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The surgical treatment of atrial fibrillation
J
THORAC CARDIOVASC SURG
1991;101:406-26
The surgical treatment of atrial fibrillation II. Intraoperative electrophysiologic mapping and description of the electrophysiologic basis of atrial flutter and atrial fibrillation Computerized mapping of atrial fibrillation was perfonned in animals and man. To study atrial fibrillation in a systematic manner, we developed a clinically relevant experimental model of atrial fibrillation. Chronic mitral regurgitation was created surgically in 25 dogs .without opening the pericardium. Mter several months of chronic mitral regurgitation, the atria became enlarged and sustained atrial fibrillation could be induced by standard programmed electrical stimulation techniques. Computerized isochronous activation maps of the atria were recorded during atrial fibrillation from 208 bipolar electrodes simultaneously. In a parallel study, human atrial fibrillation was mapped with a separate 16(khannel intraoperative mapping system in patients with paroxysmal atrial fibrillation who were undergoing surgical correction of the Wolff-Parkinson-White syndrome. The canine activation sequence maps demonstrated a spectrum of rhythm abnormalities ranging from simple atrial flutter to complex atrial fibrillation. They also showed that macroreentrant circuits within the atrial myocardium were responsible for the entire spectrum of arrhythmias. Atrial reentry was also documented during human atrial fibrillation. All patients had nonuniform conduction around regions of bidirectional block in both atria resulting in multiple discrete wave fronts. In addition, six patients had a single reentrant circuit in the right atrium in which bidirectional block of the activation wave front occurred along the sulcus terminalis between the venae cavae. The left atrium in all patients demonstrated multiple wave fronts and conduction block, but left atrial reenty could not be detected. Both the experimental study and the clinical study demonstrated that multiple wave fronts, nonuniform conduction, bidirectional block, and large (macroreentrant) reentrant circuits occur during atrial fibrillation. The presence of macroreentrant circuits and the absence of either microreentrant circuits or evidence of atrial automaticity suggests that atrial fibrillation should be amenable to surgical ablation.
James L. Cox, MD, Thomas E. Canavan, MD, Richard B. Schuessler, PhD, Michael E. Cain, MD, Bruce D. Lindsay, MD, Constance Stone, MD, Peter K. Smith, MD, Peter B. Corr, PhD, and John P. Boineau, MD, St. Louis, Mo.
From the Division of Cardiothoracic Surgery, Department of Surgery, and the Division of Cardiology, Department of Medicine, Washington University School of Medicine, Barnes Hospital, St. Louis, Mo. Supported by National Institutes of Health Grants ROI HL33722 and ROJ HL32257 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, Division of Cardiothoracic Surgery, Suite 3108, Queeny Tower, One Barnes Hospital Plaza, St. Louis, MO 63110.
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Rvious efforts at mapping atrial fibrillation have been hampered by two factors: (1) the inability to record local atrial electrograms from multiple sites simultaneously and (2) inadequate animal models of atrial fibrillation. Allessie, Bonke, and Schopman J developed a multipoint system for mapping atrial flutter and fibrillation in an isolated atrial model, but the system was not adaptable for use in human studies. Boineau and colleagues/ developed a different type of multipoint mapping system that they used to study a dog with naturally occurring spontaneous atrial flutter, but it was a multiplexed system that required several cycles of a stable rhythm to allow time for switching from one set of electrodes to another to com-
Volume 101 Number 3 March 1991
Surgical treatment ofatrial fibrillation, II 4 0 7
Fig. 1. Atrial epicardial electrode templates containing 156 bipolar electrodes. These templates. fashioned of silicone rubber (O.02-inch thickness, Dow Corning Corp., Midland, Mich.) were designed to conform to the epicardial surfaces of the atria. Fine silver wires (Quad Teflon-coated silver wire, a.005-inch diameter. Medwire, Inc., Mt. Vernon, N.Y.) were embedded in these silicone rubber templates at an interelectrode distance of 6 mm and an intraelectrode distance of I mm. The largest template, containing 80 electrodes, was placed over the postolateral right atrium and extended from the interatrial groove posteriorly to the right atrial appendage and atrioventricular groove anteriorly. A second template with 64 electrodes covered the anterior aspects of both the right and left atria immediately behind the ascending aorta in the region of the transverse sinus. The third template, also containing 64 electrodes, covered the posterior left atrium inferior to the pulmonary veins and the posterior left atrial appendage. These templates were fixed in position on the epicardial surfaces of the atria with 4-0 silk sutures. The template on the left side of A covers the lateral right atrium. The upper right template in A covers the anterior right and left atria and the medial portion of the left atrial appendage. The lower right template covers the posterior left atrium. B shows an enlarged view of the anterior left and right atrial template. The holes on the edges of each template are for suture fixation to the atrium.
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Fig. 2. Raw data recorded from a single normal sinus rhythm beat. The lower left panel shows the computer-generated outline of the atrium with activation times at each electode site. The upper left panel is the digitized standard ECG lead aVF. The boxed area over the signal is the time window that was analyzed to produce the activation map. Typical electrograms associated with various times on the activation map are illustrated. The dark vertical bar and small number at the beginning of each signal is the voltage calibration in millivolts (mV). The activation on each signal is marked with a vertical cursor and the number to the left is the activation time. The window is 248 msec in width. LA. Left atrial appendage; R; right atrial appendage; PV. pulmonary veins; SVC, superior vena cava; Il/C, inferior vena cava; M. mitral valve; T. tricuspid valve.
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Surgical treatment of atrial fibrillation, II 4 0 9
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IVC Fig. 3. Atrial epicardial activation map during normal sinus rhythm in a dog. The total atrial activation time during normal sinus rhythm in dogs with noninducible arrhythmias was 66 ± 3 msec and' in dogs with inducible arrhythmias it was 77 ± 10 msec (p = 0.076). Upperpanel; Limb lead ECG is scanned; a window containing the P wave is chosen for analysis of atrial activation data. Right lowerpanel, Electrograms recorded from surface electrodes 209 to 216 in the time window shown in the upperpanel. Activation times have been chosen by computer and are indicated by cursors (see text for details). Left lowerpanel, Activation times are plotted on a map of the atria and isochronous lines are drawn at intervals of 10 msec. This activation pattern represents normal sinus rhythm. MV, Mitral valve; TV, tricuspid valve; LAA, left atrial appendage; RAA, right atrial appendage; sve, superior vena cava; IVe, inferior vena cava; PV, pulmonary veins.
plete the mapping process. Thus their mapping system was of limited value in the study of atrial fibrillation. The lack of a suitable animal model of atrial fibrillation and the inability to map human atrial fibrillation simultaneously from multiple sites led Waldo and associates- 4 to study atrial fibrillation in humans by using temporary atrial epicardial electrodes that were left in patients after cardiac operations. Although the technique was severely limited by the number of available atrial electrodes, Waldo's group was able to identify several
different types of atrial fibrillation. Moreover, differences in the rhythms recorded at different sites within the right atrium and between the two atria have been found in studies with epicardial electrodes.l as well as byendocardial catheter techniques.v" Chen and colleagues? have reported the results of intraoperative studies with a set of epicardial electrodes placed over a limited portion of the right atrial surface. Their electrogram data were said to be suggestive of a reentry process in the right atrium in two patients.
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Cox et al.
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The Journal of Thoracic and Cardiovascular Surgery
--------------------------------
Fig. 4. A to C, Two-dimensional representation of activation sequence maps of a simple pattern of canine atrial flutter with one reentrant circuit rotating around an area of functional blockalong the sulcusterminalison the posterior right atrium. Three consecutive 120msecrevolutions of this reentrant circuitare shown. D, Three-dimensional representation of the same data, showing the reentrant circuiton the posterior right atrium (large dark arrows), with the remainder of the atrium being activated passively (small arrows). For abbreviation see Fig. 3.
Volume 101 Number 3 March 1991
Surgical treatment ofatrial fibrillation, II 4 I I
Fig. 5. A to C, Two-dimensional representation of activation sequence maps during another simple, repetitive pattern of canine atrial flutter. Three consecutive 120 msec revolutions of this reentrant circuit are shown. D to F, Threedimensional representation of three possible conduction routes of the electrical acitivty. D shows the reentrant circuit (thick black arrows) circling counterclockwise around the pulmonary veins, entering the septum posteriorly, and exiting anteriorly. The remaining portions of the atria activated passively (thin black arrows) by the reentrant circuit. In E, the reentrant circuit rotates clockwise around the SVC, entering the septum medially, between the cavae, and exiting on the anterior surface. In F, the reentrant circuit is completely contained within the septum, passively activating the epicardial surface in both atria.
Because of these limitationsin the ability to study the mechanisms of atrial fibrillation, we designed the present studiesto develop a more clinically relevantanimal modelof atrial fibrillation, to devise a meansof recordinglocal electrograms from multiple sites on both atria simultaneously, and to adapt these multipoint mapping techniques for use in humans so that clinicalatrial fibrillation could be mapped in detail. Material and methods Experimental studies. Twenty-five adult mongrel dogs weighing 20 to 25 kg underwent a sterile left thoracotomy, and
a purse-string suture was placed in the extrapericardial left superior pulmonary vein. A high-fidelity Millar catheter (Millar Instruments, Inc., Houston, Tex.) was positioned in the left atrium through the purse-string suture. A Cobe biopsy needle (Cobe Laboratories, Inc., Lakewood, Colo.) was then passed through the purse-string suture, into the left atrium, and across the mitral valve. The chordae tendineae of the mitral valve were sequentially transected with the biopsy needle until the left atrial pressure increased to a mean of 10 to 12 mm Hg from a normal baseline of 2 to 4 mm Hg. The Millar catheter and the biopsy needle were then removed and the thoracotomy was closed. After a minimum of 3 months, the animals were reanesthetized with intravenous a-chloralose (100 mg/kg) and morphine sulfate (l rug/kg). Ventilation was maintained via a cuffed endotracheal tube at an inspired oxygen concentration of
The Journal 01 Thoracic and Cardiovascular
4 1 2 Cox et al.
