Download Sample Chapter 36 from Runge: Netter`s Cardiology, 2nd Edition

Mitral Valve Disease
36 c00036
Thomas R. Griggs
s0010
s0015
itral valve leaflets consist of thin, pliable, fibrous material.
The two leaflets—anterior and posterior—open by
unfolding against the ventricular wall and close by apposition
when the pressure in the left ventricle becomes greater than that
in the left atrium. Mitral stenosis occurs when the mitral valve
leaflets become stiffened, calcified, and unable to open completely during diastole. This process often involves the chordae
tendineae in addition to the mitral valve leaflets. Mitral valve
regurgitation occurs when the leaflets are unable to close completely in systole. In the United States, more than 20,000
patients annually require surgery for manifestations of mitral
stenosis and mitral regurgitation, and thousands more require
monitoring and treatment.
Etiology and Pathogenesis
Mitral Stenosis
p0015 Rheumatic fever is responsible for a majority of cases of mitral
stenosis. The initial infection and its sequelae result in thickened
valve leaflets and fusion of the commissure between the leaflets.
Chordae tendineae are also affected and become thickened,
fused, and shortened. Most valves that are affected by rheumatic
fever show abnormalities of all these structures. Few patients
with rheumatic mitral valve disease have pure mitral stenosis;
most have a combination of stenosis and regurgitation, and
many have aortic and tricuspid involvement. Approximately two
thirds of mitral stenosis cases in the United States occur in
women.
p0020
The normal mitral valve cross-sectional area in diastole is 4
to 6 cm2. Blood flow is impaired when the valve orifice is narrowed to less than 2 cm2, creating a pressure gradient with
exertion. A valve area smaller than 1 cm2 is considered critical
mitral stenosis and results in a significant pressure gradient
across the valve at rest with chronically increased left atrial (LA)
pressures (Fig. 36-1).
p0025
Chronically increased LA pressures associated with mitral
stenosis, along with ongoing rheumatic inflammation, result in
LA enlargement and a predisposition for atrial fibrillation.
Valves affected by mitral stenosis are also vulnerable to recurrent thrombosis and implantation of bacteria that lead to infective endocarditis.
p0030
The hemodynamic effects of chronic mitral stenosis include
pulmonary venous and arterial hypertension; right ventricular
(RV) hypertrophy, dilation, and failure; peripheral edema; tricuspid regurgitation; ascites; and hepatic injury with cirrhosis
(Fig. 36-2).
s0020
Dysfunction of any component of the mitral apparatus can cause
mitral regurgitation. Mitral regurgitation also frequently occurs
in the absence of primary mitral valve disease in patients with
cardiomyopathy and ventricular dilation. When the cause of
mitral regurgitation is primarily a valve defect, valve repair or
replacement can correct the mitral regurgitation and improve
long-term prognosis. When the valve leaks because the ventricle
is dysfunctional and dilated, mitral repair or replacement may
have little or no effect on symptoms or prognosis.
With mitral regurgitation, blood is discharged during systole p0040
into the left atrium in addition to traveling its usual route
through the aortic valve and into the aorta. If the regurgitant
volume is large, LA remodeling occurs with dilation to accommodate increased volumes without intolerable LA hypertension
(Fig. 36-3). Over time, as an increasing fraction of ventricular
volume is regurgitant, the “forward” ventricular output is
reduced, and symptoms and other findings of mitral regurgitation become obvious (Fig. 36-4). Patients are generally clinically
well if the regurgitant fraction (regurgitant volume/total ejection volume) is less than 0.4. Patients with regurgitant fractions
greater than 0.5 predictably develop left ventricular (LV) failure
and have high morbidity and mortality. Any evidence of LV
failure (LV ejection fraction <60%) is also a critical marker of
poor prognosis.
