doi:10.1016/j.e

848

ATRIAL FIBRILLATION

New Insights Into the Predictors of Left AtrialStunning After Successful Direct-Current

Cardioversion of Atrial Fibrillation and FlutterRowlens M. Melduni, MD, FACC, FASE, Joseph F. Malouf, MD, FACC,

Krishnaswamy Chandrasekaran, MD, FACC, FASE, Charles J. Bruce, MD, FACC,Roger D. White, MD, Kwan-Kin Law, MD, Faisal O. Al Atawi, MD,

Virend K. Somers, MD, PhD, Bernard J. Gersh, MBChB, DPhil, David O. Hodge, MS,Paul A. Friedman, MD, FACC, James B. Seward, MD, FACC, FASE, and

Naser M. Ammash, MD, FACC, Rochester, Minnesota

Background: Direct-current cardioversion (DCCV) of atrial fibrillation and atrial flutter commonly causespost-DCCV left atrial (LA) stunning (LAS), which may potentiate thromboembolic complications. Data on LASdeterminants are inconclusive.

Methods: We prospectively evaluated LA and LA appendage function before and immediately after DCCV ofatrial fibrillation and atrial flutter in 59 consecutive patients undergoing transesophageal echocardiographi-cally guided DCCV to determine predictors of post-DCCV LAS.

Results: After exclusion of patients with pre-DCCV LAS (LA appendage emptying velocity �20 cm/s),post-DCCV LAS was observed in 32 of 45 patients (71%). Only precardioversion mitral E-wave decelerationtime significantly correlated with post-DCCV LAS (142 � 46 vs 170 � 360 milliseconds; P � .04). At 3.3 years,there was a trend toward a higher arrhythmia recurrence rate in patients with LAS compared with thosewithout (86% vs 53%; P � .063).

Conclusion: Only mitral E-wave deceleration time was predictive of post-DCCV LAS, which may be a markerof atrial fibrillation and atrial flutter recurrence.

Keywords: Atrial fibrillation, Atrial flutter, Atrial stunning, Cardioversion, Transesophageal

echocardiography

Atrial fibrillation (AF) is the most common arrhythmia encounteredin clinical practice and is often associated with adverse clinicalconsequences, including palpitations, stroke, heart failure, and re-duced quality of life. Although restoration of sinus rhythm improvescardiac hemodynamics and alleviates symptoms, direct-current car-dioversion (DCCV) of AF1,2 and, to a lesser extent, atrial flutter(AFL)3 is commonly associated with post-DCCV left atrial (LA)mechanical dysfunction, commonly referred to as LA stunning (LAS).This phenomenon may be associated with acute thrombus forma-tion1,3 and may be the underlying mechanism of post-DCCV throm-boembolic events.1,2,4 Previous studies have suggested that LASoccurs immediately after DCCV and is characterized by a reductionin LA appendage (LAA) emptying velocity (LAAEV) and the devel-

From the Division of Cardiovascular Diseases (R.M.M., J.F.M., K.C., C.J.B.,K.-K.L., F.O.A.A., V.K.S., B.J.G., P.A.F., J.B.S., N.M.A.), the Division of Cardio-vascular and Thoracic Anesthesia (R.D.W.), and the Division of Biostatistics(D.O.H.) Mayo Clinic, Rochester, Minnesota.

Reprint requests: Rowlens M. Melduni, MD, FACC, FASE, Division of Cardiovas-cular Diseases, Mayo Clinic, 200 First St SW, Rochester, MN 55905 (E-mail:melduni.rowlens@mayo.edu).

0894-7317/$34.00

Copyright 2008 by the American Society of Echocardiography.

cho.2007.12.001

opment of spontaneous echocontrast.1,2 Although the duration ofthe preceding AF and AFL has been reported as the most importantdeterminant of stunning,5,6 severe LAS has occurred in animalmodels even after brief periods (60 minutes) of AF and AFL7 and inpatients with severe precardioversion atrial dysfunction regardless ofthe duration of the arrhythmia.8-11 These observations suggest thatassessment of LA function before cardioversion may help to identifypatients at risk of LA dysfunction predisposing to thromboembolismafter reversion of AF or AFL to sinus rhythm.

