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The surgical treatment of atrial fibrillation
J
THORAC CARDIOVASC SURG
1991;101:402-5
The surgical treatment of atrial fibrillation I. Summary of the current concepts of the mechanisms of atrial flutter and atrial fibrillation Atrial fibrillation is a common arrhythmia that is frequently resistant to medical therapy and has no satisfactory surgical therapy. The development of an effective surgical procedure to treat atrial fibrillation has been hampered by the paucity of clinically relevant information on the basic mechanisms respomible for the arrhythmia. This paper summarizes the current concepts of the electrophysiologic abnormalities in atrial flutter and fibrillation.
James L. Cox, MD, Richard B. Schuessler, PhD, and John P. Boineau, MD, St. Louis, Mo.
Atrial fibrillation is a common arrhythmia that afflicts over one million persons in the United States alone. The medical treatment of atrial fibrillation is less than optimal in that it frequently fails to ablate the arrhythmia and is ultimately directed only toward the control of the ventricular response rate. This results in patients (1) continuing to experience the unpleasantness of an irregular heartbeat, (2) continuing to suffer the consequence of impaired hemodynamics because of loss of atrioventricular synchrony, and (3) remaining vulnerable to the thromboembolic complications of atrial fibrillation. Perhaps the greatest impairment to the development of an effective surgical treatment for atrial fibrillation has been the lack of understanding of the basic electrophysiologic mechanisms responsible for the genesis and perpetuation of this arrhythmia. Unfortunately, virtually all of the scientific information relating to the underlying mechanisms responsible for atrial fibrillation has been generated from animal models that bear little similarity From the Division of Cardiothoracic Surgery, Department of Surgery, Washington University School of Medicine, Barnes Hospital, St. Louis, Mo. Supported by National Institutes of Health Grants ROI HL33722 and ROI HL 32257 and an American Heart Association grant, funds contributed in part by the American Heart Association, Missouri Affiliate, Inc. Received for publication May II, 1989. Accepted for publication Sept. 26, 1990. Address for reprints: James L. Cox, MD, Evarts A. Graham Professor of Surgery, Chief, DivisionofCardiothoracicSurgery, 3108 Queeny Tower, Box 8109, One Barnes Hospital Plaza, St. Louis, M063110.
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to the clinical setting in which the arrhythmia occurs. As with other arrhythmias, it is impossible to develop an effectivesurgical therapy for atrial fibrillation without an appreciation of the relationship between atrial anatomy and atrial electrophysiology in both normal and pathologic circumstances. It is the purpose of this paper to summarize the pertinent current knowledge regarding the mechanisms of atrial fibrillation. In subsequent articles, this information will provide the basis for interpreting more recent observations that clarify the relationship between atrial anatomy and atrial fibrillation and that have allowed the development of surgical procedures designed to cure atrial fibrillation.
