REVIEW ARTICLE

Functional Mitral Regurgitation

Jan D. Schmitto, MD, PhD, Lawrence S. Lee, MD, Suyog A. Mokashi, MD, Ralph M. Bolman III, MD,
Lawrence H. Cohn, MD, and Frederick Y. Chen, MD, PhD

Abstract: Functional mitral regurgitation (MR) is a common clinical entity

which will likely increase in the future due to predicted demographic
changes. It is also associated with poor long-term survival. The anatomic
structure of the mitral valve apparatus is complex and consists of several
components, each of which can be affected by a variety of diseases resulting
in MR. In primary MR, the valvular incompetence is caused by compromised
or structurally disrupted components of the valve apparatus; the valve in
functional MR is structurally normal, with the regurgitation resulting from
failure of coaptation of the mitral valve leaflets without coexisting structural
changes of the valve itself. Therefore, we defined functional MR as a systolic
retrograde flow from the left ventricle into the left atrium due to reduction
and/or elimination of the normal systolic coaptation of the mitral valve
leaflets. A slow progression of the symptoms is typical for this valve disease
and often ends in irreversible left ventricular dysfunction. The pathophysiology and treatment of functional MR are quite complex. This article reviews
and summarizes the existing literature, with a focus on the pathophysiology
and current treatment of functional MR.
Key Words: chronic heart failure, functional mitral regurgitation, MR,
review
(Cardiology in Review 2010;18: 285291)

itral valve regurgitation (MR), defined as retrograde flow from

the left ventricle (LV) into the left atrium during systole, is
among the most common valve diseases in developed countries and
represents nearly one-third of acquired left-sided valve pathology.1
MR can be broadly classified into 2 major categories as follows:
primary and secondary MR. In primary MR, the valvular incompetence is caused by compromised or structurally disrupted components of the valve apparatus. Examples include degeneration from
rheumatic disease, myxomatous degeneration, endocarditis, chordae
tendineae rupture, and papillary muscle rupture. In secondary MR,
the valve is structurally normal with the regurgitation resulting from
failure of coaptation of the mitral valve leaflets without coexisting
structural changes of the valve itself. This form of MR is often
referred to as functional MR.
The pathophysiology of primary MR is well understood. The
incompetent valve causes volume overload in the LV, leading to
ventricular remodeling, myocardial dysfunction, and ultimately,
heart failure. The treatment of primary MR is clearly defined by
American College of Cardiology/American Heart Association
guidelines.2,3 On the other hand, the pathophysiology and treatment
of functional MR is more complex and controversial. There is a
growing general consensus that functional MR evolves from a
primarily ventricular (and not valvular) etiology, of any type, that
first causes ventricular dilatation. Ventricular dilatation in the setting
From the Division of Cardiac Surgery, Harvard Medical School, Brigham and
Womens Hospital, Boston, MA.
Correspondence: Frederick Y. Chen, MD, PhD, Division of Cardiac Surgery,
Brigham and Womens Hospital, Harvard Medical School, 75 Francis Street,
Boston, MA. E-mail: fchen@partners.org.
Copyright 2010 by Lippincott Williams & Wilkins
ISSN: 1061-5377/10/1806-0285
DOI: 10.1097/CRD.0b013e3181e8e648

of a structurally normal valve then causes the papillary muscles to be

situated too far apart, typically leading to a central area of failed
coaptation and subsequent MR. The optimal therapeutic strategy for
functional MR is currently a topic of substantial debate. Specifically,
it is unclear whether treatment should involve intervention on the
valve (ie, mitral valve repair or replacement), correction of ventricular pathology, both, or neither. Further complicating this issue is
the fact that there have been varying definitions of functional MR
used by different investigators in the past, resulting in heterogeneous patient groups that complicate the comparison of outcomes
among studies.
In this article, we review and summarize the existing literature, with a focus on the pathophysiology and current treatment of
functional MR.

