Ebsteins Anomaly

Dr Awadhesh Kumar Sharma

Sequence of presentation
Anatomy

Work up
Treatment

Embryology

Clinical Features

Tricuspid Valve Anatomy

TV annulus
The tricuspid valve is the most apically (or

caudally) placed valve with the largest

orifice among the four valves.
The tricuspid annulus is oval-shaped and

when dilated becomes more circular.

20% larger than MV annulus .
Normal TV annulus= 3.0 3.5 cm

Leaflets
The tricuspid valve has three distinct

leaflets described as septal, anterior, and

posterior.
The septal and the anterior leaflets are

larger.
The posterior leaflet is smaller and appears

to be of lesser functional significance since

it may be imbricated without impairment of
valve function.

Leaflets
The septal leaflet is in immediate proximity

of the membranous ventricular septum,

and its extension provides a basis for
spontaneous closure of the
perimembranous ventricular septal defect.
The anterior leaflet is attached to the

anterolateral margin of the annulus and is

often voluminous and sail-like in Ebsteins
anomaly.

Papillary Muscles &

Chordae
There are three sets of small papillary

muscles, each set being composed of up to

three muscles.
The chordae tendinae arising from each set
are inserted into two adjacent leaflets.
The anterior set chordae insert into half of
the septal and half of the anterior leaflets.
The medial and posterior sets are similarly
related to adjacent valve leaflets.

Transthoracic Views

Transesophageal Views

Embryologic aspect
The leaflets and tensile apparatus of the atrio ventricular

valves seem to be formed by a process of delamination of

the inner layers of the inlet zone of the ventricles.
Delamination of the right ventricular free wall, continues to
the level of AV junction.
In EA, delamination of these leaflets may have failed to
occur due to an incompletely understood mechanism
Process of delamination is incomplete and falls short of
reaching the level of the AV junction.
The apical portions of the valve tissue fail to resorb
completely.
Distortion and displacement of the tricuspid valve leaflets,
and a part of the right ventricle becomes atrialized.

DEFINITION
Congenital defect
Origins of septal or posterior

leaflets, or both, are displaced

downward into RV
Leaflets are variably deformed
Atrialization of right ventricle
Anterior leaflet is enlarged and

sail-like

Pathologic anatomy of TV
Origin of TV from AV ring & its

chordal attachments are

malpositioned
Leaflets are malformed,

dysplastic (thickened &

distorted), enlarged or reduced
in size
Septal leaflet always affected,

posterior leaflet nearly always,

and anterior leaflet seldom
Septal & posterior leaflets

displaced , maximal
displacement is usually at the
commissure

Top, Normal tricuspid valve with

anterior, posterior,
and septal leaflets in 1 plane.
Middle, Tricuspid valve in right sided
Ebsteins anomaly showing
displacement of posterior and
septal leaflets; maximal displacement
is at the crux of the posterior and
septal leaflets.
Bottom, Tricuspid valve in left-sided
Ebsteins anomaly; the displacement
of leaflets is similar to that in the
right-sided anomaly.
From Anderson et al.16 Used with
permission of the Mayo
Foundation for Medical Education
and Research.

Pathologic
anatomy of RV
Proximal
Atrialized in one fourth of hearts\dilated
When thin moves paradoxically during systole
Electrical potentials are ventricular, but pressure pulse

is atrial contoured
Distal
Smaller than normal RV
RV dilatation
Functional portion is infundibulum, trabeculated apex,

portion beneath anterior cusp

Thinner walled with fewer muscles

Severe Ebsteins
malformation of
tricuspid valve (4chamber view) showing
marked downward
displacement of shelflike posterior leaflet
with attachment to
underlying free wall by
numerous muscular
stumps (arrows),
markedly dilated
atrialized portion of
right ventricle (ARV),
small functional portion
of right ventricle (RV),
leftward bowing of
ventricular septum, and
marked dilatation of
right atrium (RA). LA
indicates left atrium; LV,
left ventricle

Epidemiology
Ebsteins anomaly occurs in 0.3-0.8% of all

congenital heart diseases

1 in 20,000-50,000 live births
Equal male: female occurrence
Mortality in children presenting in the
neonatal period is 30-50%
Mortality at all ages is 12.5%

Arch Anat Physiol 1866:23825

Associated defects
Commonly associated with:
ASD or PFO (90%)
VSD, AV canal defect
Pulmonary stenosis/atresia (20-25%)
Wolff-Parkinson-White

Syndromes:
Down, Marfan, Noonan

sumner RG, Jacoby WJ Jr, Tucker DH.