Historical perspectives important to an understanding of the mechanisms of atrial flutter and atrial fibrillation Although atrial flutter was considered to be a simpler arrhythmia than atrial fibrillation, most of the earliest experimental studies were designed to study the mechanisms of atrial fibrillation. This paradox was due to the fact that atrial flutter is more difficult to induce experimentally than is atrial fibrillation. Three theories were advanced to explain the activation of the atrium during atrial fibrillation. Rothberger and Winterberg) proposed a theory in which a single automatic ectopic focus fires at an extremely rapid rate, which causes the entire atrial myocardium to fibrillate. Garrey reasoned that if this theory were true, subdivision of the atria into several smaller segments of isolated myocardium should result in only one of the isolated segments continuing to fibrillate,
Volume 101 Number 3 March 1991
the one harboring the automatic focus. Garrey? performed such a study, found that all of the isolated segments of the atrium continued to fibrillate,and thereby disproved Rothberger's hypothesis. Englemanrr' subsequentlyproposedthat, during atrial fibrillation, there were multiple automatic foci firing independently throughout the atria, suggesting that the reason that all of Garrey's isolated segments of atrial musclecontinued to fibrillate was that they all harbored automatic foci. In answer to this theory, Garrey reasoned that if multipleautomatic fociwere responsible for atrial fibrillation, as Englemann suggested,further subdivision of the atria into even smaller segments should not terminate the fibrillation, at least not in all of the small segments. However,when he performed this experiment, he foundthat atrial fibrillation did ceasein all of the small segments and that, once an isolated segment was made small enough, atrial fibrillation simply could not be induced in that segment. Garrey's observations, made over 65 years ago, establishedtwocardinal principles of atrial fibrillation: (1) that a critical mass of tissue is necessaryfor atrial fibrillation to occur and (2) that the underlying mechanism is reentry, not automaticity.The reentry hypothesishad already been advanced by Lewis" 4 years before Garrey's observations, but because of technical limitations his hypothesiscould not be proved. Lewis had mapped atrial fibrillation in a dog with a limited number of atrial electrodes and concluded that the arrhythmia was due to a single wavefront circling the orificeof the superior vena cava. Despitethese observations, the erroneousconceptthat atrial fibrillation was caused by multiple automatic foci persistedin the medical literature for the next 35 to 40 years.In the late 1950s,however, Moe5 performeda series of elegant experiments that culminated in his so-called "multiple wavelet hypothesis" of atrial fibrillation. His most important observation was that atrial fibrillation could be initiated by a rapid succession of premature stimuli delivered to the atrium. From a practical standpoint,this observation confirmedbeyonddoubt that atrial fibrillation is a reentrant arrhythmia because, by definition, automatic arrhythmias cannot be induced by programmed electricalstimulation techniques. Moe surmised that atrial fibrillation could be induced only when the refractory periods in some areas of the atrium were markedly different from the refractory periods in other nearby areas of the atrium. Several electrophysiologic terms have been applied to this phenomenon, including among others, nonuniform recovery, nonuniform repolarization, refractory period dispersion, and inhomogeneous tissuerefractoriness. Becausemyocardiumcannot
Surgical treatment of atrialfibrillation, I 40 3
be activated (depolarized) during its refractory period, impulsepropagation is slowin areas with long refractory periods and faster in areas with short refractory periods. Moe suggestedthat the unevenconductionofa wavefront through the atria (caused by inhomogeneous tissue refractoriness) results in a dissociation of the wave front into multiple reentrant circuits or "wavelets," a condition that we recognizeas atrial fibrillation.