ANATOMY
The mitral valve apparatus is a complex structure composed
of 6 functional components, each of which can be affected by a
variety of diseases resulting in MR4: (1) anterior and posterior mitral
valve leaflets; (2) primary, secondary, and tertiary chordae tendineae; (3) anterolateral and posteromedial papillary muscles; (4) the
mitral annulus; (5) the left ventricular myocardium, from which the
papillary muscles originate, and (6) the left atrial endocardium, from
which the posterior mitral leaflet extends.
In primary MR, such as in myxomatous degeneration, more
than 1 component is typically involved. With disease progression,
other anatomic components may become affected as well. In contrast, with functional MR only the mitral annulus, abnormally
dilated, is affected without pathology of any other components of the
valve. Such annulus dilatation leads to failure of the normal systolic
coaptation between anterior and posterior mitral valve leaflets,
resulting in MR. In addition to annular dilation, it is important to
note that papillary muscle splaying also results in MR. For this
reason, echocardiography remains an important diagnostic tool to
assess leaflet tethering.

EPIDEMIOLOGY
The epidemiology of MR has changed in the last several
decades, particularly in developed countries. About 50 years ago,
rheumatic fever was the leading cause of MR. However, the substantial reduction in rheumatic heart disease and the significant
increase of coronary artery disease have altered the epidemiology of
MR. The main etiologies of MR today are classified as degenerative,
dilatative, and ischemic.57
Due to the varying definitions of functional MR in the published
literature, its prevalence has been difficult to calculate.57 Some estimates report that up to 40% of patients with heart failure caused by
dilated cardiomyopathy (DCM) will develop functional MR.57 DCM
is a disorder of the cardiac muscle in which myocyte weakness leads to
ventricular dilatation and heart failure. There are multiple etiologies of
DCM, including ischemic, genetic, toxic, viral, inflammatory, autoimmune, and idiopathic causes.8 14 As a broad category, DCM has an
incidence of 5 to 10 patients/100,0001517 and a prevalence of 36
patients/100,000 people.15,18 Future demographic changes, such as an
aging population and greater life expectancy, are expected to increase
the incidence of DCM and as a result, the incidence of functional MR.

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Schmitto et al

Thus, functional MR will likely play a growing economic and medical

role in the coming years.

PATHOPHYSIOLOGY
The pathophysiologic mechanisms are quite different in primary and functional MR. In primary MR, the incompetent valve
causes acute and/or chronic LV volume overload, leading to ventricular remodeling, myocardial dysfunction, and subsequent heart
failure. In functional MR, on the other hand, a primary ventricular
pathology leads to ventricular remodeling and dysfunction with
subsequent development of regurgitation through an anatomically
normal valve. Specifically, the ventricular remodeling and enlargement causes dilation of the mitral valve annulus. This leads to a
reduction or elimination of the normal systolic coaptation line
between anterior and posterior mitral valve leaflets, thus compromising competence of mitral valve closure. The resulting regurgitation back into the left atrium during systole increases left atrial
volume and pressure. Over time, this chronically increased preload
leads to enlargement of the left atrium. In contrast to acute regurgitation where the left atrium is mostly noncompliant, the enlarged
left atrium in functional MR is compliant and the V-wave is often
smaller.
The degree of MR can be categorized by the effective regurgitant orifice (ERO) area19 and volume overload, measured as regurgitant volume. This may be affected by the driving force, or LV systolic
pressure, and left atrial compliance.20 In functional MR, the ERO area
is dynamic during systole, particularly during the relaxation phases
when there is inadequate leaflet apposition due to reduced LV systolic
pressure.21 Changes in myocardial loading or contractility can also
affect the ERO area: decreased loading22 or inotrope administration can
cause a reduction or even elimination of the ERO area, whereas
exercise most often results in an increase.23
The total impedance to ventricular ejection is reduced in
functional MR since the LV ejects blood through 2 orifices simultaneously: through the aortic valve (forward stroke volume) into the
aorta and through the incompetent mitral valve (regurgitant stroke
volume) into the lower pressure left atrium. As a consequence, the
LV decompresses as blood is ejected into the left atrium and the LV
volume declines during isometric contraction and early systole.
Thus, in the presence of functional MR, there is no isometric phase
of ventricular systole and almost 50% of the regurgitant volume into
the left atrium occurs prior to the opening of the aortic valve.
The resultant reduction of impedance enhances LV systolic
pump function in early functional MR. Furthermore, this early
systolic ventricular emptying into the left atrium leads, according to
the Law of Laplace, to a reduction of ventricular wall stress because
of the reduction in late systolic LV radius and pressure. The
reduction in wall stress, in turn, permits a greater extent and rate of
LV systolic shortening, and total stroke volume is increased for any
given level of preload (end-diastolic volume) and contractility. It is
important to note that in MR the forward, or effective, stroke volume
is less than the total stroke volume (forward plus regurgitant).
Accordingly, the LV end-diastolic volume and total stroke volume
must be increased to fulfill normal circulatory demands. A clinical
corollary is that the reported ejection fraction (EF) in these patients
often represents a combination of both forward and regurgitant flow.
If the regurgitation continues to progress, further changes in
cardiac pathophysiology develop: the left atrium dilates and atrial
pressure increases, which results in a higher myocardial afterload,
greater end-systolic volume, and consequently, increased ventricular
systolic wall stress.24 As the atrial pressure becomes greater and the
driving force, or LV systolic pressure, decreases, the regurgitant
volume falls.25 As a result, functional MR can be clinically silent.26
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FIGURE 1. Vicious cycle of functional mitral regurgitation.