Studies investigating LAmechanical function after cardioversion ofAF and AFL have been limited by their use of indirect measures of LAfunction (peak mitral A-wave velocity and atrial ejection force) ortheir paucity of patients.1-3,5,8,11 Hence, the results do not allowdefinitive conclusions regarding the determinants of LAS. In addition,immediately after cardioversion, the relatively large LA may notgenerate detectable flow velocities by Doppler assessment of mitralinflow velocities. However, the relatively small LAA can generategreater flows with the same contractile force. Thus, the LAAEV mayprovide a more accurate reflection of LAmechanical activity than themitral inflow velocity. Therefore, our objective was to prospectivelystudy the clinical and echocardiographic predictors of LAS by use oftransthoracic echocardiography and transesophageal echocardiogra-phy (TEE) before cardioversion of AF and AFL and by use of TEE

immediately after DCCV.

Journal of the American Society of Echocardiography Melduni et al 849Volume 21 Number 7

METHODS

The study was approved by the Mayo Clinic Institutional ReviewBoard, Rochester, MN, and written informed consent was obtainedfrom all participants.

Patient SelectionPatients with AF or AFL undergoing TEE-guided DCCV in the MayoClinic Cardioversion Unit at Saint Marys Hospital, Rochester, MN,were prospectively studied between October 2000 and October2002. Patients were excluded from the study for any of the followingreasons: (1) patient had rheumatic heart disease or a prosthetic heartvalve; (2) patient was pregnant or suspected to be pregnant; (3)patient was at risk of esophageal injury or aspiration (eg, history ofreflux, obesity, reduced upper airway protective reflexes, or by thediscretion of the anesthesiologist); or (4) patient was believed by theanesthesiologist to potentially have a difficult airway to maintainduring the conduct of general anesthesia. Of the 1127 consecutivepatients evaluated during the 2-year recruitment period, 407 patientswere eligible for the study. A total of 89 patients gave informedconsent to participate in the study; of these, 27 patients wereexcluded owing to concerns raised by the anesthesiologist aboutairway issues, and in 3 other patients the TEE procedure was abortedowing to hemodynamic compromise. The remaining 59 patientsenrolled were observed through September 2006.

Relevant demographic and clinical data were collected, includingage, sex, duration of arrhythmia, hypertension, and concomitant useof any of the following drugs: antiarrhythmic drugs in class IA(quinidine, procainamide, and disopyramide), IC (propafenone andflecainide), or III (amiodarone, sotalol, ibutilide, and dofetilide);�-blockers; calcium channel blockers; statins; angiotensin-convertingenzyme inhibitors; or angiotensin receptor blockers.

ElectrocardiographyA standard precardioversion 12-lead surface electrocardiogram re-corded at a speed of 25 mm/s and an amplitude of 1 mV/cm wasperformed for all patients and reviewed by an experienced cardiolo-gist or electrophysiologist. Electrocardiograms with low-amplitudeF waves and irregularly irregular R-R intervals were classified as AF,and electrocardiograms with classic regular F waves or F waves thatwere quasiregular with regularly or irregularly irregular R-R intervalswere classified as AFL. Determination of the duration of AF or AFLwas based on the onset of symptoms and the time of documentationof arrhythmia on the electrocardiogram.

Precardioversion Echocardiography ProtocolTEE was performed immediately before cardioversion with commer-cially available ultrasonographic instruments (Sonos 5500, Phillips,Andover, MA, or Acuson Sequoia, Siemens, Mountain View, CA)and a multiplane probe. The TEE examination, including patientpreparation, has been previously described.12,13 All patients werefasting and were therapeutically anticoagulated with intravenousheparin or warfarin. Before DCCV, patients were assessed with TEEfor intracardiac thrombus (an echodense intracavitary mass distinctfrom the underlying endocardium and not caused by pectinatemuscles), spontaneous echocontrast (dynamic smokelike echoeswithin the atrial cavity with a characteristic swirling motion that couldnot be eliminated by changes in gain settings), significant valvulardisease (more than moderate regurgitation or stenosis), left ventricu-lar (LV) function, pulsed wave Doppler mitral inflow (mitral E-wave

