late embolic complications (occurring 1 day, 3 months, and 3.5 months after ablation) following 153 left-sided procedures for a complication rate of 2.0%. No patient had any alternative identifiable cause for their complication and all received heparin for anticoagulation during and aspirin for 3 months after the ablation procedure.

In this report, thromboembolic complications oc- curred in slightly > 1% of patients and procedures. Embolic complications occurred in 0.8% of patients and 0.7% of procedures, whereas the embolic com- plication rate for left-sided procedures was higher at 1.8%. Although the complication rates presented do not differ significantly from those previously re- ported, I-4 a new finding of this study is that embolic complications after RF ablation in patients without other risk factors were rare. Only 1 procedure of 830 had an associated late embolic complication in an otherwise risk-free patient. No patient without other identifiable risk factors undergoing RF ablation of a left-sided target had an associated late embolic com- plication.

The rarity of embolic complications in patients without other risk factors for systemic embolization cannot be attributed to the use of anticoagulation ei- ther during or after RF ablation, because a wide range of both inpatient and outpatient anticoagula- tion protocols were utilized by the 11 centers partic- ipating in the study, and no single protocol was as- sociated with a higher incidence of thromboembolic complications. Thakur et al4 observed that embolic complications occurred despite both intraoperative and postprocedure anticoagulation, and that at least 1 embolic complication occurred after anticoagula- tion therapy had been discontinued. Thus, data from this report combined with that of Thakur suggest that anticoagulation with aspirin is neither useful nor nec- essary after RF ablation procedures.

A potential unique feature of this study compared with prior reports l-4 is that temperature monitoring,

with its associated theoretical reduction in cqagulum formation, and hence embolic complications, was used. Because no procedure complicated by throm- boembolic events had an associated impedance, tem- perature, or power shutdown, the near elimination of impedance rises by temperature control6 did not ap- pear to be helpful in reducing the incidence of throm- boembolic events.

In the population enrolled in this study, em- bolic complications were rare following only 0.7% of procedures. In addition, no relationship existed between procedures with thromboembolic complications and anticoagulation protocol, pro- cedure time, number of RF lesions, or impedance shutdowns. Only 1 of 830 procedures had an as- sociated late embolic complication in an other- wise risk-free patient.

Acknowledgment: We are indebted to Suzan Moser, RN, Pat Yong, Peter Lichtman, and Brenda Radde for their invaluable assistance with the man- uscript and clinical study.

1. Hindricks G. The Multicentre European Radiofrequency Survey (MERFS): complications of radiofrequency catheter ablation of arrhythmias. Eur Heart J 1993;14:1644-1653. 2. Kugler JD, Danford DA, Deal BJ, Gillette PC, Perry JC, Silka MJ, Van Hare GF, Walsh EP. Radiofrequency catheter ablation for tachyarrhythmias in chil- dren and adolescents. N Engl JMed 1994;330:1481-1487.

3. Greene TO, Huang SK, Wagshal AB, Mittleman RS, Pires LA, Mazzola F, Andress JD. Cardiovascular complications after radiofrequency catheter ablation of supraventricular tachyarrhythmias. Am J Cardiol 1994;74:615- 617.

4. Thakur RK, Klein GJ, Yee R, Zardini M. Embolic complications after radiofrequency catheter ablation. Am .I Cardiol 1994;74:278- 279.

5. Hope EJ, Haigney MC, Calkins H, Resar JR. Left main coronary thrombosis after radiofrequency ablation: successful treatment with percutaneous translu- minal angioplasty.Am Hean J 1995;129:1217-1219.

6. Calkins H. Prwtowskv E. Carlson M. Klein LS. Saul JP. Gillette P. Tem- perature moiitoing dmihg radiofrequency cathete; ablation’ procedures using closed loop control. Circulafion 1994;90: 1279- 1286.

