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Right and left atrial activation during external direct-current cardioversion shocks delivered for termination of atrial fibrillation in humans
Right and Left Atrial Activation During External Direct-Current Cardioversion Shocks Delivered for Termination of Atrial Fibrillation in Humans Atul Prakash,
MD,
Sanjeev Saksena, MBBS, MD, Ryszard B. Krol, George Philip, MS
MD, PhD,
and
We examined the regional electrophysiologic effects of successful and unsuccessful direct-current cardioversion shocks on different right and left atrial regions in patients with sustained atrial fibrillation (AF). Patients with sustained AF undergoing external cardioversion underwent simultaneous mapping of the right and left atria. Electrogram changes after shock delivery, regional atrial activation, and effects of shock intensity were analyzed. Twenty-two patients with sustained AF received 52 shocks (mean 2.4/patient, 22 successful and 30 unsuccessful). The efficacy of 50, 100, 200, and 300 J was 18%, 39%, 100%, and 100%, respectively. In all 22 successful shocks, there was virtually simultaneous termination of electrical activity in all right and left atrial regions mapped. Unsuccessful shocks resulted in a significant increase in mean atrial cycle length at lateral right atrium, superior left atrium, and proximal, mid, and distal coronary sinus (p ⴝ 0.01), but not at the
interatrial septum (p >0.2), which often disappeared before the next shock. This cycle length prolongation was accompanied by reduction in fragmented and chaotic electrograms (p <0.03) and emergence of discrete electrograms at all right and left atrial regions that persisted until the next shock. The changes in electrogram morphology failed to alter the surface electrocardiographic appearance of AF. There was no correlation between the shock intensity and the magnitude of these effects. We conclude that termination of AF with external cardioversion shocks is associated with the widespread extinction of regional atrial wave fronts. Unsuccessful shocks are associated with a temporary slowing of atrial activation at all regions except at the interatrial septum and emergence of organized and/or rapidly propagating wave fronts. 䊚2001 by Excerpta Medica, Inc. (Am J Cardiol 2001;87:1080 –1088)
oth external direct-current cardioversion and catheter defibrillation have been used to restore sinus B rhythm in atrial fibrillation (AF), with efficacy rates
defibrillation protocols for use with implantable and external defibrillation devices.4 In this prospective study, we evaluated the electrophysiologic effects of external direct-current cardioversion shocks in different right and left atrial regions. Specifically, we examined the effect of these shocks on AF electrographic cycle length and atrial electrographic morphology in multiple right and left atrial regions simultaneously. We also analyzed the temporal relation of these regional effects to shock delivery and the effect of increasing shock intensity.
ranging from 60% to 100%.1,2 The mechanism of defibrillation is believed to be related to depolarization and/or hyperpolarization of a critical mass of myocardium at different atrial regions, preventing propagation of reentrant wave fronts in AF. However, human validation studies are lacking. In addition, little is known regarding atrial regions critical to successful cardioversion or defibrillation. Unlike mapping of ventricular defibrillation, the electrophysiologic effects of cardioversion shocks on different right and left atrial regions has, hitherto, not been studied in humans.3 Furthermore, the impact of unsuccessful cardioversion shocks in the atria is not known. These electrophysiologic effects are especially important when we attempt to understand the mechanism(s) underlying successful AF termination, and clinically highly relevant to the development of effective atrial From the Arrhythmia & Pacemaker Service, Cardiovascular InstituteAtlantic Health System, Passaic; and the Electrophysiology Research Foundation, Millburn, New Jersey. Manuscript received August 18, 2000; revised manusript received and accepted November 27, 2000. Address for reprints: Sanjeev Saksena, MD, Cardiovascular Institute, Atlantic Health System (Passaic), 55 Essex Street, Suite 3-2, Millburn, New Jersey 07041. E-mail: [email protected].
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©2001 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 87 May 1, 2001
METHODS
Patient selection: Consecutive patients with spontaneous AF requiring electrical cardioversion for restoration of sinus rhythm during clinically indicated electrophysiologic studies were included in this study. Patients were undergoing electrophysiologic study with biatrial mapping for evaluation of tachycardias and their mechanisms, symptoms, associated electrical disorders such as conduction system disease, and had spontaneous AF. Electrical cardioversion was clinically indicated for termination of a symptomatic episode of AF. Written informed consent was obtained from the patient for the procedure. Patients with atrial flutter at the time of cardioversion were excluded from the study. All patients had either undergone anticoagulation for a minimum of 3 weeks or had had trans0002-9149/01/$–see front matter PII S0002-9149(01)01465-5
TABLE 1 Patient Characteristics, Shock Outcome, and Arrhythmia Cycle Length by Cardiac Disease
Pt. No.
Age (yrs)
AF Duration (mo)
Heart Disease
Shocks Delivered
50 J Preshock CL (ms)
50 J Postshock CL (ms)
100 J Preshock CL (ms)
100 J Postshock CL (ms)
200/300 J Preshock CL (ms)
200/300 J Postshock CL (ms)
11 21 8 4 22 14 1 18 17 6 10 3 9 20 5 19 7 16 12 15 2 13
56 62 68 70 72 78 56 32 48 51 63 74 78 46 67 68 72 76 79 80 86 74
1 2 6 1 3 8 1 1 3 3 5 1 1 3 3 3 3 3 9 4 3 4
CAD CAD CAD CAD CAD CAD IDC O O O O O O SH SH SH SH SH SH SH SH VHD
1 1 3 2 1 2 3 3 3 2 3 3 2 3 2 3 2 1 3 2 3 3
252 176 181 157 154 161 163 148 182 199 211 195 227 191 162 172 187 178 154 155 185 180
SR SR 160 255 SR 179 172 164 222 234 234 165 260 210 171 176 243 SR 167 181 202 206
181 161 165 157 152 202 213 210 190 234 188 161 178 205 161 161 174 195
195 SR SR 190 166 224 SR 232 214 SR 214 SR 202 SR 174 SR 225 217
178 166 150 222 220 194 194 182 164 182 190
SR SR SR SR SR SR SR SR SR SR SR
CAD ⫽ coronary artery disease; CL ⫽ mean arrhythmia cycle length; IDC ⫽ idiopathic dilated cardiomyopathy; O ⫽ none; SH ⫽ systemic hypertension; SR ⫽ sinus rhythm; VHD ⫽ valvular heart disease.
FIGURE 1. Fluoroscopic location of catheter electrodes during right and left atrial mapping of cardioversion shocks. AO ⴝ aorta; CS ⴝ coronary sinus; HB ⴝ His bundle; HRA ⴝ high right atrium; IAS ⴝ interatrial septum; LA ⴝ left atrium; LLPA ⴝ left lower pulmonary artery; LLRA ⴝ low lateral right atrium; LSPV ⴝ left superior pulmonary vein os; LV ⴝ left ventricle; RA ⴝ right atrium.