Documentation of the basis of experimental atrial flutter and atrial fibrillation Although Moe's concepts of the electrophysiologic basisof atrial fibrillation wereingenious, they were largely theoretical; more important, several seminal observations were yet to be made when he formulated them. For example, the potential importance of atrial geometry to the genesisand perpetuation of atrial fibrillation was not a part of Moe's theories. Not only has atrial anatomy subsequently been shown to play an important role in normal atrial activation,but the vagaries of the geometry of the atria are now known to be important to the development of atrial flutter and atrial fibrillation. The importance of the atrial orifices was pointed out in the early atrial mapping studies of experimental atrial flutter by Lewis,Drury, and Iliescu" and later by Rosenbleuth and Garcia Ramos," Kimura and associates," and Hayden, Hurley, and Rytand.? The most persuasive argument for circus motion (reentrant circuits) about anatomic obstacleswas that of Rytand!? in a paper titled ''The Circus Movement (Entrapped Circuit Wave) Hypothesisand Atrial Flutter." Until the mid-1970s,the technologic limitations of data acquisition precluded the ability to record accurate activation maps of the atria during either atrial flutter or atrial fibrillation. Using multiplexed, simultaneous recordingsin the rabbit atria, Allessie, Banke, and Schopman!' were able to demonstrate reentrant circuits during experimentally induced flutterlike tachycardias. However, they concluded that functional block resulting from differences in local repolarization representedthe primary obstacleand that anatomic obstacles, such as the orifices of the superior and inferiorcavae, were not essentialto these arrhythmias. It could be argued that these experimental flutterlike arrhythmias correspondedmore closelyto atrial fibrillation than to true atrial flutter. Subsequently,Boineauand associates'? demonstrated two forms of circus motion reentry in a unique dog with naturally occurring atrial flutter. One type of flutter demonstrated clockwise and the other counterclockwise reentry around the orifice of the superior vena cava. The cycle lengths of these two arrhythmias were longer than most of those observedfor
404
Cox, Schuessler, Boineau
experimental atrial flutter, which resulted in greater stability or sustainability of the arrhythmias. These investigators concluded that both anatomic factors, such as atrial orifices or abnormalities in atrial myocardium, and functional factors, such as nonuniform repolarization, combined to form the substrate for reentrant atrial tachycardias. In the early 1980s, Spach and associates 13. 14 demonstrated that the conduction velocity of a wave front (in an isolated atrial myocardial preparation) depended on the relationship between the direction the wave front was traveling and the orientation of the muscle fibers within the tissue being activated. They demonstrated that these directional differences in conduction parallel and perpendicular to the fiber orientation could account for unidirectional block and reentry in atrial muscle. Conduction was faster along fibers oriented parallel to the direction of wave-front propagation and slower across fibers oriented perpendicular to the direction of wave-front propagation. Thus they predicted that this myocardial "anisotropy" was an important factor in the genesis and perpetuation of reentrant arrhythmias. Finally, in 1984, Allessie and associates" used a sophisticated multipoint computerized endocardial mapping system in an isolated, perfused atrial preparation to document the presence of multiple reentrant circuits in the atria during atrial fibrillation. Their elegant studies confirmed, for the first time, the multiple wavelet theory of Moe and documented the importance of inhomogeneous atrial refractoriness in atrial fibrillation. Summary Before summarizing the current concepts of the mechanisms of atrial flutter and atrial fibrillation, we should mention that there are serious limitations in the ability to transfer these concepts to human atrial fibrillation. Obviously, all of these concepts were developed on the basis of animal experimentation. Moreover, with the exception of Boineau's studies, most ofthese mechanisms have been described on the basis of isolated atrial preparations that depend on hyperstimulation of the vagus nerves, surgical trauma, topical arrhythmogenic agents such as aconitine, or various combinations of these interventions to induce atrial flutter and atrial fibrillation. Despite these limitations, these studies represent the only scientific information available because (1) more relevant animal models have not been developed and (2) it has not been feasible to record detailed multipoint maps of atrial flutter or atrial fibrillation in humans. Thus, within the confines of these limitations, the current concepts of the mechanisms of atrial flutter and atrial fibrillation can be summarized as follows.
