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Ann Thorac Surg 1996;61:104-112
© 1996 The Society of Thoracic Surgeons

Original Articles: Cardiovascular

Atrial Activation During Chronic Atrial Fibrillation in Patients With Isolated Mitral Valve Disease

Atsushi Harada, MD, Kenji Sasaki, MD, Takao Fukushima, MD, Masatoshi Ikeshita, MD, Tetsuo Asano, MD, Shigeo Yamauchi, MD, Shigeo Tanaka, MD, Tasuku Shoji, MD

Department of Cardiovascular Surgery, Ebina General Hospital, Kanagawa, Japan

Accepted for publication August 17, 1995.


   Abstract
Top
 Footnotes
 Abstract
Introduction
 Material and Methods
 Results
 Comment
 References
 
Background. A computerized 32-channel mapping system has been developed to investigate the characteristics of the atrial activation sequence. The system is capable of displaying sequential atrial maps and provides a rapid and dynamic means of verifying the activation sequence of atrial fibrillation.

Methods. Using this system, we performed intraoperative atrial activation mapping in 10 patients with chronic atrial fibrillation who were undergoing isolated mitral valve operations.

Results. Regular and repetitive activation (cycle length ranged from 131 to 228 milliseconds) originated in the left atrium in all 10 patients. Two patterns of repetitive activation in 2 patients and three patterns in 1 patient appeared alternately during the observation period in the left atrium. In contrast to the repetitive activation in the left atrium, the activation sequence of the right atrium was extremely complex and chaotic. In 7 of the 10 patients, the same pattern of right atrial activation was never repeated during the observation period. In 2 patients, revolution of repetitive activation in the right atrium sporadically appeared, but the pattern of activation immediately deteriorated to a complex and chaotic pattern. In 1 patient, repetitive activation emerged from the low lateral portion of the right atrium. Because our mapping technique was limited by the number of available atrial electrodes, discrete reentrant circuits or ectopic foci could not be demonstrated in the present study. However, the activation sequences during chronic atrial fibrillation suggested that (1) the left atrium would act as an electrical driving chamber for atrial fibrillation in the majority of the patients and (2) atrial activation patterns are different in each case.

Conclusions. Computerized intraoperative mapping should guide surgeons in determining the appropriate surgical procedure and facilitate operation for chronic atrial fibrillation associated with mitral valve disease.


   Introduction
Top
 Footnotes
 Abstract
 Introduction
Material and Methods
 Results
 Comment
 References
 
See also page 111.

During the past 5 years, surgery has emerged as an increasingly important modality in the treatment of atrial fibrillation (AF) [1–4]. The selection of the appropriate type of surgical procedure to ablate AF should be pertinent to mechanism of AF, verified by electrophysiologic mapping. Using a multipoint mapping system, Cox and associates [5] described atrial activation of AF in experimental models and paroxysmal AF in patients with Wolff-Parkinson-White syndrome. Their study demonstrated the presence of macroreentrant circuits in the right atrium, and multiple wave fronts and conduction blocks in the left atrium. On the basis of their electrophysiologic study, an innovative maze procedure has been developed to ablate paroxysmal AF [1, 2]. Recently, application of the maze procedure has been extended to chronic AF associated with mitral valvular disease [6] or atrial septal defect [7]. However, detailed studies of atrial activation in chronic AF associated with mitral valve disease have been relatively sparse. Intraoperative mapping of chronic AF associated with mitral valve disease has been hampered because considerable time is required in the construction of activation maps during AF to edit activation times from complex or questionable electrograms. Therefore, we have developed a 32-channel computerized mapping system capable of producing atrial activation maps during AF. The purpose of this study is to investigate the characteristics of the atrial activation sequence during chronic AF in patients who were undergoing isolated mitral valve operations.


   Material and Methods
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
Results
 Comment
 References
 
Computerized atrial activation mapping was performed in 10 patients with chronic AF complicated by isolated mitral valve disease who were undergoing mitral valve operations. Ages ranged from 33 to 65 years, and there were 4 male and 6 female patients. Four of them had rheumatic mitral stenosis, and 6 had mitral regurgitation. Fentanyl citrate was used for the induction and maintenance of anesthesia, and median sternotomy followed by pericardiotomy was performed to expose the heart. The heart was suspended in a pericardial cradle. Before the institution of cardiopulmonary bypass, intraoperative atrial mapping was performed with our newly developed atrial mapping system.