esophageal echocardiography and intravenous heparin therapy before the cardioversion protocol. Patients with atrial thrombi or significant spontaneous echo contrast on transesophageal echocardiography were not included to undertake a longer period of anticoagulation. Regional endocardial mapping: The methods of regional endocardial contact catheter mapping in our laboratory has been previously reported.5,6 To summarize, 4 to 6 multipolar catheters were positioned in the right and left atrium. A 7Fr duodecapolar (1-mm
band electrodes with 3-mm interelectrode distance, Cordis Webster, Inc., Baldwin Park, California) catheter was positioned in the right atrium (Figure 1). Two 6Fr decapolar catheters (2-mm electrodes with 5-mm interelectrode distance, Daig Corp., St. Paul, Minnesota) were positioned in the coronary sinus to record from the inferior left atrium, and in the left pulmonary artery to record the superior left atrium. Three to 5 close bipolar electrograms were obtained in each atrial region. The right atrial regions mapped were the lateral right atrium, interatrial septum, His bundle location, and coronary sinus ostium. Left atrial recordings were obtained epicardially via the coronary sinus and left pulmonary artery and directly endocardially via a patent foramen ovale or retrogradely from the left ventricle using decapolar catheters. Multiple recordings were obtained in the superior left atrium at septal and lateral locations and at the proximal, mid-, and distal coronary sinus. Simultaneous 12-lead electrocardiograms were available before and after the delivered shock(s). Multiple bipolar recordings were obtained in each region and stored digitally on a Cardio Lab system (Prucka Engineering, Inc., Houston, Texas). Electrograms were amplified and filtered between 30 and 100 Hz. Cardioversion protocol: All patients were in sustained AF at the time of the cardioversion shock attempt. Cardioversion was performed after all the catheters were in position and the recorded atrial activation was consistent with a diagnosis of AF. Patients were anesthetized with intravenous midazolam and/or propofol. External direct-current R-wave synchronous shocks were delivered using a predefined step-up defibrillation protocol using a conventional
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FIGURE 2. Panel A, regional atrial map with surface electrocardiographic leads and intracardiac recordings illustrating bipolar regional local atrial electrograms before and after a successful 100-J shock. Arrows show superior and inferior or medial to lateral activation sequence. Discrete and fractionated electrograms are seen before shock delivery. Note that there is simultaneous cessation of atrial activation at all the atrial regions mapped. No atrial region shows continuation of electrical activity with restoration of sinus rhythm, with noise or motion artifacts being present on the left lower pulmonary artery recording. Panel B, efficacy of direct-current cardioversion shocks at increasing energy levels. Patients with induced atrial flutter as a result of a previously ineffective shock were excluded from this analysis. CSd ⴝ distal coronary sinus; CSp ⴝ proximal coronary sinus; LRA ⴝ lateral right atrium; SLAd ⴝ superior lateral left atrium; SLAp ⴝ superior proximal left atrium; other abbreviations as in Figure 1.
damped sine wave defibrillator (Hewlett-Packard, CodeMaster XL, model M1722B). Shocks were delivered via cutaneous patch electrodes (Hewlett-Packard defibrillation pads M3501A, Andover, Massachusetts), which were positioned anterior to the sternum at the fourth left intercostal space and posteriorly over the spine. The initial shock energy was 50 J.5 If this 1082 THE AMERICAN JOURNAL OF CARDIOLOGY姞
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was unsuccessful a shock of 100 J was then delivered. The third shock was either 200 or 300 J (high energy). Repeat shocks were delivered within 90 to 120 seconds later, although this was not always constant. Definitions and study analysis: Shock outcome was deemed successful if there was restoration of sinus rhythm. Successful shocks were further subdivided MAY 1, 2001
FIGURE 3. Mean cycle length of local bipolar atrial electrogram before (Pre-Shock) and after (Post-Shock) delivery of unsuccessful shocks at different right and left atrial regions. Note the significant increase in the mean cycle length after shock delivery in all the mapped atrial regions except the interatrial septum (IAS). DCS ⴝ distal coronary sinus; MCS ⴝ midcoronary sinus; PCS ⴝ proximal coronary sinus; other abbreviations as in Figures 1 and 2.
into type 1 termination if sinus rhythm ensued immediately after the shock, or type 2 if the termination was within 5 seconds of shock delivery. Electrogram analysis was performed for mean cycle length and morphology on the 10 AF cycles before and the 10 cycles after an unsuccessful shock delivery. Based on morphology, the atrial electrograms were classified as discrete, fractionated, or chaotic electrical activity.5–7 Measurements were obtained at paper speed of 200 mm/s using the initial high-frequency deflection of the electrogram. Chaotic electrograms were not used for measurement. In a region with multiple recordings, the midregional bipolar recording was preferentially used for analysis: atrial fibrillation: defined on the basis of 12-lead surface electrocardiography by the absence of P waves with irregular fibrillatory waves ⬎350 beats/min; discrete electrograms: local bipolar atrial electrograms of constant morphology and regular cycle length with reproducible isoelectric intervals between successive atrial electrograms; fragmented electrograms: prolongation of duration of local bipolar atrial electrogram ⬎50 ms with or without multiple high-frequency deflections; chaotic electrical activity: local bipolar atrial electrogram with variable morphology with indistinct or absent isoelectric interval between electrograms; stable activation sequence: same activation sequence between and within each atrial region of the first and tenth AF beat after an unsuccessful cardioversion shock with a variable AA cycle length and electrogram morphology; and atrial flutter: discernable flutter waves with rates from 200 to 350 beats/min on the surface electrocardiogram with a stable activation sequence, no AA variability in cycle length, and stable electrogram morphology.
RESULTS
Patient group: Twenty-two patients (15 men, mean age 68 ⫾ 16 years) were included in the study. Sixteen patients had structural heart disease and 6 had coronary artery disease; 8 patients had hypertensive heart
disease, 1 patient had valvular heart disease, and 1 had dilated cardiomyopathy. Six patients had lone AF (Table 1). AF duration varied from 1 to 6 months. Their mean left atrial diameter was 37 ⫾ 8 mm, whereas the mean left ventricular ejection fraction was 44 ⫾ 12%. All patients had persistent or permanent AF that was sustained at the time of shock delivery and required clinically indicated cardioversion. No patient arrived in the laboratory in sinus rhythm. The mean duration of the sustained episode that was cardioverted using this protocol was 3.3 ⫾ 7.0 months.
Shock efficacy and regional mapping of successful shocks: A total of
52 shocks were delivered to 22 patients (mean 2.4 shocks/patient). Twenty-two shocks were successful, whereas 30 shocks were unsuccessful. Twenty of the 22 successful shocks resulted in type 1 termination, whereas in 2 patients, type 2 termination was observed. In all 22 successful shocks (types 1 and 2), there was virtually simultaneous termination of electrical activity in all atrial regions (Figure 2A). Type 1 and 2 terminations were not associated with discordance at the time of electrical activity in ⱖ1 atrial region. In 4 of 22 patients (18%), 50-J shocks were successful. In the remaining 18 patients, 100-J shocks were successful in 7 patients (39%). The remaining 12 patients had either a 200-J (6 patients) or a 300-J shock (6 patients) delivered, which were uniformally successful in all 12 patients (100%). Figure 2B shows the percent efficacy of the delivered intermediate energy (50 and 100 J) and high-energy (200 or 300 J) shocks. Regional mapping of unsuccessful shocks: EFFECTS ON LOCAL ATRIAL ELECTROGRAM CYCLE LENGTH: The
main finding was an increase in the mean local atrial electrogram cycle length after unsuccessful shock delivery in all right and left atrial regions, except at the interatrial septum (Figure 3). However, there was no significant difference in the magnitude of this increase among the different regions. Thirteen of 18 patients had a mean cycle length increase of ⱖ10 ms after a 50-J shock, and all 11 patients exposed to 100-J shocks had this change. Six patients (46%) with a prolongation at 50 J had AF termination at 100 J compared with 1 of 5 patients (20%) without this finding. Figure 4 shows regional atrial endocardial mapping of an unsuccessful 50-J shock. Note the immediate increase in electrogram cycle length (shown for 1 of the 10 measured cycles after the shock) at all sites except in the interatrial septum, which shows a trend toward regional organization. These effects, however, are transient with restoration of original cycle length in the later recordings. Mean AF cycle lengths for individual patients are listed in Table 1.
