250

NASPE 25TH ANNIVERSARY SERIES

Cardiac Surgery for Arrhythmias

JAMES L. COX, M.D.
From the Division of Cardiothoracic Surgery, Washington University School of Medicine, St. Louis, Missouri, USA

Cardiac Surgery for Arrhythmias. Cardiac arrhythmia surgery was initiated in 1968 with the first
successful division of an accessory AV connection for the Wolff-Parkinson-White syndrome. Subsequent
surgical procedures included the left atrial isolation procedure and right atrial isolation procedure for
automatic atrial tachycardias, discrete cryosurgery of the AV node for AV nodal reentrant tachycardia,
the atrial transection procedure, the corridor procedure, and the maze procedure for atrial fibrillation,
the right ventricular disconnection procedure for arrhythmogenic right ventricular tachycardia, and the
encircling endocardial ventriculotomy, subendocardial resection procedure, endocardial cryoablation, the
Jatene procedure, and the Dor procedure for ischemic ventricular tachycardia. Because of monumental
strides in the treatment of most refractory arrhythmias by endocardial catheter techniques during the past
decade, the only remaining viable surgical procedures for cardiac arrhythmias are the maze procedure for
atrial fibrillation and the Dor procedure for ischemic ventricular tachycardia. Nevertheless, the 25 to 30
years of intense activity in the field of cardiac arrhythmia surgery provided the essential foundation for
the development of these catheter techniques and represent one of the most exciting and productive eras
in the history of medicine. In one short professional career, we have witnessed the birth of arrhythmia
surgery, its adolescence as an “esoteric” specialty, its prime as an enlightening yet exhausting period, and
finally its waning years as a source of knowledge and wisdom upon which better methods of treatment have
been founded. One could hardly ask for a more rewarding experience. (J Cardiovasc Electrophysiol, Vol. 15,
pp. 250-262, February 2004)

intraoperative mapping, Wolff-Parkinson-White syndrome, left atrial isolation, cryosurgery, atrial fibrillation,
maze procedure, right ventricular disconnection, Dor procedure, mini-maze procedure

Perspective
During the past quarter century, surgery has played a
pivotal role in the elucidation of the anatomic and elec-
trophysiologic abnormalities responsible for supraventric-
ular and ventricular tachyarrhythmias. The development
of sophisticated electrophysiologic systems for intraopera-
tive mapping, and the anatomically precise surgical tech-
niques that were designed, resulted in the ability to cure
the majority of medically refractory cardiac arrhythmias.
Knowledge gained from the electrophysiologically guided
surgical approaches to the Wolff-Parkinson-White (WPW)
syndrome and AV nodal reentrant tachycardia contributed
in large part to the subsequent development of endocar-
dial catheter techniques capable of curing those specific
arrhythmias without the need for surgical intervention.1,2
These intellectual and technologic advances, along with the
increasing sophistication and availability of antitachycar-
dia pacemakers and implantable cardioverter defibrillators3
for refractory ventricular tachyarrhythmias, eventually nar-
rowed the indications for surgical intervention for cardiac
arrhythmias.
Despite this dramatic progress in nonsurgical interven-
tional therapy, surgery has remained an important therapeu-
Address for correspondence: James L. Cox, M.D., 13523 Rosewood Lane,
Naples, FL 34119. Fax: 239-598-4090; E-mail: jamescoxmd@aol.com
doi: 10.1046/j.1540-8167.2004.03656.x
tic modality for the treatment of cardiac arrhythmias into the
21st century. The first extensive electrophysiologic mapping
of human atrial fibrillation4 and the subsequent development
of a surgical technique for the treatment of atrial fibrilla-
tion in the late 1980s5-8 spawned a variety of new interven-
tional and surgical approaches to the treatment of this most
common of all cardiac arrhythmias.9-14 Critical to current
interventional techniques was the documentation that most
paroxysmal (i.e., intermittent) atrial fibrillation is induced
by spontaneous ectopic beats originating in or near one or
more of the pulmonary vein orifices in the left atrium.15 The
interventional treatment of continuous atrial fibrillation re-
mains problematic, but with a better understanding of the
differences between intermittent and continuous atrial fib-
rillation and modifications of the original curative surgical
techniques, the ability to cure both forms of atrial fibrillation
seems imminent. Nevertheless, any discussion of the devel-
opment and subsequent history of surgery for cardiac arrhyth-
mias must begin with God’s Gift to Electrophysiology . . . the
Wolff-Parkinson-White syndrome.
WPW Syndrome
16
Gaskell was the first to demonstrate that electrical activ-
ity propagated from the atrium to the ventricle via myocardial
tissue rather than nerves; his studies on the turtle heart were
reported in 1883. Stanley Kent17 identified muscular connec-
tions between the atria and ventricles of mammals in 1893,
but he erroneously concluded that these connections were