velocity and deceleration time), pulmonary vein flow (peak systolic

and diastolic velocities and systolic and total forward flow timevelocity integrals), and LAAEV. The LAAEV profiles were assessed bypulsed wave Doppler interrogation with a sample volume positioned1 to 2 cm within the orifice of the LAA. The peak LAAEV measure-ments were performed offline using integrated echocardiographicsoftware, and the data were averaged for 5 consecutive cycles. TheLA volume index (biplane area-length method) was measured bytransthoracic echocardiography performed within 1 month of cardio-version while patients were in AF or AFL.

Cardioversion Protocol

If no intracardiac thrombus or dense spontaneous echocontrast(sludge) was detected, the attending anesthesiologist anesthetized thepatient with sodium thiopental, and DCCV was applied according tothe established guidelines of the cardioversion unit, using a biphasiccardioversion protocol with the TEE probe left in the midesophagus.Shock protocols used a step-upmethod of 50, 75, 100, 120, 150, and200 J with a biphasic defibrillator (M Series, Zoll Medical Corp,Chelmsford, MA), which uses a biphasic rectilinear waveform de-signed to maintain a relatively constant current during the first phase.Patients who did not achieve cardioversion with the maximal shockfrom the device could receive the maximal shock from a differentdevice (Lifepak 12, Medtronic Physio-Control International Corp,Redmond, WA), which uses a biphasic truncated exponential wave-form that compensates for impedance by adjusting the leading-edgevoltage and pulse durations. A special mask, which permitted esoph-ageal intubation and delivery of high-flow oxygen to ventilate thepatient without compromising the procedure, was used. Electrocar-diograms and oxygen saturation by pulse oximetry were monitoredcontinuously during the procedure. Successful DCCV was defined asthe patient having sinus rhythm when discharged from the cardiover-sion unit. Recorded data included the amount of delivered energyand the success in restoring sinus rhythm for each shock, the numberof shocks, and the total energy delivered.

Postcardioversion Echocardiography Protocol

Immediately after DCCV, the following TEE variables were recorded:presence of spontaneous echocontrast, de novo thrombus formationin the LA or LAA, mitral E-wave and A-wave velocities, total mitraldiastolic forward flow time velocity integral and A-wave time velocityintegral, mitral E-wave deceleration time, peak systolic and diastolicpulmonary vein flow velocities, total pulmonary vein forward flowtime velocity integral, pulmonary vein atrial flow velocity, and peaklate (post-A wave) LAA diastolic emptying velocity. Measurementswere performed offline using integrated echocardiographic software,and the data were averaged for 5 consecutive cycles. LAS wasdefined as LAA peak late diastolic emptying velocities less than 20cm/s, a predictor of the development of spontaneous echocontrastand thromboembolic events.14-16 All patients were anticoagulatedaccording to the American College of Cardiology/American HeartAssociation/European Society of Cardiology guidelines.17 Patientswith AF or AFL for 48 hours or longer began anticoagulation in theCardioversion unit and were referred to the Mayo Clinic Thrombo-philia Center, Rochester, MN, on discharge for monitoring andmanagement of their anticoagulation. An international normalizedratio between 2.0 and 3.0 for 4 weeks was recommended for patientswho remained in sinus rhythm; otherwise, anticoagulation was con-tinued indefinitely. Antiarrhythmic drug therapy was left to the

discretion of the patient’s physician.

850 Melduni et al Journal of the American Society of EchocardiographyJuly 2008

Follow-upFollow-up data were obtained by electronic chart reviews from thecomprehensive medical record of the database of the Mayo Clinic,Rochester, MN, to determine arrhythmia recurrence and stroke rates.The patients’ 12-lead electrocardiograms were reviewed to docu-ment the time to the first arrhythmia recurrence. Stroke occurrencewas based on documented clinical signs of focal (or global) distur-bance of cerebral function and results of radiographic examination,including computed tomographic scan or magnetic resonance imag-ing findings. The mean follow-up period was 3.3 years.