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FIGURE 4. Regional right and left atrial mapping during delivery of a 50-J external direct-current cardioversion shock. The measured atrial cycle after shock delivery was greater at all mapped atrial sites (except at the interatrial septum) than that before shock delivery. The electrogram cycle length for 1 of the 10 measured cycles is shown just above the bipolar recording at each mapped site. Abbreviations as in Figures 1 and 2.
In a few shocks, there was acceleration or a decrease in local atrial cycle length. Acceleration in ⱖ2 atrial regions was seen in 4 shocks in 4 patients. Two of these patients subsequently had slowing with delivery of a shock of a higher energy; 1 patient had slowing with a shock at lower energy, whereas another patient had subsequent slowing at the same delivered energy during a second AF episode. Three of these 4 patients had a change in the regional activation sequence with acceleration. Thus, unsuccessful shocks invariably modified local atrial electrical activity for rate, sequence, or both. The concordant and discordant behavior of local atrial electrical activity in different atrial regions was also analyzed. Slowing after shock delivery at ⱖ2 regions without simultaneous acceleration at any other region was seen with 20 shocks (67%) in 13 patients (59%). Slowing at ⱖ2 regions, accompanied by simultaneous acceleration at another atrial region, was seen with 5 shocks (17%) in 5 patients (27%). The site of acceleration was the interatrial septum in 4 patients and distal coronary sinus in 1 patient. Figure 5 is a typical example of intracardiac recordings during delivery of a 100-J unsuccessful shock in such a patient. The shock was unsuccessful in restoring sinus rhythm, but there was an increase in the local atrial electrogram cycle length at all right and left atrial regions. 1084 THE AMERICAN JOURNAL OF CARDIOLOGY姞
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The duration of unsuccessful shock effects on local atrial electrogram cycle length was also assessed. In patients with ⱖ2 unsuccessful shocks during the protocol, the mean cycle length before the first shock was compared with the mean cycle length before shock delivery for the next 2 successive shocks. The preshock cycle length for the first shock was similar to the parameter for the second shock, and was also not significantly different from the parameter for the third shock (Figure 6). Mean time interval between the first and second shock and between the second and third shock was 150 ⫾ 27 and 102 ⫾ 43 seconds, respectively. EFFECTS OF UNSUCCESSFUL SHOCKS ON LOCAL ATRIAL ELECTROGRAM MORPHOLOGY: Our main finding was a
shift toward discrete electrogram morphologies from fractionated or chaotic electrograms in virtually all atrial regions mapped. Figure 7A and 7B illustrate the difference in local atrial electrogram morphologies before and after unsuccessful shock delivery at different right and left atrial regions. Note there is an increase in discrete atrial electrogram morphology, with a simultaneous reduction in chaotic and fractionated atrial electrogram activity in many right and left atrial regions. Furthermore, unlike the effect of slowing on atrial electrograms, this effect on the electrogram morphologies was also seen at the interatrial septum. MAY 1, 2001
FIGURE 5. Regional right and left atrial mapping of a 100-J synchronous external direct-current cardioversion shock. Arrows show superior and inferior or medial to lateral sequential bipolar recording in each region. Before shock delivery, the different atrial regions show varying cycle lengths and incoordinate activation sequences. There is an increase in cycle length at all the mapped regions and appearance of an organized atrial wave front. The magnitude of increase in cycle length is similar for the atrial regions mapped. LLPAd ⴝ left lower pulmonary artery distal recording for superior left atrial activation; LLPAp ⴝ left lower pulmonary proximal artery recording for superior left atrial activation; other abbreviations as in Figures 1 and 2.
and a change from a discrete to a fractionated or chaotic electrogram morphology in 2 patients. With shocks of 100 J, the shift to discrete electrogram morphology was seen in 8 of 12 patients (72%). There was no change in local electrogram morphology in 2 patients, whereas in 1 patient there was a reverse shift toward a more fractionated or chaotic electrogram morphology. One patient had a shift toward discrete electrograms in 1 atrial region and a shift toward fractionated electrograms in another atrial region. There was no statistically signifiFIGURE 6. Mean local atrial cycle length in different right and left atrial regions for 10 cant difference between 50 and 100 cycles preceding cardioversion shock delivery before the first, second, and third shocks J with respect to effects on local in patients receiving repetitive shocks. Note that there is no difference in the mean cyatrial electrogram morphology. cle length before shock delivery for successive shocks, indicating that the increase in The persistence of these effects mean atrial cycle length as a result of shock delivery did not persist until the delivery on electrogram morphology was of the next shock. Abbreviations as in Figures 1 to 3. analyzed. Of the 14 patients demonstrating a shift to a more discrete The shift to more discrete electrogram morpholo- local electrogram morphology with a 50-J shock, this gies was seen at ⱖ1 atrial region with a 50-J shock in discrete morphology persisted up to the delivery of the 14 of 18 (78%) patients. In the remaining 4 patients, next 100-J shock in 11 of 14 patients (78%). In the there was no change at any atrial region in 2 patients, remaining 3 patients, the morphology reverted back to ARRHYTHMIAS AND CONDUCTION DISTURBANCES/EFFECTS OF EXTERNAL DIRECT–CURRENT CARDIOVERSION
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and left atrial recordings. In the coronary sinus, chaotic fractionated activity that obscured most of the isoelectric line is replaced by discrete but fractionated electrograms with restoration of isoelectric periods. EFFECT ON ACTIVATION SEQUENCE: Twenty-one of the 22 pa-
tients had an unstable and variable right and left atrial activation sequence before first cardioversion shock delivery. In 18 patients with an unsuccessful shock of 50 J, the global atrial activation sequence became stable and repetitive in 7 patients (39%). In 2 of these 7 patients, the arrhythmia became type 1 atrial flutter. In 4 of these 7 patients, the stable activation sequence during AF persisted until the next shock of 100 J. The remaining patient reverted back to an unstable activation sequence. A 100-J shock resulted in a further 2 patients with an unstable activation sequence reverting to a stable sequence with the arrhythmia becoming sustained atrial flutter (type 1 clockwise in 1 patient and type 2 atrial flutter in 1 patient). This was terminated by the next shock. Site of initial activation after unsuccessful shock: The site of earliest
FIGURE 7. Panel A, comparison of the frequency of discrete, fractionated, and chaotic local bipolar atrial electrograms at different right atrial regions before and after cardioversion shock delivery. Both the lateral right atrium (RA) and the interatrial septum show a significant increase in discrete electrograms with a concomitant decrease in fractionated electrogram activity. Chaotic recordings are also reduced after cardioversion shocks. Panel B, comparison of the frequency of discrete, fractionated, and chaotic electrograms at 2 different left atrial sites before and after cardioversion shock delivery. As seen in right atrial regions, there is an increase in discrete electrograms with a simultaneous decrease in fractionated and chaotic electrograms at both the midcoronary sinus and distal coronary sinus recordings after shock delivery.
activation for the first AF beat after an unsuccessful shock varied from patient to patient. This was the interatrial septum in 17 shocks, crista terminalis in 5 shocks, proximal coronary sinus in 2 shocks, and mid- or distal coronary sinus in 3 shocks (p ⬍0.05 interatrial septum vs other sites). In patients with 2 unsuccessful shocks, the site of earliest activation was the same in 7 patients and different in 5 patients.