Direct-Current Cardioversion for the Conversion of Atrial Flutter

Prasad Chalasani, MD, Suzanne Cambre, RN, and Mark E. Silverman, MD

AL trial flutter was first described by Thomas ewis >80 years ago.’ Since then, multiple

modalities have been tried to convert this rhythm disturbance, including antiarrhythmic drugs,’ di- rect-current (DC) cardioversion, 3-6 atria1 pacing’s8 (intracardiac and transesophageal) , and catheter ab- lation ? In 1962 Lown et al3 introduced DC cardio-

From the Department of Medicine, Emory University School of Med- icine and Piedmont Hospital, Atlanta, Georgia. Dr. Silverman’s ad- dress is: 1968 Peachtree Road NW, Atlanta, Georgia 30309. Mon- uscript received March 30, 1995; revised manuscript received and accepted July 18, 1995

version for the treatment of atrial arrhythmia. Only a few studies have subsequently reported the role of DC cardioversion in atrial flutter.‘-7,10 There is lim- ited information regarding cardioversion in atria1 flutter in recent years since changing patterns of management and new options have become avail- able. This report presents our experience with DC cardioversion of atria1 flutter over a 15-year period in a community hospital setting.

. . . This is a retrospective study of all patients who

received elective DC cardioversion for atria1 flutter during 1979 to 1993 at Piedmont Hospital, a 500-

658 THE AMERICAN JOURNAL OF CARDIOLOGY@ VOL. 77 MARCH 15, 1996

TABLE I Etiology and Possible Contributing Factors of 85

Potients

Etiology Number of Patients Ix)

No known disease 29 (34)

Coronary artery disease 20 (24)

Hypertension 6 (7) Valvular heort disease 6 (7) Dilated cardiomyopathy 5 (61 Alcohol 5 I4 Chronic lung disease, 6 (71 Miscellaneous (congenital heort disease, 6 (71

WPW syndrome, IHSS)

Data not available 8 A

IHSS = idiopathic hypertrophic subaortic stenosis; WPW = Wolff-Parkinson-

White syndrome.

bed community hospital in Atlanta, Georgia. Adult patients (age > 18 years) with atria1 flutter of any etiology who were hemodynamically stable (defined as systolic pressure >lOO mm Hg) were included. Patients were excluded for the following reasons: ( 1) associated atria1 fibrillation or fibrillation flutter, (2) hemodynamically unstable (defined as atria1 flutter with 1: 1 conduction or systolic blood pressure < 100 mm Hg ) , and (3 ) atria1 flutter after cardiothoracic surgery. A cardioversion checklist and data collec- tion sheet were completed, Digoxin was usually held the day of DC cardioversion. Three and one half inch external electrode gel pads were placed over the apex and base of the heart in most cases. Recently, an anteroposterior approach has been used. Synchro- nized, DC countershock was applied using a stan- dard defibrillator with selected energies. Patients were followed up in the hospital or checked by phone if they underwent cardioversion as an outpa- tient. Data were obtained from cardioversion data sheets and a retrospective review of medical records. The procedure was considered successful if sinus rhythm was restored after z 1 attempt.

Ninety-eight episodes of atria1 flutter in 85 pa- tients were analyzed: 64 patients (75%) were men and 21 (25%) were women. The age range was 37 to 89 years (mean 65.6). Success was achieved in 93 of 98 episodes (95%). Underlying heart diseases and other causes possibly contributing to the atri,al flutter are listed in Table I. No apparent etiology was found in 29 of 85 patients (34%). The duration of atria1 flutter was known in 25 episodes. Seventy-nine percent of atria1 flutter episodes were originally treated with drugs to control the ventricular rate; 50% were treated with antiarrhythmic drugs. Drugs used to control the ventricular rate were digoxin (55%), a combination of digoxin, a p blocker, and a calcium blocker (20% ) , a ,f? blocker alone (3% ) , no drug (20%)) and an unknown drug ( 1% ) . An- tiarrhythmic therapy before cardioversion included no therapy (50%)) quinidine (23%)) procainamide (2 1% ) , flecainide ( 3% ) , amiodarone ( 1% ) , and di- sopyramide ( 1%) . Sixty-five percent had successful cardioversion by a single attempt, 27% required 2 shocks, and the remaining patients required ~3

