Perspective
Any attempt to describe the historical development of a specific era or discipline in the medical field is ultimately a personal view of that history. This chapter is no different. Having been present at the very beginning of cardiac arrhythmia surgery on May 2, 1968, and having spent 60 years (1964–2024) of focused interest and active participation in the evolution of surgery for cardiac arrhythmias, this chapter describes my own personal journey and is not meant to be the definitive history of cardiac arrhythmia surgery. Many of the great electrophysiologists (EPs) and surgeons who contributed to the basic knowledge that allowed us and others to devise surgical procedures to cure almost all clinical arrhythmias are not mentioned. If they were given their full due, it would take a book, not a book chapter, to describe the complete history of cardiac arrhythmia surgery. Hence, this chapter is presented as “A History,” not “The History.”
The Origins of Cardiac Arrhythmia Surgery
In 1930, the renowned Boston cardiologist Paul Dudley White visited the equally renowned London physician John Parkinson so they could update one another on the latest developments in the world of medicine. As was customary in those days, White brought along one of his young residents, Louis Wolff, to assist him on the long trans-Atlantic journey ( Fig. 1.1 ). White was anxious to show Parkinson a few electrocardiograms (ECGs) he had recorded from several healthy young people in Boston who had recurrent bouts of sudden unexplained tachycardia. White had noted that when these patients were in normal sinus rhythm (i.e., between episodes of tachycardia), their ECGs showed a short P-R interval, an early deflection off the baseline immediately preceding the QRS complex (later termed the “delta wave”), and a wide QRS complex. The tachycardia, however, was characterized by a regular, narrow-complex rate of 240 beats/min with no delta wave.
The only known photograph of (from left to right) Drs. Louis Wolff, John Parkinson, and Paul Dudley White. Date unknown.
Upon arrival in London, and much to White’s surprise, Parkinson promptly produced several similar ECGs recorded from his own patients who had similar clinical histories of sudden tachycardia. Louis Wolff, being the most junior physician in attendance, was assigned the task of researching the literature and writing a paper on their observations, which led to the designation of the condition known thereafter as the Wolff-Parkinson-White (WPW) syndrome. Even though Stanley Kent had described abnormal anatomic connections between the atria and the ventricles in mammalian hearts in 1893 2 ( Fig. 1.2 ), Drs. Wolff, Parkinson, and White did not know that these “Kent bundles” were actually responsible for their newly identified syndrome. Indeed, it took more than three decades for this association to be documented, but it eventually led to a new field of medicine… clinical electrophysiology. However, before this could happen, electrophysiologic mapping techniques and a new method of controlling the onset and termination of arrhythmias had to be developed.
Photomicrograph from Stanley Kent’s 1893 article showing an accessory atrioventricular connection (aka, “Kent bundle,” “accessory pathway”). The entire connection from atrium to ventricle is not seen because its full length was not in the exact plane of this histologic section.
For some reason, a disproportionate number of the seminal observations and developments related to the electrical activity of the heart have emanated from the Netherlands. Thus, it is not surprising that although electrophysiological mapping was first reported at the beginning of the 20th century, , the technique was not fully developed until mid-century by A.M. Scher in Seattle, who used intramural needle electrodes in the ventricle and most particularly by a Dutch physician, Dirk Durrer ( Fig. 1.3 ), who developed a method for recording local electrograms directly from the surface of the heart. Durrer realized that by comparing the timing of a “roving” handheld epicardial electrode with a fixed electrode, he could reconstruct the timing sequence of the electrical activation of the heart or at least of its epicardial surface. This became known as “activation time mapping” (see Chapter 6 ). Durrer’s protégé, Hein J.J. Wellens, who was also from the Netherlands, subsequently developed a pacing technique called “programmed electrical stimulation” that provided a means of inducing and terminating most clinical arrhythmias. Activation mapping and programmed electrical stimulation became the foundation of all subsequent clinical electrophysiology, cardiac arrhythmia surgery, and the catheter ablation of arrhythmias.
Photo of Professor Durrer taken by John Boineau during his year studying with Durrer in 1963 to 1964 as the professor was leaning out an open window of a Dutch windmill near Amsterdam.
