthopnea, and paroxysmal nocturnal dyspnea, often after significant
myocardial dysfunction has developed.
•Angina is a common complaint late in the course, especially during
sleep when heart rate slows and arterial diastolic pressure falls

78. Diagnostic Studies
•In the acute setting, TTE should be performed to confirm the
presence and severity of aortic regurgitation, the degree of
pulmonary hypertension, and the cause of valvulardysfunction.
•When aortic dissection is suspected as the cause of acute AI, TEE or
chest CT angiography may be substituted if more readily available.
•In patients with confirmed aortic dissection, cardiac catheterization
and coronary angiography are rarely indicated and can delay life-
saving urgent surgical intervention.

79. •In cases of chronic AI, the ECG frequently demonstrates left axis
deviation and, late in the course, intraventricularconduction defects
associated with left ventricular dysfunction.

80. •On chest X-ray, the left ventricle enlarges predominantly in an inferior
and leftward direction, causing marked increase in the long axis
diameter of the heart, frequently with little or no change in the
transverse diameter.
•The chest X-ray should be examined for aneurysmal dilation of the
aorta.

81. •An initial TTE should be performed to confirm the diagnosis and
severity of AI, assess the cause of AI (including valve morphology and
aortic root size and morphology), and assess the degree of left
ventricular hypertrophy, volume, and systolic function.
•Follow-up TTE is indicated on an annual or semiannualbasis in
patients with asymptomatic moderate to severe AI in order to assess
changes from baseline parameters and direct the timing of surgery.
•Any abrupt change in signs or symptoms in a patient with chronic AI is
an indication for TTE examination.

82. Indications for Operation
•Based on the morphology and severity of valve dysfunction (Table 21-
10), AV repair or replacement may be performed for the treatment of
AI (Table 21-11).
•Although the indications for AV repair and AV replacement do not
differ, it is recommended that AV repair be performed only in those
surgical centersthat have developed the appropriate technical
expertise, gained experience in patient selection, and which have
demonstrated outcomes equivalent to those of valve replacement.

83. Peri-operative evaluation
•Trans-esophageal echo (TTE) affords an excellent tool for the
diagnosis of the mechanism of aortic regurgitation and is essential
intra-operatively to assess the quality of the repair.
•The two dimensional axial and longitudinal views of the aortic root
allow measurement of the aortic annulus, ascending aorta, as well
aortic cusp free margin diameters.
•The plane of coaptationand leaflet prolapse or folding can be easily
demonstrated.

84. Aortic Valve Operative Techniques and Results
•Aortic valve surgery has traditionally been performed through a
median sternotomy with the assistance of cardiopulmonary bypass.
•However, minimally invasive incisions for aortic valve surgery have
been introduced, including mini-sternotomy and mini-thoracotomy
approaches.
•After the aorta is cross-clamped, cold blood cardioplegiais delivered
antegradethrough the aortic root and/or retrograde through the
coronary sinus.

85. Aortic Valve Replacement
•During aortic valve replacement, an aortotomyis performed, extending medially
from approximately 1 to 2 cm above the right coronary artery and inferiorly into
the noncoronarysinus.
•The valve is completely excised.
•The annulus is thoroughly debrided of calcium deposits.
•At this point, the annulus is sized and an appropriate prosthesis is selected.
•Pledgetedhorizontal mattress sutures are then placed into the aortic valve
annulus and subsequently through the sewing ring of the prosthetic valve, taking
care to avoid damage to the coronary ostia, the conduction system, and the MV
apparatus.
•The annular sutures may be placed from below the annulus, seating the valve
supra-annularly, or from above the annulus for intra-annular placement (Fig. 21-
11).

86. •The major components to increased operative risk associated with
surgical AVR include age, body surface area, diabetes, renal failure,
hypertension, chronic lung disease, peripheral vascular disease,
neurologic events, infectious endocarditis, previous cardiac surgery,
myocardial infarction, cardiogenic shock, NYHA functional status, and
pulmonary hypertension.

88. Aortic Valve Repair
•Aortic valve repair is usually performed through traditional open-
heart surgery and opening of the chest bone (sternotomy).
•Doctors wire the bone back together after the procedure to prevent
movement and aid in healing.

89. Aortic valve repair procedures may involve
several different types of repair, including:
1.Inserting tissue to patch holes or tears in the flaps (perforated
cusps) that close off the valve
2.Adding support at the base or roots of the valve
3.Separating fused valve cusps
4.Reshaping or removing tissue to allow the valve to close more
tightly
5.Tightening or reinforcing the ring around a valve (annulus) by
implanting an artificial ring (annuloplasty)

90. •Intra-operative technique
•Access to the heart is obtained via median sternotomy.
•Cardiopulmonary bypass with ascending aorta, femoral or axillary
artery cannulationmay be required depending on the specifics of
concomitant ascending arch pathology.

91. TranscatheterAortic Valve Replacement
2types of transcathetervalves
approved for commercial use:
1.Balloon-expandable valve
(Edwards)
2.Self-expandable valve
(CoreValve).

92. •A transcathetervalve may be inserted via the femoral artery, the left
subclavianartery, the ascending thoracic aorta via an upper mini-
sternotomy, or LV apex via a small left anterior thoracotomy.
•The most common route is transfemoral, making up the majority of
TAVR in most centers.
•The principle of valves placed via these routes are to place the aortic
prosthesis inside the patient’s native aortic valve.
•Rigorous preoperative planning is needed to ensure adequate sizing
of the valve as well as placement to ensure there is no risk of
coronary occlusion or malalignmentof the valve.