multiple and that they represented the normal pathways of
AV conduction. Despite this misconception, his name serves
as the eponym for the accessory AV connections responsible
for WPW syndrome (“Kent bundles”).
Perhaps the most important work delineating the special-
ized conduction system of the heart was reported in 1906
when Tawara, working in Aschoff’s laboratory in Germany,
identified and characterized the AV node, His bundle, bundle
branches, and Purkinje system.18
During the 1920s, Dr. Paul Dudley White, one of the great
teachers and clinical cardiologists of the 20th century, noted
that a small group of young, apparently normal patients with
ventricular preexcitation on standard ECG had frequent bouts
of paroxysmal tachycardia. During a trip to London, he dis-
covered that Dr. John Parkinson, an English physician, had
collected a similar series of patients. Dr. White suggested
that Dr. Louis Wolff, one of Dr. White’s fellows, combine
their series of patients and report their observations, which
he did in 1930.19 Neither the ventricular preexcitation nor
the bouts of tachycardia were explained, however, until Drs.
Wolferth and Wood reported a patient with the same clinical
syndrome in 1933 and suggested that the ECG abnormali-
ties were due to accessory pathways between the atrium and
ventricle, similar to those previously described by Kent. Al-
though they accepted Kent’s erroneous hypothesis that these
accessory pathways were normal and occurred on the right
free wall, Wolferth and Wood directed their attention to that
region in a patient with the syndrome who died. Fortuitously,
they were able to document an accessory pathway histologi-
cally at autopsy.20
Although the basis for WPW syndrome was suspected,
the issue remained controversial for many years. The picture
became somewhat clearer in 1967, when Dr. Dirk Durrer
of Amsterdam performed intraoperative mapping in a patient
with WPW syndrome and demonstrated electrical conduction
across the AV groove in the region of ventricular preexcita-
tion.21 In the same year, Dr. Howard Burchell of the Mayo
Clinic performed intraoperative mapping in a patient with
WPW syndrome who was undergoing surgery for closure of
an atrial septal defect. After identifying the suspected site of
the accessory pathway on the right free wall, he was able to
abolish ventricular preexcitation by injecting procainamide
into the AV groove at that site.22 Although the preexcitation
returned postoperatively, this procedure demonstrated for the
first time that a surgical technique might be capable of perma-
nently interrupting conduction across an accessory pathway,
thereby curing WPW syndrome. The first surgical attempt at
permanent ablation followed several months later on May 28,
1968, when Dr. Will Sealy of Duke University successfully
divided a right free-wall accessory pathway in a 31-year-old
fisherman (Fig. 1).23 Sixteen years later, Dr. Sealy published
the following comment, which gives some insight into the role
frequently played by serendipity in the advance of medical
science: “Had Kent not published what are now considered to
be incorrect observations, Wood and colleagues might never
have found the right free-wall pathway. Had the fisherman’s
anomalous pathway been anyplace other than the right free-
wall, I would not likely have found it at operation.”24 In fact,
the second patient to undergo surgery at Duke a few weeks
later died in the operating room while undergoing repeated
attempts at surgical ablation of what later was understood to
be a septal pathway, something that was completely unknown
at the time of her surgery.25
Cox Cardiac Surgery for Arrhythmias 251
Figure 1. Operative photograph of the first patient to undergo a surgical
procedure designed specifically and solely to cure a cardiac arrhythmia. The
patient was a 33-year-old fisherman from the Outer Banks of North Carolina
who underwent surgical division of a right free-wall accessory pathway (dot)
by Dr. Will C. Sealy at Duke University on May 28, 1968. (Reproduced with
permission from Cobb FR, Blumenschein SD, Sealy WC, Boineau JP, Wagner
GS, Wallace AG: Successful surgical interruption of the bundle of Kent in a
patient with Wolff-Parkinson-White syndrome. Circulation 1968;38:1018.)
Dr. Sealy’s initial surgical approach was based solely on
the electrophysiologic findings at the time of surgery, and
only approximately 60% of patients were cured by their ini-
tial operation. At the time NASPE was founded, we were
performing more than 100 WPW operations per year, with
a 100% initial cure rate using a technique that was based
on both the anatomy of the AV groove and the location of
the accessory pathway.26 The numbers continued to increase,
and hundreds of cardiac surgeons learned the surgical tech-
niques during the decade of the 1980s. As that decade ended,
however, the radiofrequency (RF) catheter techniques were
introduced, and in 1 month’s time, September 1990, our ar-
rhythmia surgical caseload at Barnes Hospital in St. Louis
dropped from approximately 12 cases per month to zero.
During the ensuing years, we operated on approximately 30
patients who had not responded to catheter therapy and found
that virtually all of them had some underlying anatomic ab-
normality that had precluded their cure by catheter ablation
alone. My last surgical procedure for WPW syndrome was
performed in 1996, and since that time, the operation has
become of historical interest only.
AV Nodal Reentrant Tachycardia
Prior to 1982, the only surgical therapy for medically
refractory AV nodal reentrant tachycardia was surgical di-
vision of the His bundle.27 The objective of elective His-
bundle ablation was to protect the ventricles from AV nodal
reentry. Because the procedure resulted in complete heart
block, however, a permanent ventricular pacemaker was re-
quired postoperatively in all patients. In 1982, Scheinman
described a technique for ablating the His bundle by intro-
ducing an electrical shock through a catheter placed adjacent
to the His bundle.28 This closed chest procedure immediately
252 Journal of Cardiovascular Electrophysiology Vol. 15, No. 2, February 2004
Figure 2. Comparison of preoperative and postoperative AV nodal con-
duction curves obtained during an atrial paced cycle length (PCL) of
400 msec in a patient with AV nodal reentrant tachycardia. The dual AV nodal
conduction pathways (slow pathway and fast pathway) that were present pre-
operatively are no longer present postoperatively as the slow pathway has
been ablated with the cryosurgery. (Reproduced with permission from Cox
JL, Holman WL, Cain ME: Cryosurgical treatment of atrioventricular node
reentry tachycardia. Circulation 1987;76:1329-1336.)
replaced the open heart surgical method for interrupting the
His bundle. However, because the catheter fulguration tech-
nique also created complete heart block, all of those pa-
tients also required implantation of permanent pacemaker
systems.
Although both the surgical technique and the catheter
ablative technique for His-bundle interruption ameliorated
the unpleasant and detrimental effects of AV nodal reentrant
tachycardia, both procedures replaced one type of arrhythmia
(tachycardia) with another (heart block). In 1982, we attained
the first clinical cure of AV nodal reentrant tachycardia using
a discrete cryosurgical technique (Fig. 2).29 Ross et al.30 sub-
sequently reported the cure of AV nodal reentrant tachycardia
using surgical dissection of the perinodal tissues. Guiraudon
and colleagues have reported success with a similar surgical
dissection technique.31
The surgical techniques designed to cure AV nodal reen-
trant tachycardia enjoyed excellent results. There were no
operative deaths in any of the three major series reported.
Following the perinodal cryosurgical procedure, smooth AV
nodal conduction curves through the remaining single con-
duction pathway were demonstrated in all patients in our se-
ries, and none of the patients had inducible AV nodal reentrant
tachycardia postoperatively.32 Moreover, all patients main-
tained normal conduction through the AV node–His-bundle
complex, with no recurrent AV nodal reentrant tachycardia.
The surgical dissection techniques were associated with low
incidences of permanent complete heart block and recur-
rent AV nodal reentrant tachycardia.30,31 Again, however, RF
catheter techniques replaced surgery for AV nodal reentrant
tachycardia,1,2 and the last known surgical procedure for this
problem was our last case in the summer of 1990.
Automatic Atrial Tachycardia
These tachycardias have a focal origin and are due to auto-
maticity, not reentry. They usually originate from the body of
the right atrium or left atrium, although occasionally they may
arise from the interatrial septum. These arrhythmias posed an
interesting and unique problem in the early years of cardiac
arrhythmia surgery. All of the available general anesthetic
agents at that time uniformly suppressed automatic atrial ar-
rhythmias; therefore, it was not unusual to be in the oper-
ating room with the patient’s median sternotomy opened in
preparation for the intraoperative mapping only to have the
arrhythmia “disappear.” This was a common problem even
for atrial tachycardias that had been incessant preoperatively.
Because automatic arrhythmias, by definition, cannot be in-
duced by programmed electrical stimulation techniques, the
surgeon was left with a perfectly normal heart and no means
of localizing and treating the arrhythmia. If nothing further
was done and the incision was closed, the arrhythmia invari-
ably would resume postoperatively as soon as the general
anesthesia “wore off” a few hours later. Therefore, in this
situation the surgeon was forced to proceed on the only in-
formation available from the preoperative studies, i.e., that
the arrhythmia was originating at a level above the AV node.
That meant that the only viable option for the surgeon was to
ablate the AV node–His-bundle complex and insert a perma-
nent pacemaker.
The first surgical advance in the treatment of automatic
atrial tachycardias occurred in the late 1970s as a result of
recognizing that most automatic atrial arrhythmias originate
in the body of the left atrium rather than from the atrial sep-
tum or right atrium. The author deduced that because the
sinus (SA) node resides in the right atrium and the AV node
is in the atrial septum, it was theoretically possible to con-
fine these left atrial tachycardias to the left atrium surgically,
thereby leaving the right atrium and both ventricles in a sinus
rhythm without the need for a pacemaker. After 2 years of an-
imal experimentation to perfect the surgical technique and to
determine the hemodynamic consequences of having normal
right atrial function but no left atrial function, we reported
the left atrial isolation procedure in 1980 (Figs. 3 and 4).33
This was an important procedure in the evolution of
surgery for supraventricular arrhythmias because the surgical
principles that were learned proved to be fundamental to the
future success of the maze procedure for treatment of atrial
fibrillation. A seminal observation was that it was impossible
to isolate the left atrium from the right atrium electrically
unless conduction through the walls of the coronary sinus
was blocked. Further, it was shown that this coronary sinus
conduction took place not in the atrial myocardial fibers sur-
rounding the coronary sinus but in the walls of the coronary
sinus itself. This information later proved to be crucial in
attaining complete conduction block through the “left atrial
isthmus” when performing the maze procedure.34
The second observation was that, in the presence of normal
ventricles, the forward cardiac output is completely indepen-
dent of left atrial transport function as long as the right atrium
remains in synchrony with the right ventricle. This surprising
observation results from the following hemodynamic phys-
iology. Following surgical isolation of the left atrium, the
right atrium continues to beat in synchrony with the right
ventricle and, as a result, the forward output of the right heart
remains normal. This normal right-sided output is delivered