Infectious endocarditis, spontaneous rupture of chordae ten- p0045
dineae, or ischemic injury of a papillary muscle may cause acute
loss of mitral valve integrity and acute mitral regurgitation. In
these cases of abruptly increased regurgitant flow, because there
is no adaptation of the left atrium or pulmonary vasculature to
the increased regurgitant volumes, acute pulmonary edema may
suddenly occur. Aggressive use of vasodilators is the emergent
treatment, but survival usually depends on emergency repair or
replacement of the valve.
AL
M
PR
SA O
M PE
PL R
E TY
C O
O F
N E
TE L
N SE
T V
- N IE
O R
T
FI
N
p0010
Mitral Regurgitation
p0035 Numerous etiologies contribute to mitral regurgitation, includ-
ing mitral valve prolapse, rheumatic heart disease, bacterial or
fungal endocarditis, and certain collagen-vascular diseases.
Clinical Presentation
s0025
Mitral Stenosis
s0030
2
Patients notice the effects of moderate (valve area = 1–2 cm ) p0050
mitral stenosis with activity. With severe stenosis, dyspnea
with minimal exertion and paroxysmal nocturnal dyspnea may
occur. In some cases a sudden, dramatic onset of atrial fibrillation produces the first symptoms, occasionally resulting in fatal
pulmonary edema. When the development of atrial fibrillation
is clinically silent, the initial event may be a stroke or other
thromboembolic event. The classic presentation of severe cor
pulmonale with ascites and edema is rarely seen today except in
medically underserved populations. Mitral valve disease increases
the risk for bacterial endocarditis, which should always be considered when symptoms worsen in a previously stable patient
with mitral valve disease.
Auscultatory findings in a patient with mitral stenosis include p0055
a loud first heart sound, an opening snap after the second heart
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T1
306 SECTION V • Valvular Heart Disease
RV
LV
AO
LA
AL
PR
SA O
M PE
PL R
E TY
C O
O F
N E
TE L
N SE
T V
- N IE
O R
T
FI
N
Mitral stenosis, viewed
from below and left: Minor
rheumatic involvement
of aortic valve
Echocardiogram demonstrating mitral stenosis.
Valve located between LA and LV is thickened,
with reduced orifice and intense signal due to
excessive calcium.
Thickened stenotic mitral
valve: Anterior cusp has
typical convexity; enlarged
left atrium; “jet lesion” on
left ventricular wall
Enlargement of right ventricle with some thickening
of wall resulting from mitral stenosis; pulmonary
artery enlarged and thickened with scattered
plaques of atheromas
Thickened, calcified,
stenotic mitral valve
demonstrated in
echocardiographic
study above
RV
LV
AO
LA
f0010 Figure 36-1 Mitral stenosis. AO, aorta; LA, left atrium; LV, left ventricle; RV, right ventricle.
T1
sound, and a low-pitched diastolic murmur with presystolic
accentuation if the patient is in sinus rhythm. The opening snap
is the sound generated by sudden full opening of the mitral
valve. It reflects the severity of the pressure gradient across the
mitral valve, because greater LA pressures generate earlier
opening than do lesser ones. Therefore, the shorter the interval
from second heart sound to opening snap, the greater the pressure gradient, and the more severe the stenosis.
p0060
The characteristic diastolic, low-frequency “rumble” or
murmur associated with mitral stenosis is best heard at the apex
with the patient in the left lateral decubitus position and the bell
over the point of maximal ventricular intensity. The rumble
occurs throughout diastole, with accentuation in late diastole
(presystole) in patients who have preserved normal sinus rhythm.
This murmur can be difficult to hear, and is soft and brief when
the stenosis is minor. Therefore, heightened awareness of possible mitral stenosis is necessary. If the murmur is inaudible, it
can be accentuated by having the patient exercise before auscultation or perform maneuvers such as isometric handgrip. This
murmur sequence—loud first sound, opening snap, and diastolic
rumble—is specific for mitral stenosis. Murmurs that mimic
mitral stenosis include the Austin Flint murmur with aortic
regurgitation, mitral diastolic murmurs in patients with large
intracardiac shunts, and occasionally murmurs that are caused
by an LA myxoma. However, none have all three components
of classic mitral stenosis.
