CLINICAL STUDIES
Intravenous sotalol decreases transthoracic cardioversion energy requirement for chronic atrial fibrillation in humans: assessment of the electrophysiological effects by biatrial basket electrodes
Ling-Ping Lai, MD, PhDa,
Jiunn-Lee Lin, MDa,
Wen-Pin Lien, MD, FACCa,
Yung-Zu Tseng, MDa and
Shoei K. Stephen Huang, MD, FACCa
a Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan
Manuscript received August 9, 1999;
revised manuscript received December 3, 1999,
accepted January 17, 2000.
Reprint requests and correspondence: Dr. Shoei K. Stephen Huang, Department of Internal Medicine, National Taiwan University Hospital, No 7, Chung-Shan South Road, Taipei, Taiwan
SKH{at}ha.mc.ntu.edu.tw
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Abstract
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OBJECTIVES
This study was undertaken to assess the effects of sotalol on the transthoracic cardioversion energy requirement for chronic atrial fibrillation (AF) and on the atrial electrograms during AF recorded by two basket electrodes.
BACKGROUND
The effects of sotalol infusion on transthoracic electrical cardioversion for chronic atrial fibrillation in humans have not been well investigated.
METHODS
We included 18 patients with persistent AF for more than three months. Atrial electrograms were recorded by two basket electrodes positioned in each atrium respectively. Transthoracic cardioversion was performed before and after sotalol 1.5 mg/kg IV infusion.
RESULTS
In the 14 patients whose AF could be terminated by cardioversion before sotalol infusion, the atrial defibrillation energy was significantly reduced after sotalol infusion (236 ± 74 jules [J] vs. 186 ± 77 J; p < 0.01). Atrial fibrillation was refractory to cardioversion in four patients at baseline and was converted to sinus rhythm by cardioversion after sotalol infusion in two of them. We further divided the patients into two groups. Group A consisted of 10 patients in whom the energy requirement was decreased by sotalol while group B consisted of eight patients in whom the energy requirement was not decreased. The mean A-A (atrial local electrogram) intervals during AF were significantly increased after sotalol infusion in both groups, but the increment of A-A interval was significantly larger in group A than it was in group B patients (36 ± 13 ms vs. 22 ± 8 ms for the right atrium; 19 ± 7 ms vs. 9 ± 7 ms for the left atrium; both p < 0.05). The spatial and temporal dispersions of A-A intervals were not significantly changed after sotalol infusion in both atria in both groups.
CONCLUSIONS
Sotalol decreases the atrial defibrillation energy requirement by increasing atrial refractoriness but not by decreasing the dispersion of refractoriness.
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Abbreviations and Acronyms
| | AF | = atrial fibrillation | | J | = joules | | LA | = left atrium | | RA | = right atrium |
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Electrical cardioversion has been an established treatment modality for converting atrial fibrillation (AF) into sinus rhythm (1,2). However, it often requires a relatively large amount of energy, which may lead to possible myocardial stunning and injury. In addition, AF may be refractory to direct current shock even with the highest energy output, especially in patients with chronic persistent atrial fibrillation for a prolonged duration (3). To increase the efficacy of electrical cardioversion, concomitant pharmacological therapy might be used to possibly decrease the energy requirement. Various antiarrhythmic agents have been reported to change the ventricular defibrillation threshold (4–7). Among them, sotalol has been reported to decrease the ventricular defibrillation threshold (8,9). However, the effects of sotalol on atrial defibrillation energy requirement remain unknown. We hypothesize that intravenous sotalol can also decrease the energy requirement for atrial defibrillation in humans. This study was undertaken to assess the effects of sotalol on the transthoracic atrial defibrillation energy requirement and on the electrical activities during AF in patients with chronic persistent AF for more than three months.
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Methods
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Patients.
From June 1997 to December 1998, 18 patients with persistent AF for more than three months were included in the study. Patients with a left ventricular ejection fraction of less than 35%, congestive heart failure of New York Heart Association functional class III or more, a left atrial thrombus as detected by transthoracic and transesophageal echocardiography as well as patients with hyperthyroidism were excluded. There were 14 men and 4 women with a mean age of 65 ± 9 years (range 44 to 81). The clinical characteristics of the patients are summarized in Table 1.