In 1963, John Boineau ( Fig. 1.4 ), a young assistant professor of pediatric cardiology at Duke University, spent a year studying with Durrer in Amsterdam. Boineau returned to Duke in the summer of 1964 to work with Dr. Madison Spach, the revered chief of pediatric cardiology at Duke, on various arrhythmia problems in children and young adults, the most important of which was WPW syndrome. Ironically, Andrew Wallace, a colleague in cardiology (and Boineau’s undergraduate classmate at Duke), had also just returned to Duke from the National Institutes of Health, where interest was also increasing in this newly emerging clinical electrophysiology field. Wallace asked Dr. Will Sealy, a renowned professor of thoracic surgery at Duke, for some space in his research laboratory where he could study the WPW syndrome, and Sealy graciously provided the necessary space. Thus, in 1964 Boineau and Wallace independently and simultaneously established two of the earliest, most productive, and most competitive electrophysiology laboratories in the world that were located less than 100 yards from one another on the Duke University campus.
Photo of a young John Boineau (c. 1964) at the time he returned to Duke University after spending a year with Durrer in the Netherlands.
Several other individuals in the United States were active in this young field of clinical electrophysiology by that time, most notably Brian Hoffman and Paul Cranefield at Columbia-Presbyterian in New York City, E. Neil Moore at the University of Pennsylvania in Philadelphia, and Dan Brody, Leo Horan, and Nancy Flowers at the University of Tennessee in Memphis. I was privileged to begin my own career in the electrophysiology laboratory of Horan and Flowers ( Fig. 1.5 ) in Memphis in that seminal year of 1964 as Boineau and Wallace were returning to Duke. In November 1966, I presented a paper at the American Heart Association (AHA) in New York City that was the first to delineate and characterize the “ischemic border zone” surrounding acute myocardial infarction (MI) and to suggest this zone as being the source of ischemic ventricular tachyarrhythmias. During that meeting, Nancy Flowers introduced me to John Boineau, a person who would have a powerful influence on me for the remainder of his life.
(From left to right) Drs. Nancy Flowers and Leo Horan, who had one of the few experimental electrophysiological laboratories in the world in the early 1960s at the University of Tennessee School of Medicine in Memphis. They believed that ischemic ventricular tachycardia secondary to myocardial infarction (MI) most likely arose from myocardium located between the dead tissue in the center and normal tissue outside of the infarct. However, such an “ischemic zone” surrounding an MI had never been documented histologically. To identify it, in 1964 they provided the author, a freshman medical student, with an assistant and a small laboratory that harbored a grocer’s standard meat slicer, a cryotome, a tank of liquid nitrogen, and a copy of Pearce’s Textbook of Histochemistry . They also provided financial support and a lot of encouragement.
In 1967, the long-standing controversy regarding the anatomic–electrophysiologic basis of the WPW syndrome was seemingly solved when Boineau and Moore provided the most convincing evidence to date that Kent bundles were indeed responsible for the abnormal electrical activation in the WPW syndrome. They first performed detailed mapping of a dog with the WPW syndrome and then asked Duke’s renowned cardiac pathologist Don Hackel to cross-section the atrioventricular (AV) groove serially in the general region of earliest ventricular activation. Hackel documented the presence of an anatomic accessory pathway (Kent bundle) that spanned the AV groove between the atrium and the ventricle at the precise anatomic site of ventricular preexcitation ( Fig. 1.6 ). Although this laboratory observation was made in 1967, it was not published until 1970. Nevertheless, it immediately convinced the EPs at Duke that accessory AV connections (aka, accessory pathways, or Kent bundles) were responsible for the WPW syndrome and suggested that the problem might be curable by surgical division.
The accessory pathway (AP) in a dog that was identified by John Boineau and Neil Moore in 1967 documenting that the Wolff-Parkinson-White syndrome was caused by these abnormal connections between the atrium and ventricle. (Reproduced from Boineau JP, Moore EN. Evidence for propagation of activation across an accessory atrioventricular connection in types A and B pre-excitation. Circulation. 1970:41(3):375–397.)
In 1967, Howard Burchell of the Mayo Clinic successfully blocked conduction across an accessory pathway in a patient undergoing surgery for closure of an atrial septal defect by Dwight Magoon ( Fig. 1.7 ). The site of the accessory pathway in the AV groove of the right free wall was first identified by intraoperative mapping, and the AV groove was then injected with lidocaine at that site. The abnormal conduction across the accessory pathway abruptly stopped and did not return until several hours after surgery when the effects of the drug had abated.