Thirty silver unipolar electrodes, 2 mm in diameter, were mounted in five rows of six on a flexible plastic rectangular sheet (card type electrode, 55 x 65 mm). All of the signals from each unipolar electrode were connected to differential amplifiers at a frequency response of 100 to 1,000 Hz. A computer stored the digitalized unipolar data and displayed the waveforms (Fig 1Go). At the time of operation, a common reference electrode for all cardiac unipolar electrodes was sewn onto the right chest wall at a distance of at least 20 cm from the heart. The card-type electrode was attached to the right atrial epicardial surface to record 30 local right atrial electrograms simultaneously. Because our 32-channel mapping system was not able to perform simultaneous right and left atrial mapping, the electrode was switched and similarly attached to the left atrial epicardial surface to record local left atrial epicardial electrograms. A computer program was used to determine local activation times from unipolar tracings. The peak negative derivative of the major deflection of the unipolar complex was defined as the time of local activation. Within 30 seconds of acquisition of the atrial epicardial electrograms, atrial activation maps for a 100-millisecond window were automatically produced from the computer analysis and displayed sequentially (Fig 2Go).



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  		Fig 1. . Electrocardiogram lead II (ECG) and 30 epicardial electrograms recorded from the left atrium during atrial fibrillation. Electrocardiogram lead II is drawn on the top of the tracings, and the lower 30 tracings are 30 unipolar electrograms recorded from the left atrium (E1, E2, ...E30 indicate electrocardiograms recorded from electrode 1, electrode 2, ...electrode 30, respectively). The marks 200 to 1000 msec indicate milliseconds from the beginning of all tracings. This chart was directly copied from the computer display. Although these left atrial epicardial electrograms were recorded during chronic atrial fibrillation, regular and repetitive local activation at a cycle length of 154 milliseconds was demonstrated in the left atrium.

 


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  		Fig 2. . Consecutive activation maps of the left atrium. Twelve activation maps directly copied from the computer display are presented. Maps A to L were constructed from epicardial electrograms in windows A to L divided by the vertical dotted lines shown in Figure 1Go. The same pattern of activation sequence emerged from the lower posterior portion of the left atrium, indicated by a closed circle, and propagated in the direction of the left atrial appendage (LAA) and the right atrium. The repetition of the same activation sequence is demonstrated in maps B, C, E, F, H, I, K, and L. Isochronous lines are drawn at intervals of 5 milliseconds, and the black arrows indicate the direction of the spread of the activation. (PV = pulmonary vein.)

 
The atrial mapping studies in patients were performed after informed consent had been obtained from each patient and approved by the institutional review board for human studies.


   Results
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
Comment
 References
 
The characteristics of atrial activation during chronic AF are summarized in Table 1Go; regular and repetitive activation in the left atrium and chaotic activation in the right atrium were observed in the majority of the patients. In all 10 patients, repetitive activation sequences at cycle lengths of 131 to 228 milliseconds persisted in the left atrium. In 3 patients, two types of regular activation sequences were observed in the left atrium. These regular activation sequences emerged from the base of the left atrial appendage, lateral to the left pulmonary veins, or in the posterior wall adjacent to the atrioventricular groove. In contrast to the regular and repetitive activation sequences in the left atrium, complex and chaotic activation sequences dominated in the right atrium. Although a sporadic, regular activation sequence was observed in the right atrium in 2 of the 10 patients, after two to three revolutions of repetitive activation, the pattern immediately deteriorated to a complex and chaotic state. In only 1 patient were regular revolutions at a cycle length of 159 milliseconds identified in the right atrium, and they originated in the low lateral portion of the right atrium.