The Journal of Thoracic and Cardiovascular Surgery
Both atrial flutter and atrial fibrillation are reentrant arrhythmias. Atrial flutter is probably always due to a single reentrant circuit that may theoretically involve either the right or left atrium. However, because of normal differences in the refractory periods of the two atria (short in the left atrium and long in the right atrium), atrial flutter is more likely to involve the right atrium. Atrial fibrillation is characterized by the presence of multiple reentrant circuits that may be active simultaneously, precluding the synchronous activation of enough atrial myocardium to generate an identifiable p wave. Either a sinus impulse or a stable atrial flutter reentrant circuit (flutter wave) may degenerate into the multiple reentrant circuits (multiple wavelets) characteristic of atrial fibrillation. Degeneration of the stable activation patterns of sinus rhythm and atrial flutter into atrial fibrillation is enhanced most dramatically when there is an abnormal disparity in the local refractory periods of closely approximated regions of atrial myocardium. However, atrial geometry, atrial anisotropy, and histopathologic changes in the atrial myocardium may also predispose to both atrial flutter and atrial fibrillation. REFERENCES 1. Rothberger CJ, Winterberg H. Uber Vorhoffiimmem und Vorhofllattem. Pfleugers Arch 1914;160:42-90. 2. Garrey WE. Auricular fibrillation. Physiol Rev 1924; 4:215-50. 3. Engelmann TW. Refraktaere Phase und kompensatorische Ruhe in ihrer Bedeutung fuer den Herzrhythmus. Pfluegers Arch Ges Physiol 1894-95;59:309-49. 4. Lewis T. Observations upon flutter and fibrillation. Part IV. Impure flutter: theory of circus movement. Heart 1920; 7:293-331. 5. Moe GK. On the multiple wavelet hypothesis of atrial fibrillation. Arch Int Pharmacodyn 1962;140:183-8. 6. Lewis T, Drury AN, Iliescu CC. A demonstration of circus movement in clinical flutter of the auricles. Heart 1921;8:341-59. 7. Rosenbleuth A, Garcia Ramos J. Studies on flutter and fibrillation. II. The influence of artificial obstacles on experimental auricular flutter. Am Heart J 1947;33:67784. 8. Kimura E, Kato K, Murao S, Ajisaka H, Koyama S. Omiya Z. Experimental studies on the mechanism of the auricular flutter. Tohoku J Exp Moo 1954;60:197-207. 9. Hayden WG, Hurley EJ, Rytand DA. The mechanism of canine atrial flutter. Circ Res 1967;20:496-505. 10. Rytand DA. The circus movement (entrapped circuit wave) hypothesis and atrial flutter. Ann Intern Moo 1966;65:12557. 11. Allessie MA, Bonke FIM, Schopman FJG. Circus movement in rabbit atrial muscle as a mechanism of tachycardia. III. The "leading circle" concept: a new mode of circus
Volume 101 Number 3 March 1991
movement in cardiac tissue without the involvementof an anatomical obstacle. Circ Res 1977;41:9-18. 12. BoineauJP, Schuessler RB, Mooney CR, et al. Natural and evokedatrial flutter due to circus movement in dogs:role of abnormal atrial pathways, slow conduction, nonuniform refractory period distribution and premature beats. Am J Cardiol 1980;45:1167-81. 13. Spach MS, Miller WT III, Geselowitz DB, Barr RC, Kootsey JM, Johnson EA. The discontinuous nature of propagation in normal canine cardiac muscle: evidencefor recurrent discontinuities of intracellular resistance that affect the membrane currents. Circ Res 1981;48:39-54.
Surgical treatment of atrial fibrillation, I
405
14. Spach MS, Dolber PC. Relating extracellular potentials and their derivativesto anisotropic propagation at a microscopic level in human cardiac muscle: evidence for electrical uncoupling of side-to-side fiber connections with increasing age. Circ Res 1986;58:356-71. 15. Allessie MA, Lammers WJEP, Bonke FIM, Hollen JM. Experimental evaluationof Moe's multiple wavelethypothesisof atrial fibrillation. In: Zipes DP, Jalife J, eds. Cardiac electrophysiology and arrhythmias. Orlando, florida: Grune & Stratton, 1985;265-75.
Bound volumes available to subscribers Bound volumes ofTHE JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY are available tosubscribers (only) forthe 1991 issues from thePublisher, at a costof$64.00 ($82.00 international) forVol. 101 (January-June) andVol. 102(July-December). Shipping charges are included. Eachbound volume contains a subject and authorindex and all advertising is removed. Copies are shipped within 60 days after publication of the last issue of the volume. The binding is durable buckram with the JOURNAL name, volume number, and year stamped ingold onthespine. Payment must accompany all orders. Contact Mosby-Year Book, Inc., Subscription Services, 11830 Westline Industrial Drive, St. Louis, Missouri 63146-3318, USA; phone (800) 325-4177, ext.4351. Subscriptions must be in force to qualify. Boond volumes are not available in place of a regular JOURNAL subscription.