through the pulmonary vasculature to the left side of the heart
where, despite no effective left atrial contraction, the left ven-
tricle immediately adapts to this preload volume by slightly
increasing its end-diastolic volume and delivering a normal
forward left-sided output (Fig. 5). This is the reason the car-
diac output following the maze procedure can still be normal
even if the left atrium is not functioning well, as long as the
right atrial function is normal and remains in synchrony with
the right ventricle.
During the 1980s, the improvement in general anesthesia
techniques and the development of computerized intraopera-
tive mapping systems35 made it possible to localize the site of
Figure 4. Following the left atrial isolation procedure, this patient’s contin-
uous left atrial tachycardia (LA) was confined to the left atrium because of
its surgical isolation. However, the remainder of the heart was in a normal
sinus rhythm, as evidenced by the His-bundle electrogram (HBE). Note that
each beat is initiated in the right atrium (RA) and then propagates through
the His bundle (H) to the ventricles (QRS complex). Also note that on the
standard peripheral lead ECG (leads I, II, and III), the p wave is created
by activation of the left atrium (which is isolated), not the right atrium. A =
atrial; GR = patient’s initials.
Cox Cardiac Surgery for Arrhythmias 253
Figure 3. Left atrial isolation procedure. A: Standard
left atriotomy incision is extended anteriorly (dashed
line) across Bachmann’s bundle to the level of the mitral
valve annulus just to the left of the right fibrous trigone.
B: Anterior extension of the standard left atriotomy has
been completed. Note that the anterior atriotomy ex-
tends across the mitral valve annulus. C: Standard left
atriotomy is extended posteriorly to the level of the
coronary sinus. The remaining portion of the incision
is made transmural from the endocardial side and ex-
tends across the mitral valve annulus posteriorly just to
the left of the interatrial septum. At this point, electrical
activity continues to be propagated in a 1:1 fashion via
the coronary sinus. D: Coronary sinus is cryoablated
circumferentially in the same plane as the posterior
atriotomy to complete the isolation of the left atrium.
The left atriotomy is closed with continuous 4-0 non-
absorbable suture. (Reproduced with permission from
Williams JM, Ungerleider RM, Lofland GK, Cox JL:
Left atrial isolation: New technique for the treatment
of supraventricular arrhythmias. J Thorac Cardiovasc
Surg 19809;80:373.)
Figure 5. Postoperative electrograms of the right atrium, left atrium, right
ventricle, and lead II ECG recorded during simultaneous monitoring of
cardiac output (aortic flow), systemic arterial blood pressure (B.P.), left
ventricular end-diastolic pressure (LVEDP), and pulmonary artery (P.A.)
pressure. In the control tracings, the right and left atria both are being paced,
but the pacing stimulus to the left atrium is delayed 30 msec to simulate
the exact activation pattern that existed preoperatively during normal sinus
rhythm. The pacing stimulus to the left atrium is then abruptly discontinued
(silent L.A.). No alterations in normal AV conduction occur, and there is
no change noted in left ventricular preload, afterload, or cardiac output.
The left atrium is paced at a rate of 300 pulses per minute (L.A. SVT)
with no alteration in normal AV conduction, preload, afterload, or cardiac
output. (Reproduced with permission from Williams JM, Ungerleider RM,
Lofland GK, Cox JL: Left atrial isolation: New technique for the treatment
of supraventricular arrhythmias. J Thorac Cardiovasc Surg 19809;80:373.)
254 Journal of Cardiovascular Electrophysiology Vol. 15, No. 2, February 2004

origin of automatic atrial tachycardias from only a single ab-

normal beat in the operating room. Because most automatic
left atrial tachycardias arise from a single focus, this made
the surgery for these arrhythmias both simple and curative.
However, most automatic right atrial tachycardias were found
to be multicentric in origin; therefore, we developed the right
atrial isolation procedure to confine them to the body of the
right atrium while allowing the sinus node to drive the re-
mainder of the heart in a normal sinus rhythm.36,37 With the
advent of RF catheter ablation techniques in the early 1990s,
surgery for automatic atrial tachycardias became extremely
rare.