Electrocardiographic changes in mitral stenosis may range p0065
from minor ST-segment and T-wave abnormalities to electrocardiographic evidence of severe pulmonary hypertension and
RV enlargement. The ECG pattern of LA and RV enlargement
is a classic indicator. Atrial fibrillation is common.
Mitral Regurgitation
s0035
Mitral regurgitation following sudden catastrophic failure of the p0070
valve apparatus is almost always immediately and severely symptomatic. In this situation, the regurgitant volume competes for
systemic blood flow and is simultaneously filling a small, noncompliant left atrium. This results in pulmonary edema often
coupled with hypotension or shock. The physical examination
will reflect the respiratory distress and evidence of poor systemic
perfusion such as tachycardia, cool extremities, and diaphoresis.
Importantly, however, the cardiac examination may not be
helpful. Any systolic murmur may be difficult to hear or be
absent. Emergent diagnosis usually requires echocardiography.
Conversely, even severe chronic mitral regurgitation may be p0075
tolerated without symptoms for years. Many cases of chronic
mitral regurgitation are discovered during routine examinations
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CHAPTER 36 • Mitral Valve Disease 307
Dyspnea
Elevated “wedge” pressure
Hemoptysis
Pulm. arteriolar constriction and/or sclerosis
Elevated pulm.-artery pressure
Elevated pulm. venous pressure
Pulmonary
congestion
Elevated left atrial pressure
Edema
Pulmonary atherosclerosis
Parasternal
lift
Pulmonary fibrosis
I Sounds II
R. ventricle
dilated
Fibrillation frequently
L. atrium
enlarged
Opening snap
Thrombosis (embolism)
I
Hypertrophy
Failure
Diminished
left ventricular
filling
Liver
enlarged,
tender
AL
Diastolic–presystolic
rumbling murmur
4th. L. interspace
Fixed leftheart
output
PR
SA O
M PE
PL R
E TY
C O
O F
N E
TE L
N SE
T V
- N IE
O R
T
FI
N
Gradient
(Ascites)
Left ventricular pressure
(Portal
hypertension)
Elevated
venous
Edema
pressure
Portal circulation
Systemic circulation
Slight cyanosis
aVR
I
V1
R
V2
V3
V5
V6
S
II
aVL
V4
III
aVF
S
Left atrial abnormality (P “mitral”) and evidence of
right ventricular hypertrophy (S in leads I and V5, R in V1)
Atrial
fibrillation
Figure 36-2 Pathophysiology and clinical aspects of mitral stenosis.
when the characteristic holosystolic murmur is noticed. Symptoms usually begin as dyspnea on exertion. Patients may also
present with acute pulmonary edema or evidence of RV failure.
Sudden decompensation can occur with the onset of atrial fibrillation or the development of bacterial endocarditis.
p0080
With chronic mitral regurgitation, the precordial cardiac
impulse may be normal or may show a displaced, sustained LV
impulse with a rapid filling wave. On auscultation the most
prominent feature is a holosystolic murmur that classically radiates to the axilla. The intensity may not correlate with the
severity of the mitral regurgitation; even severe mitral regurgitation can be associated with virtually no murmur. ECG changes
in mitral regurgitation are nonspecific and are primarily changes
of LV hypertrophy and strain; atrial fibrillation is common.
Differential Diagnosis
f0015
s0040
Primary pulmonary diseases (pneumonia, tuberculosis, chronic p0085
obstructive lung disease, and pulmonary thromboembolism)
may present similarly to mitral valve disease, with dyspnea
on exertion or pulmonary edema. Dyspnea may also be
present in chronic interstitial pulmonary diseases, pulmonary
hypertension, and malignancies that involve the chest.
Other cardiovascular conditions that present similarly include
ischemic heart disease, congenital heart disease, dilated cardiomyopathy, and hypertrophic cardiomyopathy. Chronic
pericardial disease with restriction can cause RV failure that
mimics the pulmonary hypertension associated with mitral
valve disease.