Ventricular dysfunction can be associated with large end-systolic

dimensions27,28 but is often masked by an increased ejection volume;
thus, ventricular dysfunction should be suspected with greater than
normal end-systolic dimensions even when the EF appears normal. This
phenomenon is often revealed only after surgical elimination of MR,
when there is an immediate postoperative drop in EF of approximately 10%.29,30 In addition, the LV compensates for the chronic
hemodynamic volume overload by developing eccentric ventricular
hypertrophy. There are substantial variations in the geometric distribution of this compensatory hypertrophy among individuals with
the same valvular disease.
Over time, chronic functional MR can also lead to pulmonary
hypertension31 and heart failure.32,33 During the progression of heart
failure, impaired LV function and remodeling are associated with
papillary muscle apical displacement and mitral annular enlargement. This results in decreased mitral closing forces and tenting of
the mitral valve, both of which promote MR and thus lead to a
vicious cycle (Fig. 1). Active myocardial ischemia, myocardial
asynchronism, and excessive loading conditions worsen MR at rest
and during exercise. Other factors that may contribute to the development and progression of functional MR include intraventricular
delay and LV dyssynchrony, which can create uncoordinated regional LV mechanical activation or reduce the sphincteric function
of the mitral annulus, thereby decreasing the efficiency of LV
contraction and closing forces.
In summary, the pathophysiology of functional MR results
from a dynamic interplay between chamber pressures, myocardial
forces, and cardiac morphology. Some of the significant changes
observed in functional MR include annulus enlargement, papillary
muscle displacement, reduced mitral closing forces, mitral valve
tenting, decreased forward stroke volume, increased left atrial volume and pressure, increased pulmonary arterial and venous pressures, eccentric ventricular hypertrophy, and ventricular remodeling.
A vicious cycle is created in which ventricular remodeling, from any
etiology, begets MR, which then begets more remodeling.34

DIAGNOSIS
Evaluation of the patients medical history and a careful
physical examination are the first and most useful diagnostic tools
and may, by themselves, lead to the clinical diagnosis of MR.
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Cardiology in Review Volume 18, Number 6, November/December 2010

Echocardiography is the second most useful technique for

evaluating patients with MR. According to American College of
Cardiology/American Heart Association guidelines, 2-dimensional
and Doppler echocardiography is indicated for all patients with
suspected MR to confirm its presence and determine its severity
(according to the Functional Class).2 Evaluation of the severity of
functional MR on echocardiography requires an integrated assessment of several parameters, including cardiac chamber size and
volume, regurgitant jet size by color Doppler, regurgitant jet density
by continuous-wave Doppler, and pulmonary vein and mitral valve
inflow by pulse-wave Doppler.20 Newer applications of Doppler
echocardiography allow quantitative measurement of MR, including
the regurgitant volume and the regurgitant orifice area. Color Mmode can show early systolic or bimodal (early and late systolic)
peak MR, corresponding to those time points when there is maximal
imbalance between closing and tethering forces on the mitral valve
leaflets. Chordal tethering can cause kinking of the anterior leaflet in
its midbelly, resulting in the characteristic seagull sign on echocardiography. In asymptomatic patients with significant MR, serial
echocardiography every 6 to 12 months to assess LV size and
systolic function is important for optimal timing of surgery (Class
I).2 Stress echocardiography may also be useful in these patients to
assess exercise tolerance and the response of MR severity, pulmonary pressure, and contractile reserve to exercise (Class IIa).2,35
Cardiac catheterization and angiography are usually reserved
for patients in whom noninvasive test results are inconclusive and
also to detect concomitant coronary artery disease in patients undergoing mitral valve surgery (Class I).2 Additional studies such as
cardiac magnetic resonance imaging are helpful to identify viable
myocardium (ischemic and hibernating myocardium) and may support the investigation of surgical candidates with functional MR
associated with ischemic cardiomyopathy.