Statistical AnalysisCategorical variables were compared between groups using the �2

test for independence or the Fisher exact test if the numbers weresmall. Continuous variables were compared using the Wilcoxon ranksum test. Correlations among the velocity factors were investigatedusing the Spearman correlation coefficient. Continuous data wereexpressed as mean � SD. The factors analyzed included the clinicaland echocardiographic variables mentioned above. The cumulativeprobability of AF and AFL recurrence was estimated using theKaplan-Meier method. The comparison of this probability betweenpatients with and without atrial stunning was completed using a logrank test. A P value less than .05 was considered statistically signifi-cant. Patients with precardioversion LAAEV less than 20 cm/s wereconsidered to have pre-existing LAS and were, therefore, excludedfrom the analysis.

RESULTS

Patient CharacteristicsBaseline clinical and echocardiographic characteristics of the patientsare summarized in Tables 1 and 2. The mean age was 69 � 12 years;76% (45 of 59) were male, 56% (33 of 59) had a history ofhypertension, 78% (46 of 59) had AF, and 22% (13 of 59) had AFL.

Table 1 Baseline clinical characteristics of the studypopulation (N � 59)

Characteristic Value

Age (y) 69.0 � 12.0Male 45 (76%)Duration of arrhythmia

�24 h 1 (2%)�24-48 h 1 (2%)�2-7 days 16 (27%)�1-4 wk 10 (17%)�1-12 mo 25 (43.9%)�12 mo 4 (7.0%)

Hypertension 33 (56%)Use of medication

�-Blocker 25 (42%)Calcium channel blocker 21 (36%)Antiarrhythmic drug 19 (32%)Digoxin 10 (17%)Statins 20 (34%)ACE-I or ARB 20 (34%)

ACE-I, Angiotensin-converting enzyme inhibitor; ARB, angiotensin re-ceptor blocker.Continuous data are presented as mean � SD; categorical data asnumber of patients and percentage of sample.

Approximately equal proportions of patients had their arrhythmia

from 2 days to 4 weeks and from 1 to 12 months. Only a minority ofpatients had AF or AFL outside these time frames (�48 hours or �1year). At electrical cardioversion, approximately one-third were tak-ing a �-blocker (42%), a calcium channel blocker (36%), or anotherantiarrhythmic drug (32%). Types of antiarrhythmic drugs usedincluded class IA (quinidine, 0%; procainamide, 2%; disopyramide,0%), class IC (propafenone, 10%; flecainide, 2%), and class III(amiodarone, 14%; sotalol, 7%; ibutilide, 0%; dofetilide, 0%). Signif-icant valvular heart disease was present in 10% of the patients (5 hadmitral regurgitation and none had aortic valve disease). The meanbaseline emptying velocity was 31.2 � 15.8 cm/s. Data on the LAvolume index were available for 34 of 59 patients (58%); the meanvalue was 43.1 � 24.3 mL/m2. DCCV successfully restored sinusrhythm in all 59 patients.

Incidence and Predictors of LASThe relationship of LAS to the precardioversion clinical and echocar-diographic predictors is shown in Tables 3 and 4.

With the exclusion of patients with precardioversion LAAEV lessthan 20 cm/s (n � 14; 24%), LAS occurred in 32 of 45 patients(71%) immediately after restoration of sinus rhythm (Figure 1). Thiswas associated with spontaneous echocontrast in 21 patients (47%)and thrombus in one patient (3%), with a trend toward morespontaneous echocontrast in the LAS group compared with thegroup without LAS (53% vs 31%, P � .17). No thrombus orspontaneous echocontrast was found on precardioversion TEE in 14of the 32 patients (44%) who had LAS after cardioversion. Only theprecardioversion mitral E-wave deceleration time was predictive ofLAS (142 � 46 vs 170 � 36 milliseconds in patients without LAS;P � .04). This observation most likely reflects higher LA pressure orelevated LV end-diastolic pressure in the stunning group. There wasno correlation between the occurrence of post-DCCV LAS andnumber of shocks, total energy applied, duration of arrhythmia, age,LV ejection fraction, or �-blocker or antiarrhythmic drug use.

