Valvular Heart Disease: Changing Concepts in

Disease Management
Acute Valvular Regurgitation
Karen K. Stout, MD; Edward D. Verrier, MD

cute severe valvular regurgitation is a surgical emergency, but accurate and timely diagnosis can be difficult. Although cardiovascular collapse is a common presentation, examination findings to suggest acute regurgitation
may be subtle, and the clinical presentation may be nonspecific. Consequently, the presentation of acute valvular regurgitation may be mistaken for other acute conditions, such as
sepsis, pneumonia, or nonvalvular heart failure. Although
acute regurgitation may affect any valve, acute regurgitation
of the left-sided valves is more common and has greater
clinical impact than acute regurgitation of right-sided valves.
Data to guide appropriate management of patients with
acute regurgitation are sparse; there are no randomized trials,
and much of the literature describes either small series or the
experiences of specific centers. Despite these limitations, the
available data are sufficient to allow identification of general
principles as well as development of applicable guidelines
from both the American College of Cardiology/American
Heart Association and European Society of Cardiology. The
guidelines recommend valve surgery for symptomatic patients with aortic or mitral regurgitation, including those with
acute regurgitation.13 The data and guidelines emphasize
overarching clinical principles, including the need for a high
clinical suspicion of acute regurgitation, timely use of echocardiography, and, in the majority of patients, rapid progression to surgery.

Causes
Causes of acute regurgitation overlap with causes of chronic
regurgitation and vary depending on the valve affected (Table 1).
Endocarditis may affect either the aortic or mitral valve,
whereas other causes are unique to the specific valve involved. The majority of causes of acute regurgitation present
as an acute or subacute event. However, acute regurgitation
can occur in patients with chronic regurgitation, when regurgitant severity is exacerbated by factors such as coronary
ischemia, chordal rupture, or leaflet perforation from endocarditis. Acute regurgitation of either the aortic or mitral
valve may result from procedural complications of percutaneous valve procedures. In addition, acute prosthetic valve
regurgitation is seen more frequently as more patients undergo valve surgery. Acute prosthetic valve regurgitation is

usually due to a tear of a bioprosthetic leaflet4 or thrombosis

of a mechanical valve, although perivalvular regurgitation
can occur, particularly in prosthetic valve endocarditis.
Acute aortic regurgitation is most commonly due to endocarditis, but there are a variety of less common causes as well.
Aortic dissection, whether due to Marfan syndrome, bicuspid
aortic valve, or atherosclerotic disease, may present with
aortic regurgitation. Blunt trauma may result in leaflet rupture.5 Another less common cause is rupture of a fenestration
in the aortic leaflet.6
Acute mitral regurgitation may result from either organic
or functional causes. Organic causes are those that result in
permanent structural disruption of the valve, such as leaflet
perforation from endocarditis, chordal rupture in myxomatous valve disease, or papillary muscle rupture due to myocardial infarction. Functional mitral regurgitation results from
abnormalities of the left ventricle, such as cardiomyopathies
in which the papillary muscles are laterally displaced, or
acute ischemia, in which an akinetic wall segment and
papillary muscle impair mitral valve closure. The distinction
between organic and functional causes is an important one
because treatment of organic causes requires surgical
repair, whereas functional causes may improve with treatment of the underlying myocardial ischemia, infarction, or
cardiomyopathy.
Functional mitral regurgitation is more often chronic than
acute. However, processes that result in rapid decline of
ventricular function may cause acute functional mitral regurgitation as part of the presentation of acute heart failure.
Examples include myocarditis or rapidly developing cardiomyopathies such as Takotsubo cardiomyopathy (left apical
ballooning) and peripartum cardiomyopathy.79 Emphasizing
the variability in pathological process, a study demonstrated
that mitral regurgitation in Takotsubo cardiomyopathy can
result from outflow tract obstruction and systolic anterior
mitral leaflet motion due to apical ballooning with preserved
basal ventricular function.9 Rheumatic carditis can cause
acute mitral regurgitation through a combination of leaflet
inflammation and myocardial dysfunction, with some data
suggesting that the degree of valve dysfunction drives outcomes.10 Although uncommon in industrialized nations, acute
rheumatic carditis remains a significant issue in developing
countries.11

From the University of Washington, Seattle.

Correspondence to Karen K. Stout, MD, University of Washington, Box 356422, 1959 Pacific NE, Seattle, WA 98195. E-mail stoutk@
u.washington.edu
(Circulation. 2009;119:3232-3241.)
2009 American Heart Association, Inc.
Circulation is available at http://circ.ahajournals.org

DOI: 10.1161/CIRCULATIONAHA.108.782292

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Table 1.