Electrophysiologic study.
Electrophysiologic study was performed in the fasting state after obtaining a written consent. All previous antiarrhythmic agents had been discontinued for at least five half-lives. All patients were taking warfarin achieving an International Normalized Ratio of 2 to 2.5. Intravenous propofol infusion was used to achieve general anesthesia. Two basket electrodes (Mercator, Cardiac Pathways, Sunnyvale, California) were used for global atrial mapping. The basket had eight splines and there were eight electrodes (four bipoles) on each spline (totally 32 bipoles in each basket). The interbipole distance was 8 mm, and the intrabipole electrode distance was 1 mm. The volume of the basket was either 70 or 100 ml, and the choice was dependent on the atrial size. One basket was positioned in the left atrium by transseptal atriotomy, and the other basket was positioned in the right atrium (Fig. 1). Intracardiac local electrograms from each basket were recorded by a multichannel recording system (CardioLab 4.1, Prucka Engineering Inc., Houston, Texas). Electrical cardioversion was performed using an external cardioverter defibrillator (LifePak6, Physio-Control, Redmond, Washington). The two cardioversion paddles were positioned on the midsternum and at the cardiac apex, respectively. The shock was synchronized to a QRS complex. The energy level was 100 J initially and was increased by 100 J until termination of AF or until the maximum 400 J was reached. A successful atrial defibrillation was defined as termination of AF by cardioversion. Early recurrence of atrial fibrillation after a short period of sinus rhythm (at least three beats) was still considered a successful atrial defibrillation. Atrial fibrillation was induced again by rapid atrial pacing if sinus rhythm persisted after the cardioversion. Sotalol 1.5 mg/kg was then infused intravenously over 5 min. The atrial electrograms were recorded again 15 min after the infusion, and electrical cardioversion was repeated. The cardioversion was performed by the same cardiology fellow with special attention given to assure that there were no changes in electrode paddle position or paddle pressure among all DC shocks (as judged by the cardiology fellow). In the initial eight patients, cardioversion was performed after reinduction of AF and before sotalol infusion to test whether the reinduced AF had the same defibrillation threshold as the clinical atrial fibrillation. This procedure was omitted in later patients because we found that the energy requirement was the same for both spontaneous and induced AF before sotalol infusion in the initial eight patients (Table 1).
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Figure 1 Right anterior oblique 45° and left anterior oblique 45° fluoroscopic projections during the biatrial basket study. Each basket electrode has eight splines with eight electrodes (four bipoles) on each spline. The basket electrode was positioned in the left atrium using the transseptal puncture technique. The spline with a mark at the distal third was designated as spline A, with a mark at the middle third as spline B and distal third spline C. The splines next to spline C were designated splines D, E, F, G and H serially. LAO = left anterior oblique; RAO = right anterior oblique.
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Analysis of local electrograms.
The A-A (atrial local electrogram) intervals recorded by the basket electrodes were used for analysis. The mean A-A interval at each bipole was calculated by averaging the A-A intervals in a 5-s period. Two electrograms of less than 50 ms apart were interpreted as a single activation with double potentials. The temporal dispersion of A-A intervals at each bipole was represented by the coefficiency of variation of A-A intervals in a 5-s period. The mean A-A interval of a basket was calculated by averaging the mean A-A intervals at the bipoles of the basket. The spatial dispersion of a basket was represented by the coefficiency of variation of mean A-A intervals at the bipoles of the basket.
Statistical analysis.
Data are expressed as mean ± standard deviation except for the duration of AF, which showed large deviation, and the median value was used. The coefficiency of variation was calculated as (standard deviation/mean) x 100%. Student t test was performed to compare numeric parameters except the duration of atrial fibrillation, which had a skewed distribution and was compared using Mann-Whitney-Wilcoxon rank-sum test. McNemar’s test was used to determine whether sotalol decreased the atrial defibrillation threshold.
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Results
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Atrial defibrillation threshold.