PROGNOSIS
The presence of functional MR in patients suffering from
ischemic and DCM confers a worse prognosis, serves as an independent risk factor for cardiovascular morbidity and mortality, and
limits survival in a severity-graded fashion.35 Trichon et al examined 2057 patients with ischemic MR and LV systolic dysfunction
and were able to correlate MR presence and severity with long-term
survival.36 This group revealed MR to be an independent predictor
of mortality and also found significantly lower survival rates at 1, 3,
and 5 years in heart failure patients with moderate to severe MR
versus those with mild or absent MR. Similar results were presented
by Cioffi et al in 2005.37 This group established the direct and
independent relationship between MR severity and 1-year mortality
among elderly patients with systolic heart failure, and showed that
MR was the strongest predictor of death, independent of the presence of diabetes mellitus, older age, and larger LV end-diastolic
volume. However, in this study, MR did not provide useful information regarding the risk of subsequent hospitalization for worsening heart failure.37
Larger studies have revealed similar results and have shown
that patients with functional MR have a worse prognosis than
patients with coronary artery disease and no functional MR. A study
of 11,748 cardiac catheterization patients revealed 1-year mortality
of 40% associated with severe MR, 17% for moderate MR, and 10%
for mild MR.38 If no functional MR was present at catheterization,
the 1-year mortality rate was 6%. Data from trials of thrombolysis
for acute myocardial infarction showed similarly poor prognosis for
functional MR.39 Postmyocardial infarction patients have a 1-year
mortality rate of 52% if they have severe MR, 22% if they have
mild-moderate MR, and 11% if they have no MR. The Survival and
Ventricular Enlargement study demonstrated that mild functional
2010 Lippincott Williams & Wilkins

Functional Mitral Regurgitation

MR increases the risk of cardiovascular mortality, even in patients

without congestive heart failure.40 Patients with functional MR had
a higher incidence of cardiovascular mortality (29% vs. 12%) and
heart failure (24% vs. 16%) than patients without MR at a mean of
3.5 years after myocardial infarction. Adjustment for differences in
baseline characteristics revealed that mild-to-moderate MR strongly
predicted mid-term mortality.40

TREATMENT OF FUNCTIONAL MITRAL

REGURGITATION
The management of functional MR is both challenging and
controversial. In particular, there is considerable debate and uncertainly regarding the optimal approach, timing, and effectiveness of
surgical intervention for functional MR. Various treatment strategies
for functional MR are described below, followed by a discussion of
possible future directions.

Medical Treatment
Optimal medical management is mandatory. The prognosis of
functional MR and DCM has improved significantly over the last
few decades mainly as a consequence of developments in medical
treatment options, including angiotensin-converting enzyme inhibitors, beta-blockers, digitalis, diuretics, and vasodilators. The goal
with medical therapy is to optimize cardiac performance, reduce
symptoms, and enhance survival by unloading the LV and maintaining euvolemia. When symptoms occur despite medical therapy
or LV dysfunction occurs, surgery is indicated before LV function
becomes substantially more abnormal.

Surgical Treatment
Surgical therapy plays a major role in the treatment of functional
MR and should be considered in any symptomatic patient or the
asymptomatic patient with decreased LV function. Surgery can often
restore quality of life as well as restore life expectancy.41,42 Early
detection and assessment of MR have direct consideration on surgical
therapy.2,3,43 The challenges facing the management of functional MR
include an elderly population, multiple comorbidities, timing of the
operation, and the increased incidence of heart failure.1 Although newer
interventional techniques, such as minimally invasive percutaneous
valve repair, are currently under investigation, mitral valve repair or
replacement remains the preferred method to treat severe functional MR
in most cardiac centers. With ongoing clinical trials, treatment guidelines will continue to evolve.
The major surgical therapeutic options for functional MR include mitral valve replacement, mitral valve repair, undersized mitral
annuloplasty, resynchronization therapy, implanted cardioverter defibrillators, and others.44 60 In the setting of severe LV-dysfunction and
MR, mitral valve surgery has demonstrated symptomatic improvements
and survival benefits.61 Moreover, several studies have demonstrated
that preservation of the annulo-papillary muscle continuity obtained
with mitral valve repair or replacement preserves systolic and diastolic
LV-function and improves LV geometry and wall stress.34,62 64 In
studies of patients with DCM and functional MR, mitral valve surgery
led to an improvement in mean New York Heart Association functional
class from 3.9 to 2.0, and actuarial survival was 82% at 1 year and 72%
at 2 years.65,66

