Significance of External Cardioversion InducedAtrial TachyarrhythmiasBEATRICE BREMBILLA-PERROT, DANIEL BEURRIER, PIERRE HOURIEZ, ARNAUD TERRIERDE LA CHAISE, PIERRE LOUIS, MARC NIPPERT, YIAD MUHANNA, CHRISTINESELTON-SUTY, NICOLAS SADOUL, and MARIUS ANDRONACHEFrom the Department of Cardiology, CHU of Brabois, Vandoeuvre, France

BREMBILLA-PERROT, B., ET AL.: Significance of External Cardioversion Induced Atrial Tachyarrhyth-mias. External cardioversion is used to stop VT or VF in emergency. Supraventricular tachyarrhythmiasare sometimes noted after cardioversion in patients known to be previously in sinus rhythm. The purposeof the study was to evaluate the significance of supraventricular tachyarrhythmias induced by external car-dioversion. The study population consisted of 22 patients who developed supraventricular tachyarrhyth-mias after transthoracic cardioversion (300 J) delivered to stop a VT or VF induced by electrophysio-logical study. Defibrillation used monophasic waveform. Supraventricular tachyarrhythmias complicated6% of cardioversions for VT; before cardioversion, all patients were in sinus rhythm. After cardiover-sion, three patients developed a paroxysmal reentrant supraventricular tachycardia (PSVT), which wasstopped by atrial pacing. The remaining patients developed AF that lasted from 3 minutes to 24 hours(n = 4). One patient remained in AF. AF developed after a sinus pause or bradycardia, which was dueto the interruption of VT or VF in nine patients or was noted just when VT or VF stopped (n = 10). Theanalysis of clinical data indicated that all three patients who presented a PSVT had a history of PSVT.Among patients who developed a sinus pause dependent AF, two had a history of AF. Among ten pa-tients who developed AF at the time of cardioversion, three had a history of AF. During follow-up (1–9years), no patient without a history of AF developed spontaneous AF, but patients with history of tachycar-dias had arrhythmia recurrences. The mechanism of cardioversion related tachycardias can be a pauserelated dispersion of atrial refractoriness or an adrenergic reaction induced by VT or VF, factors thatprecipitate arrhythmias in patients with history of atrial arrhythmias (one third of patients). In conclu-sion, supraventricular tachyarrhythmia is relatively frequent after external cardioversion for ventriculartachyarrhythmia, has no prognostic significance in patients without previous history of atrial arrhyth-mias, but in those with history of tachycardias is associated with a high risk of recurrence. (PACE 2003;26:2111–2115)

cardioversion, atrial fibrillation

IntroductionAtrial fibrillation (AF) or atrial flutter can oc-

cur after successful high energy transthoracic di-rect current (DC) shock given to patients withventricular tachyarrhythmias.1−3 AF also has beenreported in patients receiving defibrillation andcardioversion shocks to the heart through epi-cardial patch electrodes4−7 and following shocksusing a transvenous endocardial lead system.8−10

The purpose of this study was to evaluatethe incidence and significance of supraventric-ular tachyarrhythmias induced by external car-dioversion, which is used to stop ventricular tach-yarrhythmias in patients known to be previouslyin sinus rhythm.

Address for reprints: Beatrice Brembilla-Perrot, M.D., Cardiol-ogy, CHU of Brabois, 54500 Vandoeuvre, France. Fax: 00-33-3-83154226; e-mail: b.brembilla-perrot@chu-nancy.fr

Received October 11, 2002; revised January 6, 2003; acceptedMarch 13, 2003.

Population and MethodsThe study population consisted of 22 patients

(20 men, 2 women; age 40–75 years, mean 58 ±8.5 years) who developed supraventricular tach-yarrhythmias after transthoracic cardioversion(300 J) delivered to interrupt ventricular fibrilla-tion (VF) or syncopal ventricular tachycardia (VT)induced during an electrophysiological study.These patients were from a consecutive populationof 382 patients in whom a transthoracic cardiover-sion was performed to stop a ventricular tach-yarrhythmia. Ventricular tachyarrhythmia was in-duced by a programmed ventricular stimulationindicated (1) after a myocardial infarction (MI)(>3 weeks) to evaluate the prognosis of the pa-tient,11 (2) in patients with documented VT to re-produce the clinical tachycardia, (3) in patientscomplaining of tachycardia but without docu-mented tachycardia to elucidate the cause of symp-toms, or (4) to evaluate the mechanism of un-explained syncope. One of these patients had aWolff-Parkinson-White (WPW) syndrome and was

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Table I.