The energy requirement was summarized in Table 1. Among the 18 patients, atrial fibrillation could be terminated by cardioversion before sotalol infusion in 14 patients. In the 14 patients, the atrial defibrillation energy was significantly reduced after sotalol infusion (236 ± 74 J vs. 186 ± 77 J; p < 0.01). The mean decrease of energy requirement was 50 J (21%) (Table 1). Atrial fibrillation was refractory to the highest energy output of 400 J in four patients at baseline and was successfully converted to sinus rhythm by cardioversion after sotalol infusion in two of them. Of the 18 patients, 10 showed a decrease of energy requirement while seven showed no change, and one showed an increase. The tendency of sotalol to decrease the atrial defibrillation energy requirement was statistically significant by McNemar’s test (chi-square = 5.82, p < 0.05). We further divided the study patients into two groups. Group A consisted of 10 patients who showed a decreased energy requirement while group B consisted of eight patients in whom there was no decrease of energy requirement (no change in seven and increase in one).
Biatrial basket study.
Two basket electrodes were positioned in both atria respectively. The procedure was carried out smoothly in all patients without complications. For the 32 bipolar recordings in each basket, some recording sites showed large ventricular electrograms with very small atrial electrograms. These sites might represent the areas facing the mitral or tricuspid opening, and these recordings were excluded from analysis (Fig. 2).
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Figure 2 Atrial electrograms recorded before (A, B) and after sotalol infusion (C, D) using two basket electrodes in the RA and LA, respectively. Recordings at A4 and B4 of the RA and at B2, B3 and B4 of the LA were excluded from analysis because the atrial electrograms were too small. These areas might represent areas facing the mitral and tricuspid valve opening, and only ventricular electrograms were recorded. At baseline, the A-A intervals were shorter in the LA (157 ms) than in the RA (182 ms). Sotalol infusion caused a prolongation of the A-A intervals in both atria while the prolongation was larger in the RA (182 to 215 ms) than in the LA (157 to 174 ms). LA = left atrium; RA = right atrium.
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Changes of intraatrial recordings after sotalol infusion (Table 2).
We found that there was a significant increase of the A-A interval after sotalol infusion. The decrease was observed globally in both atria. The mean A-A interval in the right atrium (RA) basket was 170 ± 15 ms at baseline and 199 ± 15 ms after sotalol infusion (p < 0.01). There was also an increase of the mean A-A interval in the left atrium (LA) basket from 160 ± 14 ms to 175 ± 12 ms (p < 0.01). The mean increase was 30 ± 13 ms in the RA and 15 ± 8 ms in the LA. The intrabasket spatial dispersion was also compared before and after sotalol infusion. The coefficiency of variation of the RA basket was 10.9 ± 4.4% at baseline and 11.8 ± 5.4% after sotalol, while that of the LA basket was 8.5 ± 2.3% at baseline and 8.4 ± 3.5% after sotalol. The temporal dispersion of A-A interval for the RA was 19.7 ± 4.1% at baseline and 20.5 ± 3.7% after sotalol infusion and that for the LA was 20.2 ± 3.4% at baseline and 21.0 ± 5.3% after sotalol infusion. The changes of temporal dispersion were not greater in regions showing fragmented electrograms. There was no significant difference of either the spatial dispersion or temporal dispersion before and after sotalol infusion.
Differences between group A and group B patients (Table 3).
The patients in both groups did not differ significantly in their age, left atrial size, left ventricular ejection fraction and the median duration of AR (by Mann-Whitney-Wilcoxon rank-sum test) (Table 1). At baseline, the mean A-A intervals, the spatial and the temporal dispersions of both atria were not significantly different between the two groups. After sotalol infusion, the mean A-A interval was significantly increased in both atria in both groups. However, the increment of A-A interval was significantly larger in group A patients than it was in group B patients in both atria. The mean of the increment of A-A interval in the right atrium was 36 ± 13 ms for group A patients versus 22 ± 8 ms for group B patients (p < 0.01) and in the left atrium 19 ± 7 ms for group A patients versus 10 ± 7 ms for group B patients (p < 0.05). In contrast, the spatial and temporal dispersions of A-A intervals were not significantly different between the two groups.