Surgery
6
Figs. 6 and 7. For legends see page 413.
Volume 101 Number 3 March 1991
Surgical treatment ofatrial fibrillation, II 4 1 3
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8. A to F; Two-dimensionalrepresentation of activation sequence maps recorded during more complexcanine atrial fibrillation. Six separate 50 msec windows of activation are demonstrated. G, Three-dimensional representationsummarizing the major wavefronts (thick black arrows) for the 300 msecsegmentof atrial fibrillation recorded in A to F. For abbreviations see Fig. 3.
Fig. 6. A to F, Two-dimensional representation of irregular canine left atrial flutter with an irregular right atrial response and an irregular ventricularresponse (simpletype of atrial fibrillation?). The reentrant circuit involves the left atrium and atrial septum with posterior to anterior conduction through the septum(G), and the atrial septal activation requires 70 msec in each display window. If the septal activationtime of 70 msec is added to the left atrial activation time, the cycle lengthsof the completed reentrant circuits in A to F are 100 msec, 110 msec, 120 msec, 120rnsec, 120msec,respectively. The activationsequence maps of six consecutive windows of activationof approximately 100 msec each are shown. The activation pattern of the left atrium repeats regularlyand the right atrium shows a variableresponse (heavy black lines and stippled areas representblock).G, Three-dimensional representationof the same data, showing the reentrant circuit rotating counterclockwise around the pulmonaryveins, entering the septum posteriorly, and exitinganteriorly. The remainingportions of the atria are activatedirregularlywith slow conduction and variableblock. Note the similarityof the reentrant circuit in Fag. 6, G, to that in Fag. 5, D. For abbreviations see Fig. 3. Fig. 7. A to F, Two-dimensional representation of activation sequence maps during well-established, sustained canineatrial fibrillation in whicha sequenceof transientlyrepetitive reentry occurs. A showsa singlereentrant circuit similarto that in Fig.4 but the pattern doesnot repeat.B to F showthe reentrant patterns on the posteriorright atrium changing, with a second reentrant site developing on the lateral right atrium (C), By D, the circuit appears to rotate clockwise around the right atrial appendage. In E, the activationattempts to repeat in the posteriorright atrium but is blocked (stippled area). The activationthen continues at the posteroinferior right atrium near the lye. The anterior surface shows an irregular pattern with multipleareas of block (thick dark black lines) with slowconductionand collision of multiplewavefronts. Only the posterior left atrium activatesin a repetitive pattern during thisentireactivationsequence. G,Three-dimensional representation of the activationsequencein A and B. H; Threedimensional representation of the activationin e and D. For abbreviations see Fig. 3.
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The .Journalot Thoracic and Cardiovascular Surgery
Cox et al.
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Fig. 9. Two-dimensional representation of the spontaneous transition from atrial flutter (or a simple form of atrial fibrillation) to normal sinus rhythm in a dog. A to C show a regularly repeating pattern in which the activation appears to originate in the septum, activating the epicardial surface every 150 to 160 msec. In D, an apparently spontaneous electrical discharge from an independent focus in the area of the sinus node on the posterior right atrium captures the atria, and the abnormal activation pattern in A to C converts abruptly to normal sinus rhythm in D to F. For abbreviations see Fig. 3. 0.5. A median sternotomy was performed and the heart was suspended in a pericardial cradle. The standard lead II electrocardiogram (ECG) and systemic arterial blood pressure (left femoral artery catheter) were monitored continuously. Epicar dial pacing and recording electrodes were sutured onto the right and left atrial appendages. Mapping of the activation sequence of the atria during normal sinus rhythm and during atrial fibrillation was performed by means of three epicardial electrode templates containing 208 bipolar electrode pairs (Fig. 1). Atrial activation sequence maps were first recorded during sinus rhythm. Atrial fibrillation was then induced by burst pacing of the atria at a cycle length of 20 msec, a pulse width of 2.0 msec, and a stimulus strength of twice diastolic threshold. The computer system used for data acquisition during this pacing protocol has been described previously. to After sinus rhythm and at least 1000 msec of atrial fibrillation had been recorded,
the surface ECG was scanned to identify the particular windows of interest (Fig. 2, upperpanel). The electrode channels from the selected window were displayed in banks of eight on a computer screen (Fig. 2, lower right panel). The activation times were measured from the beginning of the window. The activation points within each window were chosen by the computer according to a specially designed peak detection algorithm and marked on each channel by cursors. The peak detection algorithm involvesscanning the digitized electrogram data from all 208 channels, calculating the mean and standard deviation of the voltage for each channel, identifying all areas lying outside two standard deviations from the mean, and then choosing the maximum values from these points occurring in any 50 msec interval. These computer-selected activation times were then edited by one of the investigators for accuracy. The activation rna ps were displayed on a two-dimensional line
Volume 101 Number 3 March 1991
Surgical treatment ofatrial fibrillation, II 4 1 5
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drawing in which the atria are depicted as if sectioned in a frontal plane through the superior vena cava (SYC) and then flattened. The posterior surfaces of both atria are displayed below and the anterior surfaces, or tranverse sinus area, above (Fig. 2, lower left panel). A series of maps was generated at intervals corresponding to the shortest cycle length recorded within a given window to avoid overlap of repeating activation times at one electrode point during atrial fibrillation. Hard copies of these serial maps were produced and isochronous lines were drawn at 10 msec intervals. These activation maps were then analyzed in sequence to determine the patterns of wave-front propagation during the various arrhythmias elicited. At the completion of each experiment, the animal was killed and the heart was excised. The body of each atrium and the atrial septum were separated from the remainder of the heart, debrided of fat and connective tissue, and weighed individually. All animals received humane care in compliance with the "Principles of Laboratory Animal Care" formulated by the National Society for Medical Research and the "Guide for the Care and Use of Laboratory Animals" prepared by the National Academy of Sciences and published by the National InstitutesofHealth (NIH Publication No. 80-23, revised 1978). The experimental protocol was reviewed and approved by the insti-
tutional committee for the care and use of laboratory animals. Human studies. Atrial epicardial activation mapping during induced atrial fibrillation was performed intraoperatively in 13 patients with Wolff-Parkinson- White syndrome who were operated on for divisionof an accessory atrioventricular connection. All 13 surgical procedures were primary operations. There were II male and two female patients in the study group. Ages ranged from 15 to 36 years (26.8 ± 6.5 years). All patients underwent a preoperative endocardial catheter electrophysiologic study performed with standard techniques, and each patient was found to have a single accessory atrioventricular connection. None of the patients had associated cardiac disease. Five patients had a history of spontaneous atrial fibrillation documented by standard ECG preoperatively. In one other patient, spontaneous degeneration of orthodromic reciprocating tachycardia to atrial fibrillation was observed during the preoperative electrophyisologic study. The intraoperative mapping techniques used in patients were essentially the same as those described earlier for the experimental studies, and we l 2• 13 have previously reported their use in humans. The major differences included the use of a 160-channel mapping system rather than a 208-channel system and the
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Cox et al.
The .Journat of' Thoracic and Cardiovascular Surgery
Anterior
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Fig. 11. Right atrial reentrant activation during human atrial fibrillation. The activation sequence for the window marked by the boxed area on the ECG lead a VF is shown in the lower maps. A right atrial reentrant loop is seen rotating counterclockwise around a line of bidirectional block associated with the sulcus terminalis. In the upper left panel, the dark arrow marks the site of a left free-wall accessory pathway and shows retrograde activation from the ventricle entering the posterior left atrium. The total length of the window is 420 msec. The labels on each electrogram A to G (lower right panel) correspond to the letters on the lower left enlarged map denoting the location of seven selected electrodes of the 80 electrodes covering the posterior right atrium. For abbreviations see Fig. 10.
Volume 101 Number 3 March 1991
Surgical treatment ofatrial fibrillation, II 4 1 7
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Fig. 12. Reentrant activation during human atrial fibrillation is illustrated in the left panel. Activation of the inferior posterior left atrium by retrograde conduction across a left free-wall accessory pathway is shown in the right panel. The total length of the window is 400 msec. The map on the left shows the first 240 msec, with 230 to 400 msec in the right map. For abbreviations see Fig. 10.
use of electrode templates that were larger and shaped to formfit the human atria. The bipolar electrodes on the human templates were separated by a minimun distance of 5 mm and by a maximum distance of 10 mm. Electrode density was greatest in the area of the sulcus terminalis of the right atrium. Operative exposure was gained via a median sternotomy. The venae cavae were cannulated directly to allow the entire epicardial surface of both atria to be covered by the template electrodes. Atrial fibrillation was induced before initiation of cardiopulmonary bypass in all patients by burst atrial pacing. The criteria for the presence of atrial fibrillation were (1) loss of p waves on the surface ECG, (2) the appearance of a finely undulating ECG baseline, (3) an irregularly irregular rhythm of the QRS complexes, and (4) the gross appearance of uncoordinated atrial muscle activity. Continuous atrial fibrillation was accomplished in all patients with no evidence of spontaneous resolution of the arrhythmia. After at least 30 seconds of atrial fibrillation, direct-current electrical cardioversion was used to restore sinus rhythm. The atrial mapping studies in patients were performed after informed consent had been obtained from each patient and the studies were apporved by the institutional review board for human studies.