Mitral Valve Replacement

Mitral valve replacement with either a biologic or mechanical
prosthesis was the preferred surgical approach for severe functional
MR in early studies. This treatment method involved complete
excision of the subvalvular apparatus, but subsequent studies revealed a detrimental effect on LV function and high mortality
rates.67 As a result, various surgical techniques were developed to
preserve the entire subvalvular apparatus. Given the thin and pliable
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Cardiology in Review Volume 18, Number 6, November/December 2010

valve leaflets and chordae, preserving the entire subvalvular apparatus resulted in maintenance of annulo-ventricular continuity and
improved preservation of LV function.68
Mitral valve replacement remains a reasonable surgical option
predominantly because of its reliability and reproducibility. However,
this should be considered for high-risk patients with multiple comorbidities, complex regurgitant jets (multiple or noncentral jets), failure of
mitral valve repair techniques, or severe tethering of both valve leaflets.7,69,70 Calafiore et al69 recommend mitral valve replacement when
the distance between the coaptation point of the leaflets and the plane of
the mitral annulus exceeds 10 mm.

Mitral Valve Repair

The dissatisfying results of mitral valve replacement performed 10 to 20 years ago led surgeons to favor mitral valve repair
for functional MR. Several techniques have been reported, eg,
undersized annuloplasty, edge-to-edge repair (Alfieri correction)
and/or papillary muscle repositioning, and are successfully used
with the aim of preserving the mitral valve apparatus.71
To date, there have been several retrospective studies, but no
randomized trials, comparing mitral valve repair to replacement for
functional MR.7174 The 2 largest retrospective studies are those by
Gillinov et al70 and Grossi et al.75 These investigators demonstrated that
both mitral valve repair and replacement were effective at eliminating
MR immediately postoperatively, but mitral valve repair was associated
with lower perioperative mortality. However, high-risk patients with
severe MR did as well and possibly better with mitral valve replacement.7,70 Regardless of which surgical technique was employed, 5-year
survival rates were uniformly disappointing at approximately 50%.70,75
The general consensus in the cardiac surgery community appears to be
that mitral valve repair results in lower perioperative mortality than
replacement and should be performed whenever possible over replacement.69 Along with this consensus is the acknowledgment, however,
that repair may confer a greater risk of MR recurrence. A recent study
by Al-Radi et al confirmed a lower perioperative mortality for mitral
valve repair in patients with chronic functional MR. The survival
advantage decreased over time, however, and was no longer apparent 5
years after surgery.76
In spite of the optimism generated by some studies, a recent
retrospective report showed no demonstrable decrease in long-term
mortality with mitral valve repair in patients affected by severe MR
and considerable LV dysfunction.77 These results reflect the heterogeneous nature of the disease and the etiology of MR, which is
secondary to ventricular dysfunction and not to organic disease of
leaflets. Moreover, these findings indicate that myocardial factors
are fundamental determinants of outcome in patients with DCM and
that any mitral repair based only on annuloplasty without addressing
myocardial remodeling typically result only in a temporary reduction in the severity of MR, with no effect on patient outcome.
In consideration of these findings, other groups have developed several surgical strategies for the treatment of MR secondary to
ischemic cardiomyopathy. The first is based on the relocation of
posterior papillary muscle tip to treat type IIIb leaflet motion
abnormalities.77 This procedure is based on the observation that the
displacement of the posterior papillary muscle tip after posterolateral ischemia is the main mechanism of ischemic MR.52 The second
procedure consists of the cutting of second-order chordae tendineae
to the anterior leaflet that has been shown to improve coaptation and
reduce MR.78