DISCUSSION
the fractionated or chaotic electrical activity present before the delivery of the first shock. Among the 8 patients who had the same finding with a 100-J shock, these changes persisted until delivery of the next shock in 6 patients (86%). In no patient did a reverse change toward a fractionated or chaotic electrogram morphology persist until the delivery of the next shock, suggesting spontaneous change may operate in selected patients. Figure 8 is an intracardiac recording during an unsuccessful 50-J cardioversion shock delivery. There is a marked decrease in electrogram duration in the lateral right atrium, interatrial septum, coronary sinus, 1086 THE AMERICAN JOURNAL OF CARDIOLOGY姞
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Mechanisms of efficacy and termination of atrial fibrillation with successful shocks: The
39% efficacy for the restoration of sinus rhythm with 100-J cardioversion shocks (intermediate energy), increasing to 100% with energies ⱖ200 J is similar to that reported in other studies.8,9 Termination of AF with successful shocks was associated with extinction of atrial electrical activity at virtually all the mapped sites without regional differences. This could imply that the widespread extinction of electrical wave fronts was a prerequisite for the termination of AF with the external cardioversion energies used in this study. These findings would be consistent with the concept that a critical mass of myocardium must show MAY 1, 2001
FIGURE 8. Regional right and left atrial mapping before and after delivery of a synchronous 50-J external cardioversion shock. There is a change in electrogram (EGM) morphology from fractionated to discrete at the lateral right atrium. At the interatrial septum (IAS), there is a reduction in local bipolar atrial electrogram duration and reduction in the number of its component deflections. At the proximal coronary sinus (CSp), the chaotic activity is replaced by discrete and fractionated electrograms with a clear isoelectric line between each successive electrogram. The duration of the atrial electrograms is shown above each recording site. Abbreviations as in Figures 1 and 2.
wave front interruption by shock delivery for successful defibrillation. Electrophysiologic effects and mechanisms of failure of unsuccessful cardioversion shocks: Unsuccessful car-
dioversion shocks of 50 or 100 J usually elicited slowing in multiple right and left atrial activation wave fronts, producing a shift toward more discrete atrial electrogram activity at almost all mapped regions. There may be induction of conduction delay/ block or an increase in atrial refractory periods. Alternatively, there could be fewer activation wave fronts around the recording sites. The absence of this effect at the interatrial septum implies that this region was more impervious to the effects of anteroposterior external shock vector used in the study, and may also potentially be a site for continuation or even reinitiation of AF. The slowing of the atrial cycle length by ⱖ10 ms was associated with a higher possibility of AF termination at the next energy level (46% vs 20%, p ⬍0.2). This may suggest increased vulnerability to AF termination due to the previously mentioned mechanisms. The conversion of chaotic electrograms to electrograms of a more discrete variety may represent one of several potential mechanisms. Unmasking of rapidly propagating wave fronts from rotors involved in initiation or sustenance of AF, e.g., focal atrial tachycar-
dia from pulmonary veins or atypical atrial flutter, may explain this observation. Conduction block in dead end pathways, not essential to the sustenance of AF, may also occur. Fewer activation wave fronts activating larger areas in a more cohesive fashion may potentially result in the electrograms appearing more discrete. Our bipolar electrogram findings after unsuccessful shocks correspond to a change from type 4 to a type 1 or 2 AF (Wells et al11), with concordant effects on electrogram morphology and local atrial cycle length.10 Konings et al10 suggested that discrete electrograms imply rapidly conducting activation wave fronts, whereas split or fragmented potentials may indicate slow conduction at pivot points and lines of block in the atrium. Our data could imply that unsuccessful shocks impact vulnerable regions of slow conduction or wave front pivot points. These data could also imply that organized activation wave fronts due to rotors may exist in AF and are unmasked at unsuccessful shock energies due to the disappearance of slow conduction. Jalife et al12 suggested that organized rotors exist during established AF. We reported organized atrial wave fronts at onset and termination of human AF.5,6 Our data also suggest that some atrial regions such as the septum and coronary sinus are particularly prone to fibrillatory conduction.5,6 Our
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data do not preclude induction of new tachycardias by shock delivery. Thus, the appearance of typical and atypical flutter in 4 patients could be explained either by unmasking of existing rotors or induction of new arrhythmias. However, the transformation of an unstable activation sequence to a stable activation sequence as seen in some patients in the study substantiates the view that unsuccessful shocks electrophysiologically modify the AF episode despite nondiscernable surface electrocardiographic findings. Similar effects have been seen with antiarrhythmic drug use in AF and in linear ablation in experimental studies.13,14 Study limitations: Saturation of the recording amplifiers was seen for up to 200 ms after shock delivery. For successful shocks, some atrial sites could have been activated and gone unrecognized during this period. However, despite this limitation, our data imply that ⬎1 repetitive wave front did not occur and does not change the interpretation of the data. Shocks of intermediate and lower energies could have resulted in further regional differences both for successful and unsuccessful shocks. 1. Desilva RA, Graboys TTS, Podrid PJ, Lown B. Cardioversion and defibrillation. Am Heart J 1980;100:881– 895. 2. Levy S, Lauribe P, Dolla E, Kou W, Kadish AH, Calkins H, Pagannelli F, Moyal C, Bremondy M, Schork A, Shyr Y, Das S, Shea M, Gupta N, Morady F. A randomized comparison of external and internal cardioversion of chronic atrial fibrillation. Circulation 1992;86:1415–1420.
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3. Saksena S, Pantopoulos D, Hussain SM, Gielchinsky I. Mechanisms of ventricular tachycardia termination and acceleration during transvenous cardioversion as determined by cardiac mapping in man. Am Heart J 1987;113:1495– 1506. 4. Wellens HJJ, Lau C-P, Luderitz B, Akhtar M, Waldo AL, Camm AJ, Timmermans C, Tse H-F, Jung W, Jordaens L, Ayers G, for the METRIX Investigators. Atrioverter: an implantable device for the treatment of atrial fibrillation. Circulation 1998;98:1651–1656. 5. Saksena S, Giorgberidze I, Mehra R, Hill M, Prakash A, Krol RB, Mathew P. Electrophysiology and endocardial mapping of induced atrial fibrillation in patients with spontaneous atrial fibrillation. Am J Cardiol 1999;83:187–193. 6. Saksena S, Prakash A, Krol RB, Shankar A. Regional endocardial mapping of spontaneous and induced atrial fibrillation in patients with heart disease and refractory atrial fibrillation. Am J Cardiol 1999;84:880 – 889. 7. Prakash A, Delfaut P, Krol RB, Saksena S. Regional right and left atrial activation patterns during single- and dual-site atrial pacing in patients with atrial fibrillation. Am J Cardiol 1998;82:1197–1204. 8. Lown B. Electrical reversion of cardiac arrhythmias. Br Heart J 1967;29:469 – 489. 9. Kerber RE. Energy requirements for defibrillation (abstr). Circulation 1986; 74(suppl IV):IV-117. 10. Konings KTS, Smeets JLRM, Penn OC, Wellens HJJ, Allessie MA. Configuration of unipolar atrial electrograms during electrically induced atrial fibrillation in humans. Circulation 1997;95:1231–1241. 11. Wells JL, Karp RB, Kouchoukos NT, MacLean WAH, James TN, Waldo AL. Characterization of atrial fibrillation in man: studies following open heart surgery. Pacing Clin Electrophysiol 1978;1:426 – 438. 12. Jalife J, Berenfeld O, Skanes A, Mandapati R. Mechanisms of atrial fibrillation: mother rotor or multiple daughter wavelets or both. J Cardiovasc Electrophysiol 1998;9:S2–S12. 13. Rensma PL, Allessie MA, Lammers WJAP, Bonke FI, Schlaij A. Length of excitation wave and susceptibility to reentrant atrial arrhythmias in normal conscious dogs. Circ Res 1988;62:395– 410. 14. Oritz J, Niwano S, Abe H, Rudy Y, Johnson NJ, Waldo AL. Mapping of conversion of atrial flutter to atrial fibrillation and atrial fibrillation to atrial flutter. Insights into mechanisms. Circ Res 1994;74:882– 894.