Results Experimental studies. Of 25 dogs with surgically induced mitral regurgitation, 19 had atrial flutter or fibrillation, or both. Three of these had spontaneous fibrillation after right thoracotomy or cardiac manipulation, and in the remainder fibrillation was induced by burst pacing. Fibrillation was noninducible in six dogs. In four of the 19 dogs with atrial flutter or fibrillation, the arrhythmia was not mapped because of technical difficulties. Of the 15 dogs whose atrial flutter or fibrillation was mapped, 10 dogs had spontaneous termination of atrial fibrillation and five had sustained atrial fibrillation that was terminated only by cardioversion or extensive surgical manipulation. The normal sinus rhythm maps showed no unusual conduction disturbances (Fig. 3). In three dogs maps were not obtained in sinus rhythm because of persistent atrial fibrillation. Atrial activation during fibrillation exhibited a spec-
The Journal ·01 .
4 18
Cox et al.
Anterior
Thoracic and Cardiovascular Surgery
~ 10 120 130
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Fig. 13. A right atrial reentrant circuit during human atrial fibrillation is shown. In this example, the rotation of the reentrant wave front is clockwise. The length of the window is 400 msec with the activation from the first 210 msec shown in the left map and 210 to 400 msec shown in the right map. For abbreviations see Fig. 10.
trum of abnormal patterns, ranging from the simplest pattern, in which a single reentrant circuit was present that activated the remainder of the atria, to the most complex cases, in which no consistent pattern ofactivation could be identified. An example of the simplest activation pattern is illustrated in Fig. 4. Because three-dimensional data cannot be accurately depicted in two-dimensional form, the data in Fig. 4, A to C are displayed in a more anatomic format in Fig. 4, D. The cycle length of the reentrant circuit (120 msec) corresponds to the cycle length of the atrial arrhythmia in this animal. The standard ECG recorded simultaneously with these epicardial maps showed atrial flutter with an atrial cycle length of 120 msec and 2:1 atrioventricular block. Thus Fig. 4 demonstrates a repetitive atrial activation pattern occurring during induced atrial flutter. Fig. 5 illustrates another simple pattern of atrial activation during canine atrial flutter. The cycle lengths of the reentrant circuits in both Fig. 4 and Fig. 5 are 120 msec. Both of these animals had
atrial flutter with 2:1 atrioventricular block. This flutterlike pattern occurred in seven of the animals in this study. The cycle length ofthe tachycardia in these seven animals ranged from 105 to 138 msec with an average cycle length of 124 msec. In all seven animals the arrhythmia terminated spontaneously. A more complex atrial activation pattern is illustrated in Fig. 6. There are two areas of early epicardial activation, one near the anterior septum and one near the posterior septum. The body of the left atrium and the body of the right atrium both appear to be activated passively from these two early epicardial sites. The right atrium activates irregularly, showing slow conduction and block that result in an inconsistent pattern of activation (Fig. 6, D to F). Activation of the left atrium, however, is much more regular. In the presence of such a reentrant circuit, the right atrium is passively activated. The early area of activity on the epicardial surface of the mid-posterior right atrium is consistent with a passive wave front exit-
Volume 101 Number 3 March 1991
Surgical treatment of atrial fibrillation, II 4 1 9
Fig. 14. Human atrial fibrillation in which reentry occurred fleetingly in the left atrium but could not be conclusively demonstrated in the right atrium. The length of the window is 400 msec with the first 200 msec of activation shown in the left map and the last 200 msec shown in the right map. For abbreviations See Fig. 10.
ing the reentrant circuit shortly after it enters the posterior septum. An example of sustained atrial fibrillation that was initiated by manipulation of the heart is illustrated in Fig. 7. An example of the most complex atrial epicardial activation pattern is shown in Fig. 8. Because the activation pattern is irregular, individual beats cannot be identified and each individual map shows 50 msec of activation. Cycle lengths at individual electrodes range from 60 to 167 msec. No complete reentrant loops were demonstrable and only a few repetitive patterns were suggested (Fig. 8, G). The atrial activation pattern is characterized by multiple wave fronts that are initiated and terminated spontaneously. Three to six individual wave fronts are present in each 50 msec interval. The atrial fibrillation in this animal was sustained. In this series of animals, we were unable to record spontaneous initiation of atrial flutter or atrial fibrillation. However, spontaneous termination of atrial flutter is demonstrated in Fig. 9.
Increased complexity and duration of the atrial fibrillation in this study were associated with increasing atrial enlargement; those animals exhibiting sustained atrial fibrillation had a grossly enlarged left atrium, whereas those with nonsustained patterns had more modest atrial enlargement. Also, the tissue was friable because of thinning of the atrial wall. However, there were no gross conduction disturbances in the atrial activation patterns during either sinus rhythm or atrial pacing. Human studies. Earliest atrial activation during sinus rhythm in patients also occurs in the region of the sinus node at the junction of the SVC with the right atrium (Fig. 10). Activation spreads radially across the posterior right atrium and anteriorly around the lateral border of the SV C, proceeding from right to left across Bachmann's bundle anteriorly to reach the base of the left atrial appendage at 90 msec. The wave front traversing the posterior right atrium propagates between the venae cavae onto the posterior left atrium beneath the right pulmonary veins. The apparent time gap in this region is
The Journal of Thoracic and Cardiovascular
4 20 Cox et al.
Surgery
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Fig. 15. A patient in whom reentry could not be clearlydocumentedduring atrial fibrillation. However, the repetitivesequenceof activation in the left atrium suggests that the wavefront is entering the septum posteriorly and exiting the septum anteriorly, which establishes a completereentrant loop.The length of the window is41 0 msec.The map on the left showsthe activationfrom 100-250msec and the right map shows from 250 to 410 msec. For abbreviations see Fig. 10.
the result of a slight anatomic separation of the electrode templates by the inferior vena cava (lYC), which is located between the large right atrial template and the posterior left atrial template. The posterior left atrium is activated by the anterior and posterior components of the sinus-initiated wave front that meet at the point of latest atrial activation beneath the left inferior pulmonary vein. Representative activation patterns observed during human atrial fibrillation are shown in Fig. 11 to 15. During atrial fibrillation, six of the 13 patients had atrial activation sequences in the right atrium suggestive of reentry. Although discrete reentrant circuits could not be demonstrated in the remaining patients, all seven had repetitive right atrial activation patterns. Activation sequences in the left atrium usually suggested nonuniform conduction and bidirectional block. Documentation of complete left atrial reentrant circuits was rare in patients.
Discussion Both the experimental and clinical data in this study are consistent with previous experimental studies supporting reentry as the principal mechanism of atrial fibrillation. Complete reentrant circuits were documented during atrial flutter and atrial fibrillation in dogs (Figs. 4 and 7) and in man (Figs. 11 to 14). Other data showed partial reentrant circuits, suggesting that the wave front moved through the septum and around the pulmonary veins, IYC, or SYC (Figs. 5, 6, 9, and 15). The more complex patterns, in which reentrant circuits either were not documented or were only fleeting (Figs. 8, 12, and 13), were consistent with the multiple wavelet hypothesis of Moe l 4 and the experimental data of Allessie and associates. I, 15 Although anatomic obstacles such as the pulmonary veins, IYC, and SYC were involved in the apparent reentrant circuits, Figs. 4, 7, and 11 to 14 indicate that reentry may occur in the absence of these ana-
Volume 101 Number 3
Surgicaltreatment ofatrialfibrillation, II 4 2 I
March 1991
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Fig. 16. Atrial anatomy pertinent to atrial electrophysiology and the surgical treatment of atrial arrhythmias. The entire atrial myocardium, includingthe atrial septum, is depicted as a two-dimensional rectangle, with the atrial septum separating the right atrium from the left atrium. The left atrial appendage (LAA) and right atrial appendage (RAA) are depicted as being contiguous with their respective atria. The superior vena cave (SVC) and the inferior vena cava (IVC) are depicted as black boxeswithinthe right atrium, indicating that there are twolarge anatomic "holes" (i.e., the orificesof these two vessels) around which electrical activity must propagate. The orifices of the pulmonary veins (PVs) are also indicated schematically, but because electrical activity can conduct between the orifices of each of these veins, they are illustrated with the same background as that of the left atrium. Finally, the sinoatrial node (SAN) is located at the top of the atrial septum near itsjunction with the right atrium, and the atrioventricular node (A VN) is depicted at the bottom of the atrial septum.
tomic obstacles. Functional conduction block, which is necessary for reentry, occurred throughout the atria. In some cases, the local conduction block was associated with an underlying structure in the atria, such as the crista terminalis (Figs. 4, 7, and 11 to 13), as was predicted by the isolated atrial studies ofSpach and associates. 16, 17 Allessie, Bonke, and Schopman 1 have also shown that chemically produced refractory period inhomogeneity can produce local functional block in atrial fibrillation. In the present study, no measurements of the refractory period were made. However, Fig. 6 illustrates an example in which a single left atrial reentrant circuit fails to activate all of the right atrium in a 1:I fashion with each cycle. Studies have suggested that left atrial refractory periods are shorter than right atrial refractory periods. 18 If this is true, this gross inhomogeneity in refractory peri-
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Fig. 17. During normal sinus rhythm, the electrical impulse is generated within the sinoatrial node and propagates across the right and left atria and the atrial septum to the atrioventricular node and thence to the ventricles. Note that under normal circumstances there is a collision of two portions of the sinus impulsebeneath the pulmonary veinsposteriorly(upper portion of the left atrium). (Same anatomic schema and abbreviations as in Fig. 16.)
