TRICUSPID, PULMONIC AND

MULTIVALVULAR DISEASES
Brook A. June/2016
Braunwald 10th ed.
Harrison’s 19th ed.
Other online sources
OUTLINE
 Tricuspid Valve
 Tricuspid Stenosis
 Tricuspid Regurgitation

 Pulmonic valve disorders

 Multiple/Mixed VHDs
TRICUSPID VALVE
TRICUSPID STENOSIS (TS)
 TS which is much less prevalent than MS is
generally rheumatic in origin
 More common in women than men.

 It does not occur as an isolated lesion and is

usually associated with MS.
 Hemodynamically significant TS occurs in 5–10%
of patients with severe MS
 Rheumatic TS is commonly associated with some
degree of TR.
TRICUSPID STENOSIS (TS)
 Nonrheumatic causes of TS are rare and include
 Congenital tricuspid atresia
 Right atrial tumors, which may produce a clinical
picture suggesting rapidly progressive TSand
 The carcinoid syndrome, which more frequently
produces TR.

 Rarely, obstruction to RV inflow can be caused by

 Endomyocardial fibrosis,
 Tricuspid valve vegetations,
 A pacemaker lead, or
 Extracardiac tumors.
TRICUSPID STENOSIS (TS)
 The anatomic changes of rheumatic TS resemble
those of MS
 Fusion and shortening of the chordae tendineae and
fusion of the leaflets at their edges, producing a
diaphragm with a fixed central aperture.
 However, valvular calcification is rare.

 The right atrium often is greatly dilated in TS,

and its walls are thickened.
 There may be evidence of severe passive
congestion, with enlargement of the liver and
spleen.
TS: PATHOPHYSIOLOGY
 A diastolic pressure gradient between the RA
and RV defines TS.
 It is augmented when the transvalvular blood flow
increases during inspiration and declines during
expiration.

A relatively modest diastolic pressure gradient (i.e.,

a mean gradient of only 5 mm Hg) usually is
sufficient to elevate the mean right atrial pressure
to levels that result in systemic venous congestion
and, unless sodium intake has been restricted or
diuretics have been given, is associated ultimately
with jugular venous distention, ascites, and edema.
TS: PATHOPHYSIOLOGY
 In patients with sinus rhythm, the RA a wave
may be extremely tall and may even approach the
level of the RV systolic pressure.
 The y descent is prolonged.

 The CO at rest is usually depressed, and it fails

to rise during exercise.
 The low CO is responsible for the normal or only
slightly elevated LA, PA, and RV systolic pressures
despite the presence of MS.
 Thus, the presence of TS can mask the hemodynamic
and clinical features of any associated MS
TS: PATHOPHYSIOLOGY
 A mean diastolic pressure gradient across the
tricuspid valve as low as 2 mm Hg is sufficient to
establish the diagnosis of TS.
 However, exercise, deep inspiration, and the rapid
infusion of fluids or the administration of atropine
may greatly enhance a borderline pressure gradient
in a patient with TS.
 Therefore, when this diagnosis is suspected, right
atrial and RV pressures should be recorded
simultaneously, using two catheters or a single
catheter with a double lumen, with one lumen opening
on either side of the tricuspid valve.
 The effects of respiration on any pressure
difference should be assessed as well.
TS: SYMPTOMS
 Because the development of MS generally
precedes that of TS, many patients initially have
symptoms of pulmonary congestion and fatigue.

 Characteristically, patients with severe TS

complain of relatively little dyspnea for the
degree of hepatomegaly, ascites, and edema that
they have.
TS: SYMPTOMS
 However, fatigue secondary to a low CO and
discomfort due to refractory edema, ascites,
and marked hepatomegaly are common in patients
with TS and/or TR.

 In some patients, TS may be suspected for the

first time when symptoms of right-sided failure
persist after an adequate mitral valvotomy.
TS: PHYSICAL FINDINGS
 Because TS usually occurs in the presence of
other obvious valvular disease, the diagnosis may
be missed unless it is considered.