Undersized Mitral Annuloplasty

Undersized mitral annuloplasty is the most common surgical
procedure performed for functional MR, either alone or as part of a
complex repair. The rationale of this procedure, first popularized by
Bolling et al using very small (size, 24 26 mm) rings, is that
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undersizing the mitral annulus will result in increased leaflet coaptation and decreased regurgitation.65 Although this procedure does
not fully address the ventricular causes of functional MR, it is relatively
easy to perform and will lead to symptomatic improvement. Mitral
valve annuloplasty can be performed with partial rigid rings or complete rigid rings; however, differences in ring design have not yet
demonstrated significant differences in clinical outcome.79 Although
this procedure has been widely accepted by the cardiac surgery community, several questions remain unanswered. For example, current
evidence does not reveal any definite advantage in terms of size or type
of annuloplasty ring.80 Although the initial results for undersized mitral
annuloplasty were encouraging with low perioperative mortality rates,
subsequent studies at various centers revealed significant recurrence of
MR during follow-up,66,81 83 and that recurrence is always associated
with continued LV remodeling and retethering.

Cardiac Resynchronization Therapy

Cardiac resynchronization therapy (CRT) is widely performed as
a treatment option for functional MR in cases of severe heart failure and
advanced LV dysfunction. Selected patients (heart failure with an EF
30%, right ventricular (RV)-LV-dyssynchrony, left bundle branch
block, and QRS-time 120 ms) benefit from CRT.
Mechanical RV- and LV-dyssynchrony in chronic heart failure plays an increasingly important role in the pathophysiological
mechanisms of functional MR. It must be noted that both intra- and
interventricular LV dyssynchrony may exist, and each plays an
important role in the pathophysiology of functional MR. Because of
this, important mapping techniques (eg, TSI) are used to confirm
that the LV lead is placed in the most optimal portion of the LV (the
area of latest mechanical activation), to reduce the MR.
The acute effects of CRT on functional MR were evaluated by
Breithardt et al.84 In their study of 24 patients with biventricular
pacemakers, active CRT was associated with almost a 50% reduction in
the ERO area (2513 mm2), which resulted from more coordinated LV
contraction. Long-term benefits were noted in the Cardiac Resynchronization-Heart Failure (CARE-HF) and Multicenter InSync Randomized Clinical Evaluation (MIRACLE) randomized trials of CRT.85,86
Compared with controls, CRT produced significant reductions in LV
end-systolic and end-diastolic dimensions and in MR jet area (eg, 2.7
vs. 0.5 cm2 at 6 months in MIRACLE).86
However, the benefits of CRT rapidly wane if therapy is
discontinued. The magnitude of this effect was illustrated in a report
of 20 patients with advanced heart failure who had been on CRT for
a median of 427 days.87 At 72 hours after elective temporary
cessation of biventricular pacing, there were significant increases in
mitral ERO area (4.8 9.1 mm2) and MR volume (7.8 16.0 mL) and
regurgitant fraction (13.8%27.7%). These changes were associated
with a significant and marked decline in the maximal rate of rise of
LV systolic pressure (711 442 mm Hg/s).87