Fig. 18. The three electrophysiologic components that determine the diagnosis of atrial flutter and atrial fibrillation: (1) atrial flutter-wave, (2) passiveatrial conduction, and (3) atrioventricular conduction. (Same anatomic schema and abbreviations as in Fig. 16.)
ods between the left and right atria might explain why the left atrial wave fronts fail to activate the right atrium in a 1:1 fashion. The short left atrial refractory periods allow faster reentrant circuits to form in the left atrium, but repetitive 1:1 activation of the right atrium is precluded
The Journal of Thoracic and Cardiovascular
4 2 2 Cox et al.
Electrophysiologic Components
Surgery
Findings at Intraoperative Mapping
Standard ECG
Clinical Diagnosis
Stable
.>-.,.... Regular p-wqve
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Stable Fig. 19. Electrophysiologic basis of the standard ECG findings in the simplest type of atrial flutter. (Same anatomic schema and abbreviations as in Fig. 16.)
Electrophysiologic Components
Findings at Intraoperative Mapping
Standard ECG
Clinical Diagnosis
Stable >-~ ~egular
p-wave
Stable Irregular >-~Ventricular
Atrial Flutter with Varying A-V Block
Response
Variable Fig. 20. Electrophysiologic basis of the standard ECG findings in atrial flutter with varying atrioventricular block. (Same anatomic schema and abbreviations as in Fig. 16.)
Volume 101 Number 3 March 1991
Surgicaltreatment ofatrialfibrillation. II 4 2 3
Electrophysiologic Components
Findings at Intraoperative Mapping
Variable
Standard
ECG
Regular p-wave with Varying Morphology ~.....
Stable
Stable
Clinical Diagnosis
Regular Ventricular Response
Atrial Flutter
Fig. 21. Electrophysiologic basis of the standard ECG findings in atrial flutter in which the p wave morphology varies. (Same anatomic schema and abbreviations as in Fig. 16.)
Electrophysiologic Components
Findings at Intraoperative Mapping
.....- -.......~ Variable
Stable
Standard
ECG
Clinical Diagnosis
Begular p-wave with Varying Morphology ~....~Atrial Fibrillation Irregular Ventricular Response
Variable Fig. 22. Electrophysiologic basis of the standard ECG findings in one form on "atrial fibrillation" with a single reentrant circuit in which the atrial events are identical to those in the "atrial flutter" of Fig. 21. In this case, the variable atrioventricular conduction causes an irregular ventricular response. (Same anatomic schema and abbreviations as in Fig. 16.)
424
The Journal of Thoracic and Cardiovascular
Cox et al.
Electrophysiologic Components
Surgery
Findings at Intraoperative Mapping
Standard ECG
Clinical Diagnosis
Variable """'Irregular i)-wave Atrial Fibrillation
Variable Irregular ~-..-ventricular
Stable or Variable
Response
Fig. 23. Electrophysiologic basis of the standard ECG findings in another form of "atrial fibrillation" with a single reentrant circuit that has a variable cycle length. (Same anatomic schema and abbreviations as in Fig. 16.)
by the longer refractory periods of the right atrium. Several areas of the atria were not mapped in these studies, including the pulmonary veins, atrial septum, and a small region beneath the IYC on the posterior right atrium. This is one limitation of our study and the data suggest that these regions are important. In Fig. 9, A to C (dog) and Fig. 14 (man), the activation of the epicardial surface originates in the septum, with no wave fronts reentering the septum. Therefore the mechanism responsible for the arrhythmia in these instances is completely confined to the unmapped areas. A conceptual summary of the mechanisms underlying the spectrum of arrhythmias from the simplest form of atrial flutter to the most complex form of atrial fibrillation is illustrated in Figs. 16 to 24. However, before contemplating these new concepts, one should remember that, until now, both atrial flutter and atrial fibrillation have been clinical diagnoses; that is, the diagnosis in each case has been based on the standard ECG findings or on data from a few atrial electrodes, rather than being based on the actual electrophysiologic events occurring in the atria. The present study provides more insight into the atrial events underlying these arrhythmias and documents the electrophysiologic differences between atrial flutter and atrial fibrillation, as well as the phenomena responsible for the clinical arrhythmias that occupy that
portion of the spectrum between simple flutter and complex fibrillation. To understand these electrophysiologic observations more clearly, we related them to atrial anatomy by using a schematic diagram of the atria that includes the pertinent atrial anatomy and that allows the observed electrophysiologic phenomena to be superimposed on that anatomy. As mentioned earlier, atrial flutter and atrial fibrillation are diagnosed on the basis of the standard ECG. Although there is general agreement on the clinical descriptors of simple atrial flutter and complex atrial fibrillation, there is no consensus regarding the correct terminology to be applied to the electrophysiologic findings that cause these arrhythmias. For example, it would seem to be an oversimplification to categorize atrial flutter as an arrhythmia that is caused by a single reentrant circuit and atrial fibrillation as one caused by multiple reentrant circuits, as was thought in the past. Whereas atrial flutter appears always to occur on the basis of a single reentrant circuit, some forms of atrial fibrillation may also be caused by a single reentrant circuit (see Figs. 6, 7, 11,22, and 23) and more complex forms result from multiple reentrant circuits (see Figs. 8, 12, 13, 14, and 24). Finally, both the experimental and clinical observations made in the present study consistently confirmed the
Volume 101 Number 3 March 1991
Surgical treatment ofatrial fibrillation, II 4 2 5
Electrophysiologic Components
Findings at Intraoperative Mapping
Variable Multiple Reentrant Circuits Stable or Variable
Standard ECG
Irregular p-wave
Clinical Diagnosis
Atrial Fibrillation
Irregular Ventricular Response
Fig. 24. Electrophysiologic basis of the standard ECG findings in the most complex type of atrial fibrillation. (Same anatomic schema and abbreviations as in Fig. 16.)
previous experimental observations of Moe,14 Boineau.l SpaCh,16, 17 Allessie,': 15 Waldo,4 and their associates. Our concept of the electrophysiologic mechanisms underlying atrial flutter, atrial fibrillation, and the intervening transitional arrhythmias incorporates virtuallyallof their observations, as wellas those made in the presentstudy. Although thisconceptdoesnot answerallof the questions regardingthese arrhythmias, it doesprovide the basisfor establishing a more scientific approach to the surgical treatment of atrial flutter and atrial fibrillation.
5.
6.
7. 8.
REFERENCES 1. 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 movement in cardiac tissue without the involvement of an anatomical obstacle. Circ Res 1977;41:9-18. 2. 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 CardioI1980;45:1167-81. 3. Wells JLJr, Karp RB, Kouchoukos NT, MacLean WAH, James TN, Waldo AL. Characterization of atrial fibrillation in man: studies following open heart surgery. PACE 1978;1:426-38. 4. Waldo AL, MacLean WAH. Diagnosis and treatment of
9.
10.
II.
12.
arrhythmias followingopen heart surgery: emphasis on the use of epicardial wire electrodes. New York: Futura Publishing Co., 1980:85-8. Nelson RM, Jenson CB, Davis RW. Differential atrial arrhythmias in cardiac surgical patients [Abstract]. Circulation 1968;38(Pt 2):VIl47. Leier CV, Schaal SF. Biatrial electrograrns during coarse atrial fibrillation and flutter-fibrillation. Am Heart J 1980; 99:331-41. Zipes DP, Dejoseph RL. Dissimilar atrial rhythms in man and dog. Am J CardioI1973;32:618-28. Puech P, Grolleau R, Rebuffat G. Intra-atrial mapping of atrial fibrillation in man. In: Kulbertus HE, Olsson SB, Schlepper M, eds. Atrial fibrillation. Molndal, Sweden: AB Hassell, 1982:94-109. Chen PS, Smith WM, Greer GS, Wharton JM, Vidaillet HJ Jr, Ideker RE. Activation patterns during electrically induced atrial fibrillation in humans [Abstract]. Circulation 1986;74(Pt 2):11483. Witkowski FX, Corr PB. An automated simultaneous transmural cardiac mapping system. Am J Physiol 1984; 247:H661-8. 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. Canavan TE, Schuessler RB, Boineau JP, Corr PB, Cain ME, Cox JL. Computerized global electrophysiological
of
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13.
14. 15.