 Severe TS is associated with marked hepatic

congestion, often resulting in cirrhosis, jaundice,
serious malnutrition, anasarca, and ascites.

 Congestive hepatomegaly and, in cases of severe

tricuspid valve disease, splenomegaly are
present.
TS: PHYSICAL FINDINGS
 The jugular veins are distended, and in patients
with sinus rhythm there may be giant a waves.
 The v waves are less conspicuous, and because
tricuspid obstruction impedes RA emptying during
diastole, there is a slow y descent.

 In patients with sinus rhythm there may be

prominent presystolic pulsations of the enlarged
liver as well
TS: PHYSICAL FINDINGS
 On auscultation, an OS of the tricuspid valve
may rarely be heard approximately 0.06 s after
pulmonic valve closure.

 The diastolic murmur of TS has many of the

qualities of the diastolic murmur of MS, and
because TS almost always occurs in the presence
of MS, it may be missed.
 However, the tricuspid murmur is generally heard
best along the left lower sternal border and over the
xiphoid process, and is most prominent during
presystole in patients with sinus rhythm.
TS: PHYSICAL FINDINGS
 The murmur of TS is augmented during
inspiration, and it is reduced during expiration
and particularly during the strain phase of the
Valsalva maneuver, when tricuspid transvalvular
flow is reduced.

 TS vs MS (In summary)
 Positionof the murmur
 Mid-diastolic for MS & Presystolic for TS
 Respiratory variation with TS
TS: INVESTIGATIONS
 ECG: features of RA enlargement*
 The absence of ECG evidence of right ventricular
hypertrophy (RVH) in a patient with right-sided
heart failure who is believed to have MS should
suggest associated tricuspid valve disease.

 CXR: with combined TS and MS shows particular

prominence of the RA and superior vena cava
without much enlargement of the PA and with
less evidence of pulmonary vascular congestion
than occurs in patients with isolated MS.
TS: INVESTIGATIONS
 Echocardiography: The tricuspid valve is usually
thickened and domes in diastole;
 The transvalvular gradient can be estimated
routinely by continuous wave Doppler
echocardiography.
 TTE provides additional information regarding mitral
valve structure and function, LV and RV size and
function, and PA pressure.
TS: STAGES
TS: TREATMENT
 Patients with TS generally exhibit marked
systemic venous congestion.

 Intensive salt restriction, bed rest, and diuretic

therapy are required during the preoperative
period.
 Such a preparatory period may diminish hepatic
congestion and thereby improve hepatic function
sufficiently so that the risks of operation,
particularly bleeding, are diminished.
TS: TREATMENT
 Surgical treatment of TS should be carried out
at the time of mitral valve repair or replacement
in patients with TS in whom
 The mean diastolic pressure gradient exceeds 5 mm
Hg and
 The tricuspid orifice is less than approximately 2.0
cm2.

 The final decision concerning surgical treatment

often is made at the operating table
TS: TREATMENT
 Because TS almost always is accompanied by
some TR, simple finger fracture valvotomy may
not result in significant hemodynamic
improvement but may merely substitute severe
TR for TS.

 However, open valvotomy in which the stenotic

tricuspid valve is converted into a functionally
bicuspid valve may result in substantial
improvement.
TS: TREATMENT
 The commissures between the anterior and
septal leaflets and between the posterior and
septal leaflets are opened.

 It is not advisable to open the commissure

between the anterior and posterior leaflets for
fear of producing severe TR.
TS: TREATMENT
 If open valvotomy does not restore reasonably
normal valve function, the tricuspid valve may
have to be replaced.