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T1
308 SECTION V • Valvular Heart Disease
Mitral regurgitation: Mitral valve viewed from below;
marked shortening of posterior cusp, with only slight
commissural fusion, and little fusion
and shortening of
chordae tendineae
RV
AO
LV
LA
AL
Color Doppler study demonstrating systolic aortic
outflow (blue/red) and multicolored jet of regurgitant
flow through incompetent mitral
valve into LA
PR
SA O
M PE
PL R
E TY
C O
O F
N E
TE L
N SE
T V
- N IE
O R
T
FI
N
In time, left
ventricle
dilates to
accommodate
increased
volume.
Shortened,
thickened
mitral cusps
Systolic
aortic
outflow
Left atrial
enlargement
due to mitral
regurgitation
RV
Regurgitant
jet through
incompetent
mitral valve
Calcific plate at anterolateral
commissure of mitral valve,
contributing to insufficiency
LV
Diagram of mitral regurgitation
shown in Doppler color study
above
AO
LA
f0020 Figure 36-3 Mitral regurgitation. AO, aorta; LA, left atrium; LV, left ventricle; RV, right ventricle.
s0045
Diagnostic Approach
p0090 Many pulmonary diseases can be differentiated from mitral
T1
valve disease by means of chest imaging, including both radiography and CT scanning. When an initial evaluation has focused
the differential diagnosis on mitral valve disease, the most
helpful clinical tool is echocardiography (see also Chapter 6).
p0095
In rheumatic mitral valve disease, echocardiography can
demonstrate thickening, calcification, poor valve mobility, and
thickening of subvalvular structures. The degree of valvular
stenosis or regurgitation can be estimated using Doppler ultrasonography. When necessary, the anatomy of the valve and
subvalvular apparatus can be further defined by transesophageal
echocardiography. The goals of echocardiography are to evaluate the severity of the stenosis or regurgitation, the mobility of
the valve, the involvement of subvalvular structures, and the
degree of calcification, as well as to detect intracardiac thrombi.
Echocardiography provides information about LV contractile
function and an accurate estimation of pulmonary artery pressure and RV function. It can also identify bacterial and fungal
vegetations, intracardiac masses (especially LA myxoma), and
intraventricular septal defects, conditions that can complicate
diagnosis of mitral valve disease.
p0100
Cardiac catheterization is indicated when there is a questionable diagnosis, when clinical and echocardiographic findings are
inconsistent, and in many patients for whom surgical treatment
is contemplated. Catheterization is performed to quantify the
mitral valve area, to document key elements of hemodynamics
such as cardiac output and systemic resistance, to define the
degree of pulmonary hypertension, and to determine whether
coronary artery disease is also present.
Management and Therapy
s0050
Mitral Stenosis
s0055
Asymptomatic patients in normal sinus rhythm with mild, p0105
uncomplicated mitral stenosis require only periodic monitoring
for symptoms and prophylaxis against rheumatic fever. In symptomatic patients, diuretics can help reduce pulmonary congestion. With mitral stenosis, ventricular filling time is critically
important; the heart rate should be maintained as low as is
practical with a β-blocker or a rate-affecting calcium channel
blocker. Patients with atrial fibrillation must be treated with
warfarin anticoagulation, unless it is contraindicated.