93. TranscatheterAortic Valve Replacement

94. TRICUSPID VALVE DISEASE

95. Tricuspid Stenosis and Insufficiency
•Etiology.
•Acquired tricuspid valve (TV) disease can be classified as either organic or
functional and affects approximately 0.8% of the general population.
•Tricuspid stenosis (TS) is almost always a result of rheumatic heart disease
or rarely endocarditis.
•In the case of rheumatic disease, tricuspid stenosis with or without
associated insufficiency is invariably associated with mitral valve disease.
•Other less common causes of obstruction to right atrial emptying include
congenital tricuspid atresia, right atrial tumors, and endomyocardial
fibrosis.

96. •Tricuspid insufficiency (TR) is most often a functional disease caused
by secondary dilation of the tricuspid annulus due to pulmonary
hypertension and/or right heart failure.
•This is most commonly caused by MV disease.
•Conditions such as right ventricular infarction and pulmonic stenosis
can also lead to increased right ventricular pressures and functional
TR.
•The less common causes of organic TR, with or without associated
stenosis, include endocarditis, carcinoid syndrome, radiation therapy,
trauma such as repeated endomyocardialbiopsy, and Marfan
syndrome.

97. Clinical Manifestations
•Patients with TS and severe TR develop symptoms of right heart
failure associated with chronically elevated right atrial pressures.
•The classic clinical signs and symptoms of TS and severe TR are jugular
venous distention, hepatomegaly, splenomegaly, ascites, and lower
extremity edema.
•Uncomfortable fluttering in the neck has been reported in patients
with TV disease, and sensations of throbbing in the eyeballs and
pulsatile varicose veins have been reported to occur, especially in
patients with severe TR

98. •The low cardiac output syndrome occasionally associated with TS and
severe TR can cause fatigue, weakness, and exercise intolerance in
these patients.
•In the absence of pulmonary hypertension, dyspnea is not a
prominent feature of tricuspid disease.

99. Diagnostic Studies
•Chest X-ray frequently demonstrates enlargement of the right atrium
and ventricle.
•TTE examination should be performed in patients with TV disease in
order to characterize the structure and motion of the TV, the size of
the tricuspid annulus, and other cardiac abnormalities that may affect
TV function.

100. Indications for Operation
•As an isolated lesion, mild or moderate TV disease does not require surgical
correction.
•However, patients with severe TV disease should be considered for surgical
intervention, especially in the setting of right ventricular enlargement and
impaired systolic function, as this improves life expectancy and the
development of sequelae such as heart failure and atrial fibrillation.
•Depending on the patient’s clinical status and the cause of TV dysfunction,
TV repair and TV replacement be variably recommended for the treatment
of TV dysfunction (Table 21-12).98
•In patients with TR, the valve can usually be repaired with modern
techniques.

102. Operative Techniques and Results
•TV can be approached through a median sternotomy, a right
thoracotomy, or port-based techniques.
•Surgery is performed with the assistance of cardiopulmonary bypass
and, though TV surgery is usually performed on the beating heart, a
brief period of cardioplegicarrest may be rarely needed to allow for
complete inspection of the interatrialseptum and to close any defects
that may be present.

103. •TV repair include a suture or ring annuloplastyas well as
valvuloplasty, bicuspidizationof the TV was accomplished by a figure-
of-eight suture plication of the annulus of the posterior leaflet; suture
or ring annuloplasty.

104. •Suture annuloplastyis generally performed by placing pledgeted
sutures along the base of the anterior and posterior leaflets, partially
encircling the annulus.
•Ring annuloplastycan be accomplished by suturing the TV annulus to
a variety of rigid or semirigidannuloplastyrings, which generally have
an opening at the level of the anteroseptalcommissure to avoid
passing the anchoring sutures near to the conduction system.

105. •Most surgeons favor ring over suture annuloplasty.
•In severe annular dilatation, augmentation of the anterior leaflet with
autologous pericardium has been used with some success.
•Tricuspid valvuloplastyis infrequently performed and may include
commissurotomy, triangular leaflet resection,

106. Multivalve Disease
•Pathology involving multiple valves is relatively common and may
result from diseases such as rheumatic fever, calcific disease, Marfan
syndrome, and other connective tissue disorders.

107. •In patients with multivalve disease, the clinical manifestations may be
dependent on the severity of each individual valve lesion, but this is
not always the case.
•In patients with concomitant mitral and tricuspid dysfunction, the
prominent symptoms of dyspnea, paroxysmal nocturnal dyspnea, and
orthopnea commonly associated with MV dysfunction are sometimes
diminished by associated TV dysfunction.

108. •Symptoms of multivalve disease are most commonly masked when
valvularabnormalities are of approximately equal severity,
highlighting the importance of careful examination of each valve both
preoperatively and in the operating room

109. •Surgery for multivalve disease is associated with a higher
perioperative mortality than single-valve procedures, and this risk is
exacerbated by factors such as pulmonary artery hypertension, age,
triple-valve procedures, concomitant coronary artery bypass grafting,
previous heart surgery, renal insufficiency, and diabetes.

110. •Failure to recognize significant concomitant valvulardysfunction at
the time of surgery is also associated with higher perioperative
mortality.
•Patients with multivalve involvement should undergo full
preoperative Doppler TTE or TEE evaluation and heart catheterization.
•In selected patients, procedures correcting multivalve disease
demonstrate significant clinical improvement in symptoms and
quality of life, as well as acceptable mortality and survival rates.