16.
mapping of the atrium in patients with Wolff-ParkinsonWhite syndrome. Ann Thorac Surg 1988;46:223-31. Canavan TE, Schuessler RB,Cain ME, et al. Computerized global electrophysiological mapping of the atrium in a patient with multiple supraventricular tachyarrhythmias. Ann Thorac Surg 1988;46:232-5. Moe GK. On the multiple wavelet hypothesis of atrial fibrillation. Arch Int Pharmacodyn 1962;140:183-8. Allessie MA, Lammers WJEP, Bonke FIm, Hollen JM. Experimental evaluation of Moe's multiple wavelet hypothesis of atrial fibrillation. In: Zipes DP, Jalife J, eds. Cardiac electrophysiology and arrhythmias. Orlando, Florida: Grune & Stratton, 1985:265-75. Spach MS, Miller WT III, Geselowitz DB, Barr RC,
The Journal Thoracic and Cardiovascular Surgery
Kootsey JM, Johnson EA. The discontinuous nature of propagation in normal canine cardiac muscle: evidence of recurrent discontinuities of intracellular resistance that affect the membrane currents. Circ Res 1981;48:39-54. 17. Spach MS, Dolber Pc. Relating extracellular potentials and their derivatives to anisotropic propagation at a microscopic levelin human cardiac muscles: evidence for electrical uncoupling of side-to-side fiber connections with increasing age. Circ Res 1986;58:356-71. 18. Rensma PL, Allessie MA, Lammers WJ, Bonke FI, Schalij MJ. Length of excitation wave and susceptibility to reentrant atrial arrhythmias in normal consciousdogs. Circ Res 1988;62:395-410.
THORAC CARDIOVASC SURG
1991;101:406-26
The surgical treatment of atrial fibrillation II. Intraoperative electrophysiologic mapping and description of the electrophysiologic basis of atrial flutter and atrial fibrillation Computerized mapping of atrial fibrillation was perfonned in animals and man. To study atrial fibrillation in a systematic manner, we developed a clinically relevant experimental model of atrial fibrillation. Chronic mitral regurgitation was created surgically in 25 dogs .without opening the pericardium. Mter several months of chronic mitral regurgitation, the atria became enlarged and sustained atrial fibrillation could be induced by standard programmed electrical stimulation techniques. Computerized isochronous activation maps of the atria were recorded during atrial fibrillation from 208 bipolar electrodes simultaneously. In a parallel study, human atrial fibrillation was mapped with a separate 16(khannel intraoperative mapping system in patients with paroxysmal atrial fibrillation who were undergoing surgical correction of the Wolff-Parkinson-White syndrome. The canine activation sequence maps demonstrated a spectrum of rhythm abnormalities ranging from simple atrial flutter to complex atrial fibrillation. They also showed that macroreentrant circuits within the atrial myocardium were responsible for the entire spectrum of arrhythmias. Atrial reentry was also documented during human atrial fibrillation. All patients had nonuniform conduction around regions of bidirectional block in both atria resulting in multiple discrete wave fronts. In addition, six patients had a single reentrant circuit in the right atrium in which bidirectional block of the activation wave front occurred along the sulcus terminalis between the venae cavae. The left atrium in all patients demonstrated multiple wave fronts and conduction block, but left atrial reenty could not be detected. Both the experimental study and the clinical study demonstrated that multiple wave fronts, nonuniform conduction, bidirectional block, and large (macroreentrant) reentrant circuits occur during atrial fibrillation. The presence of macroreentrant circuits and the absence of either microreentrant circuits or evidence of atrial automaticity suggests that atrial fibrillation should be amenable to surgical ablation.
James L. Cox, MD, Thomas E. Canavan, MD, Richard B. Schuessler, PhD, Michael E. Cain, MD, Bruce D. Lindsay, MD, Constance Stone, MD, Peter K. Smith, MD, Peter B. Corr, PhD, and John P. Boineau, MD, St. Louis, Mo.
From the Division of Cardiothoracic Surgery, Department of Surgery, and the Division of Cardiology, Department of Medicine, Washington University School of Medicine, Barnes Hospital, St. Louis, Mo. Supported by National Institutes of Health Grants ROI HL33722 and ROJ HL32257 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, Division of Cardiothoracic Surgery, Suite 3108, Queeny Tower, One Barnes Hospital Plaza, St. Louis, MO 63110.
12/1/25797
406
Rvious efforts at mapping atrial fibrillation have been hampered by two factors: (1) the inability to record local atrial electrograms from multiple sites simultaneously and (2) inadequate animal models of atrial fibrillation. Allessie, Bonke, and Schopman J developed a multipoint system for mapping atrial flutter and fibrillation in an isolated atrial model, but the system was not adaptable for use in human studies. Boineau and colleagues/ developed a different type of multipoint mapping system that they used to study a dog with naturally occurring spontaneous atrial flutter, but it was a multiplexed system that required several cycles of a stable rhythm to allow time for switching from one set of electrodes to another to com-
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Surgical treatment ofatrial fibrillation, II 4 0 7
Fig. 1. Atrial epicardial electrode templates containing 156 bipolar electrodes. These templates. fashioned of silicone rubber (O.02-inch thickness, Dow Corning Corp., Midland, Mich.) were designed to conform to the epicardial surfaces of the atria. Fine silver wires (Quad Teflon-coated silver wire, a.005-inch diameter. Medwire, Inc., Mt. Vernon, N.Y.) were embedded in these silicone rubber templates at an interelectrode distance of 6 mm and an intraelectrode distance of I mm. The largest template, containing 80 electrodes, was placed over the postolateral right atrium and extended from the interatrial groove posteriorly to the right atrial appendage and atrioventricular groove anteriorly. A second template with 64 electrodes covered the anterior aspects of both the right and left atria immediately behind the ascending aorta in the region of the transverse sinus. The third template, also containing 64 electrodes, covered the posterior left atrium inferior to the pulmonary veins and the posterior left atrial appendage. These templates were fixed in position on the epicardial surfaces of the atria with 4-0 silk sutures. The template on the left side of A covers the lateral right atrium. The upper right template in A covers the anterior right and left atria and the medial portion of the left atrial appendage. The lower right template covers the posterior left atrium. B shows an enlarged view of the anterior left and right atrial template. The holes on the edges of each template are for suture fixation to the atrium.
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plete the mapping process. Thus their mapping system was of limited value in the study of atrial fibrillation. The lack of a suitable animal model of atrial fibrillation and the inability to map human atrial fibrillation simultaneously from multiple sites led Waldo and associates- 4 to study atrial fibrillation in humans by using temporary atrial epicardial electrodes that were left in patients after cardiac operations. Although the technique was severely limited by the number of available atrial electrodes, Waldo's group was able to identify several
different types of atrial fibrillation. Moreover, differences in the rhythms recorded at different sites within the right atrium and between the two atria have been found in studies with epicardial electrodes.l as well as byendocardial catheter techniques.v" Chen and colleagues? have reported the results of intraoperative studies with a set of epicardial electrodes placed over a limited portion of the right atrial surface. Their electrogram data were said to be suggestive of a reentry process in the right atrium in two patients.
4 10
Cox et al.
LAA Anterior Posterior - - - - - - - - - - -- - - ---- ------ - ---
The Journal of Thoracic and Cardiovascular Surgery
--------------------------------
Fig. 4. A to C, Two-dimensional representation of activation sequence maps of a simple pattern of canine atrial flutter with one reentrant circuit rotating around an area of functional blockalong the sulcusterminalison the posterior right atrium. Three consecutive 120msecrevolutions of this reentrant circuitare shown. D, Three-dimensional representation of the same data, showing the reentrant circuiton the posterior right atrium (large dark arrows), with the remainder of the atrium being activated passively (small arrows). For abbreviation see Fig. 3.
Volume 101 Number 3 March 1991
Surgical treatment ofatrial fibrillation, II 4 I I
Fig. 5. A to C, Two-dimensional representation of activation sequence maps during another simple, repetitive pattern of canine atrial flutter. Three consecutive 120 msec revolutions of this reentrant circuit are shown. D to F, Threedimensional representation of three possible conduction routes of the electrical acitivty. D shows the reentrant circuit (thick black arrows) circling counterclockwise around the pulmonary veins, entering the septum posteriorly, and exiting anteriorly. The remaining portions of the atria activated passively (thin black arrows) by the reentrant circuit. In E, the reentrant circuit rotates clockwise around the SVC, entering the septum medially, between the cavae, and exiting on the anterior surface. In F, the reentrant circuit is completely contained within the septum, passively activating the epicardial surface in both atria.
Because of these limitationsin the ability to study the mechanisms of atrial fibrillation, we designed the present studiesto develop a more clinically relevantanimal modelof atrial fibrillation, to devise a meansof recordinglocal electrograms from multiple sites on both atria simultaneously, and to adapt these multipoint mapping techniques for use in humans so that clinicalatrial fibrillation could be mapped in detail. Material and methods Experimental studies. Twenty-five adult mongrel dogs weighing 20 to 25 kg underwent a sterile left thoracotomy, and
a purse-string suture was placed in the extrapericardial left superior pulmonary vein. A high-fidelity Millar catheter (Millar Instruments, Inc., Houston, Tex.) was positioned in the left atrium through the purse-string suture. A Cobe biopsy needle (Cobe Laboratories, Inc., Lakewood, Colo.) was then passed through the purse-string suture, into the left atrium, and across the mitral valve. The chordae tendineae of the mitral valve were sequentially transected with the biopsy needle until the left atrial pressure increased to a mean of 10 to 12 mm Hg from a normal baseline of 2 to 4 mm Hg. The Millar catheter and the biopsy needle were then removed and the thoracotomy was closed. After a minimum of 3 months, the animals were reanesthetized with intravenous a-chloralose (100 mg/kg) and morphine sulfate (l rug/kg). Ventilation was maintained via a cuffed endotracheal tube at an inspired oxygen concentration of
The Journal 01 Thoracic and Cardiovascular
4 1 2 Cox et al.