Optimum Treatment
s0060
Symptomatic mitral stenosis can be improved by percutaneous p0110
mitral balloon valvotomy (PMBV), surgical valvotomy, or
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CHAPTER 36 • Mitral Valve Disease 309
Elevated pulm. vein pressure
Dyspnea
Elevated “wedge” pressure
Systolic regurgitation
Pulmonary arteriolar constriction
Pulmonary
Pulmonary artery dilated; pressure elevated
Diminished left heart output
Edema
Right
ventricle
slightly
enlarged
I Sounds II
III
Soft, blowing pansystolic
murmur at apex
L. ventricular
pressure
PR
SA O
M PE
PL R
E TY
C O
O F
N E
TE L
N SE
T V
- N IE
O R
T
FI
N
Left
Lifting
ventricle apex
dilated beat
L. atrial pressure
AL
Failure
L. atrium
enlarged
(fibrillation
common) I
Hypertrophy
Failure
Portal circulation
Systemic circulation
S
R
Left and right ventricular enlargement
Electrocardiographic evidence of L. ventricular
hypertrophy (large S in V1, large R in V4) and minor
atrial abnormality (broad P)
Figure 36-4 Pathophysiology and clinical aspects of mitral regurgitation.
surgical replacement of the mitral valve. PMBV is the treatment
of choice in selected patients in whom there is little valvular
calcification, little involvement of the subvalvular apparatus, and
minimal or no mitral valve regurgitation. It is essential to
exclude LA thrombi by transesophageal echocardiography in
patients being considered for PMBV. The results of PMBV
depend in great part on operator experience. Longitudinal
studies in expert centers have documented event-free survival to
be greater than 70% at 7 years.
p0115
Open valvotomy is a repair procedure that involves direct
visualization of the valve by the surgeon and facilitates debridement of valve structure and reconstruction of subvalvular apparatus. This approach also permits valve replacement per the
surgeon’s judgment. Mitral valve replacement is indicated for
patients with severe mitral stenosis who are not candidates for
f0025
percutaneous commissurotomy or surgical repair (Tables 36-1,
36-2, and 36-3) (see Chapter 41).
Avoiding Treatment Errors
s0065
Many patients unknowingly minimize mitral stenosis symptoms p0555
by adopting a sedentary lifestyle. This situation may be
suspected following a careful history and documented with
exercise testing. These patients may benefit greatly from PMBV.
Alternatively, patients may report severe symptoms despite
echocardiographic data suggesting mild mitral stenosis. Exercise
testing with simultaneous echocardiography or catheterization
is indicated in this situation and may disclose dramatic worsening of atrial and pulmonary hypertension and the need for
intervention.
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T1
310 SECTION V • Valvular Heart Disease
Table 36-1 Management Approach for Patients with Asymptomatic Mitral Stenosis
Yearly Follow-up
Consider Percutaneous Mitral Balloon Valvotomy
Mild stenosis (MVA >1.5 cm )
or
MVA <1.5 cm2 but valve morphology not
favorable for PMBV
2
Moderate or severe stenosis (MVA <1.5 cm2)
and
Pulmonary artery systolic pressure >50 mm Hg
or
Exercise test results:
Pulmonary artery pressure >60 mm Hg
Pulmonary artery wedge pressure >25 mm Hg
or
New-onset atrial fibrillation
and
No LA thrombus or significant mitral regurgitation (3+ or 4+)
AL
Asymptomatic
t0010
p0560
PR
SA O
M PE
PL R
E TY
C O
O F
N E
TE L
N SE
T V
- N IE
O R
T
FI
N
LA, left atrial; MVA, mitral valve area; PMBV, percutaneous mitral balloon valvotomy.
Recommendations are from Bonow RO, Carabello B, Chatterjee K, et al. Focused update incorporated into the ACC/AHA 2006 guidelines for
the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task
Force on Practice Guidelines (Committee on Management of Patients With Valvular Heart Disease). J Am Coll Cardiol. 2008;52:1–142.
Rheumatic fever can affect all heart valves. Therefore, multiple valve disease must be considered in all patients. Special
attention should be given to the possibility that echocardiography can underestimate the degree of aortic regurgitation in
patients with severe mitral stenosis. Tricuspid stenosis may be
similarly underestimated or even undetected and may complicate the immediate postoperative recovery after mitral valve
repair or replacement.