Indication for Electrophysiological Study

Indication for Total CardioversionElectrophysiological Study Population Related SVT

Systematic after recent MI 243 8(> 3 weeks), nospontaneous VT

Spontaneous VT or VF 60 7after MI

Palpitations, no documented 45 3tachycardia + HD (no MI)

Evaluation of WPW syndrome 13 1Syncope/no HD 15 1Palpitations, no documented 6 2

tachycardia, no HD

MI = myocardial infarction; HD = heart disease; SVT =supraventricular tachycardia; VF = ventricular fibrillation; VT =ventricular tachycardia; WPW = Wolff-Parkinson-White syndrome.

studied for syncope; VF was induced by pro-grammed ventricular stimulation.12 The clinicalcauses of the patient requiring an electrophysio-logical study are summarized in Table I.

All patients were in sinus rhythm before car-dioversion.

Electrophysiological study was performed af-ter discontinuing antiarrhythmic drugs for at least5 half-lives of the drug.

Cardioversion was performed in patients afterloss of consciousness, no later than 2 minutes afterthe onset of the electrically induced VT or VF.

Defibrillation used a monophasic waveformand from 1 to 5 external shocks were performedwith an energy of 200–360 J until ventricular tach-yarrhythmia stopped. An energy of 200 J was se-lected for the first shock and increased to 300 Jand then to 360 J for subsequent shocks. Theinitial value of 360 J was at first used in pa-tients with a weight > 85 kg. The shock wasdelivered through anteroposterior adhesive elec-trodes which had been systematically positionedbefore programmed stimulation. DC shocks for VTwere synchronized. In two patients an endocardialshock was required to stop tachycardia and thesepatients were excluded.

All cardioversions were carried out by well-trained medical personnel. The cardiac rhythmwas continuously monitored before, during, andat least 3 minutes after cardioversion.

Statistical Analysis

The data were expressed as mean ± SD. Sta-tistical analysis was performed with the paired

Student’s t-test for quantitative data, with the chi-square test for discrete variables, and ordinal tests.A P value < 0.05 was considered statisticallysignificant.

ResultsIncidence of SupraventricularTachyarrhythmias After DC Shock

Supraventricular tachyarrhythmias compli-cated 6% of external cardioversions for VT.Three patients developed a reentrant paroxysmalsupraventricular tachycardia (PSVT), which wasstopped by atrial pacing. The tachycardia was re-lated to a atrioventricular nodal reentrant tachy-cardia (AVNRT) in two patients and a reentranttachycardia through an accessory pathway in thepatient with WPW syndrome.

The remaining patients developed AF thatlasted from 3 minutes to 24 hours (n = 4). Onepatient remained in permanent AF. Cardioversionwas later attempted but a prompt recurrence of AFwas noted and because the AF well tolerated, thepatient remained in permanent AF.

Analysis of Clinical Data

Patients with reentrant supraventriculartachycardia (SVT) induced cardioversion were intachycardia just after cardioversion (n = 2) or 5seconds later after a sinus bradycardia (n = 1).Two patients had no underlying heart disease andone patient had large sequelae of MI. All patientshad a history of paroxysmal tachycardias. Onepatient had WPW syndrome. Two-dimensionalechocardiogram showed a normal atrial size in allpatients.

AF induced cardioversion developed after asinus pause or bradycardia which followed the endof VT in nine patients (Fig. 1). Three patients hadno heart disease, 6 had underlying heart disease,1 had hypertrophic cardiomyopathy, and 5 patienthad old MIs. Two patients had a history of AF. Oneof them, who remained later in chronic atrial fibril-lation, had an enlarged atrial size (diameter 50-mmlong-axis at TM echocardiogram). AF induced car-dioversion was noted when VT stopped in ten pa-tients (Fig. 2). Of these patients, two had no heartdisease and eight had heart disease that was cor-rected by tetralogy of Fallot (n = 1) and old MI(n = 7).

Comparisons of Clinical Data of Patients WhoDid or Did Not Develop AF After Cardioversion

Table II shows the data of patients withor without cardioversion related supraventriculartachyarrhythmias. Age, sex, the presence of heartdisease, left ventricular ejection fraction, left atrial

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Figure 1. Complete atrioventricular block following external cardioversion and then atrial fibrillation.

size, postcardioversion pause, and the energydelivered to stop the ventricular tachyarrhyth-mia were similar in both groups. The inci-dence of previous history of supraventriculartachyarrhythmias was significantly (P < 0.001)higher in patients who developed a SVT after car-

Figure 2. Atrial fibrillation occurring just after interruption of ventricular tachyarrhythmia by external cardioversion.

dioversion than in those who remained in sinusrhythm.

Follow-UpNo patient without history of AF developed

spontaneous atrial tachyarrhythmias during the

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Table II.

Comparison of Patients with and Without Cardioversion Related Supraventricular Tachyarrhythmia

Cardioversion Related No CardioversionSupraventricular Related Supraventricular

Data Tachyarrhythmia Tachyarrhythmia Comparison

Number 22 360Age 58 ± 8.5 59 ± 11 NSFemale sex 9% 8% NSHeart disease 82% 92% NSLeft atrial size 40 ± 5 mm 38 ± 6 mm NSLVEF 45 ± 12% 43 ± 13% NSPostcardioversion pause > 2 seconds 18% 11% NSEnergy 300 ± 20 J 310 ± 25 J NSHistory of Supraventricular tachyarrhythmia 36% 5% P < 0.001

***P < 0.0001. LVEF = left ventricular ejection fraction; NS = non significant.

1- to 9-year follow-up. Patients with a historyof supraventricular tachyarrhythmias still had ar-rhythmic recurrences and were treated with antiar-rhythmic drugs and/or β-blockers.