 A large bioprosthesis is preferred to a

mechanical prosthesis in the tricuspid position
because of
 The high risk of thrombosis of the latter* and
 The longer durability of bioprostheses in the
tricuspid than in the mitral or aortic positions.
TRICUSPID REGURGITATION (TR)
 Most commonly, TR is secondary to marked
dilation of the tricuspid annulus from RV
enlargement due to PA hypertension

 Functional TR may complicate RV enlargement of

any cause, including an inferior MI that involves
the RV
TRICUSPID REGURGITATION (TR)
 Functional TR is commonly seen in
 The late stages of heart failure due to rheumatic or
congenital heart disease with severe PA hypertension
 Ischemic and idiopathic dilated cardiomyopathies

 It is reversible in part if PA hypertension can be

relieved.

 Rheumatic fever may produce organic (primary)

TR, often associated with TS
TRICUSPID REGURGITATION (TR)
 Infarction of RV papillary muscles, tricuspid
valve prolapse, carcinoid heart disease,
endomyocardial fibrosis, radiation, infective
endocarditis, and trauma all may produce TR.
 Less commonly, TR results from congenitally
deformed tricuspid valves, and it occurs with
defects of the atrioventricular canal, as well as
with Ebstein's malformation of the tricuspid
valve.
 TR also develops eventually in patients with
chronic RV apical pacing.
TRICUSPID REGURGITATION (TR)
 TR or the combination of TR and TS is an
important feature of the carcinoid syndrome
 Leads to focal or diffuse deposits of fibrous tissue
on the endocardium of the valvular cusps and cardiac
chambers and on the intima of the great veins and
coronary sinus

 Carcinoid plaques are most extensive on the right

side of the heart, where they usually are deposited
on the ventricular surfaces of the tricuspid valve and
cause the cusps to adhere to the underlying RV wall,
thereby producing TR.
TR: CLINICAL FEATURES
 In the absence of pulmonary hypertension, TR
generally is well tolerated.

 However, when pulmonary hypertension and TR

coexist, cardiac output declines and the
manifestations of right-sided heart failure
become intensified.

 Thus the symptoms of TR result from a reduced

cardiac output and from ascites, painful
congestive hepatomegaly, and massive edema.
TR: CLINICAL FEATURES
 With the onset of TR in patients with PA
hypertension, symptoms of pulmonary congestion
diminish, but the clinical manifestations of right-
sided heart failure become intensified.

 Occasionally, patients exhibit throbbing

pulsations in the neck, which intensify on effort
and are caused by jugular venous distention
 Systolicpulsations of the eyeballs also have been
described.
TR: CLINICAL FEATURES
 In the many patients with TR who have mitral
valve disease, the symptoms of the latter usually
predominate.

 Symptoms of pulmonary congestion may abate as

TR develops but are replaced by weakness,
fatigue, and other manifestations of a depressed
cardiac output.
TR: CLINICAL FEATURES
 Jugular Venous Pulse
 The neck veins are distended with prominent v waves
and rapid y descents, marked hepatomegaly, ascites,
pleural effusions, edema, systolic pulsations of the
liver, and a positive hepatojugular reflex.

A venous systolic thrill and murmur in the neck may

be present in patients with severe TR
TR: CLINICAL FEATURES
 Palpation
 The RV impulse is hyperdynamic and thrusting in
quality.

 Systolic
pulsations of an enlarged tender liver are
commonly present initially.

 However, in patients with chronic TR and congestive

cirrhosis, the liver may become firm and nontender.
Ascites and edema are frequent.
TR: CLINICAL FEATURES
 Auscultation
 Usually reveals a S3 originating from the RV, which
is accentuated by inspiration.