DISCUSSION
The timing, type, and advantages of surgical correction for
functional MR in DCM are still not clear. The operative risk is
mitigated by continued vigorous medical management and judicious
perioperative care. However, correction of functional MR and the
volume overload in a timely fashion can lead to improvement in the
physiology and perhaps a reversal of LV dysfunction. When operative treatment is under consideration, the chronic, often slowly
progressive nature of MR must be balanced against perioperative
morbidity and mortality and the long-term uncertainties of mitral
valve surgery. Perioperative morbidity and mortality depend on
surgeon experience, the patients clinical and hemodynamic status,
and the presence of associated noncardiac diseases, rather than on
which prosthetic or tissue valve or ring is used.
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The optimal timing of surgery for patients with severe functional MR has not yet been determined, nor has the optimal surgery
for this disease been defined. The difficulty in timing a valve
operation in chronic functional MR is complicated by the fact that
disabling symptoms may be the result of irreversible LV dysfunction. Clearly, the best time to intervene in functional MR is before
irreversible impairment of LV function occurs. Unfortunately, this
point cannot be determined by symptoms. Furthermore, the ejection
phase indices commonly used to assess LV performance are augmented by the reduced impedance to LV ejection associated with
MR. As the LV enlarges and performance decreases, a point is
reached where mitral valve surgery likely will not be beneficial.
With our current medical knowledge, it is not possible to define this
point prospectively in each patient. Our current practice is to offer
surgery when there is severe MR, whether there are symptoms or
not. For patients with at least moderate MR and symptoms or LV
dysfunction, surgery is also offered.
Clinical outcomes of mitral valve surgery in nonischemic
DCM are comparable with cardiac transplantation in the early-tointermediate term, but the long-term results are less satisfactory. At
the Mayo Clinic, patients undergoing mitral valve repair have a 1-,
and 3-year survival of 84% and 80%, respectively.85 Evolving
technology and research focused on methods of altering or reversing
cardiomyopathy, eg, cell transplant, may have significant impact on
the future management of this debilitating illness.88
In our opinion, surgical correction of functional MR can be
safely performed even when the LV EF is 30%. Mitral valve
repair, especially undersized annuloplasty, can be useful in these
patients, but as mentioned above, the indications are still controversial. The benefits of the simplest and shortest procedure must be
balanced against potential perioperative complications. Furthermore, in functional MR the treatment of ventricular myocardial
damage should be considered as the priority; rather than performing
mitral valve repair as an isolated intervention, patients should
undergo a concomitant procedure (ie, coronary artery bypass graft)
that targets the dysfunctional ventricle.
The correction of functional MR with mitral valve surgery
often results in symptomatic improvement, but survival benefit has
yet to be proven. Surgical intervention for functional MR, specifically mitral valve repair, is a viable option for symptomatic patients
including those with severely depressed LV function, and should be
performed as part of an overall therapeutic strategy that targets the
underlying ventricular pathology.
One of the most controversial and interesting topics regarding
surgery for functional MR is the issue of undersized annuloplasty
repair versus mitral valve replacement.34,89 92 Many think undersized annuloplasty is not effective and simply results in MR recurrence60,91,92; many others feel that valve repair is the better option
for all the reasons previously discussed.45 We feel that the crux of
the issue is the ventricular pathology and physiology. If the dysfunctional ventricle can stop remodeling and even undergo reverse
remodeling by removal of the pure volume overload that MR
represents, then we think repair will be effective and mitral valve
competence long lasting. There is strong evidence that MR recurrence is almost always associated with continued LV remodeling.92
However, if the dysfunctional ventricle is so dysfunctional that
removal of the MR volume overload does not stop remodeling, then
we submit that repair of any variety will not be long lasting and that
mitral valve replacement should be performed. Any replacement
should be performed with complete preservation of the subvalvular
apparatus to preserve ventricular function as much as possible. In
this circumstance, though the ventricle continues to dilate, there will
no longer be any MR. Such a scenario portends very poorly for the
patient.
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Functional Mitral Regurgitation

SUMMARY
The mitral valve apparatus is a complex anatomic structure
composed of several components, each of which can be affected by
a variety of diseases, resulting in MR. We define functional MR as
systolic retrograde flow from the LV into the left atrium due to
reduction and/or elimination of the normal systolic coaptation of the
mitral valve leaflets. The natural history is characterized by slowly
progressive symptoms, and often the onset of disabling symptoms is
the result of irreversible LV dysfunction. The pathophysiology and
treatment of functional MR is complex. Chronic functional MR is a
common clinical entity, which will likely increase in the future due
to predicted demographic changes. Functional MR is also associated
with poor long-term survival.
Optimal medical treatment is obviously required as standard
therapy for symptomatic patients. When symptoms persist despite
maximal medical therapy, or severe MR exists or LV dysfunction is
present, valvular surgery should be considered before LV function
becomes further depressed. What this surgery should bewhether
replacement or undersized annuloplasty repairremains a very
controversial topic. There is no completely accepted consensus in
either the cardiology or cardiac surgery communities, though most
surgeons feel that mitral valve repair results in lower perioperative
mortality than mitral valve replacement and should therefore likely
be the preferred procedure. However, this is far from an accepted
viewpoint, and there is no current standard of care. Treatment of the
underlying ventricular pathology, if possible, is equally as important
as treatment of the valve itself, though it is equally unclear whether
treatment of the functional MR will result in correction of the LV
remodeling. Functional MR should remain an active area of basic
and clinical research to define the optimal treatment strategy and to
improve outcomes for a steadily increasing patient population.
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