MAY 1, 2001
MD,
Sanjeev Saksena, MBBS, MD, Ryszard B. Krol, George Philip, MS
MD, PhD,
and
We examined the regional electrophysiologic effects of successful and unsuccessful direct-current cardioversion shocks on different right and left atrial regions in patients with sustained atrial fibrillation (AF). Patients with sustained AF undergoing external cardioversion underwent simultaneous mapping of the right and left atria. Electrogram changes after shock delivery, regional atrial activation, and effects of shock intensity were analyzed. Twenty-two patients with sustained AF received 52 shocks (mean 2.4/patient, 22 successful and 30 unsuccessful). The efficacy of 50, 100, 200, and 300 J was 18%, 39%, 100%, and 100%, respectively. In all 22 successful shocks, there was virtually simultaneous termination of electrical activity in all right and left atrial regions mapped. Unsuccessful shocks resulted in a significant increase in mean atrial cycle length at lateral right atrium, superior left atrium, and proximal, mid, and distal coronary sinus (p ⴝ 0.01), but not at the
interatrial septum (p >0.2), which often disappeared before the next shock. This cycle length prolongation was accompanied by reduction in fragmented and chaotic electrograms (p <0.03) and emergence of discrete electrograms at all right and left atrial regions that persisted until the next shock. The changes in electrogram morphology failed to alter the surface electrocardiographic appearance of AF. There was no correlation between the shock intensity and the magnitude of these effects. We conclude that termination of AF with external cardioversion shocks is associated with the widespread extinction of regional atrial wave fronts. Unsuccessful shocks are associated with a temporary slowing of atrial activation at all regions except at the interatrial septum and emergence of organized and/or rapidly propagating wave fronts. 䊚2001 by Excerpta Medica, Inc. (Am J Cardiol 2001;87:1080 –1088)
oth external direct-current cardioversion and catheter defibrillation have been used to restore sinus B rhythm in atrial fibrillation (AF), with efficacy rates
defibrillation protocols for use with implantable and external defibrillation devices.4 In this prospective study, we evaluated the electrophysiologic effects of external direct-current cardioversion shocks in different right and left atrial regions. Specifically, we examined the effect of these shocks on AF electrographic cycle length and atrial electrographic morphology in multiple right and left atrial regions simultaneously. We also analyzed the temporal relation of these regional effects to shock delivery and the effect of increasing shock intensity.
ranging from 60% to 100%.1,2 The mechanism of defibrillation is believed to be related to depolarization and/or hyperpolarization of a critical mass of myocardium at different atrial regions, preventing propagation of reentrant wave fronts in AF. However, human validation studies are lacking. In addition, little is known regarding atrial regions critical to successful cardioversion or defibrillation. Unlike mapping of ventricular defibrillation, the electrophysiologic effects of cardioversion shocks on different right and left atrial regions has, hitherto, not been studied in humans.3 Furthermore, the impact of unsuccessful cardioversion shocks in the atria is not known. These electrophysiologic effects are especially important when we attempt to understand the mechanism(s) underlying successful AF termination, and clinically highly relevant to the development of effective atrial From the Arrhythmia & Pacemaker Service, Cardiovascular InstituteAtlantic Health System, Passaic; and the Electrophysiology Research Foundation, Millburn, New Jersey. Manuscript received August 18, 2000; revised manusript received and accepted November 27, 2000. Address for reprints: Sanjeev Saksena, MD, Cardiovascular Institute, Atlantic Health System (Passaic), 55 Essex Street, Suite 3-2, Millburn, New Jersey 07041. E-mail: [email protected].
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©2001 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 87 May 1, 2001
METHODS
Patient selection: Consecutive patients with spontaneous AF requiring electrical cardioversion for restoration of sinus rhythm during clinically indicated electrophysiologic studies were included in this study. Patients were undergoing electrophysiologic study with biatrial mapping for evaluation of tachycardias and their mechanisms, symptoms, associated electrical disorders such as conduction system disease, and had spontaneous AF. Electrical cardioversion was clinically indicated for termination of a symptomatic episode of AF. Written informed consent was obtained from the patient for the procedure. Patients with atrial flutter at the time of cardioversion were excluded from the study. All patients had either undergone anticoagulation for a minimum of 3 weeks or had had trans0002-9149/01/$–see front matter PII S0002-9149(01)01465-5
TABLE 1 Patient Characteristics, Shock Outcome, and Arrhythmia Cycle Length by Cardiac Disease
Pt. No.
Age (yrs)
AF Duration (mo)
Heart Disease
Shocks Delivered
50 J Preshock CL (ms)
50 J Postshock CL (ms)
100 J Preshock CL (ms)
100 J Postshock CL (ms)
200/300 J Preshock CL (ms)
200/300 J Postshock CL (ms)
11 21 8 4 22 14 1 18 17 6 10 3 9 20 5 19 7 16 12 15 2 13
56 62 68 70 72 78 56 32 48 51 63 74 78 46 67 68 72 76 79 80 86 74
1 2 6 1 3 8 1 1 3 3 5 1 1 3 3 3 3 3 9 4 3 4
CAD CAD CAD CAD CAD CAD IDC O O O O O O SH SH SH SH SH SH SH SH VHD
1 1 3 2 1 2 3 3 3 2 3 3 2 3 2 3 2 1 3 2 3 3
252 176 181 157 154 161 163 148 182 199 211 195 227 191 162 172 187 178 154 155 185 180
SR SR 160 255 SR 179 172 164 222 234 234 165 260 210 171 176 243 SR 167 181 202 206
181 161 165 157 152 202 213 210 190 234 188 161 178 205 161 161 174 195
195 SR SR 190 166 224 SR 232 214 SR 214 SR 202 SR 174 SR 225 217
178 166 150 222 220 194 194 182 164 182 190
SR SR SR SR SR SR SR SR SR SR SR
CAD ⫽ coronary artery disease; CL ⫽ mean arrhythmia cycle length; IDC ⫽ idiopathic dilated cardiomyopathy; O ⫽ none; SH ⫽ systemic hypertension; SR ⫽ sinus rhythm; VHD ⫽ valvular heart disease.
FIGURE 1. Fluoroscopic location of catheter electrodes during right and left atrial mapping of cardioversion shocks. AO ⴝ aorta; CS ⴝ coronary sinus; HB ⴝ His bundle; HRA ⴝ high right atrium; IAS ⴝ interatrial septum; LA ⴝ left atrium; LLPA ⴝ left lower pulmonary artery; LLRA ⴝ low lateral right atrium; LSPV ⴝ left superior pulmonary vein os; LV ⴝ left ventricle; RA ⴝ right atrium.