Postcardioversion Echocardiographic Variables of theStudy PopulationThe post-DCCV echocardiographic variables are shown in Table 5.

Table 2 Baseline precardioversion echocardiographiccharacteristics of the study population (N � 59)

Characteristic Value

Significant valvular disease (�moderate mitralregurgitation)

5 (8%)

Spontaneous echocontrast (n � 47) 31 (66%)Left atrial volume index (mL/m2) (n � 34) 43.1 � 24.3Left atrial appendage velocity (cm/s) 31.2 � 15.8Mitral E-wave velocity (cm/s) 88.4 � 29.0Mitral E-wave deceleration time (ms) 153.6 � 45.4Pulmonary vein peak systolic velocity (cm/s) 28.5 � 14.4Pulmonary vein peak diastolic velocity (cm/s) 42.5 � 16.6Pulmonary vein systolic-diastolic velocity ratio 0.70 � 0.32Pulmonary vein systolic TVI (cm) 4.8 � 2.9Pulmonary vein diastolic TVI (cm) 11.7 � 5.4Pulmonary vein systolic-diastolic TVI ratio 0.42 � 0.26

TVI, Time-velocity integral.Continuous data are presented as mean � SD; categorical data asnumber of patients and percentage of sample. Unless indicated other-wise, N � 59.

We observed a significantly lower mean percentage reduction in

Journal of the American Society of Echocardiography Melduni et al 851Volume 21 Number 7

LAAEV (60% � 17% vs 4% � 58%, P � .001) and percentagemitral A-wave velocity (35% � 22% vs 57% � 35%, P � .04) inaddition to a trend toward lower mitral A-wave velocity (25.3 � 18.1vs 33.6 � 16.3 cm/s, P � .06) in patients with LAS compared withthose without LAS, which is consistent with LA and LAAmechanicaldysfunction. The overall mean percentage reduction in post-DCCVLAAEV was 44% � 42%. Post-DCCV LAS was found in 12 of 14patients (86%) with precardioversion LAAEV less than 20 cm/s. Thepost-DCCV pulmonary vein peak systolic velocity was significantlyless in patients with LAS than in those without LAS (29.8 � 17.4 vs43.7 � 17.3 cm/s, P � .02), reflecting higher LA pressure in thepatients with LAS. There was no difference in the pulmonary veinflow reversals or mitral E-wave deceleration time between the twogroups. These findings were likely the result of increased preloadamong the patients without LAS from the additional atrial kick,resulting in pronounced pulmonary vein atrial flow reversal commen-surate with a shortening of the mitral deceleration time, negating thestatistical effect one would expect in patients with LAS because ofhigher LV filling pressure.

OutcomesThe overall arrhythmia recurrence rates at 1, 2, and 3 years were57%, 67%, and 78%, respectively, regardless of antiarrhythmictherapy at discharge. The 3-year recurrence rate of AF or AFL forpatients who were receiving antiarrhythmic drug therapy at dischargecompared with those who were not was very similar (82% vs 67%,P � .97). However, after a mean follow-up of 3.3 years, the rate ofrecurrence of AF or AFL appeared to be higher in patients with LASthan in those without LAS (86% vs 53%, P � .063). There were twostrokes, both in the LAS group (6%). These effects were more evident4 years after DCCV (Figure 2).

DISCUSSION

Main FindingsThis study demonstrates that LAS after DCCV is a quantifiablephenomenon that is common, occurring in 71% of cases immedi-ately after restoration of sinus rhythm. This finding underscores the

Table 3 Univariate clinical predictors of left atrial stunning(n � 45)

VariableStunning(n � 32)

No stunning(n � 13) P value

Male 24 (75%) 11 (85%) .48Age (y) 69 � 11 66 � 17 .97Onset �4 wk 15 (47%) 7 (54%) .56Hypertension 18 (56%) 6 (46%) .54Valve disease 5 (16%) 0 .30Dilated cardiomyopathy 5 (16%) 2 (15%) .98Ischemic cardiomyopathy 6 (19%) 1 (8%) .35�-Blockers 13 (41%) 8 (62%) .20Calcium channel blockers 10 (31%) 7 (54%) .16Antiarrhythmics 9 (28%) 5 (38%) .50Statins 10 (31%) 4 (31%) .97ACE-I or ARB 9 (28%) 6 (46%) .25