Ebsteins anomaly associated with
Car-diomyopathy and Pulmonary
Hypertension. Circulation

Etiology
Congenital disease of often

uncertain cause.
Environmental factors
Maternal ingestion of lithium in first

trimester
Maternal benzodiazepine use
Maternal exposure to varnishing
substances
Maternal history of previous fetal
loss
Risk is higher in whites than in

other races.

Genetic factors
Rare cases of cardiac transcription factor NKX2.5

mutations, 10p13-p14 deletion, and 1p34.3p36.11 deletion have been described in the
anomaly .
Recently, Postma et al. reported the results of a
mutational analysis in a cohort of 141 unrelated
probands with Ebstein anomaly.
Eight were found to have a mutation in the gene
MYH7 and six of the eight patients also had left
ventricular noncompaction.
This may warrant genetic testing and family
evaluation in this subset

emanuel R, OBrien K, Ng R. Ebsteins

anomaly: genetic study of 26 families. Br Heart J 1976;38:57.

Origin
1866 A.D.
Hypothesis on single autopsy specimen
He even did not see the patient, when later

was alive
Word used in 1927 A.D.

A pencil
sketch of
Wilhelm
Ebstein
published in
the
Festschrift
celebrating
Ebsteins 70th
birthday.
Published by
permission of
the Mayo
Clinic
Proceedings,
where it was
published by
Mann RJ, Lie
JT.
The life story
of Wilhelm
Ebstein (1836
1912) and his

Clinical presentation

Presentation at various stages

of life
Fetal life:
Diagnosed incidentally by

echocardiography.
Neonatal life and infancy:
Cyanosis and/or severe

heart failure
Improve as pulmonary
vascular resistance
decreases.
Adult life:
Fatigue, exertional dyspnea,

cyanosis, tricuspid
regurgitation and/or right
heart failure, and
palpitations; arrhythmias
are common.

Neonatal presentation
Congestive heart failure
Due to TR and RV dysfunction

Cyanosis
Decreased pulmonary blood flow due to R

L shunt through ASD or PFO

Increased pulmonary vascular resistance in
the neonatal period compounds this problem
Murmur

Later presentation
Cyanosis
Due to R L shunt at atrial level

Fatigue and dyspnea

Secondary to RV failure and decreased LV

ejection fraction
Palpitations and sudden cardiac death
Incidental murmur
Paradoxical embolism

Cyanosis
Fairly common
Right-to-left shunt at the atrial level and/or severe heart

failure
Transient in neonatal life with recurrence in adult life
May appear for the first time in adult life
Transient appearance/worsening of cyanosis in adult life

due to paroxysmal arrhythmias

Once apparent, progressively worsens

Fatigue and dyspnea

Poor cardiac output secondary to right
ventricular failure and decreased left
ventricular ejection fraction.
Palpitations and sudden cardiac

death
SVT in as many as one third of patients

Fatal ventricular arrhythmias

accessory pathways

Arrhythmias
Due to right atrial enlargement and high

prevalence of accessory pathways

30-50% have evidence of WPW secondary
to the atrialized RV tissue
Mapping and ablation are difficult
Atrial dilation disrupts anatomic landmarks
Accessory pathways are often multiple

Electrophysiologic studies
25-30% have accessory pathways
5-25% have evidence of preexcitation on the

surface ECG.
Right-sided pathways are more common.
Fifty percent of the patients have multiple

pathways.
Guide ablative therapy.

Complications
Congestive heart failure
Sudden cardiac death
Bacterial endocarditis
Brain abscess
Paradoxical embolism
Transient ischemic attacks
Stroke

Pregnancy & Ebsteins

Anomaly

Pregnancy seems to be well tolerated with

adequate supervision.

