Download Managing Asymptomatic Patients With Chronic Mitral Regurgitation*

Patients With
Asymptomatic
Managing
Chronic Mitral Regurgitation*
William H. Gaasch, MD; Roy M. John, MBBS, PhD; and
Gerard P. Aurigemma, MD
(CHEST 1995; 108:842-47)
LV=left ventricular; NYHA=New York Heart Association
Key words: atrial enlargement; atrial fibrillation; cardioversion; left ventricular function; mitral regurgitation; mitral
valve repair; vasodilator therapy
/Clinicians are generally reluctant to consider surgi^^ cal correction of mitral
regurgitation in an asymp¬
tomatic patient. With nothing to gain in the way of
symptomatic improvement, such early surgery exposes
the patient to perioperative morbidity and mortality
and the long-term complications of a prosthetic valve.
waiting for the patient to ex¬
Unfortunately, however,
or
exercise
intolerance may allow
perience dyspnea
time for the development of irreversible depression of
left ventricular (LV) function. If this occurs, the patient
may be deprived of the full benefit of corrective sur¬
gery. For this reason, surgery might be considered in
an asymptomatic patient who appears to be develop¬
ing LV dysfunction.
Recognizing the complications of prosthetic valves,
in patients with depressed LV function or
especially
atrial fibrillation or both, surgical repair of the native
valve is gaining wide acceptance. Repair procedures
for the maintenance of papillary muscle and
provide
annular continuity; thus, the functional components of
the subvalvular apparatus are preserved and postop¬
erative ventricular function is better than that seen af¬
replacement. Moreover, prosthetic valve-re¬
lated complications are eliminated and long-term an¬
is not necessary. For these reasons, the
ticoagulation
decision to proceed with surgical correction, especially
in an asymptomatic patient, is somewhat easier if a
repair procedure can be substituted for a valve re¬
ter valve
placement.
It could
also be argued that corrective surgery
should be considered before the development of irre¬
versible changes in atrial size or rhythm, even in a pa-
Department of Medicine (Cardiology), the Lahey
Hitchcock Medical Center, Burlington, Mass; and the University
of Massachusetts Medical School, Worcester.
Reprint requests: Dr. Gaasch, Director, Cardiovascular Research,
Lahey Hitchcock Medical Center, 41 Mall Road, Burlington, MA
*From the
01805
tient with little or no symptoms. The rationale for this
of the
is based on
occurrence of thromboembolism in patients who ex¬
frequent
hibit persistent postoperative atrial enlargement and
atrial fibrillation. Such complications might be avoided
if surgery were performed at an earlier stage.
For almost 2 decades, vasodilator therapy has been
known to affect favorably the hemodynamics of mitral
regurgitation. While widely accepted, this notion is
on acute or short-term interventions with
largely basedvasodilators.
there is only
parenteralevidence that Unfortunately,
vasodilator
therapy
long-term
meager
can be useful in the asymptomatic patient. Obviously
such therapy, if it could delay the development of
symptoms or LV dysfunction and the need for surgery,
would be desirable.
Based on knowledge of pathophysiology and natural
history, the and
importance of LV dysfunction and atrial
the therapeutic potential of chronic
fibrillation,
vasodilator therapy, it is possible to develop a rationale
with
approach
knowledge
for the management of asymptomatic
chronic mitral regurgitation.
patients
Pathophysiology of Mitral Regurgitation
Mitral regurgitation burdens the left ventricle with
excessive volume load that leads to a series of com¬
pensatory myocardial and circulatory adjustments.1-3
These adjustments vary over the prolonged course of
the disorder, such that the changes that are operative
in acute or subacute mitral regurgitation are eventually
by other compensatory mechanisms. With
replaced
acute regurgitation and volume overload, the ventricle
uses its preload reserve and the total stroke volume
increases via the Frank-Starling mechanism. In addi¬
tion, the low resistance runoff into the left atrium
contributes to an increased ejection fraction and a de¬
crease in systolic volume; according to the law of
Laplace, systolic load (ie, afterload) declines. Thus, in
acute mitral regurgitation, an increased ejection frac¬
tion and increased total stroke volume occurs as a re¬
sult of an increase in LV preload and a decrease in af¬
terload.