 P2 accentuation: when TR is associated with and

secondary to pulmonary hypertension
TR: CLINICAL FEATURES
 Auscultation
 TR in the presence of pulmonary hypertension
 The systolic murmur usually is high-pitched, pansystolic, and
loudest in the fourth intercostal space in the parasternal
region but occasionally is loudest in the subxiphoid area.
 When it is mild, the murmur may be of short duration

 TR in the absence of pulmonary hypertension

 E.g., in infective endocarditis or after trauma
 The murmur usually is of low intensity and limited to the

first half of systole

 When the RV is greatly dilated and occupies the
anterior surface of the heart, the murmur may be
prominent at the apex and difficult to distinguish
from that produced by MR
TR: CLINICAL FEATURES
 Auscultation
 The response of the systolic murmur to respiration
and other maneuvers is of considerable aid in
establishing the diagnosis of TR.
 The murmur characteristically is augmented during
inspiration (Carvallo sign)
 However, when the failing ventricle can no longer
increase its stroke volume with the patient in the
recumbent or sitting position, the inspiratory
augmentation may be elicited by standing.
 The murmur also increases during the Mueller
maneuver*, exercise, leg raising, and hepatic
compression
TR: CLINICAL FEATURES
 Auscultation
 It demonstrates an immediate overshoot after
release of the Valsalva strain but is reduced in
intensity and duration in the standing position and
during the strain of the Valsalva maneuver.

 Increased atrioventricular flow across the tricuspid

orifice in diastole may cause a short early diastolic
flow rumble in the left parasternal region following
S3.
TR: CLINICAL FEATURES
 Auscultation
 Tricuspid valve prolapse, like MVP, causes
nonejection systolic clicks and late systolic murmurs.

 In tricuspid valve prolapse, however, these findings

are more prominent at the lower left sternal border.

 Withinspiration, the clicks occur later and the

murmurs intensify and become shorter in duration.
TR: INVESTIGATIONS
 ECG: may show changes characteristic of the
lesion responsible for the enlargement of the RV
that leads to TR, e.g., an inferior Q-wave MI or
RVH.
 Echocardiography: RV dilation and prolapsing,
flail, scarred, or displaced tricuspid leaflets; the
diagnosis and assessment of TR can be made by
color flow Doppler imaging
 Severe TR is accompanied by hepatic vein systolic
flow reversal.
 Continuous wave Doppler of the TR velocity profile is
useful in estimating PA systolic pressure.
TR: INVESTIGATIONS
 CXR: usually reveals enlargement of both the RA
and RV.

 In patients with severe TR, the CO is usually

markedly reduced, and the RA pressure pulse
may exhibit no x descent during early systole
but a prominent c-v wave with a rapid y descent.

 The mean RA and the RV end-diastolic pressures

are often elevated.
TR: TREATMENT
 Isolated TR, in the absence of PA hypertension,
such as that occurring as a consequence of
infective endocarditis or trauma, is usually well
tolerated and does not require operation.

 Indeed, even total excision of an infected

tricuspid valve may be well tolerated for several
years if the PA pressure and resistance are
normal
 Dilationof the right side of the heart usually occurs
months or years after tricuspid valvectomy (usually
carried out for acute infective endocarditis).
TR: TREATMENT
 However, functional TR in the setting of
pulmonary hypertension is associated with heart
failure and poor survival.

 Treatment of the underlying cause of left heart

failure usually reduces the severity of functional
TR, by reducing the size of the tricuspid annulus
TR: TREATMENT
 In patients with mitral valve disease and TR
secondary to PA hypertension and RV
enlargement, effective surgical correction of
the mitral valve abnormality results in lowering
of the PA pressures and a gradual reduction or
disappearance of the TR without direct
treatment of the tricuspid valve
TR: TREATMENT
 However, recovery may be more rapid in patients
with severe functional TR if, at the time of
mitral valve surgery
 TV repair (especially when there is enlargement of
the annulus) with TV annuloplasty (generally with the
insertion of a ring) or
 TV replacement: in the rare instance of severe
organic TV disease

 Tricuspid valve annuloplasty or replacement may

rarely be required for severe, primary TR.
PULMONIC VALVE
PULMONIC VALVE
 Due to its relative location within the infundibular
musculature (at the distal portion of the right
ventricular out flow tract), the pulmonary valve is
considered, in an anatomical sense, a more simple
valvar structure than the aortic valve