Causes of Acute Regurgitation

Aortic Regurgitation

Mitral Regurgitation

Endocarditis

Acute Valvular Regurgitation

Table 2. Comparison of Findings in Acute and Chronic

Severe Regurgitation
Acute

Chordal rupture
Endocarditis

Aortic regurgitation

Papillary muscle rupture

Hemodynamics

Aortic dissection (type A)

Ruptured fenestration
Blunt chest trauma
Prosthetic valve dysfunction

Chronic

Papillary displacement due to ischemia*

Cardiac output

Acute rheumatic fever with carditis

Pulse pressure

N2

Acute cardiomyopathy*
Prosthetic valve dysfunction
*Functional causes of mitral regurgitation.

Pathophysiology
Most clinicians are familiar with the pathophysiology and
hemodynamic impact of chronic regurgitation, but the stark
differences between acute and chronic regurgitation are
important to understand to make an accurate diagnosis of
acute regurgitation. Chronic regurgitation of either the aortic
or mitral valve affords time for the ventricle to dilate to
accommodate the regurgitant volume. This adaptation maintains forward stroke volume and cardiac output despite the
regurgitant volume. Correspondingly, left ventricular end-diastolic pressure remains normal unless there is coexistent
pathology that impairs diastolic function.
The lack of time for adaptation to additional blood volume
leads to the cascade of events typical of acute regurgitation.
Acute aortic and mitral regurgitation share some common
hemodynamic sequelae, despite the differences in pathogenesis and valve location within the circulation. In both circumstances, the left ventricle is not able to adequately compensate
for the regurgitant volume, and excessive backward blood
flow impairs forward stroke volume. Compensatory
tachycardia may preserve cardiac output initially, but eventually hypotension, organ failure, and other evidence of
cardiogenic shock will develop. Pulmonary capillary wedge
pressure increases abruptly and pulmonary edema develops,
although by different mechanisms depending on the valve
involved. Notably, acute exacerbation of chronic regurgitation may result in similar hemodynamic changes.

Aortic Valve Regurgitation

Acute aortic regurgitation differs from chronic aortic regurgitation in several important ways. In acute aortic regurgitation, normal ventricular size results in a marked increase in
end-diastolic pressure relative to the regurgitant volume.
Impaired forward stroke volume yields a decreased systolic
pressure and a narrow pulse pressure.12,13 Although there is
some degree of compensation by a Frank-Starling mechanism, the ventricle is functioning on a steep pressure-volume
curve because of the lack of chamber dilation. This contrasts
with chronic regurgitation, in which end-diastolic pressures
are relatively low, and the additional stroke volume manifests
as an increased systolic pressure (Table 2). Therefore, reliance on pulse pressure as an indicator of regurgitation may
significantly underestimate the severity of acute aortic regurgitation. In chronic aortic regurgitation, increased systolic
pressure results in increased afterload. This is not seen in
acute regurgitation given the low stroke volume. However, if
acute regurgitation has resulted in shock, sympathetic activa-

3233

Systolic pressure
Left ventricular
end-diastolic pressure
Left ventricular size

11

Examination
Diastolic murmur

Soft, early

Holodiastolic, decrescendo

S1

Soft

Normal

S2

Loud P2

Normal

S3

Present

Absent

Mitral regurgitation
Hemodynamics
Cardiac output

Ejection fraction

N2

N1

Left ventricular
end-diastolic pressure

11

Left atrial compliance

Left ventricular size

Soft, decrescendo

Holosystolic

Examination
Murmur
S3

May be present

Absent

V waves of CVP

May be present

Absent

N indicates normal; 1, increased from normal; 2, decreased from normal;

CVP, central venous pressure.

tion and the renin-angiotensin cascade may result in increased

systemic vascular resistance.
Abnormal mitral valve function due to acute hemodynamic
changes may further impair stroke volume. Marked elevation
of left ventricular diastolic pressure can cause early closure of
the mitral valve, and tachycardia will limit mitral inflow,
resulting in decreased ventricular filling.14
The presence of preexisting chronic aortic regurgitation
and ventricular enlargement may blunt the hemodynamic
impact of acutely worsened regurgitation. Conversely, preexisting disease processes that impair diastolic function, such as
hypertension or aortic stenosis, may result in markedly more
dramatic clinical presentation of acute aortic regurgitation.
Coronary ischemia may develop as a consequence of aortic
regurgitation. Decreased diastolic coronary flow decreases
myocardial perfusion, whereas elevated end-diastolic pressures and tachycardia increase myocardial oxygen demand.
This supply-demand mismatch is obviously further exacerbated if obstructive coronary lesions are present or if aortic
dissection impairs coronary flow.

Acute Mitral Regurgitation

Chronic regurgitation increases left atrial size and compliance, and, accordingly, left atrial pressures will be normal
despite the regurgitant volume. Conversely, acute mitral

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regurgitation increases volume into a normally compliant left

atrium, resulting in a marked increase in left atrial pressure
(Table 2).2 A significant V wave may be evident in either
condition, although it is more pronounced in acute regurgitation. Because of the increased left atrial pressure from acute
mitral regurgitation, pulmonary edema is a common consequence. Preexisting conditions may affect tolerance of
acutely increased left atrial and left ventricular volume.
Patients with a history of chronic mitral regurgitation and
preserved ventricular function may tolerate the marked increase in volume better, whereas patients with impaired
ventricular function may quickly decompensate with acute
worsening of mitral regurgitation. Those patients with pulmonary edema associated with ST-segment elevation myocardial infarction often have coexistent mitral regurgitation,
with often underappreciated severity and a poor prognosis.15
As with acute aortic regurgitation, there is some degree of
initial compensation afforded by increased preload, but the
inability of the ventricle and atrium to accommodate the
increased volume results in marked increase in left ventricular end-diastolic and left atrial pressures.