Atrial fibrillation is a frequent cause of decompensation in p0565
patients with mitral stenosis and must be anticipated and
Table 36-2 Management Approach for Patients with Symptomatic Mitral Stenosis
Mildly symptomatic
(NYHA class II)
Moderately to severely
symptomatic (NYHA
class III–IV)
T1
t0015
Consider Open
Valvotomy or Mitral
Valve Replacement
Periodic Follow-up
Consider PMBV
Mild stenosis (MVA
>1.5 cm2)
and
Exercise test results:
PASP <60 mm Hg
PAWP <25 mm Hg
MVG <15 mm Hg
or
Valve morphology not
favorable for PMBV
Mild stenosis (MVA >1.5 cm2)
and
Exercise test results:
PASP >60 mm Hg
PAWP >25 mm Hg
MVG >15 mm Hg
and
Valve morphology favorable for PMBV
and
No LA thrombus or significant mitral
regurgitation (3+ to 4+)
Moderate or severe stenosis (MVA <1.5 cm2)
and
Valve morphology favorable for PMBV
and
No LA thrombus or significant mitral
regurgitation (3+ to 4+)
Moderate or severe
stenosis (MVA <1.5 cm2)
and
Valve morphology not
favorable for PMBV
and
Pulmonary pressure
>60–80 mm Hg
Moderate or severe stenosis (MVA <1.5 cm2)
and
Valve morphology favorable for PMBV
or
High-risk surgical candidate with less than
favorable morphology for PMBV
and
No LA thrombus or significant mitral
regurgitation (3+ to 4+)
Moderate or severe
stenosis (MVA <1.5 cm2)
and
Valve morphology not
favorable for PMBV
and
Acceptable surgical risk
Moderate or severe stenosis
(MVA <1.5 cm2)
and
Valve morphology not
favorable for PMBV
and
Pulmonary pressure
<60 mm Hg
Mild stenosis (MVA
>1.5 cm2)
and
Exercise test results:
PASP <60 mm Hg
PAWP <25 mm Hg
MVG <15 mm Hg
LA, left atrial; MVA, mitral valve area; MVG, mitral valve gradient; NYHA, New York Heart Association; PASP, pulmonary artery systolic
pressure; PAWP, pulmonary artery wedge pressure; PMBV, percutaneous mitral balloon valvotomy.
Recommendations are from Bonow RO, Carabello B, Chatterjee K, et al. Focused update incorporated into the ACC/AHA 2006 guidelines for
the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task
Force on Practice Guidelines (Committee on Management of Patients With Valvular Heart Disease). J Am Coll Cardiol. 2008;52:1–142.
ISBN: 978-1-4377-0637-6; PII: B978-1-4377-0637-6.00036-2; Author: Runge & Stouffer & Patterson; 00036
http://www.us.elsevierhealth.com/Netter/Netter-Clinical-Specialties/book/9781437706376/Netters-Cardiology
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CHAPTER 36 • Mitral Valve Disease 311
Table 36-3 Management Approach for Patients with Chronic Severe Mitral Regurgitation
No subjective symptoms and
no suggestion of symptoms
by exercise testing
Mitral Valve Replacement
LV dysfunction (EF <60%,
ESD >40 mm)
or
Pulmonary hypertension
or
New-onset atrial fibrillation
LV dysfunction (EF <60%,
ESD >40 mm)
and
Mitral valve repair not
possible
EF >30%
ESD <55 mm
Intervention indicated but
mitral valve repair not
possible
PR
SA O
M PE
PL R
E TY
C O
O F
N E
TE L
N SE
T V
- N IE
O R
T
FI
N
Symptoms
Normal LV function
(EF >60% and ESD <40 mm)
and
No new-onset atrial fibrillation
and
No pulmonary hypertension
and
Mitral valve repair unlikely*
Severe LV dysfunction
(EF <30% and/or ESD >55 mm)
and
Chordal preservation not likely
Mitral Valve Repair
AL
Follow-up with Echo Every 6
Months or Medical Therapy
t0020
EF, ejection fraction; ESD, end-systolic dimension of the left ventricular chamber; LV, left ventricular.