 The left and the right leaflets of the aortic valve

face lie adjacent to the pulmonary trunk, and this
relative anatomic orientation has been used to
name the pulmonary valve leaflets: the right and
left facing leaflets and the nonfacing leaflet
PULMONIC VALVE
 Anatomically, the commissure of both the right
and left leaflets are supported by the
supraventricular crest of the right ventricle,
which separates the pulmonary valve from the
tricuspid valve

 Further, the opposite edge of the valve (i.e., the

nonfacing leaflet is supported by the anterior
wall of the infundibulum), is in general the most
anterior part of the heart
PULMONIC VALVE
 Pulmonary valve replacement is considered by
most to be less challenging than aortic valve
replacement due to the lower pressure gradient
across the valve and the relative ease of access
to the valve annulus.
 The ease of complete valve removal from the
cardiac base has led to the use as an autograft
replacement for the aortic valve in some
congenital heart patients.
 Even so, information on the valve is less
abundant and reports on variations in valve
dimensions are less comprehensive.
PULMONIC VALVE
 Capps et al. report the mean diameter of the valve
as 25.4 ± 3.2 mm in a study comparing the size of
the aortic and pulmonary valve to the overall body
surface area.

 It should be noted that these measurements were

taken on valves removed postmortem using a Hegar
dilator without annular dilation.

 By the authors’ admission, this sizing presents

limitations regarding the material properties of the
pulmonary annulus differing signi fi cantly from the
aortic
PULMONIC VALVE DISORDERS
 The pulmonic valve is affected by rheumatic
fever far less frequently than are the other
valves,
 It is uncommonly a nidus for infective endocarditis.

 The most common acquired abnormality

affecting the pulmonic valve is regurgitation
secondary to dilation of the pulmonic valve ring
as a consequence of severe PA hypertension.
PULMONIC VALVE DISORDERS
 This dilation produces the Graham Steell
murmur, a high-pitched, decrescendo, diastolic
blowing murmur along the left sternal border,
which is difficult to differentiate from the far
more common murmur produced by AR.

 Pulmonic regurgitation is usually of little

hemodynamic significance; indeed, surgical
removal or destruction of the pulmonic valve by
infective endocarditis does not produce heart
failure unless significant PA hypertension is also
present.
PULMONIC VALVE DISORDERS
 The carcinoid syndrome may cause pulmonic
stenosis and/or regurgitation.

 Pulmonic regurgitation occurs universally among

patients who have undergone childhood repair of
tetralogy of Fallot with reconstruction of the RV
outflow tract.
PULMONIC VALVE DISORDERS
 Percutaneous pulmonic valve replacement has
been successfully performed in many patients
with severe PR after childhood repair of
tetralogy of Fallot or pulmonic valve stenosis or
atresia

 This procedure was introduced clinically prior to

percutaneous aortic valve replacement
MULTIPLE/MIXED VHDS
MULTIPLE/MIXED VHDS
 Multivalvular involvement frequently is caused by
rheumatic fever, and various clinical and
hemodynamic syndromes can be produced by
different combinations of valvular abnormalities.
 Other causes:-
 Myxomatous MR
 With associated pulmonary hypertension is a leading cause of
concomitant TR, often with dilation of the tricuspid annulus.
 Marfan syndrome and other connective tissue disorders
 May cause multivalve prolapse and dilation, resulting in
multivalvular regurgitation.
 Degenerative calcification of the aortic valve may be
associated with degenerative mitral annular
calcification, resulting in concomitant AS and MR.
MULTIPLE/MIXED VHDS
 Different pathologic conditions may affect two
valves in the same patient (e.g., infective
endocarditis on the aortic valve causing AR and
ischemia causing MR).