Clinical Presentation
The majority of patients with acute aortic or mitral regurgitation will present with dyspnea, hemodynamic instability,
and symptoms of shock, including weakness, dizziness, and
altered mental status. Symptoms at presentation may also
reflect the underlying pathogenesis of acute regurgitation,
such as severe chest pain from aortic dissection or fever from
endocarditis. A subset of patients with acute mitral regurgitation may present solely with new-onset dyspnea, without
evidence of impending cardiovascular collapse, and may
therefore be misdiagnosed with a noncardiogenic pulmonary
process or heart failure from another cause (Figure 1).
On examination, tachycardia, hypotension, peripheral vasoconstriction, and other evidence of cardiogenic shock are
common. As listed in Table 2, examination findings typically
seen in chronic regurgitation may be absent or subtle. For the
aforementioned reasons, the findings of chronic regurgitation
related to ventricular enlargement, such as apical displacement, are typically absent, and murmurs are frequently soft.
The presence of tachycardia and tachypnea further impairs
the detection of faint murmurs.
In acute aortic regurgitation, the rapid equilibration of left
ventricular and aortic diastolic pressures results in a faint
early diastolic murmur, in contrast to the louder decrescendo
diastolic murmur of chronic significant aortic regurgitation.
Early closure of the mitral valve due to elevated left ventricular end-diastolic pressures yields a soft S1, lack of aortic
leaflet coaptation during valve closure results in a soft A2,
and, if pulmonary hypertension is present, there may be a
loud P2, findings not typical of chronic regurgitation. The
eponymous peripheral signs associated with chronic aortic
regurgitation typically reflect increased pulsatility from increased stroke volume and wide pulse pressure. Because of
the diminished stroke volume and decreased pulse pressure of
acute aortic regurgitation, these signs are not typically present. With acute severe mitral regurgitation, rapid equilibration of ventricular and atrial pressures during systole results

Figure 1. Transesophageal echocardiography of acute mitral

regurgitation due to perforation of the mitral leaflet from endocarditis. A 70-year-old man presented with hypotension and
dyspnea 3 weeks after treatment for infection of an indwelling
venous catheter. He was in shock, was intubated, and was
begun on pressors and antibiotics. He was clinically believed to
have sepsis and pneumonia. His clinical condition did not
improve, and although his examination did not suggest a cardiac abnormality, because of concerns about his prior catheter
infection, an echocardiogram was ordered. The transthoracic
images showed severe mitral regurgitation with normal left ventricular size and function. A vegetation was seen on the mitral
leaflet and there was an apparent perforation. He was taken
emergently to the operating room for mitral valve replacement;
this transesophageal echocardiogram was obtained before initiation of cardiopulmonary bypass. The image shows a large vegetation and associated leaflet perforation, resulting in significant
regurgitation. VEG indicates vegetation; MV, mitral valve; MR,
mitral regurgitant jet; AV, aortic valve; LV, left ventricle; and LA,
left atrium.

in a faint systolic murmur rather than the holosystolic

murmur typically heard with chronic mitral regurgitation.
Reliance on examination findings alone to diagnose acute
regurgitation or estimate severity is fraught with potential
error, and therefore additional diagnostic testing is needed.

Diagnostic Testing
Electrocardiography typically demonstrates sinus tachycardia
with nonspecific ST- and T-wave abnormalities. Evidence of
ischemic ST changes may be seen if regurgitation is mediated
by ischemia or if the hemodynamic circumstances exacerbate
coronary insufficiency.
Chest x-ray will typically demonstrate a normal-sized left
heart and pulmonary edema. Those patients with preexisting
left ventricular dilation may have cardiomegaly, whereas
those with aortic dissection may have a widened mediastinum. Rarely, acute mitral regurgitation may direct regurgitant
flow preferentially to a single pulmonary vein, with edema
seen most prominently in that lung segment.16 This finding is
easily confused with pneumonia, particularly if the patient
has endocarditis or is not profoundly ill.
The diagnosis of acute regurgitation is made by echocardiography. The presence of severe aortic or mitral regurgitation and normal left ventricular size should immediately raise
the possibility of acute regurgitation. Further suspicion
should be raised if ventricular function appears normal or

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Table 3.