Nonischemic Ventricular Tachycardia

Although idiopathic cardiomyopathy, Uhl syndrome, and
a few other even more esoteric conditions can cause non-
ischemic ventricular tachycardias, the majority are caused
by arrhythmogenic right ventricular dysplasia, which was
first described by Guy Fontaine and associates in 1979.38
This syndrome is a congenital cardiomyopathy character-
ized by transmural infiltration of adipose tissue resulting in
weakness and aneurysmal bulging of the infundibulum, apex,
and/or posterior basilar region of the right ventricle. Clini-
cally, patients have intractable ventricular tachycardia orig-
inating from one or all of the three pathologic areas of the
right ventricle and severely decreased right ventricular con-
tractility. Hypertrophic muscular bands in the infundibulum
and anterior right ventricular wall result in apparent pseudo-
diverticula, the so-called feathering appearance of the right
ventricular outflow tract.
Our initial experience with this problem was in 1979,
when we performed localized isolation procedures in the in-
fundibulum of the right ventricle in a 16-year-old girl, and
a few months later a localized isolation procedure of ap-
proximately one third of the RV free wall was performed
in a 66-year-old man. Because arrhythmogenic right ventric-
ular dysplasia commonly presented with multiple morpho-
logic types of ventricular tachycardia, all involving only the
right ventricular free wall, we subsequently combined the two
operations into a surgical procedure that isolated the entire
right ventricular free wall from the remainder of the heart
(Fig. 6).29 This rather drastic but very successful procedure
was capable of confining ventricular tachycardia to the right
ventricle while leaving the remainder of the heart in sinus
rhythm (Fig. 7). Two 16-year-old boys who underwent this
procedure in 1982, one of whom had undergone more than
250 episodes of full cardiopulmonary resuscitation and place-
ment of one of the first implantable automatic defibrilla-
tors, were still alive and well at the time of final follow-up
17 years later. However, with the increased availability of
cardiac transplantation and the improvement in automatic
defibrillators beginning in the mid-1980s, total surgical dis-
connection of the right ventricle from the remainder of the
heart became only a dramatic historical footnote. Neverthe-
less, the physiology learned from this operation contributed
to a better understanding of the interplay between the right
ventricle, ventricular septum, and left ventricle in patients
requiring mechanical left and/or right heart assist devices.
Indeed, the popular contemporary practice of biventricular
pacing for heart failure owes much to the observations that
were made following the performance of this procedure in
Figure 6. Right ventricular disconnection procedure. A: Transmural right
ventriculotomy is placed parallel to and 5 mm from the interventricular
septum, extending from just across the pulmonic valve annulus anteriorly
to the tricuspid valve posteriorly. After identification of the location of the
His bundle and right bundle branch, a second transmural incision is placed
from the posterior pulmonic valve annulus to the anterior medial tricus-
pid valve annulus, exposing the underlying aortic root. B: The posterior
papillary muscle of the tricuspid valve is transferred from the right ventric-
ular free wall to the septum. C: The incisions are closed with a continuous
nonabsorbable suture. (Reproduced with permission from Cox JL: Surgery
for cardiac arrhythmias. In: Current Problems in Cardiology, Volume VIII,
Number 4. Chicago: Year Book Medical Publishers, 1983.)
animal experiments and in patients more than 20 years ago
(Fig. 8).
Ischemic Ventricular Tachyarrhythmias
Our experimental studies in the mid- and late 1960s docu-
mented the heterogeneity of tissue injury in acute myocardial
infarction,39 and the reentrant basis of ischemic ventricular
tachyarrhythmias was confirmed.40-46 Thus, with the advent
of coronary bypass surgery in the late 1960s, it seemed ap-
parent that ischemic ventricular tachycardia would be eas-
ily corrected by this new procedure, because the basis for
the arrhythmia (myocardial ischemia) could be alleviated
by myocardial revascularization. During the 1970s, how-
ever, it became apparent that neither revascularization nor
resection of the injured myocardium resulted in acceptable
cure rates. In addition, the operative mortality rates reported
when these procedures were performed primarily for ven-
tricular tachycardia control were prohibitively high.47 Al-
though the demonstration that ischemic ventricular tach-
yarrhythmias occurred on a reentrant basis improved our
concept of the arrhythmia, there remained a profound igno-
rance of the uncharted interplay between the autonomic ner-
vous system, endogenous humoral stimulants, intracellular

Figure 7. Surface recordings and intracardiac electrograms in a 16-year-
old boy during an episode of right ventricular (RV) tachycardia following
the right ventricular disconnection procedure. The limb lead (I–III) and pre-
cordial lead (V 1 and V 6 ) electrograms demonstrated normal sinus rhythm in
the remainder of the heart documented by right atrial (RA) activity preced-
ing each left ventricular complex. (Reproduced with permission from Cox
JL, Bardy GH, Damiano RJ, et al: Right ventricular isolation procedures
for nonischemic ventricular tachycardia. J Thorac Cardiovasc Surg 1985;
90:212.)
electrophysiology, extracellular electrophysiology, the spe-
cialized conduction system, coronary artery disease, myocar-
dial ischemia and infarction, and normal myocardial conduc-
tion, all of which undoubtedly play a role in the genesis and
perpetuation of ischemic ventricular tachyarrhythmias.
Because of the lack of efficacy of myocardial revascular-
ization and/or resection in controlling ischemic ventricular
tachycardia, several groups began to approach the problem in
a more direct surgical manner. In 1969, both our group48 and
Kaiser et al.49 independently reported intraoperative mapping
in patients with ischemic heart disease to localize the area of
ischemic injury. Fontaine et al.50 performed intraoperative
mapping prior to performing a standard aneurysmectomy in
1974, but in 1975 Wittig and Boineau51 and Gallagher et al.52
first reported the use of intraoperative mapping specifically
to guide the attempted surgical ablation of ischemic ventricu-
Figure 8. By completely isolating the right ventricle from the rest of the heart
surgically, it became possible to evaluate the importance of synchronous
biventricular activation. Optimal cardiac hemodynamics occur when the
right ventricle (RV) activates a few milliseconds before the left ventricle
(LV). Earlier or later activation of the RV in relation to activation of the
LV results in a decrease in the cardiac index. (Reproduced with permission
from Damiano RJ, Asano T, Smith PK, Ferguson TB, Douglas JM, Cox JL:
Electrophysiologic effects of surgical isolation of the right ventricle. Ann
Thorac Surg 1986;42:65-69.)
Cox Cardiac Surgery for Arrhythmias 255
lar tachycardia. In 1978, Guiraudon described the encircling
endocardial ventriculotomy (Fig. 9C), a procedure he had
successfully used to ablate ventricular tachycardia in five pa-
tients.53 Shortly thereafter, Harken and associates described
the endocardial resection procedure (Fig. 9D),54 modifica-
tions of which were the mainstay of surgery for the treatment
of ischemic ventricular tachycardia for the next 15 years.
In the mid-1980s, new surgical techniques were devel-
oped for the surgical resection and repair of left ventricular
aneurysms (Fig. 10).55,56 These techniques were designed
to restore the normal contour of the left ventricle, eliminate
the adverse effects of the septal component of the aneurysm,
and realign the myofibrils of the left ventricular free wall
to restore their optimal contractile function. The functional
improvement of the left ventricle following these reparative
procedures was dramatic and remarkable when compared to
the old technique of simply resecting the aneurysm and clos-
ing the ventricle. The most unexpected and unintended “side
effect” of these procedures was that they essentially cured
ischemic ventricular tachyarrhythmias without the need for
intraoperative mapping or extensive endocardial surgery.57
Their continued success, along with that of interventional
catheter techniques, has obviated the need for the complex
and extensive direct surgical procedures for ischemic ventric-
ular tachycardia that were so popular at the time that NASPE
was founded.
Atrial Fibrillation
Although atrial fibrillation is considered by many to be an
innocuous arrhythmia, it is associated with significant mor-
bidity and mortality due to its three detrimental sequelae: (1)
an irregularly irregular heartbeat, which causes patient dis-
comfort and anxiety; (2) loss of synchronous AV contraction,
which compromises cardiac hemodynamics resulting in vary-
ing levels of congestive heart failure; and (3) stasis of blood
flow in the left atrium, which increases the vulnerability to
thromboembolism.
Optimal medical therapy of atrial fibrillation includes the
use of drugs directed toward rhythm control, i.e., the con-
version of atrial fibrillation to normal sinus rhythm. Unfor-
tunately, these drugs frequently fail, and the therapeutic goal
shifts to rate control, i.e., slowing the ventricular response
rate to atrial fibrillation. Although the ventricular response
rate usually can be controlled medically, it is important to rec-
ognize the fact that the atria are still fibrillating and, therefore,
all three of the detrimental sequelae associated with atrial fib-
rillation persist. Obviously, the hemodynamic compromise is
not as great with a controlled ventricular response rate to atrial
fibrillation, but just as obviously, cardiac hemodynamics are
not restored to normal because of the absence of the atrial
“kick.” Thus, in a large number of patients with atrial fibril-
lation, pharmacologic therapy is less than optimal. Because
medical therapy frequently fails to control atrial fibrillation,
several surgical procedures were introduced in the 1980s to
either ablate the arrhythmia or ameliorate its attendant detri-
mental sequelae.
Initial Surgical Procedures for Atrial Fibrillation
Although the early procedures developed for the surgical
treatment of atrial fibrillation are no longer used, it is virtu-
ally impossible to understand the vagaries of treating atrial
256 Journal of Cardiovascular Electrophysiology Vol. 15, No. 2, February 2004