THORAC CARDIOVASC SURG
1991;101:402-5
The surgical treatment of atrial fibrillation I. Summary of the current concepts of the mechanisms of atrial flutter and atrial fibrillation Atrial fibrillation is a common arrhythmia that is frequently resistant to medical therapy and has no satisfactory surgical therapy. The development of an effective surgical procedure to treat atrial fibrillation has been hampered by the paucity of clinically relevant information on the basic mechanisms respomible for the arrhythmia. This paper summarizes the current concepts of the electrophysiologic abnormalities in atrial flutter and fibrillation.
James L. Cox, MD, Richard B. Schuessler, PhD, and John P. Boineau, MD, St. Louis, Mo.
Atrial fibrillation is a common arrhythmia that afflicts over one million persons in the United States alone. The medical treatment of atrial fibrillation is less than optimal in that it frequently fails to ablate the arrhythmia and is ultimately directed only toward the control of the ventricular response rate. This results in patients (1) continuing to experience the unpleasantness of an irregular heartbeat, (2) continuing to suffer the consequence of impaired hemodynamics because of loss of atrioventricular synchrony, and (3) remaining vulnerable to the thromboembolic complications of atrial fibrillation. Perhaps the greatest impairment to the development of an effective surgical treatment for atrial fibrillation has been the lack of understanding of the basic electrophysiologic mechanisms responsible for the genesis and perpetuation of this arrhythmia. Unfortunately, virtually all of the scientific information relating to the underlying mechanisms responsible for atrial fibrillation has been generated from animal models that bear little similarity From the Division of Cardiothoracic Surgery, Department of Surgery, Washington University School of Medicine, Barnes Hospital, St. Louis, Mo. Supported by National Institutes of Health Grants ROI HL33722 and ROI HL 32257 and an American Heart Association grant, funds contributed in part by the American Heart Association, Missouri Affiliate, Inc. Received for publication May II, 1989. Accepted for publication Sept. 26, 1990. Address for reprints: James L. Cox, MD, Evarts A. Graham Professor of Surgery, Chief, DivisionofCardiothoracicSurgery, 3108 Queeny Tower, Box 8109, One Barnes Hospital Plaza, St. Louis, M063110.
12/1/25798
402
to the clinical setting in which the arrhythmia occurs. As with other arrhythmias, it is impossible to develop an effectivesurgical therapy for atrial fibrillation without an appreciation of the relationship between atrial anatomy and atrial electrophysiology in both normal and pathologic circumstances. It is the purpose of this paper to summarize the pertinent current knowledge regarding the mechanisms of atrial fibrillation. In subsequent articles, this information will provide the basis for interpreting more recent observations that clarify the relationship between atrial anatomy and atrial fibrillation and that have allowed the development of surgical procedures designed to cure atrial fibrillation.