Acute Valvular Regurgitation

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Echo Findings of Acute Regurgitation

Aortic Regurgitation

Mitral Regurgitation

Vena contracta 6 mm

Vena contracta 7 mm

Pressure 1/2 time 200 ms

Reversed pulmonary vein flow

Holodiastolic flow reversal in

abdominal aorta

Disrupted mitral valve apparatus

Decreased aortic valve opening

Premature mitral valve closure

Normal left ventricular size and function

Normal left ventricular size

and function

hyperdynamic because ejection fraction is typically not significantly decreased in acute regurgitation.17 Echocardiographic findings of acute severe aortic and mitral regurgitation are shown in Table 3. Quantitative measures of
regurgitant severity that are useful in chronic regurgitation
are less useful in acute regurgitation. Measures of effective
regurgitant orifice area and regurgitant volume can be inaccurate in acute regurgitation, particularly in the face of
tachycardia. Hemodynamic data have demonstrated the variability in effective regurgitant orifice area and regurgitant
volume in acute regurgitation depending on afterload and
loading conditions.18,19 Thus, rarely will quantitative measures contribute significantly to management decisions in
acute regurgitation.
In addition to assessment of severity and ventricular
function, transthoracic echocardiography should also demonstrate the mechanism of regurgitation, such as dissection or
ruptured mitral chordae. The acuity of regurgitation may be
difficult to assess by echocardiography alone in patients with
a history of chronic regurgitation because ventricular size is
enlarged, and Doppler findings may be present because of
chronic regurgitation. In these cases, comparison with prior
studies and clinical examination of the patient will aid in
determination of acuity.
Color Doppler on transthoracic echocardiography may
underestimate regurgitation severity, particularly if the jet is
eccentric. Transesophageal echocardiography may be indispensable in identifying the severity and mechanism of regurgitation if a transthoracic study is inconclusive, particularly
with prosthetic valve dysfunction. Additionally, transesophageal echocardiography is important in planning operative
repair options, including identification of leaflet or annulus
involvement, and in establishing annular size to guide valve
replacement options. Particularly if one plans to use an aortic
homograft or to evaluate the feasibility of a Ross repair,
transesophageal echocardiographic data on annular size are
important. However, if the transesophageal echocardiography
results will not materially change the decision to pursue
surgery, transesophageal echocardiography can be done in the
operating room (Figures 1 and 2).
Cardiac catheterization is generally not indicated in the
preoperative assessment of patients with acute regurgitation.
The exception is patients with acute coronary syndromes
complicated by acute mitral regurgitation, for whom revascularization alone may improve regurgitation or for whom
both revascularization and mitral valve surgery are needed.
For those patients without ischemia as a potential underlying
mechanism of regurgitation, such as those with mitral regur-

Figure 2. Intraoperative view of leaflet perforation and vegetation. This image demonstrates the perforation and nearby vegetation, which resulted in severe valve destruction and mitral regurgitation. The valve was replaced with a tissue prosthesis,
and the patient tolerated surgery well and was transferred to the
intensive care unit in hemodynamically stable condition. Ventricular function was preserved, and the mitral prosthesis functioned well without evidence of recurrent infection.

gitation due to chordal rupture or aortic regurgitation, the

time to obtain a cardiac catheterization and the contrast load
may be poorly tolerated. For those with aortic dissection,
cardiac catheterization is rarely needed and may worsen
dissection. Additional imaging to evaluate possible underlying causes of acute regurgitation, such as computed tomography or magnetic resonance imaging, may be needed,
particularly if aortic dissection is a concern not addressed
fully by echocardiography.20
Rapid diagnosis is of the utmost importance because the
mortality of acute severe regurgitation is high if untreated.
Therefore, any diagnostic modality needed to make an
accurate timely diagnosis should be used, but once the
diagnosis is made, definitive treatment should not be delayed
for diagnostic studies that will not significantly alter the
course of care. Acute coronary syndromes and ischemia
benefit diagnostically from cardiac biomarkers, and brain
natriuretic peptide results can help to distinguish cardiac from
noncardiac causes of dyspnea and shock. This is particularly
true in those patients presenting with unilateral pulmonary
edema.16

Treatment
Medical Therapy
The treatment of acute aortic regurgitation is surgery to repair
or replace the valve. Medical therapy may be used to stabilize
the patient en route to surgery; however, surgery should not
be delayed in favor of efforts at medical management.16
While the surgical team is being readied, vasodilators such as
nitroprusside may be used to improve forward flow, and
inotropes such as dobutamine may improve cardiac output.
Medical therapy is not a substitute for surgery, however.21,22
Intra-aortic balloon pump use is contraindicated in acute
aortic regurgitation because balloon inflation during diastole
is detrimental to left ventricular hemodynamics.