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  		Table 1. . Activation Sequence in Patients With Chronic Atrial Fibrillation
 
Figure 1Go shows the lead II electrocardiogram and 30 unipolar epicardial electrograms recorded from the left atrium during chronic AF in a 58-year-old woman with mitral regurgitation (patient 2 in Table 1Go). In this patient, a regular activation sequence at a cycle length of 156 milliseconds was repeated. Twelve left atrial activation maps (see Fig 2Go) were constructed from the epicardial electrograms shown in Figure 1Go. The maps demonstrated that the activation arose in the lower posterior wall of the left atrium and propagated in the directions of the left atrial appendage and the right atrium. However, shortly after, the pattern of activation changed: an activation, at a cycle length of 181 milliseconds, emerged from the upper base of the left atrial appendage and propagated to the body of the left atrium (Fig 3Go). These two patterns of activation shown in Figures 2 and 3GoGo alternately appeared during the observation period. In this patient, in contrast to the regular and repetitive activation in the left atrium, activation in the right atrium was more complex and chaotic (Fig 4Go), and multiple wave fronts emerged fleetingly and spread in the right atrium. The electrograms from each electrode were not sequential, and the same activation pattern never repeated during the observation period (Fig 5Go). In 7 of the 10 patients, the activation sequences of the right atrium were extremely complex and chaotic, as in patient 2.



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  		Fig 3. . Activation maps of the left atrium. Four activation maps of the left atrium and 10 of 30 epicardial electrograms used in the same patient as in Figures 1 and 2GoGo are demonstrated. The chart is directly copied from the computer display. Maps A, D, G, and J were constructed from the epicardial electrograms in windows A, D, G, and J divided by vertical dotted lines on the electrograms. The earliest activation sites where the repetitive activation emerged are indicated by closed circles. Isochronous lines are drawn at intervals of 5 milliseconds. The black arrows indicate the direction of the spread of the activation from its origin. (For abbreviations see Figure 2Go.)

 


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  		Fig 4. . Electrocardiogram lead II (ECG) and 30 epicardial electrograms recorded from the right atrium in the same patient used in Figures 1Go–3. In contrast to the repetitive activation of the left atrium, electrical discharges in each epicardial electrogram are fleeting and independent. (For abbreviations see Figure 1Go.)

 


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  		Fig 5. . Activation maps of the right atrium during atrial fibrillation. Maps C, D, E, and F were constructed from the epicardial electrograms in windows C, D, E, and F divided by the vertical dotted line in Figure 4Go. The activation of the right atrium during atrial fibrillation is complex and intricate. The same pattern of activation was never repeated during the observation period. The numbers on the isochrones are times in milliseconds. (ECG = electrocardiogram lead II; IVC = inferior vena cava; PV = pulmonary vein; RA = right atrium; RAA = right atrial appendage; SVC = superior vena cava.)

 
Three patterns of activation sequence were observed in the left atrium in a 54-year-old woman with rheumatic mitral stenosis (patient 7 in Table 1Go). The first pattern of activation emerged from the left atrial appendage and propagated in the direction of the left atrium (Fig 6AGo). The second pattern of activation originated on the side of the left pulmonary vein (Fig 6B,CGo). The third pattern of activation simultaneously arose in the left atrial appendage and adjacent to the left pulmonary vein (Fig 6DGo). These three patterns of activation were observed alternately during the observation period.



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  		Fig 6. . Activation maps of the left atrium (LA) in a 54-year-old woman with chronic atrial fibrillation associated with rheumatic mitral stenosis. The boxed areas on the electrocardiogram lead II (ECG) are the 100-millisecond windows of the data analyzed to construct atrial activation maps. See text for details. (For abbreviations, see Figure 2Go.)

 
In only 1 of the 10 patients (patient 9 in Table 1Go) was a regular activation sequence in the right atrium demonstrated. The activation emerged from the low lateral portion of the right atrium, and spread throughout the right atrium (Fig 7A,BGo). From the pattern of activation, it was suspected that the mechanism of the repetitive activation in the right atrium could be ectopic or microreentrant. Although the regular activation sequence perpetuated at a cycle length of 159 milliseconds, the regular activation often competed or interfered with activation wave fronts spreading from the other portions of the right atrium (Fig 7C,DGo). In this patient, the repetitive activation emerged from the upper portion of the left atrial appendage at a cycle length of 148 milliseconds.



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  		Fig 7. . Activation maps of the right atrium in a 44-year-old man with chronic atrial fibrillation associated with mitral regurgitation. The boxed areas on the electrocardiogram lead II (ECG) are the 100-millisecond windows of the data analyzed to construct atrial activation maps A, B, C, and D. (For abbreviations see Figure 5Go.)