The major change that occurs during the evolution
from acute to chronic mitral regurgitation is an en¬
new steady state
largement of the ventricle. As thischamber
of acute
the
small
hyperkinetic
develops,
an
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Reviews
mitral regurgitation is converted into a large compliant
chamber that is well suited to deliver a large stroke
volume. This comes about through a rearrangement of
myocardial fibers in association with the addition of
new sarcomeres and the development of eccentric LV
As a result, preload at the sarcomere level
hypertrophy.
returns toward normal. Moreover, the systolic un¬
loadingis that is characteristic of acute mitral regurgita¬
tion
gradually replaced by normal systolic wall
stresses. Thus, the enhanced total stroke volume, seen
in chronic compensated mitral regurgitation, is "me¬
diated through a normal performance of each unit of
an enlarged circumference."6 At this time, LV con¬
tractility, loading conditions, and ejection fraction re¬
main in the range of normal; stroke volume is high as
a result of the large end-diastolic volume. An enlarged
atrium is also seen, but rhythm disturbances
compliant
are uncommon. During this compensated phase of the
disease, most patients remain asymptomatic and sur¬
gery should be postponed.
A most elusive and poorly understood aspect of the
of mitral regurgitation is the nature of
pathophysiology
the transition from the compensated to a decompensated state. Such a change may occur as a consequence
of progressive increments in the regurgitant volume or
chamber size or both. This decompensated state is
characterized by substantial and progressive ventricu¬
lar enlargement with high LV diastolic pressure,
increased systolic wall stress, and a decline in the
ejection fraction; the fall in ejection fraction occurs as
a consequence of a depressed contractile state and af¬
terload excess. Progressive atrial enlargement and
atrial arrhythmias are seen, pulmonary hypertension
and the patient becomes symptomatic. At
develops,
late
this
(ie, decompensated) stage, there may be irre¬
versible depression of ventricular and atrial function;
thus, it may be too late to expect an optimal result from
corrective surgery.
Ventricular Enlargement and Dysfunction
In the transition from the compensated to decom¬
state, the ventricle progressively enlarges and
pensatedfunction
In spite of this, the ejection
systolic tends todeclines.
remain within the broad range of
fraction
"normal." Some patients experience fatigue, a limited
exercise tolerance, or even dyspnea during this transi¬
tion; in such patients, the decision to proceed with
surgery is relatively easy and the results are generally
good. On occasion, a patient may proceed through the
transition and show evidence of LV dysfunction with
minimal or no symptoms. If an optimal response to
surgery is the goal, it is important to identify such a
patient before the development ofirreversible changes
in ventricular function. This can be achieved by con¬
ventricle and
sidering the markers of afordecompensated
of the
the
identification
developing guidelines
transitional stage of chronic mitral regurgitation.
Schuler et al7 studied the temporal changes in left
ventricular size and function before and after mitral
valve replacement in 16 patients with chronic mitral
corrective surgery was
regurgitation. In 12 of the 16,LV
associated with a decrease in chamber size and a
regression of myocardial hypertrophy; the
significantfraction
fell but remained within the normal
ejection
range. In four patients, LV function progressively de¬
teriorated after surgery. These two groups exhibited
different preoperative echocardiographic in¬
distinctly
dices of ventricular size and function; the four patients
with a poor response to valve replacement could be
identified (preoperative data) by an end-diastolic di¬
mension exceeding 70 mm, an end-systolic dimension
exceeding 50 mm, and a low-normal or depressed
ejection fraction.
Zile et al8 made similar observations in 20 patients.