Drs. Howard Burchell (top) and Dwight Magoon (bottom) of the Mayo Clinic were the first to temporarily block conduction across an accessory pathway in a patient with the Wolff-Parkinson-White syndrome in early 1968. The site of earliest ventricular and atrial preexcitation is on the right free-wall at the curvature of the right ventricle. See text for further description.
(Reproduced from Burchell HB, Frye RL, Anderson MW, et al. Atrial-ventricular and ventricular-atrial excitation in Wolff-Parkinson-White syndrome (type B): temporary ablation at surgery. Circulation. 1976:36:663.)
Documentation of the anatomic-physiologic relationship between accessory AV connections and the WPW syndrome by Boineau and Moore, coupled with the clinical experiment of Burchell and McGoon, emboldened the involved parties at Duke University to attempt a surgical approach in a patient with the WPW syndrome. As a result, on May 2, 1968, with Drs. John Boineau performing the preliminary intraoperative mapping procedure, Dr. Will Sealy performed the first operation ever devised specifically for the treatment of a cardiac arrhythmia. He divided the accessory pathway responsible for the WPW syndrome in a fisherman from the outer banks of North Carolina ( Fig. 1.8 ). The fisherman lived for another 32 years and never again experienced a single episode of tachycardia.
John P. Boineau (bottom) and Will C. Sealy (top) of Duke University were the first to permanently block conduction across an accessory pathway on May 2, 1968. This successful operation initiated the era of surgery for cardiac arrhythmias. The right atrioventricular groove was dissected from the epicardial approach for approximately 1 cm on either side of the mapped location of the accessory pathway (black dot) . See text for further discussion.
Despite the success of this famous landmark surgical procedure, the second patient, on whom I was the third surgical assistant as a surgical intern at Duke, was not so fortunate. Her accessory pathway was located in an area that was later designated as the “anterior septal space,” but at the time of her surgery the septum had not yet been recognized as a potential site of accessory pathways. Long hours of intraoperative mapping and surgical dissection resulted in her perioperative death, and a gloom settled over the entire concept of subjecting patients to such a risky surgical procedure to cure an elusive problem that was not life threatening.
The Maturing of Cardiac Arrhythmia Surgery
I went to Duke in 1967 not because of my interest in electrophysiology but as a surgical intern interested in being trained as a cardiothoracic surgeon by David C. Sabiston, Jr. Nevertheless, having already spent 3 years during medical school in the electrophysiology research laboratory of Horan and Flowers in Memphis, I became involved rather early in my surgical residency with the electrophysiology pioneers at Duke who were quietly creating this new specialty of clinical electrophysiology. During my second year of surgical training, John Boineau came up to me in the surgical intensive care unit one day and asked if I was the same person who had worked with Horan and Flowers whom he had met at the AHA meeting in New York 2 years earlier. When I answered yes, he asked if I would consider working in his research laboratory, and thus began our lifelong association.
Boineau’s laboratory ( Fig. 1.9 ) was primarily focused on further elucidating the genesis of ischemic ventricular arrhythmias in the “ischemic border zone” surrounding acute myocardial infarctions, , the subject of my previous research with Horan and Flowers. , Also during that year, we continued to try to explain the vagaries and persistent mysteries of the WPW syndrome. Even though Boineau and Moore had already demonstrated the anatomic basis of the syndrome in its simplest form and Sealy had cured a patient with surgery based on that knowledge, the syndrome was still poorly understood. In fact, many authorities persisted in their belief that the WPW syndrome was caused by a phenomenon called “longitudinal dissociation in the His bundle.” Thus, in the summer of 1969, the elucidation of the basis of the WPW syndrome with all its ramifications remained a challenge.
John Boineau’s electrophysiology laboratory crew at Duke University in 1969. Boineau and the author are identified. The man in the yellow shirt is Jack Kasell, who built all of the electrical stimulators, electrodes, and mapping devices used in the laboratory to study arrhythmias. The man kneeling in the center is Dr. Tom Daniel, who was also a Duke surgical resident several years senior to me in the program. Dr. Sabiston called us into his office one day and asked Tom if we wanted to be an “arrhythmia surgeon” in the future. Tom said he wasn’t exactly sure what that meant, so he answered “no.” Dr. Sabiston then asked me the same question and I answered “yes” even though the meaning of the designation “arrhythmia surgeon” was not clear to me either. Tom later became a highly respected professor of thoracic surgery at the University of Virginia.