 For the majority of patients with mixed valve

disease, there is usually a predominant valve
lesion (i.e., stenosis or regurgitation); further,
the symptoms and pathophysiology resemble
those of a pure dominant lesion
MULTIPLE/MIXED VHDS
 In patients with multivalvular disease, the clinical
manifestations depend on the relative severity of
each of the lesions
 When the valvular abnormalities are of approximately
equal severity, clinical manifestations produced by
the more proximal (upstream) of the two valvular
lesions (i.e., the mitral valve in patients with
combined mitral and aortic valvular disease and the
tricuspid valve in patients with combined tricuspid
and mitral valvular disease) are generally more
prominent than those produced by the distal lesion.
 Thus the proximal lesion tends to mask the distal
lesion
MULTIPLE/MIXED VHDS
 It is important to recognize multivalvular
involvement preoperatively because failure to
correct all significant valvular disease at the
time of operation increases mortality
considerably.

 In patients with multivalvular disease, the

relative severity of each lesion may be difficult
to estimate by clinical examination and
noninvasive techniques because one lesion may
mask the manifestations of the other
MULTIPLE/MIXED VHDS
 Therefore patients suspected of having
multivalvular involvement and who are being
considered for surgical treatment should
undergo careful clinical evaluation and full
Doppler echocardiographic evaluation and right
and left cardiac catheterization and angiography.
MULTIPLE/MIXED VHDS
 If there is any question concerning the presence
of significant AS in patients undergoing mitral
valve surgery, the aortic valve should be
inspected because overlooking this condition can
lead to a high perioperative mortality.

 Similarly, it is useful to palpate the tricuspid

valve at the time of mitral valve surgery.
AS/AR
 Mixed aortic disease and predominant AS
A high gradient and small valve area will be present.

 Pressureoverload results in concentric LV

myocardial hypertrophy, usually without chamber
enlargement except in late stages of the disease.

 Symptoms may be present in patients with

predominant AS with or without alterations in
chamber morphology.
AS/AR
 Mixed aortic disease and predominant AR
 The aortic velocity and gradient may be significantly
elevated due to regurgitation in the setting of AS,
but the aortic valve area is relatively large.

 Patientswith predominant AR will have both

pressure and volume overload, resulting in marked
increases in LV volume.

 In these patients, symptoms may be relatively latent

due to preload recruitment with compensatory
hypertrophy.
MS/MR
 Mixed mitral disease and predominant MS
A high transmitral gradient and small valve area will
be present.
 Left atrial enlargement occurs with relative
preservation of the LV chamber size.

 Mixed mitral disease and predominant MR

 LV remodeling will occur in addition to left atrial
enlargement.
 These patients frequently have high transmitral
gradients due to the regurgitant flow, but the valve
area may be relatively large.
MS & AV DISEASE
 Aortic valve involvement is present in
approximately one third of patients with
rheumatic MS.

 Rheumatic aortic valve disease may result in

primary regurgitation, stenosis, or mixed
stenosis and regurgitation.

 AR is evident on physical examination in

approximately two thirds of patients with severe
MS, but only approximately 10% of patients with
MS have severe rheumatic AR.
MS & AV DISEASE
 On physical examination, a proximal lesion may
mask signs of a distal lesion.
 For example, significant AR may be missed in
patients with severe MS because the widened pulse
pressure may be absent.
 On the other hand, MS may be missed or, conversely,
may be falsely diagnosed on clinical examination of
patients with obvious AR.
 An accentuated S1 and an OS in a patient with AR
should suggest the possibility of mitral valvular
disease.
MS & AV DISEASE
 AS is evident on physical examination based on
the typical murmur, even when MS is present;
however, cardiac output tends to be reduced
more than in patients with isolated AS.

 On physical examination, a S4 (which is common

in patients with pure AS) usually is not present.