Historical perspectives important to an understanding of the mechanisms of atrial flutter and atrial fibrillation Although atrial flutter was considered to be a simpler arrhythmia than atrial fibrillation, most of the earliest experimental studies were designed to study the mechanisms of atrial fibrillation. This paradox was due to the fact that atrial flutter is more difficult to induce experimentally than is atrial fibrillation. Three theories were advanced to explain the activation of the atrium during atrial fibrillation. Rothberger and Winterberg) proposed a theory in which a single automatic ectopic focus fires at an extremely rapid rate, which causes the entire atrial myocardium to fibrillate. Garrey reasoned that if this theory were true, subdivision of the atria into several smaller segments of isolated myocardium should result in only one of the isolated segments continuing to fibrillate,
Volume 101 Number 3 March 1991
the one harboring the automatic focus. Garrey? performed such a study, found that all of the isolated segments of the atrium continued to fibrillate,and thereby disproved Rothberger's hypothesis. Englemanrr' subsequentlyproposedthat, during atrial fibrillation, there were multiple automatic foci firing independently throughout the atria, suggesting that the reason that all of Garrey's isolated segments of atrial musclecontinued to fibrillate was that they all harbored automatic foci. In answer to this theory, Garrey reasoned that if multipleautomatic fociwere responsible for atrial fibrillation, as Englemann suggested,further subdivision of the atria into even smaller segments should not terminate the fibrillation, at least not in all of the small segments. However,when he performed this experiment, he foundthat atrial fibrillation did ceasein all of the small segments and that, once an isolated segment was made small enough, atrial fibrillation simply could not be induced in that segment. Garrey's observations, made over 65 years ago, establishedtwocardinal principles of atrial fibrillation: (1) that a critical mass of tissue is necessaryfor atrial fibrillation to occur and (2) that the underlying mechanism is reentry, not automaticity.The reentry hypothesishad already been advanced by Lewis" 4 years before Garrey's observations, but because of technical limitations his hypothesiscould not be proved. Lewis had mapped atrial fibrillation in a dog with a limited number of atrial electrodes and concluded that the arrhythmia was due to a single wavefront circling the orificeof the superior vena cava. Despitethese observations, the erroneousconceptthat atrial fibrillation was caused by multiple automatic foci persistedin the medical literature for the next 35 to 40 years.In the late 1950s,however, Moe5 performeda series of elegant experiments that culminated in his so-called "multiple wavelet hypothesis" of atrial fibrillation. His most important observation was that atrial fibrillation could be initiated by a rapid succession of premature stimuli delivered to the atrium. From a practical standpoint,this observation confirmedbeyonddoubt that atrial fibrillation is a reentrant arrhythmia because, by definition, automatic arrhythmias cannot be induced by programmed electricalstimulation techniques. Moe surmised that atrial fibrillation could be induced only when the refractory periods in some areas of the atrium were markedly different from the refractory periods in other nearby areas of the atrium. Several electrophysiologic terms have been applied to this phenomenon, including among others, nonuniform recovery, nonuniform repolarization, refractory period dispersion, and inhomogeneous tissuerefractoriness. Becausemyocardiumcannot
Surgical treatment of atrialfibrillation, I 40 3
be activated (depolarized) during its refractory period, impulsepropagation is slowin areas with long refractory periods and faster in areas with short refractory periods. Moe suggestedthat the unevenconductionofa wavefront through the atria (caused by inhomogeneous tissue refractoriness) results in a dissociation of the wave front into multiple reentrant circuits or "wavelets," a condition that we recognizeas atrial fibrillation.