 
More recently, the 32-channel system has been extended to a 64-channel system capable of simultaneous right and left atrial mapping. The newly designed electrodes are shown in Figure 8Go: 64 silver unipolar electrodes were mounted on three sets of silicone rubber sheets designed to conform to the entire epicardial surface of both the right and left atria. With this system atrial mapping was performed in 1 patient (patient 10 in Table 1Go). As in the activation pattern of the majority of the patients, simultaneous mapping revealed regular and repetitive activation in the left atrium and complex and chaotic activation in the right atrium (Fig 9Go).



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  		Fig 8. . Atrial epicardial templates containing 64 unipolar electrodes mounted on silicon rubber sheets designed to conform to the entire epicardial surface of the atria. The template on the left side covers the posterolateral surface of the left atrium. The template in the middle covers the anterior surface of the left and right atria including the Bachmann's bundle. The template on the right side covers the lateral surface of the right atrium.

 


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  		Fig 9. . Entire activation maps in a 62-year-old woman with chronic atrial fibrillation associated with rheumatic mitral valve stenosis. The boxed areas on the electrocardiogram lead II (ECG) are the 100-millisecond windows of the data analyzed to construct atrial activation maps A and B. As in other cases, a regular activation sequence at a cycle length of 152 milliseconds originated in the left atrial appendage and propagated to the body of the left atrium. However, in the right atrium, more complex and irregular activation was observed, and the same pattern of activation was never repeated during the observation period. (MV = mitral valve; TV = tricuspid valve; for other abbreviations see Figures 2 and 5GoGo.)

 

   Comment
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
References
 
The advent of surgical procedures for the treatment of medically refractory arrhythmias has led to a substantial improvement in the treatment of patients with these arrhythmias. As the selection of the appropriate type of surgical procedure should be pertinent to the mechanism of the arrhythmias, intraoperative mapping is essential for definitive surgical treatment. During the past two decades, sophisticated cardiac mapping systems have been developed to identify the site to which surgical procedures should be applied [5, 8–10]. Electrophysiologically guided operation has resulted in a low postoperative inducibility and reduced recurrence of both ventricular and supraventricular tachyarrhythmias. Computerized multichannel mapping systems are capable of constructing intraoperative activation maps for Wolff-Parkinson-White syndrome and ventricular tachycardia, in which one activation map from a single atrial or ventricular beat is required to determine the earliest activation site. However, intraoperative mapping of AF has been hampered, and currently surgical ablation of AF is performed without intraoperative atrial mapping. As the atrial activation of AF is extremely complex and inconstant, the rapid display of consecutive isochronous maps is required to verify the atrial activation of AF. Our 32-channel mapping system was initially designed according to the computer system developed at Washington University and has been used to construct activation maps of Wolff-Parkinson-White syndrome or ventricular tachycardia. However, the system was not adaptable for analysis of the activation sequence of AF, because the system software was not suitable for data analysis in AF. New software was developed to produce sequential atrial maps so that detailed analysis of the activation pattern of AF is possible. In our mapping system, 1,200-millisecond data from 30 epicardial electrograms were divided into twelve 100-millisecond windows, and 12 isochronous maps corresponding to each 100-millisecond window were automatically constructed within 30 seconds of acquisition of the data. Generally, 60 to 120 consecutive activation maps are required to determine the activation pattern of AF.

A historical study of the atrial activation of AF has been reported by Cox and associates [5]. Based on atrial activation sequence of electrically induced AF in experimental models and patients with Wolff-Parkinson-White syndrome, Cox and associates demonstrated the presence of macroreentrant circuits and the absence of both microreentrant circuits and evidence of atrial automaticity. Although various concepts of reentry and ectopic focus for the mechanism of AF have been proposed and introduced by several investigators [5, 11–14], the mechanism or activation sequence of chronic AF associated with mitral valve disease is still unknown.