Surgery
6
Figs. 6 and 7. For legends see page 413.
Volume 101 Number 3 March 1991
Surgical treatment ofatrial fibrillation, II 4 1 3
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8. A to F; Two-dimensionalrepresentation of activation sequence maps recorded during more complexcanine atrial fibrillation. Six separate 50 msec windows of activation are demonstrated. G, Three-dimensional representationsummarizing the major wavefronts (thick black arrows) for the 300 msecsegmentof atrial fibrillation recorded in A to F. For abbreviations see Fig. 3.
Fig. 6. A to F, Two-dimensional representation of irregular canine left atrial flutter with an irregular right atrial response and an irregular ventricularresponse (simpletype of atrial fibrillation?). The reentrant circuit involves the left atrium and atrial septum with posterior to anterior conduction through the septum(G), and the atrial septal activation requires 70 msec in each display window. If the septal activationtime of 70 msec is added to the left atrial activation time, the cycle lengthsof the completed reentrant circuits in A to F are 100 msec, 110 msec, 120 msec, 120rnsec, 120msec,respectively. The activationsequence maps of six consecutive windows of activationof approximately 100 msec each are shown. The activation pattern of the left atrium repeats regularlyand the right atrium shows a variableresponse (heavy black lines and stippled areas representblock).G, Three-dimensional representationof the same data, showing the reentrant circuit rotating counterclockwise around the pulmonaryveins, entering the septum posteriorly, and exitinganteriorly. The remainingportions of the atria are activatedirregularlywith slow conduction and variableblock. Note the similarityof the reentrant circuit in Fag. 6, G, to that in Fag. 5, D. For abbreviations see Fig. 3. Fig. 7. A to F, Two-dimensional representation of activation sequence maps during well-established, sustained canineatrial fibrillation in whicha sequenceof transientlyrepetitive reentry occurs. A showsa singlereentrant circuit similarto that in Fig.4 but the pattern doesnot repeat.B to F showthe reentrant patterns on the posteriorright atrium changing, with a second reentrant site developing on the lateral right atrium (C), By D, the circuit appears to rotate clockwise around the right atrial appendage. In E, the activationattempts to repeat in the posteriorright atrium but is blocked (stippled area). The activationthen continues at the posteroinferior right atrium near the lye. The anterior surface shows an irregular pattern with multipleareas of block (thick dark black lines) with slowconductionand collision of multiplewavefronts. Only the posterior left atrium activatesin a repetitive pattern during thisentireactivationsequence. G,Three-dimensional representation of the activationsequencein A and B. H; Threedimensional representation of the activationin e and D. For abbreviations see Fig. 3.
4 14
The .Journalot Thoracic and Cardiovascular Surgery
Cox et al.
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Fig. 9. Two-dimensional representation of the spontaneous transition from atrial flutter (or a simple form of atrial fibrillation) to normal sinus rhythm in a dog. A to C show a regularly repeating pattern in which the activation appears to originate in the septum, activating the epicardial surface every 150 to 160 msec. In D, an apparently spontaneous electrical discharge from an independent focus in the area of the sinus node on the posterior right atrium captures the atria, and the abnormal activation pattern in A to C converts abruptly to normal sinus rhythm in D to F. For abbreviations see Fig. 3. 0.5. A median sternotomy was performed and the heart was suspended in a pericardial cradle. The standard lead II electrocardiogram (ECG) and systemic arterial blood pressure (left femoral artery catheter) were monitored continuously. Epicar dial pacing and recording electrodes were sutured onto the right and left atrial appendages. Mapping of the activation sequence of the atria during normal sinus rhythm and during atrial fibrillation was performed by means of three epicardial electrode templates containing 208 bipolar electrode pairs (Fig. 1). Atrial activation sequence maps were first recorded during sinus rhythm. Atrial fibrillation was then induced by burst pacing of the atria at a cycle length of 20 msec, a pulse width of 2.0 msec, and a stimulus strength of twice diastolic threshold. The computer system used for data acquisition during this pacing protocol has been described previously. to After sinus rhythm and at least 1000 msec of atrial fibrillation had been recorded,
the surface ECG was scanned to identify the particular windows of interest (Fig. 2, upperpanel). The electrode channels from the selected window were displayed in banks of eight on a computer screen (Fig. 2, lower right panel). The activation times were measured from the beginning of the window. The activation points within each window were chosen by the computer according to a specially designed peak detection algorithm and marked on each channel by cursors. The peak detection algorithm involvesscanning the digitized electrogram data from all 208 channels, calculating the mean and standard deviation of the voltage for each channel, identifying all areas lying outside two standard deviations from the mean, and then choosing the maximum values from these points occurring in any 50 msec interval. These computer-selected activation times were then edited by one of the investigators for accuracy. The activation rna ps were displayed on a two-dimensional line
Volume 101 Number 3 March 1991
Surgical treatment ofatrial fibrillation, II 4 1 5
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drawing in which the atria are depicted as if sectioned in a frontal plane through the superior vena cava (SYC) and then flattened. The posterior surfaces of both atria are displayed below and the anterior surfaces, or tranverse sinus area, above (Fig. 2, lower left panel). A series of maps was generated at intervals corresponding to the shortest cycle length recorded within a given window to avoid overlap of repeating activation times at one electrode point during atrial fibrillation. Hard copies of these serial maps were produced and isochronous lines were drawn at 10 msec intervals. These activation maps were then analyzed in sequence to determine the patterns of wave-front propagation during the various arrhythmias elicited. At the completion of each experiment, the animal was killed and the heart was excised. The body of each atrium and the atrial septum were separated from the remainder of the heart, debrided of fat and connective tissue, and weighed individually. All animals received humane care in compliance with the "Principles of Laboratory Animal Care" formulated by the National Society for Medical Research and the "Guide for the Care and Use of Laboratory Animals" prepared by the National Academy of Sciences and published by the National InstitutesofHealth (NIH Publication No. 80-23, revised 1978). The experimental protocol was reviewed and approved by the insti-
tutional committee for the care and use of laboratory animals. Human studies. Atrial epicardial activation mapping during induced atrial fibrillation was performed intraoperatively in 13 patients with Wolff-Parkinson- White syndrome who were operated on for divisionof an accessory atrioventricular connection. All 13 surgical procedures were primary operations. There were II male and two female patients in the study group. Ages ranged from 15 to 36 years (26.8 ± 6.5 years). All patients underwent a preoperative endocardial catheter electrophysiologic study performed with standard techniques, and each patient was found to have a single accessory atrioventricular connection. None of the patients had associated cardiac disease. Five patients had a history of spontaneous atrial fibrillation documented by standard ECG preoperatively. In one other patient, spontaneous degeneration of orthodromic reciprocating tachycardia to atrial fibrillation was observed during the preoperative electrophyisologic study. The intraoperative mapping techniques used in patients were essentially the same as those described earlier for the experimental studies, and we l 2• 13 have previously reported their use in humans. The major differences included the use of a 160-channel mapping system rather than a 208-channel system and the
4 16
Cox et al.
The .Journat of' Thoracic and Cardiovascular Surgery
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Fig. 11. Right atrial reentrant activation during human atrial fibrillation. The activation sequence for the window marked by the boxed area on the ECG lead a VF is shown in the lower maps. A right atrial reentrant loop is seen rotating counterclockwise around a line of bidirectional block associated with the sulcus terminalis. In the upper left panel, the dark arrow marks the site of a left free-wall accessory pathway and shows retrograde activation from the ventricle entering the posterior left atrium. The total length of the window is 420 msec. The labels on each electrogram A to G (lower right panel) correspond to the letters on the lower left enlarged map denoting the location of seven selected electrodes of the 80 electrodes covering the posterior right atrium. For abbreviations see Fig. 10.
Volume 101 Number 3 March 1991
Surgical treatment ofatrial fibrillation, II 4 1 7
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aVF
Fig. 12. Reentrant activation during human atrial fibrillation is illustrated in the left panel. Activation of the inferior posterior left atrium by retrograde conduction across a left free-wall accessory pathway is shown in the right panel. The total length of the window is 400 msec. The map on the left shows the first 240 msec, with 230 to 400 msec in the right map. For abbreviations see Fig. 10.
use of electrode templates that were larger and shaped to formfit the human atria. The bipolar electrodes on the human templates were separated by a minimun distance of 5 mm and by a maximum distance of 10 mm. Electrode density was greatest in the area of the sulcus terminalis of the right atrium. Operative exposure was gained via a median sternotomy. The venae cavae were cannulated directly to allow the entire epicardial surface of both atria to be covered by the template electrodes. Atrial fibrillation was induced before initiation of cardiopulmonary bypass in all patients by burst atrial pacing. The criteria for the presence of atrial fibrillation were (1) loss of p waves on the surface ECG, (2) the appearance of a finely undulating ECG baseline, (3) an irregularly irregular rhythm of the QRS complexes, and (4) the gross appearance of uncoordinated atrial muscle activity. Continuous atrial fibrillation was accomplished in all patients with no evidence of spontaneous resolution of the arrhythmia. After at least 30 seconds of atrial fibrillation, direct-current electrical cardioversion was used to restore sinus rhythm. The atrial mapping studies in patients were performed after informed consent had been obtained from each patient and the studies were apporved by the institutional review board for human studies.