After surgery, LV end-diastolic dimension fell to nor¬
mal in 16 of the 20 patients; these patients exhibited a
dramatic reduction in LV mass and gratifying improve¬
ment in symptoms. In four patients, LV end-diastolic
dimension and mass were unchanged after surgery; all
four remained symptomatic despite continued medical
of Schuler et al,7 the patients
therapy. As in the studies
with a poor surgical result exhibited larger preopera¬
tive end-diastolic and end-systolic chamber dimen¬
sions than those with a good response. An end-systolic
dimension exceeding 45 to 50 mm had a high predic¬
tive value for identifying patients that were destined to
have a poor surgical result. Wisenbaugh et al9 later
confirmed a poor outcome in patients with an enddimension exceeding this range. These dimen¬
systolic
sions translate into an end-systolic volume of 55 to 65
mL/m2, which is in close agreement with the data re¬
byal.12Borow et al,10 Carabello et al,11 and Craw¬
ported
et
ford
Patients who exhibit one or more of these markers
of a decompensated ventricle are at high risk of
persistent postoperative LV enlargement, depressed
postoperative ventricular function, and a poor or sub-
result. While these considerations do
optimal clinical
not identify the optimal time for mitral valve replace¬
ment or repair, they do enable the clinician to predict
a poor LV response to corrective surgery and, in this
fashion, provide a picture of the options of surgical or
nonsurgical treatment. Thus, asymptomatic patients
with only modest LV enlargement and normal systolic
function (ie, compensated mitral regurgitation) can be
treated. By contrast, those with evi¬
conservatively
dence of a decompensated ventricle would have little
to gain by postponing surgery, even though such
patients may not expect an optimal surgical result. In
therefore, corrective surgery should be per¬
principle,
formed during the transition from a compensated to
decompensated state.
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843
Guidelines for the identification of patients who are
entering the transitional stage are shown in Table 1.
The compensated, transitional, and decompensated
stages are defined on the basis of published (preoper¬
ative) data, which distinguish patients who are most
those who will
likely to havea a suboptimal result from
result.
Thus, defini¬
experience satisfactory surgical
tion of these stages relies on measurements of LV
chamber size at end-diastole and end-systole and the
ejection fraction; the stages are not based on semiquantitative assessments of the severity of regurgita¬
tion that are obtained from cineangiography or Dop¬
echocardiography. Recognizing that these stages
pler
and their prognostic implications have not been sta¬
tistically validated in a prospective fashion, they should
be used only as general guidelines in a decision anal¬
ysis that includes other clinical data including patient
preferences.
Atrial Enlargement
and
Fibrillation
Chronic mitral regurgitation often is complicated by
the development of atrial fibrillation. If the ventricle is
the rate is not excessive, such
compensated and
notice
patients merely
palpitations. Except for the in¬
creased risk of stroke and on occasion an increase in the
regurgitant volume, there is generally little or no clin¬
ical disability. Certainly, there is a role for direct cur¬
rent cardioversion and antiarrhythmic therapy in such
patients. It can be argued, however, that surgery
should be performed before atrial fibrillation is per¬
sistent or resistant to cardioversion. This notion is
based on the observation that persistent atrial fibrilla¬
tion after corrective surgery places the patient at
especially high risk for atrial thrombus and arterial
embolism. For this reason, it becomes important to
identify factors that influence the maintenance of sinus
after corrective surgery.
rhythm
Betriu et al13 reported their experience with atrial
fibrillation after valve replacement surgery in 685 pa¬
tients. Atrial fibrillation was present before surgery in
148 of the 589 survivors. Of the 148, most (n=94) un¬
derwent mitral valve replacement; aortic valve replace¬
ment was performed in 12 and multiple valves were
replaced in 42. Within 6 months of surgery, 52 patients
converted to sinus rhythm; 38 converted spontane¬
ously, and 14 required cardioversion. The remaining
96 patients remained in or reverted to atrial fibrillation
after an initially successful cardioversion. The preop¬
erative variables that were associated with persistence
of atrial fibrillation after surgery were a prolonged
duration of the arrhythmia (ie, exceeding 1 year) and
left atrial enlargement. When preoperative left atrial
dimension (echocardiography) was normal, 85% of
patients returned to sinus rhythm after surgery; by
contrast, when the left atrial size exceeded 50 mm, less
than half of the patients returned to sinus rhythm.