Prenatal presentation
Difficult to diagnose prenatally
Fetal presentation is variable: possible

features include cardiomegaly, RA

enlargement, tricuspid regurgitation or
dysplasia, arrhythmia, or fetal hydrops
Prognosis for the fetus diagnosed in
utero with significant tricuspid valve
disease is very poor (20% survival)
Progressive right heart dilatation
Cardiac failure
Lung hypoplasia
Pulmonary stenosis/atresia

Cardiothoracic area ratio at 33 (A)

and 35 (B) weeks gestational age. A
indicates anterior; P, posterior; R,
right; and L, left.
Circulation September 23, 2003

Prognosis & management

Prenatal prognosis could be significantly

influenced by the ability of foramen ovale

to decompress the right atrium
Arrythmia due to extreme dilatation of the
RA might be a cause of sudden intrauterine
death
Ebsteins anomaly without cardiac failure or
hydrops: vaginal delivery
Cesarean section

Physical Examination
Cyanosis and clubbing - Varying degrees of

cyanosis at various times in life and transient

worsening with arrhythmias
Precordial asymmetry
Usually left parasternal prominence and occasionally

right parasternal prominence

Absent left parasternal (ie, right ventricular) lift an

important negative sign

Jugular venous pulse
May be normal
Large a and v waves late in the course of the

disease, with development of right heart failure

Physical Examination
Arterial pulses
Usually normal
Diminished volume

Heart sounds
First heart sound
widely split with loud tricuspid component
Mitral component may be soft or absent in the presence of
prolonged PR interval.
Second heart sound
usually is normal
widely split when the pulmonary component is delayed due to

RBBB.

Physical Examination
Additional heart sounds and murmurs
Third and fourth heart sounds
commonly present, even in the absence of congestive heart
failure (CHF).
Summation of third and fourth heart sounds, especially with
prolonged PR interval, can mimic an early diastolic murmur.

The holosystolic murmur of tricuspid regurgitation

At the lower left parasternal area and sometimes at

the apex
Murmur intensity and duration increase during
inspiration.

Routine investigation
protocal

12-lead ECG
Rhythm
Usually normal sinus findings
Intermittently SVT, paroxysmal

SVT, atrial flutter, atrial

fibrillation, ventricular tachycardia
Abnormal P waves consistent

with right atrial enlargement

Himalayan P waves

PR interval
Most commonly prolonged
May be normal or short in
patients with WPW (B) syndrome

QRS complex
RBBB

Low voltage in many patients

Chest XRay
Cardiomegaly

( Rounded or Box-like
contour )
Small aortic root

and main
pulmonary artery
shadow
Decreased

pulmonary
vasculature
Large right atrium

Echocardiogram
Standard for diagnosis.
M-mode
Paradoxical septal motion
Dilated right ventricle
Delayed closure of tricuspid valve leaflets

more than 65 milliseconds after mitral valve

closure

Roberson DA, Silverman NH. Ebsteins

anomaly: echocardiographic and
clinical features in the fetus and
neonate. J Am Coll Cardiol

Echocardiogram
Two-dimensional
Apical displacement of the septal leaflet of

greater than 8 mm/m2

Abnormalities in morphology and septal

attachment of the septal and anterior

tricuspid leaflets
Eccentric leaflet coaptation
Dilated right atrium
Dilated right ventricle with decreased

contractile performance
Various left heart structural abnormalities

Echocardiogram
Doppler studies
Varying degrees of tricuspid regurgitation
Excludes associated shunts

Echocardiogram
Assessment of severity and surgical options
Functional right ventricular area less than 35% of total right ventricular area or an

atrialized to functional right ventricular ratio greater than 0.5 associated with
unfavorable prognosis
Functional right ventricular size
Degree of septal leaflet displacement
Amount of leaflet tethering
Magnitude of leaflet deformity and dysplasia
Aneurysmal dilatation of right ventricular outflow tract (right ventricular outflow

tract-to-aortic root ratio of >2:1 on parasternal short axis view)

Moderate-to-severe tricuspid regurgitation

Cardiac MRI
CMR imaging has emerged as another tool

for evaluation of Ebsteins patients

It provides quantitative measurement of

right atrial and ventricular size and systolic

function even in the presence of significant
distortion of right ventricular anatomy.

Yalonetsky S, Tobler D, Greutmann M,

et al. Cardiac magnetic resonance
imaging and the assessment of
Ebstein anomaly in adults. Am J

Cardiac Catheterization
No longer required to make/confirm the

diagnosis
The most diagnostic characteristicTypical atrial pressure & ventricular
intracardiac ECG in the atrialized portion of
the RV
Elevated RAP
R-L atrial shunting with systemic
desaturation
Elevated RVEDP

Natural history

Natural history
It is not uncommon for Ebsteins anomaly to be

undiagnosed until adulthood.