 The midsystolic murmur characteristic of AS

may be reduced in intensity and duration because
the stroke volume is reduced by the MS.
MS & AV DISEASE
 Echocardiography is of decisive value in the
evaluation of patients with rheumatic disease
 It allows accurate diagnosis of the presence and
severity of multivalve involvement, taking into
consideration the altered flow conditions with serial
lesions.

 For example, the gradient across the stenotic aortic

valve may be relatively low when MS is present
because of a low cardiac output; valve area
calculations are especially helpful in this setting.
MS & AV DISEASE
 Because double-valve replacement is associated
with increased short- and long-term risks, BMV
can be the first procedure if MS is the
predominant lesion, with subsequent AVR when
needed.

 If percutaneous BMV is not an option or

concurrent AVR is needed, surgical valvotomy
may be considered as an option.
MS & AV DISEASE
 It is vital to recognize the presence of
hemodynamically significant aortic valvular
disease (i.e., AS and/or AR) preoperatively in
patients who are to undergo BMV.

 This procedure may be hazardous because it can

impose a sudden hemodynamic load on the left
ventricle that had previously been protected by
the MS and may lead to acute pulmonary edema.
AS & MR
 AS is often accompanied by MR caused by MVP,
annular calcification, rheumatic disease, or functional
MR.
 The increased LV pressure secondary to LV outflow
obstruction may augment the volume of MR flow,
whereas the presence of MR may diminish the
ventricular preload necessary for maintenance of the
LV stroke volume in patients with AS.
 The result is a reduced forward cardiac output and
marked left atrial and pulmonary venous hypertension.
 The development of AF (caused by left atrial
enlargement) has an adverse hemodynamic effect in
the presence of AS.
AS & MR
 Physical findings may be confusing because it
may be difficult to recognize two distinct
systolic murmurs.
 However, on echocardiography, the cause and
severity of AS and MR can be accurately
diagnosed.
 In most cases, MR is mild to moderate and it is
appropriate to treat AS alone.
 When MR is severe or there is significant
structural mitral valve disease, concurrent mitral
repair (whenever possible) or valve replacement
at the time of AVR should be considered
AR & MR
 The relatively infrequent combination of AR and MR
may be caused by rheumatic heart disease, prolapse
of both the aortic and the mitral valves secondary to
myxomatous degeneration, or dilation of both annuli
in patients with connective tissue disorders.

 The left ventricle usually is greatly dilated

 The clinical features of AR usually predominate, and

it is sometimes difficult to determine whether the
MR is caused by organic involvement of this valve or
by dilation of the mitral valve ring secondary to LV
enlargement.
AR & MR
 When both valvular leaks are severe, this
combination of lesions is poorly tolerated.

 The normal mitral valve ordinarily serves as a backup

to the aortic valve, and premature (diastolic) closure
of the mitral valve limits the volume of reflux that
occurs in patients with acute AR.

 With severe combined regurgitant lesions,

regardless of the cause of the mitral lesion, blood
may reflux from the aorta through both chambers
of the left side of the heart into the pulmonary
veins.
AR & MR
 Physical and laboratory examinations usually show
evidence of both lesions.

 An S3 and a brisk arterial pulse frequently are

present.

 The relative severity of each lesion can be

assessed best by Doppler echocardiography and
contrast angiography.

 This combination of lesions leads to severe LV

dilation.
AR & MR
 MR that occurs in patients with AR secondary to
LV dilation often regresses after AVR alone.

 If severe, the MR may be corrected by

annuloplasty at the time of AVR.

 An intrinsically normal mitral valve that is

regurgitant because of a dilated annulus should
not be replaced.
FOLLOW-UP
 For patients with mixed valve disease, there is a
paucity of data on the natural history of such
coexistent conditions.

 Consequently, the appropriate timing for serial

evaluations of these patients remains uncertain.