ACE-I, Angiotensin-converting enzyme inhibitor; ARB, angiotensin re-ceptor blocker.Continuous data are presented as mean � SD; categorical data asnumber of patients and percentage of sample.

importance of continuing anticoagulation in the postcardioversion

period to prevent de novo thrombus formation and to reduce the riskof subsequent embolic events.18 We found that LAS occurs morecommonly in patients with elevated filling pressure, which wasmanifested by a short mitral E-wave deceleration time. This suggeststhat the already tense LA may not be able to handle the increasedhemodynamic load that occurs with synchronized atrial contractionafter cardioversion as it converts from a conduit to a pumpingchamber.

In this study, LAS appears to be a marker of AF and AFLrecurrence after DCCV. Although the recurrence rate of AF and AFLwas similar when compared with the rates in previous reports,19-21

findings from patients with LAS trended toward higher recurrencerates than those from patients without LAS. This most likely suggestsmore severe disease in the LAS group as reflected by higher LVend-diastolic pressure.

Predictors of LASIn our study, the only significant echocardiographically measuredpredictor of LAS is a significantly shorter precardioversion mitralE-wave deceleration time recorded during AF or AFL. This is mostlikely a reflection of higher LA pressure or reduced LV compliance inpatients with LAS. Because the mitral E-wave deceleration time isconsidered a measure of net atrioventricular compliance, it may belogical to postulate that LAS is affected by the hemodynamic diastolicproperties of the LV irrespective of systolic function. This may explainwhy the LAS group had a lower (but not statistically significant)pulmonary vein systolic-diastolic velocity ratio. Reduced systolic flowin the pulmonary veins, commonly observed in AF and AFL, couldalso reflect a higher LA pressure congruent with the shorter mitralE-wave deceleration time. Although not statistically significant be-tween the two groups, the lower LV ejection fraction in the stunninggroup probably reflects more advanced disease.

Previous Related WorkPrevious studies have reported conflicting results regarding the pre-dictors of atrial stunning.3,5 Manning et al,5 using serial transthoracicDoppler studies, evaluated the time course of the recovery of LAmechanical function after successful cardioversion of AF to sinusrhythm in 60 patients and found that the duration of the precedingAF was the most important determinant of atrial stunning. Con-versely, in a prospective study of 47 patients with AFL, Irani et al3

found that the duration of AFL was not a predictor of postcardiover-sion atrial stunning. Similarly in our study, unlike the study byManning et al,5 there was no relationship between the duration of AFor AFL and the development of LAS after cardioversion. This differ-ence may be related to the different methods used to assess atrialfunction. In the study reported by Manning et al,5 the mitral A wavewas used to assess atrial function. The mitral A velocity is an indirectmeasure of LA function. It has multiple determinants, which areindependent of LA contractility, including LV diastolic characteristicsand loading conditions, whereas in our study we used the LAAEV.Although LAAEV is not a load-independent index, it is a directmeasure of LAA function and, hence, a reflection of global LAfunction.22 Moreover, as many as 50% of cases of AF or AFL can besilent. Therefore, the pre-existing state or the duration of AF or AFLcannot be ascertained or even assumed in many patients undergoingDCCV because it is based mainly on symptomatic episodes.23-25

Potential Mechanisms of LASThe mechanism of LA mechanical contractile dysfunction immedi-

ately after restoration of sinus rhythm is not clearly understood.

Color figure online.