*Mitral valve repair may be an option for asymptomatic patients with normal LV function in an experienced center.
Recommendations are from Bonow RO, Carabello B, Chatterjee K, et al. Focused update incorporated into the ACC/AHA 2006 guidelines for
the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task
Force on Practice Guidelines (Committee on Management of Patients With Valvular Heart Disease). J Am Coll Cardiol. 2008;52:1–142.
managed aggressively. Similarly, pregnancy increases requirements for cardiac output and requires special planning and management. In women with rheumatic or congenital mitral stenosis,
initial symptoms often manifest with pregnancy. Bacterial endocarditis should be considered whenever symptoms worsen in
patients with mitral stenosis.
s0070
Mitral Regurgitation
p0570 Primary mitral regurgitation is a structural problem causing
valve incompetency that can only be corrected adequately by
valve repair or replacement. Therefore, the physician’s primary
role is to monitor patients with mitral regurgitation for development of symptoms and evidence of LV dysfunction, events that
portend the need for intervention. The most promising medical
therapies for chronic mitral regurgitation, vasodilators and
β-blockers, have not been adequately documented to delay the
need for surgery and thus are not recommended for this purpose
alone. Aggressive treatment of hypertension is useful in patients
with chronic mitral regurgitation.
s0075 Optimum Treatment
p0575 The timing of surgical intervention for patients with chronic
mitral regurgitation is critical. In most cases, mitral regurgitation is well tolerated, and patients are asymptomatic for many
years. Delaying surgery as long as possible avoids the trauma,
expense, and risk of surgery. However, every effort must be
made to proceed with surgery before ventricular function has
degenerated. LV systolic function is estimated using one of
several methods for determining the LV ejection fraction. The
unique accommodating effects of ventricular dilation and myocardial remodeling with chronic mitral regurgitation allow the
ejection fraction to be preserved late into the disease course;
therefore, any decrement in ejection fraction may represent a
considerable decrease in myocardial functional reserve. In
general, mitral valve surgery should be considered in patients
with known moderate to severe mitral regurgitation when they
are symptomatic or there is objective evidence of decreased LV
function (LV ejection fraction <60%).
Valve repair for severe mitral regurgitation lessens mortality p0580
and decreases the frequency of complications. Valves must be
relatively free of calcification and have pliable leaflets with
chordae tendineae that can be separated, reinforced, or reattached as needed. Placement of a reinforcing mitral ring is
frequently included in the repair. Valve repair, as opposed to
replacement, preserves functional subvalvular components,
including the papillary muscles, and significantly improves postoperative LV function. Additionally, natural valves are resistant
to thrombus formation, obviating the need for long-term
anticoagulation.
Avoiding Treatment Errors
s0080
Mitral regurgitation resulting from dilated cardiomyopathy is p0585
caused by dilation of the mitral ring and ventricles with anatomic deformity of the spatial and functional relationship of the
papillary muscles and chordae tendineae to the mitral valve
leaflets. In severe LV dysfunction, mitral valve repair or replacement may fail to improve symptoms and is associated with a
high risk of operative death. New surgical and percutaneous
approaches for correction of mitral regurgitation in this circumstance are in clinical trials to determine safety and efficacy.
Coronary heart disease can cause mitral regurgitation by p0590
several mechanisms. The mitral valve is tethered to papillary
muscles that depend on myocardial blood flow. Acute ischemia
of the papillary muscles can cause temporary mitral regurgitation and be corrected with coronary vascular interventions,
either surgical or percutaneous. Acute myocardial infarction
that involves a papillary muscle frequently causes acute, lifethreatening mitral regurgitation, with mortality rates near 30%.
These are managed, usually surgically, with both repair of the
valve and subvalvular apparatus and simultaneous revascularization. In some circumstances, an infarction results in rupture of
the tip of the papillary muscle with acute mitral regurgitation.
This is almost always fatal unless surgically corrected.