Results Experimental studies. Of 25 dogs with surgically induced mitral regurgitation, 19 had atrial flutter or fibrillation, or both. Three of these had spontaneous fibrillation after right thoracotomy or cardiac manipulation, and in the remainder fibrillation was induced by burst pacing. Fibrillation was noninducible in six dogs. In four of the 19 dogs with atrial flutter or fibrillation, the arrhythmia was not mapped because of technical difficulties. Of the 15 dogs whose atrial flutter or fibrillation was mapped, 10 dogs had spontaneous termination of atrial fibrillation and five had sustained atrial fibrillation that was terminated only by cardioversion or extensive surgical manipulation. The normal sinus rhythm maps showed no unusual conduction disturbances (Fig. 3). In three dogs maps were not obtained in sinus rhythm because of persistent atrial fibrillation. Atrial activation during fibrillation exhibited a spec-
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Anterior
Thoracic and Cardiovascular Surgery
~ 10 120 130
Posterior
Fig. 13. A right atrial reentrant circuit during human atrial fibrillation is shown. In this example, the rotation of the reentrant wave front is clockwise. The length of the window is 400 msec with the activation from the first 210 msec shown in the left map and 210 to 400 msec shown in the right map. For abbreviations see Fig. 10.
trum of abnormal patterns, ranging from the simplest pattern, in which a single reentrant circuit was present that activated the remainder of the atria, to the most complex cases, in which no consistent pattern ofactivation could be identified. An example of the simplest activation pattern is illustrated in Fig. 4. Because three-dimensional data cannot be accurately depicted in two-dimensional form, the data in Fig. 4, A to C are displayed in a more anatomic format in Fig. 4, D. The cycle length of the reentrant circuit (120 msec) corresponds to the cycle length of the atrial arrhythmia in this animal. The standard ECG recorded simultaneously with these epicardial maps showed atrial flutter with an atrial cycle length of 120 msec and 2:1 atrioventricular block. Thus Fig. 4 demonstrates a repetitive atrial activation pattern occurring during induced atrial flutter. Fig. 5 illustrates another simple pattern of atrial activation during canine atrial flutter. The cycle lengths of the reentrant circuits in both Fig. 4 and Fig. 5 are 120 msec. Both of these animals had
atrial flutter with 2:1 atrioventricular block. This flutterlike pattern occurred in seven of the animals in this study. The cycle length ofthe tachycardia in these seven animals ranged from 105 to 138 msec with an average cycle length of 124 msec. In all seven animals the arrhythmia terminated spontaneously. A more complex atrial activation pattern is illustrated in Fig. 6. There are two areas of early epicardial activation, one near the anterior septum and one near the posterior septum. The body of the left atrium and the body of the right atrium both appear to be activated passively from these two early epicardial sites. The right atrium activates irregularly, showing slow conduction and block that result in an inconsistent pattern of activation (Fig. 6, D to F). Activation of the left atrium, however, is much more regular. In the presence of such a reentrant circuit, the right atrium is passively activated. The early area of activity on the epicardial surface of the mid-posterior right atrium is consistent with a passive wave front exit-
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Surgical treatment of atrial fibrillation, II 4 1 9
Fig. 14. Human atrial fibrillation in which reentry occurred fleetingly in the left atrium but could not be conclusively demonstrated in the right atrium. The length of the window is 400 msec with the first 200 msec of activation shown in the left map and the last 200 msec shown in the right map. For abbreviations See Fig. 10.
ing the reentrant circuit shortly after it enters the posterior septum. An example of sustained atrial fibrillation that was initiated by manipulation of the heart is illustrated in Fig. 7. An example of the most complex atrial epicardial activation pattern is shown in Fig. 8. Because the activation pattern is irregular, individual beats cannot be identified and each individual map shows 50 msec of activation. Cycle lengths at individual electrodes range from 60 to 167 msec. No complete reentrant loops were demonstrable and only a few repetitive patterns were suggested (Fig. 8, G). The atrial activation pattern is characterized by multiple wave fronts that are initiated and terminated spontaneously. Three to six individual wave fronts are present in each 50 msec interval. The atrial fibrillation in this animal was sustained. In this series of animals, we were unable to record spontaneous initiation of atrial flutter or atrial fibrillation. However, spontaneous termination of atrial flutter is demonstrated in Fig. 9.
Increased complexity and duration of the atrial fibrillation in this study were associated with increasing atrial enlargement; those animals exhibiting sustained atrial fibrillation had a grossly enlarged left atrium, whereas those with nonsustained patterns had more modest atrial enlargement. Also, the tissue was friable because of thinning of the atrial wall. However, there were no gross conduction disturbances in the atrial activation patterns during either sinus rhythm or atrial pacing. Human studies. Earliest atrial activation during sinus rhythm in patients also occurs in the region of the sinus node at the junction of the SVC with the right atrium (Fig. 10). Activation spreads radially across the posterior right atrium and anteriorly around the lateral border of the SV C, proceeding from right to left across Bachmann's bundle anteriorly to reach the base of the left atrial appendage at 90 msec. The wave front traversing the posterior right atrium propagates between the venae cavae onto the posterior left atrium beneath the right pulmonary veins. The apparent time gap in this region is
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V
M
~
0
/
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I
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290
"
Posterior
Fig. 15. A patient in whom reentry could not be clearlydocumentedduring atrial fibrillation. However, the repetitivesequenceof activation in the left atrium suggests that the wavefront is entering the septum posteriorly and exiting the septum anteriorly, which establishes a completereentrant loop.The length of the window is41 0 msec.The map on the left showsthe activationfrom 100-250msec and the right map shows from 250 to 410 msec. For abbreviations see Fig. 10.
the result of a slight anatomic separation of the electrode templates by the inferior vena cava (lYC), which is located between the large right atrial template and the posterior left atrial template. The posterior left atrium is activated by the anterior and posterior components of the sinus-initiated wave front that meet at the point of latest atrial activation beneath the left inferior pulmonary vein. Representative activation patterns observed during human atrial fibrillation are shown in Fig. 11 to 15. During atrial fibrillation, six of the 13 patients had atrial activation sequences in the right atrium suggestive of reentry. Although discrete reentrant circuits could not be demonstrated in the remaining patients, all seven had repetitive right atrial activation patterns. Activation sequences in the left atrium usually suggested nonuniform conduction and bidirectional block. Documentation of complete left atrial reentrant circuits was rare in patients.
Discussion Both the experimental and clinical data in this study are consistent with previous experimental studies supporting reentry as the principal mechanism of atrial fibrillation. Complete reentrant circuits were documented during atrial flutter and atrial fibrillation in dogs (Figs. 4 and 7) and in man (Figs. 11 to 14). Other data showed partial reentrant circuits, suggesting that the wave front moved through the septum and around the pulmonary veins, IYC, or SYC (Figs. 5, 6, 9, and 15). The more complex patterns, in which reentrant circuits either were not documented or were only fleeting (Figs. 8, 12, and 13), were consistent with the multiple wavelet hypothesis of Moe l 4 and the experimental data of Allessie and associates. I, 15 Although anatomic obstacles such as the pulmonary veins, IYC, and SYC were involved in the apparent reentrant circuits, Figs. 4, 7, and 11 to 14 indicate that reentry may occur in the absence of these ana-
Volume 101 Number 3
Surgicaltreatment ofatrialfibrillation, II 4 2 I
March 1991
LAA
LAA ATR ......... . - - - - - - - - , I
III
={ ELJ
LEFT ATRIUM
A L
RIGHT ATRIUM
RAA
Fig. 16. Atrial anatomy pertinent to atrial electrophysiology and the surgical treatment of atrial arrhythmias. The entire atrial myocardium, includingthe atrial septum, is depicted as a two-dimensional rectangle, with the atrial septum separating the right atrium from the left atrium. The left atrial appendage (LAA) and right atrial appendage (RAA) are depicted as being contiguous with their respective atria. The superior vena cave (SVC) and the inferior vena cava (IVC) are depicted as black boxeswithinthe right atrium, indicating that there are twolarge anatomic "holes" (i.e., the orificesof these two vessels) around which electrical activity must propagate. The orifices of the pulmonary veins (PVs) are also indicated schematically, but because electrical activity can conduct between the orifices of each of these veins, they are illustrated with the same background as that of the left atrium. Finally, the sinoatrial node (SAN) is located at the top of the atrial septum near itsjunction with the right atrium, and the atrioventricular node (A VN) is depicted at the bottom of the atrial septum.
tomic obstacles. Functional conduction block, which is necessary for reentry, occurred throughout the atria. In some cases, the local conduction block was associated with an underlying structure in the atria, such as the crista terminalis (Figs. 4, 7, and 11 to 13), as was predicted by the isolated atrial studies ofSpach and associates. 16, 17 Allessie, Bonke, and Schopman 1 have also shown that chemically produced refractory period inhomogeneity can produce local functional block in atrial fibrillation. In the present study, no measurements of the refractory period were made. However, Fig. 6 illustrates an example in which a single left atrial reentrant circuit fails to activate all of the right atrium in a 1:I fashion with each cycle. Studies have suggested that left atrial refractory periods are shorter than right atrial refractory periods. 18 If this is true, this gross inhomogeneity in refractory peri-
RAA
Fig. 17. During normal sinus rhythm, the electrical impulse is generated within the sinoatrial node and propagates across the right and left atria and the atrial septum to the atrioventricular node and thence to the ventricles. Note that under normal circumstances there is a collision of two portions of the sinus impulsebeneath the pulmonary veinsposteriorly(upper portion of the left atrium). (Same anatomic schema and abbreviations as in Fig. 16.)