This problem was substantially clarified by two fortuitous events that occurred that year. First, Neil Moore, a PhD, DVM, and EP from the University of Pennsylvania, brought a huge black dog with a ventricular septal defect and the WPW syndrome down to Duke in the back of his station wagon one day so that he and Boineau could map its electrical abnormality. That study revealed for the first time that accessory pathways could occur in the septum , which was unknown at the time. It was an observation that many years later would be recognized by John Gallagher as the source of the problem that had occurred with Sealy’s second patient who had died during surgery. In retrospect, she had an unrecognized anterior septal pathway that could simply not be reached surgically from the epicardial surface of the heart.
A few weeks later, Boineau received a call from Bowman-Gray Medical School at Wake Forest University in Winston-Salem, North Carolina, about one of the rhesus monkeys in their arteriosclerosis colony that had the pattern of the WPW syndrome on its ECG. The next day, Boineau and I drove to Winston-Salem, some 80 miles away, and transported the monkey back to his laboratory in Durham in the back seat of the car. We mapped the monkey extensively that very evening and Boineau finally deduced that the monkey had not one, but two accessory pathways. This finding, along with that from Neil Moore’s dog, provided most of the final pieces of the puzzle of the WPW syndrome in humans.
In 1970, John Gallagher became the head of Duke’s newly formed “Clinical Electrophysiology Service” ( Fig. 1.10 ) as I was beginning a 2-year tour of active military duty in the US Army. Dr. Sealy was still working on developing surgical techniques for the different types of the WPW Syndrome. Unfortunately for me, Boineau left Duke for the University of Southern California during the 2 years that I was away from Duke on active duty in the Army. During the subsequent decade of the 1970s, while I was completing my residency in cardiothoracic surgery at Duke, Sealy and Gallagher continued to clarify the anatomic–electrophysiologic basis of WPW syndrome and its surgical treatment.
John Gallagher, chief of clinical electrophysiology at Duke University from 1970 to 1983. It was primarily through his efforts, brilliance, and devotion that cardiac arrhythmia surgery eventually developed into an identifiable subspecialty of clinical medicine.
Surgery for All Cardiac Arrhythmias Except Atrial Fibrillation (Non–Atrial Fibrillation Arrhythmias)
Because of the enormous strides that were made in clinical electrophysiology from Durrer’s first activation time mapping in 1957, through the seminal experimental observations of the 1960s, to the ability to cure the WPW syndrome surgically on a routine basis in the 1970s, the stage was set to develop surgical procedures that would cure all other clinical cardiac arrhythmias. The interest in surgery for cardiac arrhythmias shifted in the late 1970s from the WPW syndrome to ischemic ventricular tachycardia (VT) primarily because of the efforts in Paris of Dr. Gerard Guiraudon (surgeon) and Guy Fontaine (EP) ( Fig. 1.11 ). Guiraudon visited Duke in 1976, and Drs. Sealy, John Gallagher, Guiraudon, and I had a memorable dinner one evening when we spent several hours cutting napkins into multiple patterns trying to create a way to treat ischemic VT. Shortly thereafter, Guiraudon and I performed an “encircling endocardial ventriculotomy” together in Paris for ischemic VT ( Fig. 1.12 ). Almost simultaneously and totally independently, Drs. Alden Harken (surgeon) and Mark Josephson (EP) at the University of Pennsylvania ( Fig. 1.13 ) performed a “subendocardial resection,” which quickly became the procedure of choice for the surgical treatment of ischemic VT.
Drs. Gerard Guiraudon (left) and Guy Fontaine (right) of Pitié Salpêtrière Hospital of the Sorbonne in Paris, two of the earliest pioneers in the surgical treatment of ischemic ventricular tachycardia (VT), who developed the encircling endocardial ventriculotomy. The procedure was soon abandoned because of the unacceptable operative mortality rate, but nevertheless, it contributed significantly to the understanding of ischemic VT and its surgical treatment. Fontaine was also the first to describe arrhythmogenic right ventricular dysplasia, a frequent cause of non-ischemic VT.
Guiraudon and the author performing one of the earliest encircling endocardial ventriculotomies together in Paris on November 22, 1978. Both John Gallagher and Guy Fontaine were in the operating room with us and Gallagher took this photo during the operation. Photo by John J. Gallagher, MD.