Documentation of the basis of experimental atrial flutter and atrial fibrillation Although Moe's concepts of the electrophysiologic basisof atrial fibrillation wereingenious, they were largely theoretical; more important, several seminal observations were yet to be made when he formulated them. For example, the potential importance of atrial geometry to the genesisand perpetuation of atrial fibrillation was not a part of Moe's theories. Not only has atrial anatomy subsequently been shown to play an important role in normal atrial activation,but the vagaries of the geometry of the atria are now known to be important to the development of atrial flutter and atrial fibrillation. The importance of the atrial orifices was pointed out in the early atrial mapping studies of experimental atrial flutter by Lewis,Drury, and Iliescu" and later by Rosenbleuth and Garcia Ramos," Kimura and associates," and Hayden, Hurley, and Rytand.? The most persuasive argument for circus motion (reentrant circuits) about anatomic obstacleswas that of Rytand!? in a paper titled ''The Circus Movement (Entrapped Circuit Wave) Hypothesisand Atrial Flutter." Until the mid-1970s,the technologic limitations of data acquisition precluded the ability to record accurate activation maps of the atria during either atrial flutter or atrial fibrillation. Using multiplexed, simultaneous recordingsin the rabbit atria, Allessie, Banke, and Schopman!' were able to demonstrate reentrant circuits during experimentally induced flutterlike tachycardias. However, they concluded that functional block resulting from differences in local repolarization representedthe primary obstacleand that anatomic obstacles, such as the orifices of the superior and inferiorcavae, were not essentialto these arrhythmias. It could be argued that these experimental flutterlike arrhythmias correspondedmore closelyto atrial fibrillation than to true atrial flutter. Subsequently,Boineauand associates'? demonstrated two forms of circus motion reentry in a unique dog with naturally occurring atrial flutter. One type of flutter demonstrated clockwise and the other counterclockwise reentry around the orifice of the superior vena cava. The cycle lengths of these two arrhythmias were longer than most of those observedfor
404
Cox, Schuessler, Boineau
experimental atrial flutter, which resulted in greater stability or sustainability of the arrhythmias. These investigators concluded that both anatomic factors, such as atrial orifices or abnormalities in atrial myocardium, and functional factors, such as nonuniform repolarization, combined to form the substrate for reentrant atrial tachycardias. In the early 1980s, Spach and associates 13. 14 demonstrated that the conduction velocity of a wave front (in an isolated atrial myocardial preparation) depended on the relationship between the direction the wave front was traveling and the orientation of the muscle fibers within the tissue being activated. They demonstrated that these directional differences in conduction parallel and perpendicular to the fiber orientation could account for unidirectional block and reentry in atrial muscle. Conduction was faster along fibers oriented parallel to the direction of wave-front propagation and slower across fibers oriented perpendicular to the direction of wave-front propagation. Thus they predicted that this myocardial "anisotropy" was an important factor in the genesis and perpetuation of reentrant arrhythmias. Finally, in 1984, Allessie and associates" used a sophisticated multipoint computerized endocardial mapping system in an isolated, perfused atrial preparation to document the presence of multiple reentrant circuits in the atria during atrial fibrillation. Their elegant studies confirmed, for the first time, the multiple wavelet theory of Moe and documented the importance of inhomogeneous atrial refractoriness in atrial fibrillation. Summary Before summarizing the current concepts of the mechanisms of atrial flutter and atrial fibrillation, we should mention that there are serious limitations in the ability to transfer these concepts to human atrial fibrillation. Obviously, all of these concepts were developed on the basis of animal experimentation. Moreover, with the exception of Boineau's studies, most ofthese mechanisms have been described on the basis of isolated atrial preparations that depend on hyperstimulation of the vagus nerves, surgical trauma, topical arrhythmogenic agents such as aconitine, or various combinations of these interventions to induce atrial flutter and atrial fibrillation. Despite these limitations, these studies represent the only scientific information available because (1) more relevant animal models have not been developed and (2) it has not been feasible to record detailed multipoint maps of atrial flutter or atrial fibrillation in humans. Thus, within the confines of these limitations, the current concepts of the mechanisms of atrial flutter and atrial fibrillation can be summarized as follows.