Fig. 18. The three electrophysiologic components that determine the diagnosis of atrial flutter and atrial fibrillation: (1) atrial flutter-wave, (2) passiveatrial conduction, and (3) atrioventricular conduction. (Same anatomic schema and abbreviations as in Fig. 16.)
ods between the left and right atria might explain why the left atrial wave fronts fail to activate the right atrium in a 1:1 fashion. The short left atrial refractory periods allow faster reentrant circuits to form in the left atrium, but repetitive 1:1 activation of the right atrium is precluded
The Journal of Thoracic and Cardiovascular
4 2 2 Cox et al.
Electrophysiologic Components
Surgery
Findings at Intraoperative Mapping
Standard ECG
Clinical Diagnosis
Stable
.>-.,.... Regular p-wqve
~-t-'!~
Stable
Regular
Atrial Flutter
~-Ventricular
Response
Stable Fig. 19. Electrophysiologic basis of the standard ECG findings in the simplest type of atrial flutter. (Same anatomic schema and abbreviations as in Fig. 16.)
Electrophysiologic Components
Findings at Intraoperative Mapping
Standard ECG
Clinical Diagnosis
Stable >-~ ~egular
p-wave
Stable Irregular >-~Ventricular
Atrial Flutter with Varying A-V Block
Response
Variable Fig. 20. Electrophysiologic basis of the standard ECG findings in atrial flutter with varying atrioventricular block. (Same anatomic schema and abbreviations as in Fig. 16.)
Volume 101 Number 3 March 1991
Surgicaltreatment ofatrialfibrillation. II 4 2 3
Electrophysiologic Components
Findings at Intraoperative Mapping
Variable
Standard
ECG
Regular p-wave with Varying Morphology ~.....
Stable
Stable
Clinical Diagnosis
Regular Ventricular Response
Atrial Flutter
Fig. 21. Electrophysiologic basis of the standard ECG findings in atrial flutter in which the p wave morphology varies. (Same anatomic schema and abbreviations as in Fig. 16.)
Electrophysiologic Components
Findings at Intraoperative Mapping
.....- -.......~ Variable
Stable
Standard
ECG
Clinical Diagnosis
Begular p-wave with Varying Morphology ~....~Atrial Fibrillation Irregular Ventricular Response
Variable Fig. 22. Electrophysiologic basis of the standard ECG findings in one form on "atrial fibrillation" with a single reentrant circuit in which the atrial events are identical to those in the "atrial flutter" of Fig. 21. In this case, the variable atrioventricular conduction causes an irregular ventricular response. (Same anatomic schema and abbreviations as in Fig. 16.)
424
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Cox et al.
Electrophysiologic Components
Surgery
Findings at Intraoperative Mapping
Standard ECG
Clinical Diagnosis
Variable """'Irregular i)-wave Atrial Fibrillation
Variable Irregular ~-..-ventricular
Stable or Variable
Response
Fig. 23. Electrophysiologic basis of the standard ECG findings in another form of "atrial fibrillation" with a single reentrant circuit that has a variable cycle length. (Same anatomic schema and abbreviations as in Fig. 16.)
by the longer refractory periods of the right atrium. Several areas of the atria were not mapped in these studies, including the pulmonary veins, atrial septum, and a small region beneath the IYC on the posterior right atrium. This is one limitation of our study and the data suggest that these regions are important. In Fig. 9, A to C (dog) and Fig. 14 (man), the activation of the epicardial surface originates in the septum, with no wave fronts reentering the septum. Therefore the mechanism responsible for the arrhythmia in these instances is completely confined to the unmapped areas. A conceptual summary of the mechanisms underlying the spectrum of arrhythmias from the simplest form of atrial flutter to the most complex form of atrial fibrillation is illustrated in Figs. 16 to 24. However, before contemplating these new concepts, one should remember that, until now, both atrial flutter and atrial fibrillation have been clinical diagnoses; that is, the diagnosis in each case has been based on the standard ECG findings or on data from a few atrial electrodes, rather than being based on the actual electrophysiologic events occurring in the atria. The present study provides more insight into the atrial events underlying these arrhythmias and documents the electrophysiologic differences between atrial flutter and atrial fibrillation, as well as the phenomena responsible for the clinical arrhythmias that occupy that
portion of the spectrum between simple flutter and complex fibrillation. To understand these electrophysiologic observations more clearly, we related them to atrial anatomy by using a schematic diagram of the atria that includes the pertinent atrial anatomy and that allows the observed electrophysiologic phenomena to be superimposed on that anatomy. As mentioned earlier, atrial flutter and atrial fibrillation are diagnosed on the basis of the standard ECG. Although there is general agreement on the clinical descriptors of simple atrial flutter and complex atrial fibrillation, there is no consensus regarding the correct terminology to be applied to the electrophysiologic findings that cause these arrhythmias. For example, it would seem to be an oversimplification to categorize atrial flutter as an arrhythmia that is caused by a single reentrant circuit and atrial fibrillation as one caused by multiple reentrant circuits, as was thought in the past. Whereas atrial flutter appears always to occur on the basis of a single reentrant circuit, some forms of atrial fibrillation may also be caused by a single reentrant circuit (see Figs. 6, 7, 11,22, and 23) and more complex forms result from multiple reentrant circuits (see Figs. 8, 12, 13, 14, and 24). Finally, both the experimental and clinical observations made in the present study consistently confirmed the
Volume 101 Number 3 March 1991
Surgical treatment ofatrial fibrillation, II 4 2 5
Electrophysiologic Components
Findings at Intraoperative Mapping
Variable Multiple Reentrant Circuits Stable or Variable
Standard ECG
Irregular p-wave
Clinical Diagnosis
Atrial Fibrillation
Irregular Ventricular Response
Fig. 24. Electrophysiologic basis of the standard ECG findings in the most complex type of atrial fibrillation. (Same anatomic schema and abbreviations as in Fig. 16.)
previous experimental observations of Moe,14 Boineau.l SpaCh,16, 17 Allessie,': 15 Waldo,4 and their associates. Our concept of the electrophysiologic mechanisms underlying atrial flutter, atrial fibrillation, and the intervening transitional arrhythmias incorporates virtuallyallof their observations, as wellas those made in the presentstudy. Although thisconceptdoesnot answerallof the questions regardingthese arrhythmias, it doesprovide the basisfor establishing a more scientific approach to the surgical treatment of atrial flutter and atrial fibrillation.
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7. 8.
REFERENCES 1. 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 movement in cardiac tissue without the involvement of an anatomical obstacle. Circ Res 1977;41:9-18. 2. 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 CardioI1980;45:1167-81. 3. Wells JLJr, Karp RB, Kouchoukos NT, MacLean WAH, James TN, Waldo AL. Characterization of atrial fibrillation in man: studies following open heart surgery. PACE 1978;1:426-38. 4. Waldo AL, MacLean WAH. Diagnosis and treatment of
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arrhythmias followingopen heart surgery: emphasis on the use of epicardial wire electrodes. New York: Futura Publishing Co., 1980:85-8. Nelson RM, Jenson CB, Davis RW. Differential atrial arrhythmias in cardiac surgical patients [Abstract]. Circulation 1968;38(Pt 2):VIl47. Leier CV, Schaal SF. Biatrial electrograrns during coarse atrial fibrillation and flutter-fibrillation. Am Heart J 1980; 99:331-41. Zipes DP, Dejoseph RL. Dissimilar atrial rhythms in man and dog. Am J CardioI1973;32:618-28. Puech P, Grolleau R, Rebuffat G. Intra-atrial mapping of atrial fibrillation in man. In: Kulbertus HE, Olsson SB, Schlepper M, eds. Atrial fibrillation. Molndal, Sweden: AB Hassell, 1982:94-109. Chen PS, Smith WM, Greer GS, Wharton JM, Vidaillet HJ Jr, Ideker RE. Activation patterns during electrically induced atrial fibrillation in humans [Abstract]. Circulation 1986;74(Pt 2):11483. Witkowski FX, Corr PB. An automated simultaneous transmural cardiac mapping system. Am J Physiol 1984; 247:H661-8. 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. Canavan TE, Schuessler RB, Boineau JP, Corr PB, Cain ME, Cox JL. Computerized global electrophysiological
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Kootsey JM, Johnson EA. The discontinuous nature of propagation in normal canine cardiac muscle: evidence of recurrent discontinuities of intracellular resistance that affect the membrane currents. Circ Res 1981;48:39-54. 17. Spach MS, Dolber Pc. Relating extracellular potentials and their derivatives to anisotropic propagation at a microscopic levelin human cardiac muscles: evidence for electrical uncoupling of side-to-side fiber connections with increasing age. Circ Res 1986;58:356-71. 18. Rensma PL, Allessie MA, Lammers WJ, Bonke FI, Schalij MJ. Length of excitation wave and susceptibility to reentrant atrial arrhythmias in normal consciousdogs. Circ Res 1988;62:395-410.