esophageal echocardiography and intravenous heparin therapy before the cardioversion protocol. Patients with atrial thrombi or significant spontaneous echo contrast on transesophageal echocardiography were not included to undertake a longer period of anticoagulation. Regional endocardial mapping: The methods of regional endocardial contact catheter mapping in our laboratory has been previously reported.5,6 To summarize, 4 to 6 multipolar catheters were positioned in the right and left atrium. A 7Fr duodecapolar (1-mm
band electrodes with 3-mm interelectrode distance, Cordis Webster, Inc., Baldwin Park, California) catheter was positioned in the right atrium (Figure 1). Two 6Fr decapolar catheters (2-mm electrodes with 5-mm interelectrode distance, Daig Corp., St. Paul, Minnesota) were positioned in the coronary sinus to record from the inferior left atrium, and in the left pulmonary artery to record the superior left atrium. Three to 5 close bipolar electrograms were obtained in each atrial region. The right atrial regions mapped were the lateral right atrium, interatrial septum, His bundle location, and coronary sinus ostium. Left atrial recordings were obtained epicardially via the coronary sinus and left pulmonary artery and directly endocardially via a patent foramen ovale or retrogradely from the left ventricle using decapolar catheters. Multiple recordings were obtained in the superior left atrium at septal and lateral locations and at the proximal, mid-, and distal coronary sinus. Simultaneous 12-lead electrocardiograms were available before and after the delivered shock(s). Multiple bipolar recordings were obtained in each region and stored digitally on a Cardio Lab system (Prucka Engineering, Inc., Houston, Texas). Electrograms were amplified and filtered between 30 and 100 Hz. Cardioversion protocol: All patients were in sustained AF at the time of the cardioversion shock attempt. Cardioversion was performed after all the catheters were in position and the recorded atrial activation was consistent with a diagnosis of AF. Patients were anesthetized with intravenous midazolam and/or propofol. External direct-current R-wave synchronous shocks were delivered using a predefined step-up defibrillation protocol using a conventional
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FIGURE 2. Panel A, regional atrial map with surface electrocardiographic leads and intracardiac recordings illustrating bipolar regional local atrial electrograms before and after a successful 100-J shock. Arrows show superior and inferior or medial to lateral activation sequence. Discrete and fractionated electrograms are seen before shock delivery. Note that there is simultaneous cessation of atrial activation at all the atrial regions mapped. No atrial region shows continuation of electrical activity with restoration of sinus rhythm, with noise or motion artifacts being present on the left lower pulmonary artery recording. Panel B, efficacy of direct-current cardioversion shocks at increasing energy levels. Patients with induced atrial flutter as a result of a previously ineffective shock were excluded from this analysis. CSd ⴝ distal coronary sinus; CSp ⴝ proximal coronary sinus; LRA ⴝ lateral right atrium; SLAd ⴝ superior lateral left atrium; SLAp ⴝ superior proximal left atrium; other abbreviations as in Figure 1.
damped sine wave defibrillator (Hewlett-Packard, CodeMaster XL, model M1722B). Shocks were delivered via cutaneous patch electrodes (Hewlett-Packard defibrillation pads M3501A, Andover, Massachusetts), which were positioned anterior to the sternum at the fourth left intercostal space and posteriorly over the spine. The initial shock energy was 50 J.5 If this 1082 THE AMERICAN JOURNAL OF CARDIOLOGY姞
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was unsuccessful a shock of 100 J was then delivered. The third shock was either 200 or 300 J (high energy). Repeat shocks were delivered within 90 to 120 seconds later, although this was not always constant. Definitions and study analysis: Shock outcome was deemed successful if there was restoration of sinus rhythm. Successful shocks were further subdivided MAY 1, 2001
FIGURE 3. Mean cycle length of local bipolar atrial electrogram before (Pre-Shock) and after (Post-Shock) delivery of unsuccessful shocks at different right and left atrial regions. Note the significant increase in the mean cycle length after shock delivery in all the mapped atrial regions except the interatrial septum (IAS). DCS ⴝ distal coronary sinus; MCS ⴝ midcoronary sinus; PCS ⴝ proximal coronary sinus; other abbreviations as in Figures 1 and 2.
into type 1 termination if sinus rhythm ensued immediately after the shock, or type 2 if the termination was within 5 seconds of shock delivery. Electrogram analysis was performed for mean cycle length and morphology on the 10 AF cycles before and the 10 cycles after an unsuccessful shock delivery. Based on morphology, the atrial electrograms were classified as discrete, fractionated, or chaotic electrical activity.5–7 Measurements were obtained at paper speed of 200 mm/s using the initial high-frequency deflection of the electrogram. Chaotic electrograms were not used for measurement. In a region with multiple recordings, the midregional bipolar recording was preferentially used for analysis: atrial fibrillation: defined on the basis of 12-lead surface electrocardiography by the absence of P waves with irregular fibrillatory waves ⬎350 beats/min; discrete electrograms: local bipolar atrial electrograms of constant morphology and regular cycle length with reproducible isoelectric intervals between successive atrial electrograms; fragmented electrograms: prolongation of duration of local bipolar atrial electrogram ⬎50 ms with or without multiple high-frequency deflections; chaotic electrical activity: local bipolar atrial electrogram with variable morphology with indistinct or absent isoelectric interval between electrograms; stable activation sequence: same activation sequence between and within each atrial region of the first and tenth AF beat after an unsuccessful cardioversion shock with a variable AA cycle length and electrogram morphology; and atrial flutter: discernable flutter waves with rates from 200 to 350 beats/min on the surface electrocardiogram with a stable activation sequence, no AA variability in cycle length, and stable electrogram morphology.
RESULTS
Patient group: Twenty-two patients (15 men, mean age 68 ⫾ 16 years) were included in the study. Sixteen patients had structural heart disease and 6 had coronary artery disease; 8 patients had hypertensive heart
disease, 1 patient had valvular heart disease, and 1 had dilated cardiomyopathy. Six patients had lone AF (Table 1). AF duration varied from 1 to 6 months. Their mean left atrial diameter was 37 ⫾ 8 mm, whereas the mean left ventricular ejection fraction was 44 ⫾ 12%. All patients had persistent or permanent AF that was sustained at the time of shock delivery and required clinically indicated cardioversion. No patient arrived in the laboratory in sinus rhythm. The mean duration of the sustained episode that was cardioverted using this protocol was 3.3 ⫾ 7.0 months.
Shock efficacy and regional mapping of successful shocks: A total of
52 shocks were delivered to 22 patients (mean 2.4 shocks/patient). Twenty-two shocks were successful, whereas 30 shocks were unsuccessful. Twenty of the 22 successful shocks resulted in type 1 termination, whereas in 2 patients, type 2 termination was observed. In all 22 successful shocks (types 1 and 2), there was virtually simultaneous termination of electrical activity in all atrial regions (Figure 2A). Type 1 and 2 terminations were not associated with discordance at the time of electrical activity in ⱖ1 atrial region. In 4 of 22 patients (18%), 50-J shocks were successful. In the remaining 18 patients, 100-J shocks were successful in 7 patients (39%). The remaining 12 patients had either a 200-J (6 patients) or a 300-J shock (6 patients) delivered, which were uniformally successful in all 12 patients (100%). Figure 2B shows the percent efficacy of the delivered intermediate energy (50 and 100 J) and high-energy (200 or 300 J) shocks. Regional mapping of unsuccessful shocks: EFFECTS ON LOCAL ATRIAL ELECTROGRAM CYCLE LENGTH: The
main finding was an increase in the mean local atrial electrogram cycle length after unsuccessful shock delivery in all right and left atrial regions, except at the interatrial septum (Figure 3). However, there was no significant difference in the magnitude of this increase among the different regions. Thirteen of 18 patients had a mean cycle length increase of ⱖ10 ms after a 50-J shock, and all 11 patients exposed to 100-J shocks had this change. Six patients (46%) with a prolongation at 50 J had AF termination at 100 J compared with 1 of 5 patients (20%) without this finding. Figure 4 shows regional atrial endocardial mapping of an unsuccessful 50-J shock. Note the immediate increase in electrogram cycle length (shown for 1 of the 10 measured cycles after the shock) at all sites except in the interatrial septum, which shows a trend toward regional organization. These effects, however, are transient with restoration of original cycle length in the later recordings. Mean AF cycle lengths for individual patients are listed in Table 1.