LA, Left atrial; LAA, left atrial appendage; LVEF, left ventricular ejection fracContinuous data are presented as mean � SD; categorical data as number

852 Melduni et al Journal of the American Society of EchocardiographyJuly 2008

Several experimental and clinical studies have provided insights intothis phenomenon. Consistent with a previous report,26,27 our studydemonstrates that atrial function is not affected by electrical energy ornumber of shocks applied to restore sinus rhythm, suggesting that thisphenomenon is related to the restoration of sinus rhythm itself. LAAflow velocity decreases even after pharmacologic and spontaneouscardioversion of AF or AFL to sinus rhythm.6,28,29 These observa-tions suggest that this transitional atrial dysfunction likely results fromphysiologic atrial remodeling after restoration of sinus rhythm. Thecurrent study implicates that elevated LV filling pressure beforecardioversion may be a significant contributor to the mechanism ofLAS.

Other studies have suggested that the rapid cellular membranedepolarization of AF and AFL causes intracellular calcium over-load in the atria.30 Therefore, this process may result in down-regulation of calcium receptors and a subsequent decrease ofcalcium sensitivity in the atria. Restoration of sinus rhythm prob-ably eliminates the state of calcium overload, resulting in atransient deficit of calcium and in atrial hypocontractility untilcontractile materials, including calcium receptors, have been re-stored to their basal levels.31

Clinical ImplicationsThe risk of LAS can be determined before cardioversion by echocar-diography. Our data showed that 24% of patients with AF and AFLhad LAAEV less than 20 cm/s even before DCCV. LAS was ob-served in 86% of these patients immediately after DCCV. Thisfinding suggests that patients who are at high risk of postcardioversionLAS (eg, high LV filling pressure), as determined by precardioversionechocardiography, should undergo the usual anticoagulation for 3 to4 weeks before cardioversion even if the duration of AF or AFL is lessthan 48 hours.

Our data also showed that LAS does not occur in all patients afterDCCV and that duration of AF or AFL does not predict LAS afterelectrical cardioversion. These findings raise several important ques-tions. First, should precardioversion variables, as measured by echo-cardiography, be the determining factor for timing of cardioversionrather than duration of AF or AFL, a variable mainly based onsymptomatic episodes, which cannot be ascertained in 50% of thecases? Second, do all patients with AF or AFL of more than 48 hours

ing (n � 45)

� 32) No stunning (n � 13) P value

%) 4 (31%) .121 42.3 � 20.5 .27

86 � 14 .35170 � 36 .0436 � 17 .1640 � 12 .80

7 0.91 � 0.40 .082 5.77 � 3.51 .391 12.68 � 5.31 .464 0.43 � 0.12 .30(n � 18) 35 � 11 (n � 9) .70

55 � 12 .122.7 � 2.1 .96188 � 159 .9994 � 58 .75

tion; TVI, time-velocity integral.of patients and percentage of sample.

Figure 1 Doppler flow velocity profiles in left atrial appendage(LAA) before (A) and immediately after (B) direct-current cardio-version in patient with atrial fibrillation, illustrating atrial stunningphenomenon. Note marked reduction in late (post-A wave) LAAdiastolic emptying velocity after restoration of in sinus rhythm.

Table 4 Univariate echocardiographic predictors of left atrial stunn

Variable Stunning (n

Spontaneous echocontrast 18 (56LAA emptying velocity (cm/s) 33.3 � 11.Mitral E-wave velocity (cm/s) 84 � 30Mitral E-wave deceleration time (ms) 142 � 46Pulmonary vein systolic velocity (cm/s) 28 � 13Pulmonary vein diastolic velocity (cm/s) 40 � 16Pulmonary vein systolic-diastolic velocity ratio 0.72 � 0.2Pulmonary vein systolic TVI (cm) 4.61 � 2.8Pulmonary vein total TVI (cm) 10.61 � 4.8% Pulmonary vein systolic TVI (cm) 0.45 � 0.3LA volume index (mL/m2) 41 � 21LVEF (%) 49 � 15No. of shocks 2.3 � 1.2Total electrical energy (J) 170 � 133Maximal electrical energy (J) 85 � 56

need anticoagulation after DCCV to reduce the risk of thromboem-

Journal of the American Society of Echocardiography Melduni et al 853Volume 21 Number 7

bolic events caused by LAS as recommended by the AmericanCollege of Chest Physicians and the American College of Cardiology/American Heart Association/European Society of Cardiology? Third,rather than the usual one-size-fits-all approach, should anticoagula-tion therapy be individualized for patients undergoing electricalcardioversion?