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Patients with organic causes of mitral regurgitation are

similar to those with acute aortic regurgitation. Although
supportive therapy may provide some stability en route to the
operating room, the fundamental abnormality is structural and
requires surgical intervention. Thus, the most important
distinction in assessing acute mitral regurgitation is determining the underlying cause. If organic, with disruption of the
normal valve structure, surgery is the mainstay of therapy. If
functional, medical therapy may be sufficient to avoid operative intervention; however, if medical therapy fails, surgical
options need to be reexplored. Additionally, revascularization
is a necessity in those patients undergoing surgery for acute
mitral regurgitation if significant obstructive coronary disease
is present. Unlike in acute aortic regurgitation, the intra-aortic
balloon pump may be beneficial in acute mitral regurgitation.
Medical therapy for patients with acute functional mitral
regurgitation is directed at the underlying pathophysiology. In
patients with ischemia or infarction, restoration of blood flow
to the affected territory may be sufficient to improve regurgitation. Data suggest that severe mitral regurgitation in
patients with cardiogenic shock is not uncommon, approaching 7% of patients in the Should We Emergently Revascularize Occluded Coronaries in Cardiogenic Shock (SHOCK)
registry, and that the presence of acute mitral regurgitation in
these patients is a very poor prognostic sign, with an observed
mortality of 55%, improving to only 39% in patients selected
for emergency surgery.23 The SHOCK trial demonstrated that
early revascularization improves outcomes at 6 months in
patients with cardiogenic shock and acute myocardial infarction,24 and further analysis demonstrated the prognostic
importance of mitral regurgitation in these patients. Shortand long-term survival was inversely related to the degree of
mitral regurgitation, arguing for more aggressive treatment of
those patients with significant mitral regurgitation in the
setting of acute infarction, with improved mortality in those
patients undergoing early revascularization.25 Thus, if surgical revascularization is needed, the presence of severe mitral
regurgitation should encourage rather than discourage surgical intervention.
In those with acute regurgitation in the setting of acutely
developing or worsening cardiomyopathies, aggressive heart
failure therapy may be sufficient to improve the degree of
mitral regurgitation. In addition to pharmacotherapy, mechanical support may be of use in patients with functional
mitral regurgitation. The intra-aortic balloon pump can be an
effective support mechanism in patients with acute functional
mitral regurgitation of any cause but is particularly useful for
those patients with underlying myocardial ischemia or cardiomyopathy. The role of left ventricular assist devices is not
well studied in acute mitral regurgitation but can be used in
the setting of acutely decompensated heart failure not responsive to medical therapy.
For patients with valve thrombosis resulting in acute
regurgitation, thrombolytic therapy may be an alternative to
surgery. However, both the American College of Cardiology/
American Heart Association and European Society of Cardiology guidelines recommend surgery as first-line treatment in
patients with significant symptomatic prosthetic valve dysfunction, with thrombolytics reserved for proven valve

thrombosis when surgery is high risk or unavailable or if

there is a small thrombus burden and few symptoms.13

Surgical Treatment: Acute Aortic Regurgitation

Anesthetic Considerations
Anesthetizing a critically ill patient with acute aortic regurgitation can be a significant challenge. Induction is particularly risky, and the surgical team should be present in the
room at the time of induction, ready to initiate early cardiovascular support if necessary.
The pathophysiology of acute aortic regurgitation presents
unique challenges to the anesthesiologist. Low diastolic
pressure, tachycardia, and increased wall stress may impair
coronary flow, and if induction further reduces blood pressure, coronary ischemia may exacerbate patient instability.
Consequently, the anesthesiologist must attempt to avoid
tachycardia and hypotension during intubation and induction
of anesthesia because there may not be latitude to accelerate
care to compensate for worsened hypotension and coronary
ischemia. Hemodynamic monitoring is also crucial, and in
many cases monitoring lines will have been placed before
arrival in the operating room. The rational use of inotropic
drugs, vasoconstrictors, sedatives, and anesthetic agents is
essential to ensure optimal outcomes.
Surgical Considerations
In the aortic position, surgical options are defined by the
pathophysiology of disease, anatomy, and anticipated longterm outcomes. Myocardial protection is a significant concern
in this setting because the incompetent aortic valve and
possible associated aortic root pathology make antegrade
cardioplegia ineffective or possibly dangerous. Reliable
placement of a retrograde coronary sinus cannula for delivery
of cardioplegia is essential. Adjuvant handheld cardioplegia
can be delivered subsequently via coronary ostia after the
aortic valve and root have been properly assessed. Additionally, use of a left ventricular vent, placed via the right superior
pulmonary vein, may aid in ventricular decompression and
induction of a diastolic arrest. Other protective adjuncts such
as systemic hypothermia on cardiopulmonary bypass or
topical cooling have been used frequently but have unclear
overall value.
Aortic Valve Endocarditis
Intraoperative transesophageal echocardiography and direct
assessment of annular involvement are important in planning
the surgical procedure. Careful assessment of the annulus is
essential to ensure that (1) it is intact and (2) there are no
undrained abscesses. In cases of aortic annulus involvement,
the use of a homograft is generally indicated (Figure 3).
Although aortic homografts are also at risk for prosthetic
valve endocarditis, the additional tissue included with the
homograft, including the left ventricular outflow tract and the
anterior leaflet of the mitral valve, is sometimes essential for
successful aortic root reconstruction. In cases of endocarditis
limited to the valve leaflets, leaflet excision and aortic valve
replacement are indicated, without additional annular procedures. There is no evidence that a mechanical versus a
bioprosthetic valve has a differential rate of infection after
replacement for endocarditis.26