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FIGURE 4. Regional right and left atrial mapping during delivery of a 50-J external direct-current cardioversion shock. The measured atrial cycle after shock delivery was greater at all mapped atrial sites (except at the interatrial septum) than that before shock delivery. The electrogram cycle length for 1 of the 10 measured cycles is shown just above the bipolar recording at each mapped site. Abbreviations as in Figures 1 and 2.
In a few shocks, there was acceleration or a decrease in local atrial cycle length. Acceleration in ⱖ2 atrial regions was seen in 4 shocks in 4 patients. Two of these patients subsequently had slowing with delivery of a shock of a higher energy; 1 patient had slowing with a shock at lower energy, whereas another patient had subsequent slowing at the same delivered energy during a second AF episode. Three of these 4 patients had a change in the regional activation sequence with acceleration. Thus, unsuccessful shocks invariably modified local atrial electrical activity for rate, sequence, or both. The concordant and discordant behavior of local atrial electrical activity in different atrial regions was also analyzed. Slowing after shock delivery at ⱖ2 regions without simultaneous acceleration at any other region was seen with 20 shocks (67%) in 13 patients (59%). Slowing at ⱖ2 regions, accompanied by simultaneous acceleration at another atrial region, was seen with 5 shocks (17%) in 5 patients (27%). The site of acceleration was the interatrial septum in 4 patients and distal coronary sinus in 1 patient. Figure 5 is a typical example of intracardiac recordings during delivery of a 100-J unsuccessful shock in such a patient. The shock was unsuccessful in restoring sinus rhythm, but there was an increase in the local atrial electrogram cycle length at all right and left atrial regions. 1084 THE AMERICAN JOURNAL OF CARDIOLOGY姞
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The duration of unsuccessful shock effects on local atrial electrogram cycle length was also assessed. In patients with ⱖ2 unsuccessful shocks during the protocol, the mean cycle length before the first shock was compared with the mean cycle length before shock delivery for the next 2 successive shocks. The preshock cycle length for the first shock was similar to the parameter for the second shock, and was also not significantly different from the parameter for the third shock (Figure 6). Mean time interval between the first and second shock and between the second and third shock was 150 ⫾ 27 and 102 ⫾ 43 seconds, respectively. EFFECTS OF UNSUCCESSFUL SHOCKS ON LOCAL ATRIAL ELECTROGRAM MORPHOLOGY: Our main finding was a
shift toward discrete electrogram morphologies from fractionated or chaotic electrograms in virtually all atrial regions mapped. Figure 7A and 7B illustrate the difference in local atrial electrogram morphologies before and after unsuccessful shock delivery at different right and left atrial regions. Note there is an increase in discrete atrial electrogram morphology, with a simultaneous reduction in chaotic and fractionated atrial electrogram activity in many right and left atrial regions. Furthermore, unlike the effect of slowing on atrial electrograms, this effect on the electrogram morphologies was also seen at the interatrial septum. MAY 1, 2001
FIGURE 5. Regional right and left atrial mapping of a 100-J synchronous external direct-current cardioversion shock. Arrows show superior and inferior or medial to lateral sequential bipolar recording in each region. Before shock delivery, the different atrial regions show varying cycle lengths and incoordinate activation sequences. There is an increase in cycle length at all the mapped regions and appearance of an organized atrial wave front. The magnitude of increase in cycle length is similar for the atrial regions mapped. LLPAd ⴝ left lower pulmonary artery distal recording for superior left atrial activation; LLPAp ⴝ left lower pulmonary proximal artery recording for superior left atrial activation; other abbreviations as in Figures 1 and 2.
and a change from a discrete to a fractionated or chaotic electrogram morphology in 2 patients. With shocks of 100 J, the shift to discrete electrogram morphology was seen in 8 of 12 patients (72%). There was no change in local electrogram morphology in 2 patients, whereas in 1 patient there was a reverse shift toward a more fractionated or chaotic electrogram morphology. One patient had a shift toward discrete electrograms in 1 atrial region and a shift toward fractionated electrograms in another atrial region. There was no statistically signifiFIGURE 6. Mean local atrial cycle length in different right and left atrial regions for 10 cant difference between 50 and 100 cycles preceding cardioversion shock delivery before the first, second, and third shocks J with respect to effects on local in patients receiving repetitive shocks. Note that there is no difference in the mean cyatrial electrogram morphology. cle length before shock delivery for successive shocks, indicating that the increase in The persistence of these effects mean atrial cycle length as a result of shock delivery did not persist until the delivery on electrogram morphology was of the next shock. Abbreviations as in Figures 1 to 3. analyzed. Of the 14 patients demonstrating a shift to a more discrete The shift to more discrete electrogram morpholo- local electrogram morphology with a 50-J shock, this gies was seen at ⱖ1 atrial region with a 50-J shock in discrete morphology persisted up to the delivery of the 14 of 18 (78%) patients. In the remaining 4 patients, next 100-J shock in 11 of 14 patients (78%). In the there was no change at any atrial region in 2 patients, remaining 3 patients, the morphology reverted back to ARRHYTHMIAS AND CONDUCTION DISTURBANCES/EFFECTS OF EXTERNAL DIRECT–CURRENT CARDIOVERSION
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and left atrial recordings. In the coronary sinus, chaotic fractionated activity that obscured most of the isoelectric line is replaced by discrete but fractionated electrograms with restoration of isoelectric periods. EFFECT ON ACTIVATION SEQUENCE: Twenty-one of the 22 pa-
tients had an unstable and variable right and left atrial activation sequence before first cardioversion shock delivery. In 18 patients with an unsuccessful shock of 50 J, the global atrial activation sequence became stable and repetitive in 7 patients (39%). In 2 of these 7 patients, the arrhythmia became type 1 atrial flutter. In 4 of these 7 patients, the stable activation sequence during AF persisted until the next shock of 100 J. The remaining patient reverted back to an unstable activation sequence. A 100-J shock resulted in a further 2 patients with an unstable activation sequence reverting to a stable sequence with the arrhythmia becoming sustained atrial flutter (type 1 clockwise in 1 patient and type 2 atrial flutter in 1 patient). This was terminated by the next shock. Site of initial activation after unsuccessful shock: The site of earliest
FIGURE 7. Panel A, comparison of the frequency of discrete, fractionated, and chaotic local bipolar atrial electrograms at different right atrial regions before and after cardioversion shock delivery. Both the lateral right atrium (RA) and the interatrial septum show a significant increase in discrete electrograms with a concomitant decrease in fractionated electrogram activity. Chaotic recordings are also reduced after cardioversion shocks. Panel B, comparison of the frequency of discrete, fractionated, and chaotic electrograms at 2 different left atrial sites before and after cardioversion shock delivery. As seen in right atrial regions, there is an increase in discrete electrograms with a simultaneous decrease in fractionated and chaotic electrograms at both the midcoronary sinus and distal coronary sinus recordings after shock delivery.
activation for the first AF beat after an unsuccessful shock varied from patient to patient. This was the interatrial septum in 17 shocks, crista terminalis in 5 shocks, proximal coronary sinus in 2 shocks, and mid- or distal coronary sinus in 3 shocks (p ⬍0.05 interatrial septum vs other sites). In patients with 2 unsuccessful shocks, the site of earliest activation was the same in 7 patients and different in 5 patients.