Figure 9. Diagrammatic cross-section of an anterior

left ventricular aneurysm showing more proximal ex-
tension of the associated fibrosis at the endocardial
level than at the epicardial level (A). Because the
reentrant circuits responsible for ischemic ventricular
tachycardia occur most commonly at the junction of
this endocardial fibrosis and normal myocardium, a
standard left ventricular aneurysm resection (B) does
not ablate or excise them. The encircling endocardial
ventriculotomy (C), localized endocardial (or “suben-
docardial”) resection (D), and endocardial cryoabla-
tion (E) procedures were all introduced specifically
to ablate ventricular tachycardia associated with left
ventricular aneurysms or infarcts. (Reproduced with
permission from Cox JL: Anatomic-electrophysiologic
basis for the surgical treatment of refractory ischemic
ventricular tachycardia. Ann Surg 1983;198:119.)

fibrillation in the operating room without understanding the
lessons of those initial efforts. Most of the failures of con-
temporary catheter and surgical techniques in ablating atrial
fibrillation result from a lack of knowledge of the problems
that were identified, elucidated, and solved in the early days
of development of these surgical procedures.
In 1980, we described the left atrial isolation procedure
(Fig. 3),33 which was capable of confining atrial fibrillation
to the left atrium while leaving the remainder of the heart in
normal sinus rhythm (Fig. 11). This procedure was success-
ful in restoring a regular ventricular rhythm without the need
for a permanent pacemaker. Unexpectedly, it also restored
normal cardiac hemodynamics as described earlier. Thus,

Figure 10. The Dor procedure. After opening the anteroseptal left ventric-
ular aneurysm, the endocardial scar over the distal ventricular septum is
undermined and resected. If either spontaneous or inducible ventricular
tachycardia was present preoperatively, the junction of the scar and normal
myocardium laterally is cryoablated. A circumferential pursestring suture
is placed around the entire base of the aneurysm at the junction of endocar-
dial scar and normal myocardium. When tied down at the proper tension,
this suture restores the normal orientation of the uninvolved muscle fibers
of the ventricle exclusive of the aneurysm. An endocardial patch then is an-
chored at the level of the circumferential pursestring suture to complete the
closure of the ventricle. (Reproduced with permission from Dor V, Saab M,
Coste P, et al: Left ventricular aneurysm. A new surgical approach. Thorac
Cardiovasc Surg 1989;37:11-19.)
Figure 11. Following the left atrial isolation Procedure (see Fig. 3), atrial
fibrillation is confined to the left atrium while the rest of the heart remains
in normal sinus rhythm. Note that the right atrium and right ventricle are
beating in synchrony. The p waves are inconspicuous on the lead II ECG be-
cause of loss of synchronous contraction of the left atrial mass. (Reproduced
with permission from Williams JM, Ungerleider RM, Lofland GK, Cox JL:
Left atrial isolation: New technique for the treatment of supraventricular
arrhythmias. J Thorac Cardiovasc Surg 19809;80:373.)