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Figure 3. Operative technique for replacement of the aortic

valve and root in complicated aortic endocarditis with annular
abscess. A, Technique of aortic root replacement and
homograft reconstruction. The infected valve is excised, and all
infected and necrotic tissue is radically debrided. The coronary
ostia are preserved as buttons. B, The defect is reconstructed
by suturing the homograft mitral valve leaflet below the level of
the infection. From Sabik JF, Lytle BW, Blackstone EH, et al.
Aortic root replacement with cryopreserved allograft for prosthetic valve endocarditis. Ann Thorac Surg. 2002;74:650 659.
Modified from Sellke F, Swanson S, del Nido P, eds. Sabiston
and Spencer, Surgery of the Chest. 7th ed. Amsterdam, Netherlands: Elsevier; 2005, copyright 2005, with permission from
Elsevier.

In some centers, particularly in children, the use of a

pulmonary autograft (Ross procedure) may be used. This is
controversial, however. As with elective aortic valve surgery,
the risk and benefits of the Ross repair are debatable.
Theoretically, there is a benefit of providing a durable aortic
valve replacement that may grow with a child and not require
future intervention. However, the exchange of single-valve
disease for 2-valve disease and data suggesting that the
neoaortic valve requires replacement in 10% to 20% of
patients within 10 years of operation27,28 may argue that the
long-term outcomes offset the potential benefit. This is a
particularly important decision in the case of an unstable
patient who may not tolerate the additional bypass time
necessary to successfully perform a Ross repair. Consequently, the use of a Ross repair in the acute setting is limited
to a very specific patient population in specific centers with
extensive surgical success in Ross repairs. Finally, depending
on the clinical status of the patient and the overall status of the
aortic root, some patients benefit from a simple valve replacement with anticipated root reconstruction after the patient has
had an opportunity to recover from multisystem organ failure.
Aortic Dissection
The pathophysiology of acute aortic regurgitation in the
setting of a type A aortic dissection varies. The strategy for
addressing the acute aortic regurgitation in that setting is
dependent on its pathogenesis. In the setting of a normal
trileaflet aortic valve, aortic valve resuspension and interposition graft replacement of the ascending aorta can frequently
address valvular regurgitation by raising the commissural
heights to normal and reattaching the sinuses of Valsalva to
the aortic wall. When an aortic dissection is present in the
setting of an abnormal aortic valve, such as a bicuspid aortic
valve or an ascending aortic aneurysm, our practice is to

Acute Valvular Regurgitation

3237

perform a modified Bentall procedure using a valved conduit

and direct coronary reimplantation. One center reported their
experience with aortic root replacement using mechanical
conduits and aortic allografts, noting no difference in 1- and
5-year survival based on conduit choice, including those
patients with aortic dissection.29 Both aortic root remodeling
procedures (Yacoub procedure) and aortic root reimplantation procedures (David procedures) have been used successfully in the setting of aortic dissection as well but require
more experienced surgical expertise for consistently excellent
results. The possibility of coronary ischemia due to coronary
artery involvement from dissection or technical problems
with the coronary artery reimplantation needs to be considered in repair options to achieve optimal outcomes.
Fenestration/Trauma
Disrupted leaflets due to trauma or a ruptured fenestration can
be repaired in certain instances. A leaflet perforation can be
patched with sutures and an appropriately sized piece of
autologous or bovine pericardium. However, a low threshold
for valve replacement should be the norm. Blunt chest trauma
resulting in aortic valve regurgitation is most often a result of
loss of commissural suspension, leaflet perforation, or dissection.30 As with other causes of acute aortic regurgitation,
surgical therapy is tailored to the intraoperative anatomy.

Surgical Treatment: Acute Mitral Regurgitation

Anesthetic Considerations
Although patients with acute mitral regurgitation often are
not as unstable as patients with acute aortic regurgitation,
these patients nonetheless remain hemodynamically tenuous
and can demonstrate acute cardiopulmonary collapse at any
time. As with acute aortic regurgitation, all members of the
surgical team should be present during induction in case
urgent initiation of cardiopulmonary bypass is needed. If the
cause of acute mitral valvular regurgitation is profound
ongoing myocardial ischemia or infarction with either significant systolic or diastolic dysfunction, additional anesthetic
considerations must be made to optimize myocardial oxygen
supply and demand, preload and afterload, and coronary
perfusion pressure. If not done before arrival in the operating
room, placement of an intra-aortic balloon pump to improve
coronary perfusion may be considered before induction of
anesthesia.
Surgical Considerations
The pathogenesis of acute mitral regurgitation determines its
management. In a series of acute mitral regurgitation, the
causes were acute myocardial infarction (45%), degenerative
valvular disease (26%), and infective endocarditis (28%);
each of these causes is managed by different strategies, and
each has different outcomes.20 Unlike aortic regurgitation, for
which repair is rarely possible, mitral regurgitation may be
treated with either repair or replacement.
Surgical exposure of the mitral valve is critical, and both
surgical incision approaches may need to be considered: a
median sternotomy or an anterolateral or full lateral right
thoracotomy incision. Minimally invasive approaches to
acute mitral valvular regurgitation should be considered by
only the most experienced surgeons. Expeditious use of