ISBN: 978-1-4377-0637-6; PII: B978-1-4377-0637-6.00036-2; Author: Runge & Stouffer & Patterson; 00036
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T1
312 SECTION V • Valvular Heart Disease
Bacterial vegetations first appear along
“contact line” of mitral valve but spread
to involve atria and chordae tendineae
with subsequent rupture and shrinkage
of the latter.
Bacterial perforation
of anterior mitral cusp
AL
Perforation of
aortic valve cusp
PR
SA O
M PE
PL R
E TY
C O
O F
N E
TE L
N SE
T V
- N IE
O R
T
FI
N
Thickening and erosion of mitral valve with stumps
of ruptured chordae tendineae resulting in valvular
incompetence, regurgitation, and atrial enlargement
Valve adhesion to ventricular wall
Acute
Chronic
Left ventricular
hypertrophy
Late sequelae of bacterial endocarditis may
result in mitral regurgitation via destruction
of mitral valve cusps or by widening of
annular valve ring due to left ventricular
enlargement due to aortic insufficiency
Vegetations of bacterial
endocarditis on underside
as well as atrial surface of
mitral valve
Adhesion of mitral valve
cusp to ventricular wall
resulting from vegetations
on undersurface of valve
f0030 Figure 36-5 Bacterial endocarditis in mitral valvular disease.
p0595
s0085
Any structural abnormality of the valve can result in flow
aberrations that promote deposition of microthrombi. These
can be the nidus for a bacterial or fungal infection resulting in
further damage from endocarditis (Fig. 36-5). Endocarditis can
affect valve competency because of interference in valve function by vegetations or by destruction or fenestration of the
valve leaflets. Although endocarditis is usually managed with
antibiotics, the damage effected by the bacteria is permanent,
as is the resultant mitral regurgitation. Indications for surgery
after cured bacterial endocarditis are identical to those for other
causes for mitral regurgitation. In addition, acute surgical care
is indicated for extremely large vegetations, when heart failure
is otherwise unmanageable, when a myocardial abscess is documented, and for patients with persistent bacteremia.
Future Directions
p0600 Improving worldwide morbidity and mortality associated with
T1
rheumatic heart disease necessitates better systems of hygiene
and improved prophylactic treatment of streptococcal infection,
especially the current drug-resistant strains. Mitral regurgitation’s prevalence will increase as the population ages, spurring
improvements in several areas: imaging with more accurate estimates of ventricular reserve, surgical technology with early
repair of severely regurgitant valves, balloon valvotomy with
improved patient selection and equipment, and minimally invasive surgical techniques with reduced recovery time and morbidity. Better treatment for atrial fibrillation and improved therapies
for prevention of thrombosis will greatly improve the quality of
life for patients with mitral valve disease and valve prostheses.
Additional Resources
Carabello BA. Modern management of mitral stenosis. Circulation. 2005;
112:432–437.
Carabello BA. The current therapy for mitral regurgitation. J Am Coll
Cardiol. 2008;52:319–326.
State-of-the-art reviews by a noted expert.
p0605
Evidence
Bonow RO, Carabello B, Chatterjee K, et al. 2008 Focused update
incorporated into the ACC/AHA 2006 guidelines for the management
of patients with valvular heart disease: a report of the American College
of Cardiology/American Heart Association Task Force on Practice
Guidelines (Committee on Management of Patients With Valvular
Heart Disease). J Am Coll Cardiol. 2008;52:1–142.
In this recently updated report from a panel of experts assembled by the ACC
and AHA, the authors cite more than 1000 articles and provide a comprehensive review of the diagnosis and management of valvular heart disease. Tables
and algorithms provide easy access to the practical aspects of patient care.
p0610
ISBN: 978-1-4377-0637-6; PII: B978-1-4377-0637-6.00036-2; Author: Runge & Stouffer & Patterson; 00036
http://www.us.elsevierhealth.com/Netter/Netter-Clinical-Specialties/book/9781437706376/Netters-Cardiology
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