the left atrial isolation procedure alleviated two of the three
detrimental sequelae of atrial fibrillation, namely, the irregu-
lar heartbeat and the compromised hemodynamics. Unfortu-
nately, because the left atrium may continue to fibrillate, the
vulnerability to systemic thromboembolism was unchanged
following this procedure.
In 1982, Scheinman introduced catheter fulguration of
the His bundle as a means of controlling the irregular cardiac
rhythm associated with atrial fibrillation and other refractory
supraventricular arrhythmias.28 This procedure was also a
type of isolation procedure in that it isolated the supraven-
tricular arrhythmia to the atria and away from the ventricles.
Catheter fulguration eventually was abandoned in favor of
the less traumatic RF ablative techniques that still are in use
today. Elective His-bundle ablation necessitates the implan-
tation of a permanent ventricular pacemaker, which restores
a normal ventricular rhythm. However, the atria continue to
fibrillate following His-bundle ablation; therefore, this tech-
nique alleviates only one of the detrimental sequelae of atrial
fibrillation, the irregular heartbeat. The hemodynamic com-
promise due to loss of AV synchrony and the vulnerability to
thromboembolism are unaffected by His-bundle ablation.
In 1985, Guiraudon described the corridor procedure for
treatment of atrial fibrillation,58 an open heart technique that
isolated a strip of atrial septum (the “corridor”) harboring
both the SA node and the AV node, thereby allowing the SA
node to drive the ventricles. This procedure corrected the ir-
regular heartbeat associated with atrial fibrillation, but both
atria either continued to fibrillate postoperatively or devel-
oped their own asynchronous intrinsic rhythm because they
both were totally isolated from the septal “corridor.” In addi-
tion, both atria were isolated from their respective ventricles,
thereby precluding the possibility of AV synchrony on ei-
ther side of the heart. Therefore, neither the hemodynamic
compromise nor the vulnerability to thromboembolism asso-
ciated with atrial fibrillation were alleviated by the corridor
procedure, and it was soon abandoned.
All three of the surgical and/or catheter techniques devel-
oped up to that time had attempted to isolate and confine atrial
fibrillation to a certain region of the atria so that its effects on
the ventricles could be minimized. It was obvious that a much
better approach would be to try to ablate the atrial fibrillation
itself and thus restore the heart’s normal sinus rhythm. Using
our best canine model for atrial fibrillation,59 the first ablative
surgical procedure tried was a simple incision encompassing
all of the orifices of the pulmonary veins to totally isolate
them from the remainder of the heart.7 Unfortunately, this
incision had no effect whatsoever on the ability of the atria to
fibrillate in any of the animals. This is particularly interesting
in view of the subsequent demonstration of the importance of
the pulmonary vein orifices in serving as the “initiating site”
for intermittent atrial fibrillation.
The second series of experiments incorporated pulmonary
vein isolation plus a lateral incision to the level of the mitral
valve annulus and a medial incision to the interatrial septum.
This surgical technique also had no effect on the ability of the
atria to fibrillate. The third approach incorporated pulmonary
vein isolation with the left lateral incision, a medial incision
from the pulmonary veins to the interatrial septum posterior
to the superior vena cava orifice and across the anterior limbus
of the fossa ovalis down to the level of the tendon of Todaro.
These incisions prevented the ability of the atria to fibrillate
in every animal. However, once these left atrial and septal in-
Cox Cardiac Surgery for Arrhythmias 257
cisions were completed, the animals immediately converted
from atrial fibrillation to stable atrial flutter. Because we sus-
pected that the atrial “flutter wave” was occurring in the right
atrium, we simply extended the medial left atriotomy across
the body of the left atrium between the superior vena cava
and inferior vena cava posteriorly and down to the level of the
right free-wall tricuspid valve annulus. In the animal model
we were using, this so-called atrial transsection procedure
invariably prevented the induction and maintenance of atrial
fibrillation or atrial flutter in every animal.7 Unfortunately,
the procedure was effective but not curative in its clinical ap-
plication. It was apparent by this time that the surgical cure of
atrial fibrillation would require a more complete understand-
ing of the underlying electrophysiology of atrial fibrillation.
Anatomic-Electrophysiologic Basis of Atrial Fibrillation
Our experimental and clinical studies during the mid-
1980s documented that there are three interacting compo-
nents in atrial flutter and atrial fibrillation that determine
the findings on the peripheral ECG and, therefore, dictate
the clinical diagnosis. These three components are (1) a
macroreentrant circuit(s), (2) passive atrial conduction in that
portion of the atrium not involved in the macroreentrant cir-
cuit, and (3) AV conduction. The electrophysiologic charac-
teristics of these three components define a spectrum of atrial
arrhythmias, extending from simple atrial flutter, through
several types of transitional arrhythmias, to complex atrial
fibrillation.6
In addition to elucidating the mechanism of atrial flutter
and atrial fibrillation, these experimental and clinical elec-
trophysiologic studies also documented that our initial hopes
of obtaining computerized electrophysiologic maps of atrial
fibrillation and using them to guide the specific surgical tech-
nique, as we had done in other arrhythmias, was not feasi-
ble. Because the macroreentrant circuits responsible for atrial
flutter and atrial fibrillation are so fleeting in nature, it was
recognized that it would be impossible to use activation maps
to guide surgery even with online maps. As a result, we sought
to develop a surgical technique that would be capable of in-
terrupting any and all macroreentrant circuits that potentially
might develop in the atria, thereby precluding the ability of
the atrium to flutter or fibrillate. In addition, it was recognized
that the surgical incisions would have to be placed so that the
SA node could resume activity postoperatively and “direct”
the propagation of the sinus impulse throughout both atria.
This would allow all of the atrial myocardium to be activated
postoperatively, resulting in preservation of atrial transport
function, which is a prerequisite for the restoration of normal
cardiac hemodynamics and the prevention of stasis of blood
flow in the left atrium with the resultant potential for throm-
boembolism. The surgical procedure that was conceived to