The Journal of Thoracic and Cardiovascular Surgery
Both atrial flutter and atrial fibrillation are reentrant arrhythmias. Atrial flutter is probably always due to a single reentrant circuit that may theoretically involve either the right or left atrium. However, because of normal differences in the refractory periods of the two atria (short in the left atrium and long in the right atrium), atrial flutter is more likely to involve the right atrium. Atrial fibrillation is characterized by the presence of multiple reentrant circuits that may be active simultaneously, precluding the synchronous activation of enough atrial myocardium to generate an identifiable p wave. Either a sinus impulse or a stable atrial flutter reentrant circuit (flutter wave) may degenerate into the multiple reentrant circuits (multiple wavelets) characteristic of atrial fibrillation. Degeneration of the stable activation patterns of sinus rhythm and atrial flutter into atrial fibrillation is enhanced most dramatically when there is an abnormal disparity in the local refractory periods of closely approximated regions of atrial myocardium. However, atrial geometry, atrial anisotropy, and histopathologic changes in the atrial myocardium may also predispose to both atrial flutter and atrial fibrillation. REFERENCES 1. Rothberger CJ, Winterberg H. Uber Vorhoffiimmem und Vorhofllattem. Pfleugers Arch 1914;160:42-90. 2. Garrey WE. Auricular fibrillation. Physiol Rev 1924; 4:215-50. 3. Engelmann TW. Refraktaere Phase und kompensatorische Ruhe in ihrer Bedeutung fuer den Herzrhythmus. Pfluegers Arch Ges Physiol 1894-95;59:309-49. 4. Lewis T. Observations upon flutter and fibrillation. Part IV. Impure flutter: theory of circus movement. Heart 1920; 7:293-331. 5. Moe GK. On the multiple wavelet hypothesis of atrial fibrillation. Arch Int Pharmacodyn 1962;140:183-8. 6. Lewis T, Drury AN, Iliescu CC. A demonstration of circus movement in clinical flutter of the auricles. Heart 1921;8:341-59. 7. Rosenbleuth A, Garcia Ramos J. Studies on flutter and fibrillation. II. The influence of artificial obstacles on experimental auricular flutter. Am Heart J 1947;33:67784. 8. Kimura E, Kato K, Murao S, Ajisaka H, Koyama S. Omiya Z. Experimental studies on the mechanism of the auricular flutter. Tohoku J Exp Moo 1954;60:197-207. 9. Hayden WG, Hurley EJ, Rytand DA. The mechanism of canine atrial flutter. Circ Res 1967;20:496-505. 10. Rytand DA. The circus movement (entrapped circuit wave) hypothesis and atrial flutter. Ann Intern Moo 1966;65:12557. 11. Allessie MA, Bonke FIM, Schopman FJG. Circus movement in rabbit atrial muscle as a mechanism of tachycardia. III. The "leading circle" concept: a new mode of circus
Volume 101 Number 3 March 1991
movement in cardiac tissue without the involvementof an anatomical obstacle. Circ Res 1977;41:9-18. 12. BoineauJP, Schuessler RB, Mooney CR, et al. Natural and evokedatrial flutter due to circus movement in dogs:role of abnormal atrial pathways, slow conduction, nonuniform refractory period distribution and premature beats. Am J Cardiol 1980;45:1167-81. 13. Spach MS, Miller WT III, Geselowitz DB, Barr RC, Kootsey JM, Johnson EA. The discontinuous nature of propagation in normal canine cardiac muscle: evidencefor recurrent discontinuities of intracellular resistance that affect the membrane currents. Circ Res 1981;48:39-54.
Surgical treatment of atrial fibrillation, I
405
14. Spach MS, Dolber PC. Relating extracellular potentials and their derivativesto anisotropic propagation at a microscopic level in human cardiac muscle: evidence for electrical uncoupling of side-to-side fiber connections with increasing age. Circ Res 1986;58:356-71. 15. Allessie MA, Lammers WJEP, Bonke FIM, Hollen JM. Experimental evaluationof Moe's multiple wavelethypothesisof atrial fibrillation. In: Zipes DP, Jalife J, eds. Cardiac electrophysiology and arrhythmias. Orlando, florida: Grune & Stratton, 1985;265-75.
Bound volumes available to subscribers Bound volumes ofTHE JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY are available tosubscribers (only) forthe 1991 issues from thePublisher, at a costof$64.00 ($82.00 international) forVol. 101 (January-June) andVol. 102(July-December). Shipping charges are included. Eachbound volume contains a subject and authorindex and all advertising is removed. Copies are shipped within 60 days after publication of the last issue of the volume. The binding is durable buckram with the JOURNAL name, volume number, and year stamped ingold onthespine. Payment must accompany all orders. Contact Mosby-Year Book, Inc., Subscription Services, 11830 Westline Industrial Drive, St. Louis, Missouri 63146-3318, USA; phone (800) 325-4177, ext.4351. Subscriptions must be in force to qualify. Boond volumes are not available in place of a regular JOURNAL subscription.