Study LimitationsAlthough the current investigation is one of the largest prospectivestudies of LAS in a mixed population, the sample of 59 patients isrelatively small when compared with the number of patients in thecardiology literature; this may explain why not all differences in thestudied covariates were statistically significant. The duration of AFand AFL was unequally distributed. We suggest caution in interpret-ing the negative association of duration of AF or AFL as a predictor ofLAS. Another limitation is that the study population included patients

Table 5 Postcardioversion echocardiographic variables of thestunning)

Variable Stunn

Spontaneous echocontrast 1Acute thrombus formationLAAEV (cm/s) 12.5Mean reduction in post-DCCV LAAEV (%) 6Mitral E-wave velocity (cm/s) 77Mitral E-wave deceleration time (ms) 150Mitral A-wave velocity (cm/s) 25% Mitral A-wave velocity 3Mitral A-wave TVI 2Pulmonary vein peak systolic velocity (cm/s) 29Pulmonary vein peak diastolic velocity (cm/s) 38Pulmonary vein systolic-diastolic velocity ratio 0.7Pulmonary vein systolic TVI (cm) 4Pulmonary vein diastolic TVI (cm) 10Pulmonary vein systolic-diastolic TVI ratio 0.4Pulmonary vein atrial reversal (n � 32) 13

DCCV, Direct-current cardioversion; LAAEV, left atrial appendage emptyiContinuous data are presented as mean � SD; categorical data as nn � 45.

Figure 2 Arrhythmia recurrence after cardioversion in patientswith and without left atrial stunning (LAS) (Kaplan-Meier test,P � .063). AF, Atrial fibrillation; AFL, atrial flutter.

with both AF and AFL. This may have influenced our findings

because the association of LAA dysfunction after DCCV is not asstrong in AFL as in AF.32 The correlation of transmitral decelerationtime with LAS identified in our study strongly suggests that thisphenomenon is associated with diastolic dysfunction and elevatedLA pressure at the time of cardioversion. LA volume or LA areameasurements to support this observation were not available for 25patients. However, in the remaining 34 patients, the LA volumeindex did not differ between the two groups. Mitral annular tissueDoppler velocity, a relatively load-independent variable comparedwith mitral E-wave deceleration time, was not available. Severalfactors other than atrial function can influence the mitral E-wavedeceleration time, including the loading conditions of the heart,ventricular compliance, heart rate, and appropriate placement of thesample volume. Therefore, the mitral E-wave deceleration time maynot be a direct or ideal measure of atrial function. Despite a cleartrend toward a higher arrhythmia recurrence rate in the LAS group,the power to detect this difference was limited owing to our relativelysmall patient population. In addition, data on antiarrhythmic drugswere only available at the time of cardioversion or dismissal from thehospital, which may have influenced the rate of recurrence of AF orAFL.

CONCLUSION

Patients with high LV filling pressure, as reflected by short mitralE-wave deceleration time, are more likely to develop LAS immedi-ately after DCCV for AF or AFL. LAS after DCCV may be a markerof AF and AFL recurrence and may be linked to strokes. LAS likelyreflects more severe disease predisposing to these complications.

We gratefully acknowledge Drs Mark J. Callahan, Daniel D.Borgeson, and Lawrence J. Sinak for their assistance in performing thetransesophageal echocardiographic studies.

Editing, proofreading, and reference verification were provided by

y population (n � 45) (left atrial stunning vs no left atrial

� 32) No stunning (n � 13) P value

%) 4 (31%) .17) 0 1.04.29 34.4 � 15.9 �.00117 4 � 58 �.00126.8 69.0 � 27.5 .3245.0 153.4 � 41.4 .9218.1 33.6 � 16.3 .0622 57 � 35 .041.8 3.4 � 1.7 .1117.4 43.7 � 17.3 .0216.4 36.1 � 11.1 .840.27 0.91 � 0.40 .082.8 5.8 � 3.5 .394.8 12.7 � 5.3 .460.34 0.43 � 0.12 .305.5 14.1 � 4.5 .54

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