shocks. The initial energy used was: < 100 J (25,50, and 75 J) in 66% of episodes; 100 J, but <200 J, in 20%; and 200 J in 13%. The initial success rate was related to the level of energy used (Table II). Among 5 unsuccessful episodes, 3 remained in atria1 flutter, 1 converted to atria1 fibrillation, and 1 to a slow junc- tional escape rhythm. Diazepam was used in 54% of these episodes, sodium methohexital in 42%, and midazolam in 4% as anesthetic agents. Twelve of 98 atria1 flutter cardioversions (12%) required >5 minutes of assisted ventilation with an Ambu bag (InterTech, Fort Meyers, Florida) because of ~90% oxygen saturation or clinical evidence of hypoven- tilation. There was no aspiration, and intubation was not required. DC cardioversion was well tolerated, and very few patients had a memory of the shock. One patient had conversion into a very slow junc- tional escape rhythm requiring a temporary trans- venous pacemaker. Atria1 fibrillation after initial DC cardioversion occurred in 15 episodes ( 15%) ; 11 of 15 of these episodes (73%) occurred at low energy (<lOO J) compared with 4 of 15 (27%) when the energy was >lOO J (p = 0.01). Only 10 of 85 pa- tients ( 12%) underwent anticoagulation before DC cardioversion. There were no embolic complications immediately after cardioversion or up to 24 hours. No other complications were documented within 24 hours of DC cardioversion.

. . . Atria1 flutter is a common problem confronting

the clinician, although much less frequent than atria1 fibrillation. Atria1 flutter is usually associated with organic heart or lung disease. In our series of 85 patients, 55% had an associated heart or lung disease (Table I). Coronary artery disease was seen often in our series than in previous series in which rheumatic heart disease was more prevalent.s.6 In about one third of our patients, no apparent etiology was found. This may represent a changing pattern of disease over the last 3 decades. Ninety-five percent of our patients without apparent heart or lung disease were aged ~70 years. In these patients, atria1 flutter may be a manifestation of a sick sinus syndrome.

Few randomized studies have demonstrated the utility of antiarrhythmic drug therapy to terminate atria1 flutter. Most studies have combined patients with atria1 fibrillation with those with flutter. The success rate for these combined studies with antiar- rhythmic drug therapy ranges from 40% to 69%.” No single drug has been shown to be effective in the conversion of atria1 flutter to sinus rhythm.” In our series, 50% of patients were taking antiarrhythmic therapy before cardioversion and can be considered drug failures although drugs were not pushed to tol- erable limits.

The DC cardioversion success rate was 95% in our series, the largest series of cardioversion of atria1 flutter reported. This is in concordance with other smaller studies that have shown a success rate of 93% to 100%.4-7~‘” The success rate of radiofrequency catheter ablation of atria1 flutter is operator-dependent and was 69% in a small study? Transesophageal atria1 pacing

BRIEF REPORTS 659

TABLE II Initial Level of Energy Used for DirectCurrent Cardioversion

Result

Group I (65 episodes)-25,

50,75 J

or < 1OOJ

No. of Episodes (%)

Group II (20 episodes)- 100,

150J

or 100-200 J

No. of Episodes (%)

Group III (13 episodes)-

200 J or

> 200J

No. of Episodes (%)

Successful 37 (57) 15 (75)* 11 (85)+ Unsuccessful 28 (43) 5 (251 2 (151 I

are much lower than reported in other small series.4-7 It is not our practice to administer anticoagulant therapy to patients whose rhythm is pure atrial flutter. We did not encounter any car- diac embolic event in the first 24 hours after DC cardioversion, even though only 10 of 85 patients ( 12%) underwent anticoanulation: however.

* Group I versus group II, p = 0.14; + group I versus group Ill, p = 0.05. our study was not iontrolled and pa: tients were not followed for 2-1