Comparison between the two atria (Tables 2 and 3).
We found that the mean A-A interval was significantly shorter in the LA than it was in the RA before sotalol infusion (160 ± 14 ms vs. 170 ± 15 ms; p < 0.05). This finding was observed in every study patient. The mean A-A interval of RA remained significantly longer than that of the LA after sotalol infusion (199 ± 15 ms vs. 175 ± 12 ms; p < 0.05). Sotalol infusion caused a prolongation of A-A intervals in both atria. The degree of A-A interval prolongation was significantly larger in the RA than it was in the LA (30 ± 13 ms vs. 15 ± 8 ms; p < 0.01). The percentage of increment of the A-A interval was also significantly larger in the RA than it was in the LA (17.9 ± 8.9% vs. 9.7 ± 5.4%, p < 0.05). This finding was observed in both groups of patients. In contrast, the spatial and temporal dispersions were not significantly different between the two atria.
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Discussion
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In this study, we found that intravenous sotalol significantly decreased the transthoracic atrial defibrillation energy requirement in patients with chronic persistent AF lasting for more than three months. We also showed that some of the AF refractory to maximum energy output in transthoracic cardioversion could be successfully converted after sotalol infusion. Furthermore, we used two basket electrodes to record the right and left atrial electrical activities. We showed that the decrease of energy requirement by sotalol was related to an increase of A-A intervals during AF, and there were no changes of spatial and temporal dispersions of A-A intervals by sotalol.
Antiarrhythmic agents and defibrillation threshold.
The effects of antiarrhythmic drugs on the defibrillation threshold were mostly studied in ventricular fibrillation while information regarding the drug’s effects on atrial defibrillation is sparse. In ventricular defibrillation, drugs with sodium channel blocking effect, including amiodarone, have been reported to increase the energy requirement in animals as well as in humans (10–17). In contrast, antiarrhythmic agents with potassium channel blocking effects, such as sotalol and ibutilide, have been shown to reduce the energy requirement (18–21). However, it is unclear whether the same rule can be applied to atrial defibrillation. Early studies regarding the effects of quinidine on the atrial defibrillation energy showed contradicting results (22–24). It has been reported that procainamide is not effective in enhancing the success of atrial defibrillation (25). Guarnieri et al. (26) and Van Gelder et al. (27) both reported that flecainide increases atrial defibrillation threshold. In a more recent study in acute AF, ibutilide decreased transthoracic cardioversion energy requirement (28). With regard to sotalol, there has been a report showing that intravenous sotalol decreases the transvenous atrial defibrillation threshold in dogs (29). Lau et al. (30) also reported that intravenous sotalol was effective in decreasing the transvenous atrial defibrillation threshold in patients with acute AF. This study further showed that intravenous sotalol decreased the transthoracic atrial defibrillation threshold in patients with chronic persistent AF. Therefore, it is likely that antiarrhythmic agents with potassium channel blocking effects, such as sotalol and ibutilide, reduce the energy requirement for atrial defibrillation as well as for ventricular defibrillation.
Mechanisms of decrease of energy requirement.
We attributed the decrease of atrial defibrillation energy to the increase of atrial refractoriness for several reasons. First, the increase of A-A intervals was the major electrophysiological finding observed after sotalol infusion. There have been reports showing that A-A intervals during atrial fibrillation correlate well with atrial refractory periods (31,32). Sotalol is a class III antiarrhythmic agent. It prolongs the refractory period with minimal changes of conduction velocity (33). Therefore, the increased A-A interval was most likely caused by the increased refractory period. Furthermore, we divided our study patients into two groups according to whether the defibrillation energy level was decreased. The two groups were not significantly different in age, left atrial size, left ventricular function, AF duration or baseline A-A intervals in both atria. The increase of A-A interval by sotalol was the only parameter that differed significantly between the two groups. Therefore, it is likely that the decrease of the atrial defibrillation energy requirement was a result of the increase of A-A intervals.