Table 1.Left Ventricular Size and Function in the
Three Stages of Chronic Mitral Regurgitation
Compensated
Cardiac catheterization
End-diastolic
Transitional
<110
>160
120-150
End-systolic
<45
>60
50-55
Ejection
>60
<50
53-57
<63
>70
65-68
<42
44-45
>47
>34
<30
31-32
Decompensated
volume, mL/m2
volume, mL/m2
fraction,
%
Echocardiography
End-diastolic
dimension, mm
End-systolic
dimension, mm
Fractional
shortening,
%
et al14 came to similar conclusions in a
Flugelman
with mitral stenosis and atrial fi¬
of 40
patients
group
brillation. After corrective surgery and cardioversion,
sinus rhythm was maintained in 24 patients while atrial
fibrillation returned in 16. Those that maintained a
normal sinus rhythm were younger, had a shorter du¬
ration of symptoms, and had a smaller left atrium when
with that of the group with persistent atrial
compared
fibrillation. These authors also suggested that the
functional state of the left ventricle influenced the
with which sinus rhythm could be restored
frequency
and maintained.
Reed et al15 assessed preoperative clinical, echocar¬
and hemodynamic data in 176 symptom¬
diographic,
atic patients who underwent mitral valve replacement
for chronic mitral regurgitation. Their goal was to de¬
termine preoperative predictors of postoperative car¬
diac mortality. The atrial size was significantly smaller
in those that survived compared with that in nonsur¬
vivors (47±6 vs 52±5 cm). Although this study does
not address the issue of restoration of sinus rhythm
after surgery, these and other data support the concept
of a malefic effect of atrial fibrillation after corrective
surgery.
These studies and anecdotal clinical experience
support the concept that if postoperative atrial fibril¬
lation and its complications are to be minimized or
avoided, corrective surgery shouldbe consideredwithin
months of the development of persistent atrial fibril¬
lation or before substantial atrial enlargement is
present. This issue assumes its greatest importance in
the patient with borderline indications for surgery.
Atrial fibrillation is not necessarily an indication for
surgery in an asymptomatic patient with compensated
ventricular function, but the burden of this arrhythmia
in a patient with borderline ventricular function might
be used as an indication for surgery, especially if the
risk of surgery is low and the valve appears to be ame¬
nable to repair.
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Mitral Valve Replacement Vs Repair
Mitral valve replacement with a mechanical or tissue
prosthesis can provide remarkable clinical benefits in
selected patients with mitral valve disease. Unfortu¬
nately, the early benefits of tissue valves tend to be
neutralized by a gradual increase in the need for
reoperation after 7 to 10 years; mechanical valves are
more durable and they function satisfactorily for the
lifetime of most patients. However, thromboembolic
complications occur at the rate of 1 to 2% per year;
when atrial fibrillation is present in a patient with a
valve, this complication is approximately
prosthetic
twice as frequent. In patients receiving anticoagulants,
occurs at the rate of 1 to
clinically
significant
bleeding
The
such
2% per year.
risk of
thromboembolic and
bleeding complications form the basis for the decision
to proceed with surgery before atrial fibrillation is es¬
tablished. Other complications of mitral valve replace¬
ment include mechanical dysfunction, paravalvular
leaks, and endocarditis; while rare, prosthetic valve
endocarditis carries a 50% mortality. Prosthetic valves,
therefore, are associated with major clinical complica¬
at
of at least 3%
occur
the rate
per year.16
Consideration of these issues, not to mention periop¬
erative morbidity and mortality, tempers any enthusi¬
asm for mitral valve replacement in asymptomatic pa¬
tions that
tients.
Mitral repair procedures are increasinglybeing used
the treatment of mitral regurgitation. This trend
developed in part to avoid the complications of pros¬
thetic valves. Another advantage of the repair proce¬
dure is that LV function is better maintained than af¬
ter valve replacement.2,5 The decline in LV ejection
fraction that is almost always seen after mitral valve
is primarily related to disruption of the
replacement
functional components of the subvalvular apparatus;
chordal transection abolishes the continuity between
muscles and annulus, and the ejection frac¬
papillary
tion declines by an average often percentage units.117
To be sure, the postoperative ejection fraction is not
after valve repair.18 Most studies,
always preserved
indicate
that the ejection fraction remains
however,
after
valve
repair. Finally, perioperative
unchanged
mortality appears to be lower with repair than replace¬
in
ment.17"20
Patients are selected for repair procedure on the
basis of echocardiographic descriptions of valve dis¬
ease. Calcification and scarring of the leaflets and
chordae or, on occasion, infection of the valve or an¬
nulus can preclude repair. When mitral prolapse is
present and there is little or no calcification, experi¬
enced surgeons can repair the valve with an 80 to 90%
success rate. Rheumatic mitral regurgitation can be
less amenable to repair. Thus, factors determining the
success of the procedure include a careful selection of
patients and an experienced surgeon.