TABLE III Costs Involved for Cardioversion

Item cost

Cardioversion charge (hospital) $50.00

Medicines $50.00 Intravenous set and needles $33.00

Physicon fee $175.00

Respiratory therapist fee $23.00

Total $33 1 .oo

has been successful in a small series (73%). No study has addressed the optimal initial energy for converting atrial flutter to sinus rhythm. Ninety-three percent of our patients required only 1 to 2 shocks to convert attial flutter to sinus rhythm. If r3 DC countershocks were tried, only 3 of 7 atrial flutter episodes had successful cardioversion. In our analysis, if 2200 J was used as an initial energy setting, there is a statistically signifi- cant likelihood of converting to stable sinus rhythm with 1 attempt. In our series, 15% of atrial flutter ep- isodes transiently converted to atrial fibrillation when <200 J was chosen initially. All but 1 were then con- verted to sinus rhythm using a higher energy. Atrial fibrillation developed more often when the DC car- dioversion energy was < 100 J (p = 0.01). This has been noted by others in about 6%.“ It is postulated that during synchronized cardioversion, when the R wave is synchronized to the delivered electricity, the atria may be in a vulnerable period where fibrillation is more likely to occur. Despite the common practice of begin- ning with 25 to 50 J, which may work, we believe that 200 J is the optimal initial energy level because fewer shocks are required. No major complications were noted in our study. Twelve percent of patients required temporary respiratory support with an Ambu bag. In- tubation was never required, and aspiration did not oc- cur in our series. We have found that sodium methoh- exit01 provides the quickest sedation and the most effective amnestic response, but may require Ambu support for several minutes after DC cardioversion. One patient had a very slow junctional escape rhythm requiring a temporary pacemaker. These complications

week. The expense of cardioversion is shown in Table RI.

The total cost was about $330 in our hospital. Many of our patients had DC cardioversion as an outpatient procedure. In our experience, as well as in other series, drug therapy is not often successful. When drug ther- apy is tried first, the time to ultimate cardioversion is often delayed several days, thus increasing the cost re- lated to hospitalization. In addition, the patient is ex- posed to the adverse effects and expense of the drugs. Therefore, we believe that elective DC cardioversion should be performed in most patients as the initial ther- apy in an outpatient or observational setting. In our extensive experience with DC cardioversion ( > 1,000 cardioversion procedures), we believe that an experi- enced respiratory therapist trained in intubation is all that is required for safe assistance. If an anesthesiolo- gist is mandated, the cost of cardioversion is signifi- cantly increased.

Hemodynamically stable atrial flutter should be treated with DC cardioversion using 200 J as an initial setting. This can be accomplished in an out- patient setting, saving the cost of hospitalization and avoiding the hazards of drug therapy.

1. Jolly WA, Ritchie WJ. Auriculat flutter and fibrillation. Heart 1910;2:177-221. 2. Suttorp MJ, Kingma H, Jessurum ER. The value of class IC antiarrhytbmic drugs for acute conversion of paroxysmal atrial fibrillation or flutter to sinus rhythm. 3 Am Co11 Curdiol 1990;16:1722-1727. 3. Lawn B, Amara Bingham R, Neuman J. New method for terminating cardiac arrhythmias. JAMA 1962;182:548-551, 4. Castellanos A, Lemberg L, Gosselin A, Fonseca EJ. Evaluation of counter- shock treatment of atrial flutter. Arch Intern Med 1965;115:426-433. 5. Frithz G, Aberg H. Direct current conversion of atrial flutter. Acta Med Scmd 1970;187:271-274. 6. Morris JJ, Kong Y, North WC, McIntosh HD. Experience with “cardiover- sion” of atrial fibrillation and flutter. Am J Cardiol 1964;14:94-100. 7. Tucker KJ, Wilson C. A comparison of tramesophageal atria1 pacing and direct current cardioversion for the termination of atrial flutter: a prospective, randomized clinical trial. Br Heart J 1993;69:530-535. 8. Peters RW, Weiss DN, Carliner NH, Feliciano Z, Shorofsky SR, Gold M. Overdrive pacing for atria1 flutter. Am J Cardiol 1994;74: 1021- 1023. 9. Calkins H, Leon AR, Dearn G, Kalbfleisch SJ, Langberg JL, Morady F. Catheter ablation of atrial flutter using radiofrequency energy. Am J Cardiol 1994;73:353-356. 10. VanGelder IC, Crijns HJ, VanGilst WH, Verwer R, Lie KI. Prediction of une- ventful cardioversion and maintenance of sinus rhythm from direct current electrical cardiovemion of chronic atrial fibrillation and flutter. Am J Cardiol1991;68:41-46. 11. Olshonsky B, Wilber DT, Hariman RJ. Atria1 flutter-update on the mech- anism and treatment. PACE 1992;15:2308-2335.

660 THE AMERICAN JOURNAL OF CARDIOLOGY’s’ VOL. 77 MARCH 15, 1996