DiscussionThe occurrence of a supraventricular tach-

yarrhythmia after external cardioversion for ven-tricular tachyarrhythmias is relatively frequent(6%). This incidence is higher than in previ-ous studies concerning external cardioversion.Waldeker et al.,3 in a series of 99 patients treatedfor ventricular tachyarrhythmias, showed thatonly one patient developed AF, and another pa-tient had circus movement incorporating an acces-sory atrioventricular pathway. In patients with epi-cardial leads, the incidence of AF or atrial flutterinduced by implantable defibrillator shocks wassimilar to the incidence observed in the presentstudy (5%).7 This incidence in patients with endo-cardial leads varied from 0%7 to 2.6%9 or 10.3%8

or 23% in other studies.10 These variations couldbe related to the nature of the atrial electrode andthe possible detection of the atrial electrogram toavoid delivering shocks during the vulnerable pe-riod of the atria; ventricular shocks could induceAF if they are timed between an atrial effective re-fractory period of − 60–40, − 40–60, − 40–60, and− 20–60 ms in the epicardial monophasic, epicar-dial biphasic, endocardial monophasic, and endo-cardial biphasic configurations, respectively.13

The potential mechanisms of shocked in-duced supraventricular tachyarrhythmias are de-batable. In the present study, the cardioversion re-lated supraventricular tachyarrhythmias could bedue to the pause related dispersion of atrial refrac-toriness (9/19) or to an adrenergic reaction to VT,

factors facilitating arrhythmias in patients with ahistory of SVT, or to the energy delivery during theatrial vulnerable period.

This last mechanism is generally consideredas the main cause of AF or atrial flutter induced byventricular defibrillator shocks; for Katz et al.,13

the mechanism postulated for AF induction byventricular cardioversion or defibrillation is en-ergy delivery during the atrial vulnerable period.In the present study, other causes could be morefrequent. Several studies has previously reportedon the relationships between the neurocardio-genic system and supraventricular tachyarrhyth-mias.14−16 Supraventricular tachyarrhythmia canbe pause dependent with different causes of ar-rhythmias as an effect of vagal activity or increaseand dispersion of atrial refractoriness and con-duction velocity; supraventricular tachyarrhyth-mia can be adrenergic related with a decrease anda dispersion of atrial refractoriness and conduc-tion velocity. Recently,16 AF was shown to dependon the variations of the autonomic tone with a pri-mary increased tone followed by an abrupt shift to-ward vagile predominance. This phenomenon wasdemonstrated to occur after rapid ventricular pac-ing.17 In patients with preserved autonomic tone,a sinus tachycardia related to adrenergic tone andthen a sinus bradycardia related to vagile tone wasreported at the termination of a rapid ventricularpacing (200 beats/min). This mechanism could beapplied in the present study. However, the patientsin the present study who developed cardioversioninduced AF and who had a history of AF did nothave a clear correlation with a vagal or adrenergicoccurrence of their tachycardias.

The only factor which was significantly pre-dictive for cardioversion induced supraventricular

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tachyarrhythmias was the history of previous clin-ical occurrence of SVT. Therefore, in those witha history of AF who develop a cardioversion in-duced AF and who remain in AF a second car-dioversion after general anesthesia or an internalcardioversion at low energy should be discussed.In addition, in these patients who had inducibleventricular tachyarrhythmias and in whom an im-plantable cardioverter defibrillator is indicated,the risk of supraventricular tachyarrhythmias ishigh. Atrial therapy with use of atrial pacingshould also be discussed. Recent studies report areduction of atrial arrhythmia burden in such pa-tients.18,19 A specific algorithm to prevent postcar-dioversion pause and therapies using burst pac-ing to stop the supraventricular tachyarrhythmiashould be discussed.20

ConclusionsSupraventricular tachyarrhythmia is rela-

tively frequent after external cardioversion for ven-tricular tachyarrhythmia; AF can persist for sev-eral hours and requires immediate reduction. Inpatients without a previous history of supraven-tricular tachyarrhythmias, the cardioversion in-duced supraventricular tachyarrhythmias have noprognostic significance. In those with a historyof supraventricular tachyarrhythmias, the recur-rence of the tachycardia might be expected aftercardioversion. The mechanisms are multiple and41% of them had pause dependent supraventricu-lar tachyarrhythmias. The risk and its preventioncan be applied to the patients with implantablecardioverter defibrillators in whom a specific al-gorithm of pacing can be discussed.

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