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cardiopulmonary bypass, optimal myocardial protection, excellent valve exposure, and short pump runs will lead to the
best results and are less likely achieved through a minimally
invasive approach. Flexibility in the approach to the mitral
valve can also be important, and a variety of techniques
should be considered, particularly if there is complex endocarditis and extensive annular reconstruction is needed. Potential approaches may include the most standard lateral
Sonnegaards groove incision in the left atrium, biatrial
incisions, anterior approaches beneath the aortic root, or
transection of the superior vena cava with a more anterolateral approach to the left atrium, which is particularly useful if
endocarditis is more complex and the annular reconstructions
are more extensive.
Ischemic Mitral Regurgitation
Repair or replacement of the mitral valve in the setting of
acute regurgitation due to myocardial ischemia mandates
attention to revascularization. Careful review of preoperative
coronary angiography, if available, and preparation for aortocoronary bypass grafting are essential. Because these patients tend to be hemodynamically tenuous, time taken for left
internal mammary preparation may be ill advised, and bypass
grafting can be completed with venous conduits. Myocardial
protection in the setting of acute myocardial infarction is
challenging. Both antegrade and retrograde cardioplegia are
usable in this setting. Delivery of antegrade cardioplegia via
newly placed venous conduits can augment myocardial protection. Given the ischemic nature of the myocardium,
metabolically enhanced, slow warm induction may have
beneficial effects. Furthermore, controlled reperfusion at the
conclusion of the operation may also allow for more brisk
recovery of myocardial function. In general, intra-aortic
balloon counterpulsation is maintained for at least 24 hours
after the conclusion of the operation.
Papillary muscle rupture is a rare complication of myocardial infarction, occurring in 1% to 3% of myocardial infarctions, with a mortality of 80% with medical therapy alone.31,32
Historically, operative mortality was as high as 67%, and
patients were frequently denied surgery. With the addition of
bypass grafting to mitral valve replacement or repair, operative mortality now is 10%.33
Mitral Valve Endocarditis
When endocarditis is the underlying cause of acute regurgitation, the principle of excising all sites of active infection
drives the therapeutic approach. Once the infection is excised,
then the decision to repair (leaflet), replace (chord or entire
valve), or reconstruct (annulus) will be critical. The most
difficult reconstructions involve the fibrous trigone of the
heart, where the annular support of both the aortic and mitral
valves is involved, the tissues are edematous and friable, and
the 3-dimensional visualization for the reconstruction can be
difficult, even for the experienced surgeon. Availability of
aortic homografts may be optimal in cases of infective
endocarditis, in which both the mitral and aortic annuli are
involved with active infection or abscess.
Reoperative mitral valve surgery, such as in the case of
prosthetic valve endocarditis, poses unique challenges to the
surgeon. Manipulation of the mitral annulus, coupled with

Figure 4. Operative technique for repair of rupture posterior

mitral valve chordae. A, A flail portion of the posterior leaflet is
treated by resection of the unsupported portion of the leaflet. B,
One or 2 pledgetted sutures are used to reinforce the annulus at
the site of leaflet resection, and the leaflet is repaired with running 5-0 multifilament nonabsorbable sutures. Although the middle scallop of the posterior leaflet is most commonly affected,
up to 60% of the posterior leaflet may be resected. A posterior
annuloplasty completes the repair. This illustration is typical of a
Carpentier quadrangular repair, most often used with mitral
valve prolapse and ruptured chord. The repair technique may
also be used in other situations, such as endocarditis. Modified
from Gillinov M, Cosgrove D. Mitral valve repair. Operative
Techniques in Thoracic and Cardiovascular Surgery.
1998;3:95108.

ongoing infection and previous scar, can result in atrioventricular disruption with even the most gentle of maneuvers.
This catastrophic event is highly lethal and must be considered and anticipated if possible.
Mitral Valve Repair
Valve repair is always preferable to valve replacement, when
possible. Valve repair is more likely to be an option in acute
mitral regurgitation than in acute aortic regurgitation. Once
again, therapeutic options and surgical priorities must be
judged on the basis of pathogenesis, acute pathophysiology,
underlying pathology, and comorbidities. Keys to success are
accurate assessment of preoperative data, good surgical
judgment, and expeditious operations. When the technical
results are unacceptable with the initial procedure, use of a
second pump run and repeated repair or replacement are
necessary. Thus, repair should be undertaken only in those
situations in which procedural success is likely because an
unstable patient may not tolerate additional bypass time. In
those situations with confounding myocardial ischemia or
infarction, additional attention to detail must come into play
in planning and executing the operation, including optimal
myocardial protection, appropriate coronary revascularization, rational use of inotropic drugs, and selected use of
mechanical circulatory assistance. The extent and priorities of
the operation will be affected by many issues, including the
presence of papillary muscle rupture; chordal rupture; annular
dilation; hibernating, stunned, or infarcted myocardium; and
the severity of coronary artery disease.
All techniques for mitral valve repair can come into play:
annuloplasty with rings, annular reconstruction with pericardium, leaflet resection, leaflet reconstruction with pericardium, chordal replacement, vegetation excision, and edge to