In this communication, our study on atrial activation during chronic AF in patients with isolated mitral valve disease demonstrated regular and repetitive activation in the left atrium and intricate activation in the right atrium. Because our mapping system was limited to a 32-channel system and simultaneous right and left atrial mapping was not performed in the majority of the patients, the detailed mechanisms, whether ectopic or reentrant, were not determined in the present study. Moreover, the origins of repetitive activation fronts demonstrated by intraoperative mapping might not be all origins of AF. A more sophisticated mapping system capable of simultaneous mapping of both right and left atria is required to analyze the detailed mechanism of AF. However, this study suggested that reentrant circuit or ectopic focus might discharge repetitive wave fronts in the left atrium. Presumably, these regular activation fronts in the left atrium propagate through the Bachmann's bundle, the posterior portion of the left atrium, or the interatrial septum and are conducted to the right atrium. Multiple wave fronts reaching the right atrium through different pathways at different times could interfere with each other and result in the intricate activation in the right atrium (Fig 10Go). We do not believe the alternate explanation that the intricate activation in the right atrium propagates to the left atrium and results in the repetitive activation in the left atrium.



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  		Fig 10. . Hypothesis for atrial activation of chronic atrial fibrillation associated with isolated mitral valve disease. See text for details. (For abbreviations see Figures 2, 5, and 9GoGoGo.)

 
On the basis of our current study, we suggest that chronic AF associated with isolated mitral valve disease might be caused by electrical discharges in the left atrium in the majority of patients. Therefore, surgical procedures to ablate chronic AF should be applied to the left atrium, but are not required in the right atrium because repetitive activation caused by either reentrant circuit or ectopic focus was identified in the left atrium but not in the right atrium. Graffigna and associates [4] reported on the electrophysiologic effects of left atrial isolation [15] for AF associated with mitral valve operation in which the left atrium is electrically isolated from the remainder of the heart, and the reentrant circuit and ectopic focus are confined to the left atrium. They performed left atrial isolation in 100 patients with chronic AF complicated by mitral valve disease, and sinus rhythm was successfully restored in 79 (81.4%) of 97 survivors. From their report, we can assume that in more than 80% of chronic AF cases complicated by mitral valve disease, the left atrium plays an important role for maintaining AF but the right atrium does not. In the remaining 20% (those in whom left atrial isolation failed to ablate AF) the right atrium or interatrial septum might also play an important role. The success rate of left atrial isolation reported by Graffigna and associates is in approximate accord with our electrophysiologic study demonstrating repetitive activation of the left atrium and intricate activation of the right atrium in 90% of chronic AF cases with isolated mitral valve disease.

Current surgical procedures to ablate AF are performed without intraoperative atrial mapping [3, 4, 6], even though surgical treatment for other tachyarrythmias requires intraoperative mapping. There has been some debate on whether intraoperative mapping should be needed for surgical ablation of AF. One of the reasons why intraoperative mapping is not performed for AF operations might be that the analysis of the activation sequence of AF requires a sophisticated and expensive mapping system and a special investigator with considerable experience. Sophisticated mapping systems are owned by few institutions where AF operations are performed. Therefore, in the majority of the institutions without intraoperative mapping systems, complex surgical incisions or cryolesions are applied to all place of the atria where reentrant circuits and ectopic focus are considered to exist. Atrial fibrillation operations without intraoperative mapping would consist of both indispensable and dispensable procedures because the existence of reentrant circuit or ectopic focus is presumed but not identified by intraoperative mapping in each case. Indeed, our present study suggested a general tendency for reentrant circuit or ectopic focus to exist in the left atrium but not in the right atrium in the majority of the patents with chronic AF complicated by isolated mitral valve disease. This suggests that surgical procedures should be applied to the left atrium but might not be necessary in the right atrium. Moreover, the repetitive activation patterns of the activation sequence in the left atrium differ in each patient. Therefore, surgical procedures applied to the left atrium should differ depending on the pattern of activation. Recently, we have begun a program of intraoperative map-guided operations, and 3 patients with chronic atrial fibrillation have been operated on by different surgical procedures depending on the activation patterns of the atria [16]. These 3 patients have maintained sinus rhythm for 6 to 13 months after operation.

Although AF is an extremely complex and intricate arrhythmia, we advocate performing intraoperative atrial mapping to investigate the detailed mechanism of this complex arrhythmia. The fact that AF operations are performed without intraoperative mapping is a great obstacle to the progress of both cardiac electrophysiology and arrhythmia surgery.