accomplish these goals is based on the concept of a maze7
and, as a result, was named the “maze procedure.”8
Maze Procedure
The original surgical technique, the maze-I procedure,8
was modified to become the maze-II procedure because of
late chronotropic problems with the SA node and intra-atrial
conduction delays that resulted in decreased left atrial con-
traction. However, the maze-II procedure proved to be ex-
ceedingly difficult to perform technically. As a result, it was
modified again to become the maze-III procedure (Fig. 12),
258 Journal of Cardiovascular Electrophysiology Vol. 15, No. 2, February 2004
Figure 12. The maze-III procedure proved to be the
ideal pattern of lesions to ablate atrial fibrillation with-
out adverse side effects, such as those seen with the
maze-I and maze-II procedures. The original maze-
III lesions are shown in the right panel, with all four
pulmonary veins being encircled as a unit. More re-
cently, the lesion pattern shown in the left panel has
been used because it isolates less of the posterior
left atrium and results in somewhat better left atrial
transport function postoperatively. (Reproduced with
permission from Cox JL, Boineau JP, Schuessler RB,
Lappas DG: Modification of the maze procedure for
atrial flutter and atrial fibrillation. I. Rationale and sur-
gical results. J Thorac Cardiovasc Surg 1995;110:473-
484.)
which soon became the surgical technique of choice for the
treatment of medically refractory atrial flutter and atrial fib-
rillation.60,61 Most of the incisions originally performed as
part of the maze-III procedure eventually were replaced by
cryolesions so that the procedure could be performed by min-
imally invasive techniques.62
Between September 25, 1987, and April 16, 1992, 32 pa-
tients underwent the maze-I procedure and 15 patients the
maze-II procedure. For the reasons mentioned earlier, the
maze-III procedure became the standard thereafter, and by
July 1, 2000, 308 patients had undergone the maze-III pro-
cedure for treatment of atrial flutter and/or atrial fibrillation.
The operative mortality rate was 2.9%, with the indepen-
dent determinants of operative death being (1) preoperative
congestive heart failure, (2) preoperative hypertension, and
(3) performance of the maze procedure concomitantly with a
double-valve replacement. The most common perioperative
complication following the maze procedure was postoper-
ative arrhythmias, usually atrial flutter or atrial fibrillation,
which occurred in 37% of patients. As described earlier, the
maze procedure was designed to interrupt the macroreentrant
circuits that must be able to form for the atria to fibrillate. The
actual physical size of these circuits is determined by the du-
ration of the refractory period at any given site in the atria.
Normally, atrial refractory periods are relatively long; as a re-
sult, the macroreentrant circuits are relatively large, i.e., over
6 to 7 cm in diameter. During the immediate postoperative
period and until the atrial heal from surgery, local refractory
periods may be much shorter and, therefore, the macroreen-
trant circuits can be much smaller. As a result, it is possible to
form macroreentrant circuits between the suture lines of the
maze procedure and, therefore, to have postoperative atrial
fibrillation even after a technically perfect operation.
Because there is a critical relationship between the size of
the macroreentrant circuits, the distance between the maze
suture lines, and the effectiveness of the procedure in curing
atrial fibrillation, this same concept explains why the maze
procedure may fail when performed in extremely large atria.
Because the pattern of incisions is always the same, even in
the presence of normal long atrial refractory periods (and,
therefore, of large macroreentrant circuits), the distance be-
tween the incisions may be so great in large atria that reentrant
circuits still can form between them following the surgery.
This is why the “cut-and-sew” technique is recommended for
extremely large atria so that before the incisions are closed,
atrial muscle can be resected to decrease the distance between
the maze suture lines.
The most surprising of all results is the extremely low in-
cidence (0.7%) of perioperative neurologic events that occur
in association with the maze procedure.63 Preoperatively, all
of these patients of course had atrial fibrillation, and nearly
20% of them had suffered some type of significant throm-
boembolic event due to the atrial fibrillation. Because these
patients have early postoperative atrial fibrillation as often as
other cardiac surgery patients, we believe that careful clo-
sure of the left atrial appendage during surgery most likely
explains this apparent paradox.
In our series, 98% of patients were cured of atrial fibril-
lation by the maze procedure alone and half of the other 2%
of patients were cured with a combination of surgery and
postoperative drug therapy, for an overall initial cure rate of
99%.63 A recent study of the long-term follow-up of these pa-
tients revealed a 15-year cure rate of >95%.64 Interestingly,
the cure rate at 15 years was the same for patients with and
those without concomitant cardiac disease, putting to rest ear-
lier suggestions that the maze procedure was less effective in
patients with mitral valve disease than in those with no appar-
ent structural heart disease.9 Other groups that have adhered
to the concept of the maze procedure have attained similar re-
sults.65-67 Groups that have chosen to modify the procedure
by violating the basic concept of the maze procedure have
suffered poorer results.10,68
One of the major benefits of the maze procedure is that
it essentially abolishes the threat of stroke associated with
atrial fibrillation.69,70 The long-term stroke rate following the
maze procedure is 0.1% per year (Fig. 13). Overall, 15% of
our patients who have pacemakers required pacemakers post-
operatively, but virtually all of them already had pacemak-
ers implanted before surgery, were known to have sick sinus
syndrome preoperatively, or had abnormal SA nodes “un-
masked” by abolishing the patient’s atrial fibrillation. Never-
theless, the need for postoperative pacemakers is higher in our
own series than in most other series,65-67 probably because
of the more extensive extracardiac dissection that we per-
form routinely in “preparing” the field for performance of the
maze procedure itself. This suspicion seems to be confirmed
by the fact that only 6% of our patients required pacemakers
after undergoing the maze procedure using minimally inva-
sive techniques in which we perform very little extracardiac
dissection.
In our series, all patients were documented to have both
right atrial and left atrial transport function in the immedi-
ate postoperative period that contributed to forward cardiac
output. On late follow-up evaluation, 98% of patients have