However, late diagnosis is associated with
reduced survival.
The mean age of diagnosis in a study of the
natural history of 72 unoperated patients, was
23.9 10.4 years.
In this group of patients, arrhythmias were the
most common clinical presentation (51%) .
The estimated cumulative overall survival rates
were 89%, 76%, 53%, and 41% at 1, 10, 15, and
20 years of follow-up, respectively.

Natural history
Predictors of cardiac-related death on univariate

analysis included:
Cardiothoracic ratio of 0.65
Increasing severity of TV displacement on
echocardiography
New York Heart Association (NYHA) class III or IV
Cyanosis
Severe TR
Younger age at diagnosis
In a multivariate model, younger age at diagnosis, male
sex, cardiothoracic ratio of 0.65, and the severity of
TV leaflet displacement on echocardiography were
predictors of late cardiac mortality.

Management
Severity Assessment
Guideline/Indications
Medical management
Surgical management
Post operative functional status

Severity assessment

Celermajer Index
Celermajer et al. described an echocardiographic

grading score for neonates with Ebsteins anomaly,

the Great Ormond Street Echocardiography (GOSE)
score, with grades 1 to 4.
The ratio of the combined area of the RA and
atrialized RV is compared to the functional RV and
left heart. This classification is particularly helpful
with neonatal Ebsteins anomaly.
Grade 1: ratio <0.5
Grade 2: ratio of 0.5 to 0.99
Grade 3: ratio of 1.0 to 1.49
Grade 4: ratio 1.5

Celermajer DS, Bull C, Till JA, et al.

Ebsteins anomaly: presentation and
outcome from fetus to adult J Am Coll

GOSE score
Grade
1
2
3

Ratio
<0.5
0.50.99
1-1.49

Mortality
8%
9%

1-1.49

100%

>1.5

100%

(acyanoti
c)

10% (neonatal)
45% (later)

(cyanotic
)

Carpentiers classification
In 1988, Carpentier et al. proposed the

following classification of Ebsteins anomaly

Type A: The volume of the true RV is
adequate
Type B: A large atrialized component of
the RV exists, but the anterior leaflet of the
TV moves freely
Type C: The anterior leaflet is severely
restricted in its movement and may cause
significant obstruction of the RVOT
Type D: Almost complete atrialization of

EBSTEINS ANOMALY
(Carpentiers classification)

TYPE A (M+ C+)

TYPE (M- C -)

M mobility

C - contractility

TYPE B (M+ C -)

TYPE D (tricuspid suck)

CANADIAN CARDIOVASCULAR
SOCIETY
CANADIAN CARDIOVASCULAR SOCIETY
2009 CONSENSUS CONFERENCE
UPDATE ON THE GUIDELINES FOR
THE MANAGEMENT OF ADULTS WITH
CONGENITAL HEART DISEASE

EBSTEIN ANOMALY
Class I
The following situations warrant intervention:
Limited exercise capacity (New York Heart Association class
greater than II) (Level of Evidence: B)
Increasing heart size (cardiothoracic ratio greater than
65%) (Level of Evidence: B)
Important cyanosis (resting oxygen saturations < 90%)
(Level of Evidence: B)
Severe tricuspid regurgitation with symptoms (Level of
Evidence: B)
Transient ischemic attack or stroke (Level of Evidence: B)
Patients who require operation for Ebstein anomaly should be
operated on by congenital heart surgeons who have
substantial specific experience and success with this
operation. Every effort should be made to preserve the
native TV. (Level of Evidence: C)
Presentation at Annual CCS Meeting in Edmonton 2009

Neonatal Ebstein
Neonatal Ebstein
Poor prognosis
Reported survival only 68%
Indiactions for surgury Heart failure
Profound cyanosis

J Clin Invest 1999;104:15671573

Initial management
Prostaglandin infusion
Placement of umbilical catheters
Initiation of mechanical ventilation
Minimum possible mean airway pressure
Tidal volumes of 10-15 ml/kg to overcome

atelectasis
Management of pulmonary hypertension
Diuretics for CHF

Management of pulmonary
hypertension
Nitric oxide
Reduces after load of right ventricle

Sedation
Other pulmonary vasodilators

The surgical options include(a) Biventricular repair (Knott-Craig

approach)
(b) Single ventricle pathway with right
ventricular exclusion (Starnes approach)
(c) Cardiac transplantation.