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Stout and Verrier

Acute Valvular Regurgitation

3239

Figure 5. An approach to the general evaluation

and management of acute valvular regurgitation.
CXR indicates chest x-ray; ECG, electrocardiogram; TTE, transthoracic echocardiogram; TEE,
transesophageal echocardiogram.

edge (Alfieri) approximation. Valve repair is more common

in situations in which acute annular dilation is the cause, such
as ischemia, or in which the pathology only involves the
posterior leaflet, such as myxomatous valve disease or
endocarditis (Figure 4), with or without annular dilation. The
ability to repair the mitral valve dramatically lessens when
there is annular involvement with infection or anterior leaflet
involvement with degenerative disease.
Mitral Valve Replacement
Mitral valve replacement is needed when repair is not
possible or there is likely to be significant residual mitral
regurgitation after attempted repair. Patients with acute mitral
regurgitation are unlikely to tolerate reexploration and replacement after an unsuccessful repair, particularly if the
attempted repair was complex and time consuming. Therefore, mitral valve replacement may be the preferable choice if
valve anatomy is unfavorable or when the only option for
repair is complex. This is especially true with tissue destruction due to endocarditis, in which case, more commonly than
not, annular involvement precludes simple repair with predictable excellent initial results. The important surgical goal

in valve replacement is to avoid a periprosthetic leak because

of inadequate visualization or poor tissue quality and to
preserve both posterior and anterior chords whenever possible. There is no specific benefit of mechanical versus bioprosthetic prosthesis in degenerative, ischemic, or infectious
situations, although mechanical prostheses are usually preferred for durability, low profile, ease of insertion, and the
possible need for anticoagulation for other acute or chronic
reasons, such as arrhythmia.

Clinical Outcomes
Broadly applicable clinical outcomes in acute valvular regurgitation are difficult to ascertain. The cause of acute valvular
regurgitation is variable for both aortic and mitral valves, the
time to intervention is quite variable, the complexity of
intraoperative repair is unique, and comorbid conditions are
common; outcomes are dependent on multiple factors. Variability in outcomes is also due to incidence and prevalence of
the disease entity, patient selection, era of reporting, and
surgeon experience. Despite the difficulties, certain disease
entities have some available data. A recent report of the
outcomes of endocarditis in a multinational patient cohort

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3240

Circulation

June 30, 2009

emphasized the high mortality of the disease, despite improved medical and surgical therapy.34 Although mortality
has decreased over time, 30-day mortality remains 15% to
20%.34,35 In a series with 48% of patients undergoing surgery,
mortality was increased in those with pulmonary edema but
decreased in those who underwent surgery.34 The SHOCK
trial emphasizes the need for early revascularization to
improve long-term outcomes of patients with acute mitral
regurgitation in acute myocardial infarction.25 Mortality remains high in patients with aortic dissection, with 31.4%
mortality for unstable patients undergoing surgery for type A
dissections.36 The presence of shock increases the risk of poor
outcomes, and therefore, when possible, operative intervention before the onset of shock is one means of improving
results. The cause of acute regurgitation also drives outcomes, as demonstrated by a recent report of a series of
patients undergoing surgery for acute severe mitral regurgitation that demonstrated an overall 30-day mortality of 22.5%
with the best outcomes in those patients with degenerative
disease.20

Conclusion
Acute valvular regurgitation is a surgical emergency that
requires appropriate diagnosis and rapid intervention for
optimal outcomes (Figure 5). Because the examination findings of acute regurgitation are different and often more subtle
than those of chronic regurgitation, the diagnosis is often
missed when a patient presents with dyspnea and shock. A
high index of suspicion and echocardiography are important
in rapid diagnosis, and surgical treatment should proceed as
quickly as possible. Surgical mortality remains high; however, medical therapy is not sufficiently effective to obviate
the need for surgery.

Acknowledgments

3.

4.

5.

6.

7.

8.

9.

10.

11.
12.

13.

14.

15.

We thank Nahush Mokadam, MD, for his assistance with surgical

diagrams.
16.

Disclosures
None.
17.

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KEY WORDS: aortic valve

mitral valve insufficiency

aortic valve insufficiency mitral valve

valvular heart diseases valves

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Acute Valvular Regurgitation

Karen K. Stout and Edward D. Verrier
Circulation. 2009;119:3232-3241
doi: 10.1161/CIRCULATIONAHA.108.782292
Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright 2009 American Heart Association, Inc. All rights reserved.
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