The atrial refractory period has long been known to be an important determinant in AF. According to the multiple wavelet theory proposed by Moe et al. (34,35), multiple simultaneous reentrant wavelets are needed for the maintenance of AF. An increased atrial refractory period results in a longer fibrillation wavelet wavelength (wavelength = refractory period x conduction velocity). There will be fewer simultaneous wavelets in the atria because the size (wavelength) of the wavelet increases, and the atrial size remains constant. This may increase the tendency toward termination of AF. In this study, we found that the increase of A-A interval was significantly larger in group A patients than it was in group B patients. This is another example showing that the increase of A-A interval (and, hence, the increase of atrial refractory period and the decrease of wavelet number) is important for the decrease of the atrial defibrillation threshold.
The dispersion of refractoriness is also important for the induction and maintenance of AF (36–39). In Moe’s computer model of AF, heterogeneity in refractoriness was required for the occurrence of AF (35). Sato et al. (40) also found that an increased dispersion of refractoriness was associated with inducibility of AF in dogs. In this study, we found that the spatial dispersion of A-A intervals was not significantly changed after sotalol infusion. This observation is similar to that reported by Nattel et al. (39) in dogs. Thus, it appears that changes in the dispersion of refractoriness play little role in the decrease of the atrial defibrillation threshold by sotalol.
Sotalol has antiadrenergic action in addition to its antiarrhythmic action. The influence of adrenergic activity on the ventricular defibrillation threshold has been addressed in several studies (41,42). It has been shown that decreased adrenergic action is associated with an increase of the ventricular defibrillation threshold. However, the influence of adrenergic activity has not been well investigated in atrial defibrillation. Although it is not likely that the antiadrenergic action of sotalol contributes to the decrease of energy requirement during atrial defibrillation, we cannot completely exclude the possibility.
Clinical implications.
Electrical cardioversion of AF often requires high energy shock. We demonstrated that sotalol infusion can decrease the energy requirement and, therefore, may minimize the injury and myocardial stunning caused by the shock. Some patients may be refractory to the highest energy output, especially patients with atrial fibrillation of longer duration. In this study, AF was refractory to an energy output of 400 J in four patients at baseline and was successfully converted to sinus rhythm after sotalol infusion in two (50%) of them. In such patients, internal cardioversion could also be tried and might be effective (43,44). However, this procedure is invasive and is not widely available. We suggest that sotalol infusion be used before trying another cardioversion after a failed cardioversion. This simple management can be successful in some patients with chronic persistent atrial fibrillation refractory to transthoracic cardioversion.
With the advent of implantable cardioverter defibrillator, an implantable atrial defibrillator offers a potentially useful alternative therapy for patients with recurrent AF refractory to conventional drug treatment. However, patient discomfort caused by the shock is a major limitation for the application of an atrial defibrillator. Concomitant sotalol administration may decrease the energy requirement and may reduce pain during electric shock (30). Further investigation on this hypothesis is promising.
Study limitations.
Atrial effective refractory periods were not directly measured in the study because direct measurement of the atrial effective refractory period during atrial fibrillation is difficult. However, the local A-A intervals have been shown to correlate well with the atrial effective refractory periods in the literature (31,32). Sotalol has been documented to increase the atrial refractory period and has little effect on the conduction velocity (33). Therefore, we attributed the prolongation of A-A intervals after sotalol infusion to the prolongation of the atrial refractory period.
The measurement of the atrial defibrillation threshold was not very precise because we increased the energy output by 100 J at a time rather than 50 J or less. We feel that a more precise measurement with less increment may result in more electrical shocks and may not be feasible in humans because of ethical reasons. Third, for a failed 400 J DC shock, the exact energy requirement could not be determined. We, therefore, excluded the four patients who experienced a failed 400 J shock from energy calculation. However, the decrease of the energy requirement in the remaining 14 patients was obvious, and the difference was highly significant.
Serum concentration of sotalol was not measured. A correlation between the reduction of the energy requirement and serum sotalol concentration could not be performed. The analysis of atrial electrograms was based on the measurement of A-A intervals. Frequency domain and spectral analysis was not performed.
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Footnotes
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This study was supported, in part, by the Grant NCHCPF-87002 from the New Century Health Care Promotion Foundation, Taipei, Taiwan.
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References
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