 For patients with predominant lesions (i.e.,

stenosis or regurgitation), serial evaluations in
accordance with recommendations for the
predominant valve lesion are generally
recommended.
FOLLOW-UP
 Nonetheless, it is important to recognize that
the coexistence of stenosis and regurgitation
may have pathological consequences that are
incremental to the effects of either of these
disease states alone.

 As a result, patients with mixed disease may

require serial evaluations at intervals earlier
than recommended for single valve lesions
MULTIPLE/MIXED VHDS
SURGERY
 Combined AVR and mitral valve replacement
usually is associated with a higher risk and
poorer survival than replacement of either of
the valves alone.
 The operative risk of double-valve replacement
is approximately 70% higher than for single-
valve replacement
 STS National Database Committee
 Multivalve replacement: 9.6% for multiple
 Isolated AVR: 3.2% and

 Isolated MVR: 5.7%

 The long-term survival depends strongly on the

preoperative functional status
MULTIPLE/MIXED VHDS
SURGERY
 Patients operated on for combined AR and MR
have poorer outcomes than patients undergoing
double-valve replacement for any of the other
combinations of lesions, presumably because
both AR and MR may produce irreversible LV
damage.

 Mitral valve repair or BMV performed in

combination with AVR is preferable to double-
valve replacement and should be carried out
whenever possible
MULTIPLE/MIXED VHDS
SURGERY
 Risk factors that reduce long-term survival
after double-valve replacement include
 Advanced age,
 Less favorable functional status,
 Decreased LV ejection fraction,
 Greater LV enlargement, and
 Accompanying ischemic heart disease requiring
coronary artery bypass grafting
MULTIPLE/MIXED VHDS
SURGERY
 In view of the higher risks, a higher threshold is
required for multivalvular versus single-valve
surgery.

 Thus patients generally are advised not to undergo

multivalvular surgery until they reach late NYHA
class II or class III, unless they exhibit evidence of
declining LV function.

 Despite a detailed noninvasive and invasive workup,

the decision to treat more than one valve often is
made on the basis of findings on palpation or direct
inspection at the operating table.
MULTIPLE/MIXED VHDS
SURGERY
 Hemodynamically significant disease involving the
mitral, aortic, and tricuspid valves is uncommon
and typically is caused by rheumatic heart
disease.

 Patients with trivalvular disease may present in

advanced heart failure with marked
cardiomegaly, and surgical correction of all three
valvular lesions is imperative.

 However, triple-valve replacement is a long and

complex operation.
MULTIPLE/MIXED VHDS
SURGERY
 Early in the experience with this procedure, the
mortality rate was 20% for patients in NYHA
class III and 40% for patients in class IV.

 More recently, the mortality rate has declined;

nevertheless, triple-valve replacement should be
avoided if possible.

 In many patients with trivalvular disease, it is

possible to replace the aortic valve, repair the
mitral valve, and perform a tricuspid annuloplasty
or valvuloplasty.
MULTIPLE/MIXED VHDS
SURGERY
 Patients who survive triple-valve replacement surgery
usually experience substantial clinical improvement
during the early postoperative period, and postoperative
catheterization studies show marked reductions in
pulmonary arterial and capillary pressures.

 However, some patients die of arrhythmias or

congestive heart failure in the late postoperative period
despite three normally functioning prostheses.

 The cause of cardiac failure in this situation is unknown,

but may be related to intraoperative myocardial
ischemia, microemboli from the multiple prostheses, or
continued subclinical episodes of rheumatic myocarditis
MULTIPLE/MIXED VHDS
SURGERY
 When multiple prosthetic valves must be inserted, it
is logical to select two bioprostheses or two
mechanical prostheses for the left side of the
heart.

 If the patient is to be exposed to the hazards of

anticoagulants for one mechanical prosthesis, it
seems unreasonable to add the potential risks of
early failure of a bioprosthesis.

 However, if two mechanical prostheses are selected

for the left side of the heart, the use of a
bioprosthesis in the tricuspid position is suggested.
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