DISCUSSION
the fractionated or chaotic electrical activity present before the delivery of the first shock. Among the 8 patients who had the same finding with a 100-J shock, these changes persisted until delivery of the next shock in 6 patients (86%). In no patient did a reverse change toward a fractionated or chaotic electrogram morphology persist until the delivery of the next shock, suggesting spontaneous change may operate in selected patients. Figure 8 is an intracardiac recording during an unsuccessful 50-J cardioversion shock delivery. There is a marked decrease in electrogram duration in the lateral right atrium, interatrial septum, coronary sinus, 1086 THE AMERICAN JOURNAL OF CARDIOLOGY姞
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Mechanisms of efficacy and termination of atrial fibrillation with successful shocks: The
39% efficacy for the restoration of sinus rhythm with 100-J cardioversion shocks (intermediate energy), increasing to 100% with energies ⱖ200 J is similar to that reported in other studies.8,9 Termination of AF with successful shocks was associated with extinction of atrial electrical activity at virtually all the mapped sites without regional differences. This could imply that the widespread extinction of electrical wave fronts was a prerequisite for the termination of AF with the external cardioversion energies used in this study. These findings would be consistent with the concept that a critical mass of myocardium must show MAY 1, 2001
FIGURE 8. Regional right and left atrial mapping before and after delivery of a synchronous 50-J external cardioversion shock. There is a change in electrogram (EGM) morphology from fractionated to discrete at the lateral right atrium. At the interatrial septum (IAS), there is a reduction in local bipolar atrial electrogram duration and reduction in the number of its component deflections. At the proximal coronary sinus (CSp), the chaotic activity is replaced by discrete and fractionated electrograms with a clear isoelectric line between each successive electrogram. The duration of the atrial electrograms is shown above each recording site. Abbreviations as in Figures 1 and 2.
wave front interruption by shock delivery for successful defibrillation. Electrophysiologic effects and mechanisms of failure of unsuccessful cardioversion shocks: Unsuccessful car-
dioversion shocks of 50 or 100 J usually elicited slowing in multiple right and left atrial activation wave fronts, producing a shift toward more discrete atrial electrogram activity at almost all mapped regions. There may be induction of conduction delay/ block or an increase in atrial refractory periods. Alternatively, there could be fewer activation wave fronts around the recording sites. The absence of this effect at the interatrial septum implies that this region was more impervious to the effects of anteroposterior external shock vector used in the study, and may also potentially be a site for continuation or even reinitiation of AF. The slowing of the atrial cycle length by ⱖ10 ms was associated with a higher possibility of AF termination at the next energy level (46% vs 20%, p ⬍0.2). This may suggest increased vulnerability to AF termination due to the previously mentioned mechanisms. The conversion of chaotic electrograms to electrograms of a more discrete variety may represent one of several potential mechanisms. Unmasking of rapidly propagating wave fronts from rotors involved in initiation or sustenance of AF, e.g., focal atrial tachycar-
dia from pulmonary veins or atypical atrial flutter, may explain this observation. Conduction block in dead end pathways, not essential to the sustenance of AF, may also occur. Fewer activation wave fronts activating larger areas in a more cohesive fashion may potentially result in the electrograms appearing more discrete. Our bipolar electrogram findings after unsuccessful shocks correspond to a change from type 4 to a type 1 or 2 AF (Wells et al11), with concordant effects on electrogram morphology and local atrial cycle length.10 Konings et al10 suggested that discrete electrograms imply rapidly conducting activation wave fronts, whereas split or fragmented potentials may indicate slow conduction at pivot points and lines of block in the atrium. Our data could imply that unsuccessful shocks impact vulnerable regions of slow conduction or wave front pivot points. These data could also imply that organized activation wave fronts due to rotors may exist in AF and are unmasked at unsuccessful shock energies due to the disappearance of slow conduction. Jalife et al12 suggested that organized rotors exist during established AF. We reported organized atrial wave fronts at onset and termination of human AF.5,6 Our data also suggest that some atrial regions such as the septum and coronary sinus are particularly prone to fibrillatory conduction.5,6 Our
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data do not preclude induction of new tachycardias by shock delivery. Thus, the appearance of typical and atypical flutter in 4 patients could be explained either by unmasking of existing rotors or induction of new arrhythmias. However, the transformation of an unstable activation sequence to a stable activation sequence as seen in some patients in the study substantiates the view that unsuccessful shocks electrophysiologically modify the AF episode despite nondiscernable surface electrocardiographic findings. Similar effects have been seen with antiarrhythmic drug use in AF and in linear ablation in experimental studies.13,14 Study limitations: Saturation of the recording amplifiers was seen for up to 200 ms after shock delivery. For successful shocks, some atrial sites could have been activated and gone unrecognized during this period. However, despite this limitation, our data imply that ⬎1 repetitive wave front did not occur and does not change the interpretation of the data. Shocks of intermediate and lower energies could have resulted in further regional differences both for successful and unsuccessful shocks. 1. Desilva RA, Graboys TTS, Podrid PJ, Lown B. Cardioversion and defibrillation. Am Heart J 1980;100:881– 895. 2. Levy S, Lauribe P, Dolla E, Kou W, Kadish AH, Calkins H, Pagannelli F, Moyal C, Bremondy M, Schork A, Shyr Y, Das S, Shea M, Gupta N, Morady F. A randomized comparison of external and internal cardioversion of chronic atrial fibrillation. Circulation 1992;86:1415–1420.
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3. Saksena S, Pantopoulos D, Hussain SM, Gielchinsky I. Mechanisms of ventricular tachycardia termination and acceleration during transvenous cardioversion as determined by cardiac mapping in man. Am Heart J 1987;113:1495– 1506. 4. Wellens HJJ, Lau C-P, Luderitz B, Akhtar M, Waldo AL, Camm AJ, Timmermans C, Tse H-F, Jung W, Jordaens L, Ayers G, for the METRIX Investigators. Atrioverter: an implantable device for the treatment of atrial fibrillation. Circulation 1998;98:1651–1656. 5. Saksena S, Giorgberidze I, Mehra R, Hill M, Prakash A, Krol RB, Mathew P. Electrophysiology and endocardial mapping of induced atrial fibrillation in patients with spontaneous atrial fibrillation. Am J Cardiol 1999;83:187–193. 6. Saksena S, Prakash A, Krol RB, Shankar A. Regional endocardial mapping of spontaneous and induced atrial fibrillation in patients with heart disease and refractory atrial fibrillation. Am J Cardiol 1999;84:880 – 889. 7. Prakash A, Delfaut P, Krol RB, Saksena S. Regional right and left atrial activation patterns during single- and dual-site atrial pacing in patients with atrial fibrillation. Am J Cardiol 1998;82:1197–1204. 8. Lown B. Electrical reversion of cardiac arrhythmias. Br Heart J 1967;29:469 – 489. 9. Kerber RE. Energy requirements for defibrillation (abstr). Circulation 1986; 74(suppl IV):IV-117. 10. Konings KTS, Smeets JLRM, Penn OC, Wellens HJJ, Allessie MA. Configuration of unipolar atrial electrograms during electrically induced atrial fibrillation in humans. Circulation 1997;95:1231–1241. 11. Wells JL, Karp RB, Kouchoukos NT, MacLean WAH, James TN, Waldo AL. Characterization of atrial fibrillation in man: studies following open heart surgery. Pacing Clin Electrophysiol 1978;1:426 – 438. 12. Jalife J, Berenfeld O, Skanes A, Mandapati R. Mechanisms of atrial fibrillation: mother rotor or multiple daughter wavelets or both. J Cardiovasc Electrophysiol 1998;9:S2–S12. 13. Rensma PL, Allessie MA, Lammers WJAP, Bonke FI, Schlaij A. Length of excitation wave and susceptibility to reentrant atrial arrhythmias in normal conscious dogs. Circ Res 1988;62:395– 410. 14. Oritz J, Niwano S, Abe H, Rudy Y, Johnson NJ, Waldo AL. Mapping of conversion of atrial flutter to atrial fibrillation and atrial fibrillation to atrial flutter. Insights into mechanisms. Circ Res 1994;74:882– 894.
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