Biventricular Repair (KnottCraig Approach)

TV is repaired and the atrial septum is

partially closed.
This repair is typically a mono cusp type
based on a satisfactory anterior leaflet
Routine right atrial reduction is important
to reduce the size of the markedly enlarged
heart to allow room for the lungs.
Although early mortality is high (about
25%), the intermediate outcome appears to
be promising.
Survival to hospital dismissal was 74% with
no late
Ann Thorac Surg 2002;73:17861

Right Ventricular Exclusion

Starnes Approach
Starnes et al. pioneered the right ventricular

exclusion approach, which involves:

(a) fenestrated patch closure of the TV orifce,
(b) enlarging the interatrial communication,
(c) right atrial reduction, and
(d) placing a systemic-to-pulmonary artery shunt.
Particularly useful when there is anatomic RVOT
obstruction.
Right ventricular decompression is required as it
passively fills from thebesian venous drainage, this
is usually accomplished with a 4- to 5-mm punch
fenestration in the TV patch
starnes VA, Pitlick PT, Bernstein D, et
al. Ebsteins anomaly appear-ing in
the neonate. A new surgical
approach. J Thorac Cardiovasc Surg

Modified Starnes Repair (Total Ventricular

Exclusion)
Sano et al. modified the Starnes single-

ventricle approach by performing a total

right ventricular exclusion in which the free
wall of the RV is resected and closed
primarily or with a poly tetrafluoroethylene
patch .
This simulates a large right ventricular

plication, which may improve the left

ventricular filling and provide adequate
decompression to the lungs and LV.

Cardiac Transplantation
With the improved results of the

biventricular and single ventricle

approaches, transplantation rarely is
performed in the current era.
Cardiac transplantation remains an option
in the most severe forms of Ebsteins
anomaly, particularly when there is
significant left ventricular dysfunction.

Children & Adults

Children and Adults

Medical
Bacterial endocarditis prophylaxis may be

required in the presence of prosthetic

materials or patches that were used for the
repair.
In mild Ebsteins anomaly, with nearly
normal heart size, and in absence of
arrhythmias, athletes can participate in all
sports.
However, in severe Ebsteins anomaly,
activity is restricted unless it has been
optimally repaired with near normal heart
size and no arrhythmias.

Surgery
INDICATIONS FOR SURGERY
Presence of symptoms,
Cyanosis,
Paradoxical embolization.
Patients who have decreased exercise performance
Progressive increase in cardiothoracic ratio
Progressive right ventricular dilatation and

dysfunction
Onset or progression of arrhythmias
Presence of class III or IV NYHA or significant
symptoms

PRINCIPLES OF SURGERY FOR

EBSTEINS ANOMALY
The following principles are the goals of

surgery:
(a) Closure of any intra cardiac
communications
(b) TV repair or replacement
(c) Ablation of arrhythmias
(d) Selective plication of the atrialized RV
from apex to base,
(e) Reduction right atrioplasty
(f) Repair of associated defects (e.g.,
closure VSD).

Tricuspid Valve Repair

The goal of operation is to obtain a
competent TV, preserve right ventricular
contractility, and to decrease the risk of
late rhythm disturbances.

Danielson Repair
This repair technique was reported in 1979

and was based on the creation of a

monocusp valve using the anterior leaflet.
This consisted of Plication of the free wall of the atrialized RV
Posterior tricuspid annuloplasty
Right reduction atrioplasty

Danielson GK, Maloney JD, Devloo RA.

Surgical repair of Ebsteins anom-aly.
Mayo Clin Proc 1979;54:185192.

Modified Danielson Repair

Modifications involves Bringing the anterior papillary muscle(s) toward the

ventricular septum, which facilitates coaptation of the

leading edge of the anterior leaflet with the ventricular
septum.
Generally, an antero posterior tricuspid purse string or
ringed annuloplasty is used, and atrialized right
ventricular plication is performed selectively. This results
in a TV repair at the level of the functional annulus, in
contrast to the original repair, which brought the hinge
point of the functional annulus up to the true annulus.
A more recent modification includes patch augmentation
of the mid-anterior leaflet with surgical delamination of
attachments to the anterior and/or inferior leafets.