Figure 13. The maze procedure abolishes the risk of stroke due to atrial
fibrillation (AF). Minor risk factors that increase the likelihood of having a
stroke and/or transient ischemic attack (TIA) due to AF include hypertension,
old age, diabetes mellitus, ischemic heart disease, and congestive heart
failure. The major risk factor is a previous history of stroke and/or TIA.
AC = anticoagulation; I = patients with at least one minor risk factor and
a history of TIA and/or stroke; II = patients with one or more of the minor
risk factors but no history or stroke or TIA; Lone AF = atrial fibrillation
in the absence of any other demonstrable heart disease. (Reproduced with
permission from Cox JL, Ad N, Palazzo T: Impact of the Maze procedure on
the stroke rate in patients with atrial fibrillation. J Thorac Cardiovasc Surg
1999;118:883-840.)
continued to have right atrial transport function, and 93%
of patients who underwent the maze-III procedure also had
documented left atrial function. Because documentation of
atrial transport function is difficult, we have used multiple
tests in various combinations to arrive at these figures. These
tests include transthoracic and transesophageal echocardio-
graphy, dynamic magnetic resonance imaging, and AV se-
quential pacing versus ventricular only pacing, with multiple
determinations of cardiac output.
In 1996, we developed a minimally invasive maze proce-
dure that is performed through a 7-cm incision in the right
anterior fourth intercostal space and uses cryosurgery rather
than surgical incisions for creation of the atrial lesions of the
maze procedure (Fig. 14).62 This newer, less invasive surgical
approach has resulted in earlier extubation, shorter stays in the
intensive care unit, shorter hospitalizations, quicker recuper-
ation and return to work, a decreased need for postoperative
pacemakers (6% vs 17% following median sternotomy), and
Cox Cardiac Surgery for Arrhythmias 259
a decreased incidence of perioperative atrial fibrillation (22%
vs 37% following median sternotomy).
Despite the obvious efficacy of the maze procedure, it has
never been widely adopted by either surgeons or cardiologists
because of its complexity. As a result, we have attempted to
“streamline” the procedure without adversely affecting its
efficacy and now confine our lesion pattern to that of the
so-called mini-maze procedure (Fig. 15). During the past
6 months, we have used a technique that utilizes high-
intensity focused ultrasound to encircle the pulmonary veins
or create the lesion pattern of the mini-maze procedure in
65 patients (Champseur et al., unpublished data). This tech-
nique is performed without cardiopulmonary bypass and adds
an average of only 2 minutes to the overall operative time in
patients undergoing concomitant mitral valve surgery. Per-
formed as a minimally invasive procedure for standalone
atrial fibrillation, it takes only 10 to 12 minutes to complete
the atrial lesions. We now are developing methods to adapt
this technology for use via endoscopy and robotic surgical
techniques to make it even less invasive.
Changing Concepts of the Electrophysiology
of Atrial Fibrillation
The electrophysiology of atrial fibrillation described ear-
lier in which multiple macroreentrant circuits are present in
the atria is relevant once atrial fibrillation has begun. Thus,
the macroreentrant circuits in the atria during atrial fibrilla-
tion are responsible only for the maintenance of atrial fibril-
lation, not for the induction of atrial fibrillation. Therefore,
the real objective of the maze procedure can best be described
as creating atrial lesions that preclude the ability of the atria
to fibrillate by preventing the possibility of macroreentrant
circuit formation. The idea was that if the atria cannot har-
bor macroreentrant circuits, then by definition they cannot
fibrillate.
For a variety of reasons, we were never able to docu-
ment the spontaneous onset of atrial fibrillation in any of
our extensive experimental or clinical studies. However, in
1998, Haissaguerre and colleagues15 published a seminal ar-
ticle documenting that atrial fibrillation usually is induced by
stimulation from a site within the orifice of one or more of
Figure 14. The minimally invasive maze procedure is
performed through a 7-cm right submammary incision
with access through the fourth intercostal space. Lin-
ear cryoprobes are used to create the atrial lesions.
Because cryosurgery is ineffective from the epicardial
surface off pump because of the heat sink effect of the
atrial blood pool, pursestring sutures are placed at crit-
ical points in the atrium to allow the cryoprobe to be in-
serted into the inside of the atrium. The cryoprobe then
is lifted upward against the endocardium of the atrial
wall, and cryothermia is applied from endocardium to
epicardium to ensure complete transmurality. (Repro-
duced with permission from Cox JL: The minimally
invasive maze-III procedure. Oper Tech Thorac Car-
diovasc Surg 2000;5:79-92.)
260 Journal of Cardiovascular Electrophysiology Vol. 15, No. 2, February 2004
the pulmonary veins. This article is at once one of the most
important and one of the most poorly understood articles
ever published in the electrophysiology literature. The find-
ings were completely compatible with our earlier findings; in
fact, they completed the picture of the electrophysiology of
atrial fibrillation. The article by Haissaguerre et al. showed
how atrial fibrillation is induced, and our earlier work showed
how atrial fibrillation is maintained. Unfortunately, the article
was taken by many to mean that all that was needed to cure
atrial fibrillation was to isolate the orifices of the pulmonary
veins, a misconception that led to the development of our
own first surgical procedure to ablate atrial fibrillation (see
earlier). What resulted from the misinterpretation of this ar-
ticle was the development of a variety of surgical devices
and procedures designed to encircle the pulmonary veins
as the sole treatment for atrial fibrillation, an approach that
has resulted in a predictable and unacceptable 30% failure
rate.
This unfortunate misinterpretation of the article by
Haissaguerre et al. ignores the fact that chronic (continuous)
atrial fibrillation, of say 10 years’ duration, does not require
any type of induction stimulus because the atria are always in
atrial fibrillation. It also ignores the seminal work of Wijffels
and Allessie showing that once the atria begin to fibrillate,
they undergo a process of electrical “remodeling” in which
the more they fibrillate, the more they will fibrillate in the fu-
ture, or, as those authors state, “Atrial fibrillation begets atrial
fibrillation.”71,72 These established facts negate any impor-
tance of the pulmonary veins in continuous atrial fibrillation,
which represents approximately one half of the patients who
suffer from atrial fibrillation. Therefore, simple encirclement
of the pulmonary veins is not a scientifically sound surgi-
cal approach to the treatment of chronic atrial fibrillation.
On the other hand, pulmonary vein isolation for the treat-
ment of paroxysmal atrial fibrillation is firmly grounded in
science because of Haissaguerre’s observations and can be
expected to cure upward of 90% of patients with that spe-
cific type of atrial fibrillation if Haissaguerre’s observations
in his highly selected group of patients can be applied to
the general population. Thus, if surgeons are to treat atrial
fibrillation effectively, it is extremely important that they un-
derstand the difference between induction of atrial fibrilla-
tion and maintenance of atrial fibrillation and the difference
between paroxysmal (intermittent) and chronic (continuous)
atrial fibrillation.
Figure 15. The so-called mini-maze procedure, which
is proposed as a streamlined version of the original
maze procedure. It now is believed, although not yet
proven, that the most critical lesions required to ablate
virtually all forms of atrial fibrillation are (1) the pul-
monary vein encircling incision, (2) a lesion from the
bottom of the encircling incision down to the level of the
mitral valve annulus across the “left atrial isthmus,”
(3) circumferential lesion in the coronary sinus in the
same plane as the left atrial isthmus lesion, and (4)
a lesion across the “right atrial isthmus” to preclude
later atrial flutter. (Reproduced with permission from
Cox JL: Atrial fibrillation: II: Rationale for surgical
treatment. (Editorial) J Thorac Cardiovasc Surg 2003;
126:1693-1699.)
Techniques for Ablating Atrial Fibrillation
During Mitral Valve Surgery
Following the phenomenal success of RF catheter abla-
tion for WPW syndrome, AV nodal reentrant tachycardia,
and other supraventricular arrhythmias in the 1990s, clini-
cal electrophysiologists began to apply it for the attempted
treatment of atrial fibrillation.11,12,73 Largely because of
the availability of RF catheters and the initial reports of
Haissaguerre’s studies, surgeons began to use these RF
catheters intraoperatively in an effort to ablate atrial fibril-
lation in patients who already were undergoing surgery for
mitral valve disease.9,10,13,14 The major objective in some of
these approaches10,13 was no longer to create a maze pro-
cedure but rather to encircle the pulmonary veins. Unfortu-
nately, the RF lesions were frequently not transmural, thereby
offering at best only a temporary barrier to electrical conduc-
tion. In addition, pulmonary vein isolation was used in many
patients with continuous atrial fibrillation; thus, the 30% fail-
ure rate was predictable. Unfortunately, without properly un-
derstanding the underlying electrophysiology of atrial fibril-
lation, several medical device companies developed products
designed to do nothing more than encircle the pulmonary
veins even though pulmonary vein encirclement, even when
accomplished by completely transmural lesions, is effective
in only 90% of 50% of the patients with atrial fibrillation.
In actuality, pulmonary vein encirclement alone occasionally
can ablate continuous atrial fibrillation if the isolated “cuff”
of left atrium surrounding the pulmonary veins is so large that
it inadvertently ablates all of the surrounding macroreentrant
circuits in the left atrium. The problem with this scenario is
that so much of the left atrium is excluded by the isolated cuff
that there may be not effective left atrial contraction postop-
eratively. Nevertheless, the overall atrial fibrillation ablation
rate of 70% to 80% that now is being accomplished in some
centers certainly is an improvement over simply ignoring
atrial fibrillation in patients undergoing mitral valve surgery,
as has been the practice in the past.
We continue to apply the complete maze procedure in pa-
tients with atrial fibrillation who require mitral valve surgery,
using the cryosurgical technique rather than the old “cut-
and-sew” technique to avoid leaving suture lines in the pos-
terior left atrium. The technique presently advocated adds
only 20 minutes to the overall procedure and is, as it has
always been, just as effective in patients with mitral valve

disease as it is in patients without mitral valve or other cardiac
disease.74
Summary
The anatomy and physiology learned from the decades
of surgical treatment of WPW syndrome, AV nodal reentrant
tachycardia, automatic atrial tachycardias, ischemic and non-
ischemic ventricular tachyarrhythmias, and atrial fibrillation
provided a rich basis of knowledge and experience for the
eventual success of catheter ablative techniques for cardiac
arrhythmias. A question still remains regarding the ultimate
nonpharmacologic manner in which atrial fibrillation will be
treated. The extremely minimally invasive surgical proce-
dures, including endoscopic and robotic techniques, being
developed are challenging the catheter techniques in their
level of noninvasiveness while proving to be much quicker
and more effective than the catheter approaches. History has
shown, however, that both cardiologists and cardiac surgeons
invariably respond to a challenge by developing ingenious in-
terventional schemes; therefore, the next quarter century of
NASPE should be just as exciting as the first one has been.
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