Ifvalve repair is not possible, valve replacement with
chordal preservation has distinct advantages over valve
part of the
replacement alone. Retention aof at leasteffect
on LV
subvalvular apparatus provides salutary
seen
when
that
is
not
and
fraction
geometry ejection
the chordae are severed. Thus, postoperative ventric¬
ular function is similar to that seen with valve repair.
Chordal preservation can be especially important in
patients with decompensated mitral regurgitation in
which case attempts should be made to avoid or min¬
imize a postoperative decline in ventricular function.21
Vasodilator Therapy
provide
a dra¬
Intravenous vasodilator therapy can
matic hemodynamic improvement in patients with se¬
mitral regurgitation, especially those with con¬
re¬
gestive heart failure. Thus, sodium nitroprusside
duces the regurgitant volume and pulmonary venous
pressure while augmenting forward blood flow.22
Based on such observations, it would seem reasonable
to use oral vasodilators in patients with mild to mod¬
erate mitral regurgitation who are not yet candidates
for surgery. If a beneficial hemodynamic effect could
be sustained over months or years, it might be possi¬
ble to delay the development of LV dysfunction or
symptoms or both; surgery could also be postponed.
Unfortunately, the efficacy of long-term oral vasodila¬
tor therapy in patients with mitral regurgitation, espe¬
those without symptoms, is not well-defined.
cially
Before reviewing the potential use of oral vasodila¬
tor therapy in patients with chronic mitral regurgita¬
tion, it is important to emphasize that the volume of
regurgitant flow is determined hydraulically by the size
of the regurgitant orifice and the magnitude and
duration of the systolic pressure gradient across the
valve. Recognizing that the pressure gradient across
the valve is variable and that the regurgitant orifice area
may change, it is possible to explain the effects of he¬
modynamic interventions and therapies on regurgitant
volume.23"25 For example, venodilators and peptidyl
dipeptidase A (angiotensin-converging enzyme) inhib¬
itors can be ofvalue in reducing mitral regurgitant flow
in patients with ventricular enlargement and papillary
muscle dysfunction; the beneficial effect is brought
about by reducing ventricular size and the functional
regurgitant orifice area. In some patients with mitral
valve prolapse or hypertrophic cardiomyopathy, how¬
ever, venodilators may augment mitral regurgitant flow
through an influence on ventricular size and mitral
leaflet coaptation; a beta-blocker, by contrast, might
have an opposite and beneficial effect. In patients with
fixed-orifice mitral regurgitation (ie, those with rheu¬
matic or calcific disease), venodilation could produce
a fall in pulmonary venous pressure in association with
vere
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845
an increase in the regurgitant volume; this can occur
if the fall in left atrial pressure were greater than the
reduction in LV systolic pressure. By contrast, a pure
reduction in LV systolic pressure would reduce mitral
regurgitation, especially in the hypertensive patient.
These considerations of the dynamic determinants of
the mitral regurgitant volume are particularly relevant
to any discussion of vasodilator therapy for patients
with chronic mitral regurgitation.
Schon et al26 studied the effect of a peptidyl dipep¬
tidase A inhibitor in 12 patients with chronic mitral
regurgitation of mixed causes; nine of the 12 patients
were symptomatic (New York Heart Association
[NYHA] class 2-3). The LV size and function were
evaluated in the baseline state and again after 1 year of
(10 to 20 mg/d). Systemic arterial
quinapril therapy
from
fell
a
mean of 140/84 to 117/75 mm Hg.
pressure
There was a reduction in regurgitant fraction and re¬
gurgitant volume; LV end-diastolic volume fell from
146 to 109 mL/m2. The ejection fraction and cardiac
output did not change, but there was evidence of im¬
proved hemodynamics during exercise.