   Footnotes
Top
 Footnotes
Abstract
 Introduction
 Material and Methods
 Results
 Comment
 References
 
Address reprint requests to Dr Harada, Department of Cardiovascular Surgery, Ebina General Hospital, 1320 Kawaraguchi Ebina-City, Kanagawa, 243-04, Japan.


   References
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 References
 

  1. Cox JL, Schuessler RB, D'Agostino HJ Jr, et al. The surgical treatment of atrial fibrillation. III. Development of a definitive surgical procedure. J Thorac Cardiovasc Surg 1991;101:569–83.[Abstract]
  2. Cox JL. The surgical treatment of atrial fibrillation. IV. Surgical technique. J Thorac Cardiovasc Surg 1991;101: 584–92.[Abstract]
  3. Guiraudon GM, Campbell CS, Jones DL, McLellan DG, MacDonald JL. Combined sino-atrial node atrio-ventricular isolation: a surgical alternative to His bundle ablation in patients with atrial fibrillation. Circulation 1985;72(Suppl 3):220.
  4. Graffigna A, Pagnai F, Minizioni G, Salerno J, Vigano M. Left atrial isolation associated with mitral valve operations. Ann Thorac Surg 1992;54:1093–8.[Abstract]
  5. Cox JL, Canavan TE, Schuessler RB, et al. The surgical treatment of atrial fibrillation. II. Intraoperative electrophysiologic mapping and description of the electrophysiologic basis of atrial flutter and atrial fibrillation. J Thorac Cardiovasc Surg 1991;101:406–26.[Abstract]
  6. McCarthy PM, Castle LW, Maloney JD, et al. Initial experience with the maze procedure for atrial fibrillation. J Thorac Cardiovasc Surg 1993;105:1077–8.[Abstract]
  7. Bonchek LI, Burlingame MW, Worley SJ, Vazales BE, Lundy EF. Cox/maze procedure for atrial septal defect with atrial fibrillation: management strategies. Ann Thorac Surg 1993;55:607–10.[Abstract]
  8. Downar E, Parson ID, Mickleborough LL, Cameron DA, Yao LC, Waxman MB. On-line epicardial mapping of intraoperative ventricular arrhythmias: initial clinical experience. J Am Coll Cardiol 1984;4:703–14.[Abstract]
  9. Kramer JB, Corr PB, Cox JL, Witkowski FX, Cain ME. Simultaneous computer mapping to facilitate intraoperative localization of accessory pathways in patients with Wolff-Parkinson-White syndrome. Am J Cardiol 1985;56:571–6.[Medline]
  10. Harada A, Tweddell JS, Schuessler RB, Branham BH, Boineau JP, Cox JL. Computerized potential distribution mapping: a new intraoperative mapping technique for ventricular tachycardia surgery. Ann Thorac Surg 1990;49: 649–55.[Abstract]
  11. Moe GK. On the multiple wavelet hypothesis of atrial fibrillation. Arch Int Pharmacodyn Ther 1962;140:183–8.
  12. Allessie MA, Bonke FIM, Schopman FJG. Circus movement in rabbit muscle as a mechanism of tachycardia. III. The ``leading circle'' concept. A new mode of circus movement in cardiac tissue without the involvement of an anatomical obstacle. Circ Res 1977;41:9–18.[Free Full Text]
  13. Chen PS, Smith WM, Greer GS, et al. Activation patterns during electrically induced atrial fibrillation in humans. Circulation 1986;74(Suppl 2):483.
  14. D'Agostino HJ Jr., Harada A, Schuessler RB, Boineau JP, Cox JL. Global epicardial mapping of atrial fibrillation in a canine model of chronic mitral regurgitation. Circulation 1987;76(Suppl 4):165.
  15. Williams JM, Ungerleider RM, Lofland GK, et al. Left atrial isolation: new technique for the treatment of supraventricular arrhythmias. J Thorac Cardiovasc Surg 1980;80:373–80.[Abstract]
  16. Harada A, Sasaki K, Fukushima T. Combined operation for mitral valve stenosis and chronic atrial fibrillation. Ther Res 1994;14:163–6.

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