Dearani JA, Danielson GK. Tricuspid

valve repair for Ebsteins anomaly.
Oper Tech Thorac Cardiovasc Surg

THE BRAZIL EXPERIENCE (da SILVA

APPROACH)
The cone repair described by Dr. da Silva from Brazil

when the anatomy allows, as this technique is the most

anatomic of all the repair techniques described.
Specially, some septal leaflet should be present, which
facilitates this repair technique.
The cone technique represents the most anatomic repair
by completion of the delamination process of the TV,
providing 360 degrees of leafet tissue around the AV
junction with its hinge point at the AV groove (true
annulus).
Although not initially described with this technique,
some do supplement the repair with a flexible anterior
annuloplasty band from anteroseptal commissure to
inferseptal commissure whenever possible.

Operative steps for Ebstein's anomaly repair

da Silva J. P. et al.; J Thorac Cardiovasc Surg 2007;133:215-223

Copyright 2007 The American Association for Thoracic Surgery

Relative contraindications to the

cone reconstruction technique
Age >50 years
Moderate pulmonary hypertension
Significant left ventricular dysfunction:

ejection fraction <30%

Complete failure of delamination of the
septal and posterior leaflets with poor
delamination of the anterior leaflet (<50%)
Severe right ventricular enlargement
Severe TV annular dilatation

THE VENTRICULIZATION
PROCEDURE
Ullmann et al. published their results with

the ventriculization procedure in 2004.

This is characterized by reintegration of the
atrialized portion of the RV into the right
ventricular cavity (ventricularization).
This can be obtained by orthotopic
transposition of the detached septal and
posterior leaflets of the TV.
The reimplanted septal leaflet serves as an
opposing structure for coaptation of the
reconstructed AV valve.

Tricuspid Valve
Replacement
Every effort should be made to repair the

TV rather than replacing it, but if TV repair

is not feasible, then porcine bioprosthetic
valve replacement remains a good
alternative.
Most prefer bioprostheses to mechanical

valves due to the relatively good durability

and the lack of need for anticoagulation .
Kiziltan HT, Theodoro DA, Warnes CA,
et al. Late results of biopros-thetic
tricuspid valve replacement in
Ebsteins anomaly. Ann Thorac Surg

One and Half Ventricle

Repair
The BDCPA does two important things in

the setting of Ebsteins anomaly.

First, it reduces venous return to the
enlarged, dysfunctional RV by
approximately one-third
Second, it provides sufficient preload to
the LV to sustain adequate systemic
perfusion when right-sided output is low.
Surgens usually prefer it if the left
ventricular end-diastolic pressure (LVEDP) is
Kopf GS, Laks H, Stansel
HC, et al.
<12 mm Hg, the transpulmonary
gradient
Thirty-year follow-up of superior vena
<10 mm Hg, and the mean
pulmonary
cava-pulmonary
artery (Glenn)
J Thorac
Cardiovasc Surg
arterial pressure <16 shunts.
mm Hg,
before

Indications for the BDCPA

include
Severe RV enlargement and/or dysfunction
Squashed LV (D-shaped LV)
Moderate degree of TV stenosis (mean

gradient >6 mm Hg) as a result of

reduction in the valve orifice area after
repair
RA:LA pressure ratio >1.5, which indicates
poor RV function.
Preoperative cyanosis at rest or with
Chauvaud S, Fuzellier JF, Berrebi A et
exercise
al. Bi-directional cavopulmonary
shunt associated with ventriculo and
valvuloplasty in Ebsteins anomaly:
benefits in high risk patients. Eur J

Heart Transplantation
Heart transplantation rarely is necessary

for Ebsteins anomaly.

Indication for transplantation is usually the
presence of severe biventricular
dysfunction (left ventricular ejection
fraction <25%).

Arrythmia management
The most common atrial tachyarrhythmias in

Ebsteins anomaly are atrial fibrillation and flutter.

Most surgens used successfully the right-sided
cut-and-sew lesions of Cox-maze III procedure in
Ebsteins anomaly.
With the availability of newer devices such as
radiofrequency or cryoablation, the procedure
time for maze procedure is shortened significantly.
A biatrial maze procedure, performed particularly
when there is chronic atrial fibrillation, left atrial
dilation, or concomitant mitral regurgitation.

FUNCTIONAL OUTCOME AFTER

SURGERY