The patients in this study were likely in the stage of
transition from compensated to decompensated mitral
regurgitation; most were symptomatic. Such patients
are generally considered to be candidates for mitral
valve replacement or repair, but based on the results
of this study, it is possible that surgery could be post¬
poned while attempting a trial of intense medical
therapy.
Certainly, vasodilator therapy is an appropri¬
ate choice in a symptomatic patient who did not wish
to undergo surgery. This study, however, does not ad¬
dress
of the
management
asymptomatic patient with
the effects of capto¬
Wisenbaugh et al2' compared
in
to
32
(25
tid)
pril mg
placebo patients with chronic
chronic mitral regurgitation.
mitral regurgitation. The patients were largely asymp¬
(NYHA class I-II) and most had rheumatic
disease. After 6 months, there was no difference in
systemic arterial pressure, LV end-diastolic volume,
end-systolic volume, or ejection fraction between the
two groups. The authors concluded that the adminis¬
tration of captopril had "no effect on LV size or per¬
formance in patients with severe mitral regurgitation
but mild or no symptoms."
Several differences in these two studies may be re¬
sponsible for the disparate results. First, Wisenbaugh
tomatic
et
al27 performed a randomized, double-blind, place¬
bo-controlled study, while Schon et al,26 did not. Sec¬
ond, Schon et al26 treated patients that were more
symptomatic and had slightly larger ventricles than
those treated by Wisenbaugh et al.27 Third, the
patients of Schon et al26 exhibited higher baseline ar¬
terial pressures that fell significantly during the ad¬
ministration of quinapril. By contrast, the patients of
Wisenbaugh et al27 had lower arterial pressure that did
respond to captopril. Other differences, such as
age, gender, concomitant medical therapy, and cause
of the
not
mitral regurgitation, also may have contributed
the different results of these two studies.
Vasodilator therapy provides the most benefit in
patients with the largest hearts, the poorest systolic
function, and the most disabling symptoms. For ex¬
ample, hydralazine can produce substantial
symptom¬
atic and hemodynamic improvement in patients who
are in NYHA functional class 2-4.28 By contrast, there
was no significant change in LV size or function in the
NYHA class I-II patients reported by Wisenbaugh et
al.27 The patients reported by Schon et al26 lie some¬
where between these two extremes. Therefore, al¬
is possible that vasodilator therapy might
thoughtheit onset
or LV dysfunction, a sal¬
delay effect of of symptoms
vasodilator
utary
long-term
therapy in asymp¬
tomatic patients with compensated mitral regurgita¬
tion remains to be proven.
to
Conclusion
with normal LV systolic
modest
chamber
(ie,
only
enlargement are
of
chronic
mitral
compensated stage
regurgitation)
not candidates for corrective surgery. In the absence of
systemic arterial hypertension, there is no evidence
that vasodilator therapy has a salutary effect on the
course of such patients. However, hypertensive pa¬
tients with mitral valve prolapse can be treated with a
beta-blocker or perhaps a calcium channel blocker
with the goal of reducing the arterial pressure while
avoiding an increase in the degree of prolapse; those
with rheumatic or coronary heart disease also may
benefit from these agents or peptidyl dipeptidase A
inhibitors. Whether or not vasodilators are used, serial
and evaluation of exercise tolerance
echocardiography
and certainly endocarditis prophylaxis are appropriate.
Patients who show progressive LV enlargement and
thus appear to be in a stage of transition are generally
to be candidates for corrective surgery, even
thought
if they are not yet symptomatic. A stronger argument
for surgery, preferably valve repair, can be made if left
atrial enlargement and atrial fibrillation also are present.
If, because of patient preference or other consider¬
ation, conservative vasodilator therapy is selected, fre¬
Asymptomatic patients
function and
quent follow-up examinations are mandatory.
Most patients develop exercise intolerance,
dysp¬
before serious changes in ventricular
fatigue
function are present (ie, before the decompensated
stage). Occasionally, however, an asymptomatic pa¬
tient presents with marked ventricular enlargement
and mildly depressed ejection fraction. Although it
may be too late to expect an optimal result, most such
patients are candidates for surgery after a short period
of intensive medical therapy that includes vasodilator
nea,
or
agents.
846
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Reviews
rhythm after mitral valve surgery for mitral
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