Long-term outcome of electrical cardioversion in patients with chronic atrial flutter.

OBJECTIVE: To determine the long-term outcome of serial electrical cardioversion therapy in patients with chronic atrial flutter. DESIGN: Prospective study, case series. SETTING: University hospital. PATIENTS: 50 consecutive patients with chronic (> 24 hours) atrial flutter without a previous relapse on antiarrhythmic drugs. INTERVENTIONS: Elective electrical cardioversion therapy, if necessary repeated, to obtain and keep patients in sinus rhythm. If the first cardioversion resulted in sinus rhythm, patients were not given antiarrhythmic drugs. Relapses were managed by repeated cardioversions then anti-arrhythmic drugs were used serially in a set sequence. MAIN OUTCOME MEASURE: Maintenance of sinus rhythm. RESULTS: Mean (SD) follow up was 3.5 (1.7) years. The first cardioversion was successful in 48 patients (96%). After a single shock and without antiarrhythmic drugs being used, 42% of the patients maintained sinus rhythm in the long-term. Only left atrial size was inversely related to the efficacy of one shock (P = 0.025). With serial cardioversion 90% of the patients were kept in sinus rhythm for 5 years. Univariate analysis showed that a long duration of arrhythmia and impaired cardiac function were both related to poor outcome. During follow up 3 patients died of progression of heart failure and another 5 died suddenly. None of these 5 patients was on antiarrhythmic drugs. CONCLUSIONS: Electrical cardioversion was an effective and safe method of converting chronic atrial flutter to sinus rhythm. To maintain sinus rhythm, more than half of the patients required multiple shocks and prophylactic antiarrhythmic drugs. Sudden death was relatively frequent in the study population; the limited data available from this study suggest that such deaths were caused by the underlying disease and not drug related proarrhythmia.     

Determinants of recurrent atrial flutter after cardioversion.

Eighteen male patients (mean age 59 years) who were electrically cardioverted for pure atrial flutter were retrospectively studied to determine those factors influencing the maintenance of regular sinus rhythm or reversion to atrial flutter. Six months after successful cardioversion, 10 patients (55%) had recurrent atrial flutter and eight patients (45%) were still in sinus rhythm. The two groups were not significantly different with respect to age, symptomatology, abnormalities on the 12 lead electrocardiogram (during sinus rhythm), or the administration of digoxin and a class Ia antiarrhythmic agent (after cardioversion). There was a trend for those patients with recurrent atrial flutter to have a higher incidence of underlying heart disease and previous episodes of atrial flutter than the non-recurrent group. There were statistically significant differences between the recurrent and non-recurrent groups with respect to echocardiographically determined left atrial size and left ventricular ejection fraction. Patients with a left atrial size greater than 45 mm or with an ejection fraction less than 45% were all at high risk for recurrent atrial flutter after successful cardioversion.     

Foetal atrial flutter management-the role of electrical cardioversion

We report a successful electrical cardioversion of a foetal atrial flutter (AFL) immediately post delivery. We describe the diagnostic tools, assessment and the management antenatally. Then, we review the literature and discuss the debate about management. We stress the point that if the flutter wave is not progressing, the foetal heart will tolerate till term and we can try electrical cardioversion with confidence after delivery.     

Cardiac troponin T does not increase after electrical cardioversion for atrial fibrillation or atrial flutter

Objective—To determine whether cardiac troponin T increases after electrical cardioversion in patients with atrial fibrillation or atrial flutter.
Design—Serum creatine kinase (CK), creatine kinase-MB (CKMB), and cardiac troponin T were measured before, 24 hours, and 48 hours after cardioversion in 15 patients with atrial fibrillation or atrial flutter.
Results—12 of the 15 patients (80%) were successfully cardioverted to sinus rhythm. The median number of shocks was three (range one to six), the median cumulative energy 710 J (50 to 1430 J), and the median peak energy 300 J (50 to 360 J). Total CK increased from a baseline median concentration of 92 (45 to 259) to 1324 (96 to 6660) U/l at 24 hours and 1529 (120 to 4774) U/l at 48 hours after cardioversion. There was a small increase in CKMB but the ratio of CKMB to CK did not increase. There was no increase in cardiac troponin T in any patient.
Conclusions—Following electrical cardioversion of atrial fibrillation or atrial flutter, cardiac troponin T remains unchanged despite a large rise in total CK, indicating that the CK is derived from skeletal muscle and that myocardial injury does not occur. If cardiac troponin T is increased after cardioversion for atrial arrhythmias then other causes of myocardial damage should be sought.

Keywords: atrial fibrillation; atrial flutter; cardioversion; troponin T     

Serial antiarrhythmic drug treatment to maintain sinus rhythm after electrical cardioversion for chronic atrial fibrillation or atrial flutter

The sequential use of different types of antiarrhythmic drugs may improve arrhythmia prognosis in chronic atrial fibrillation or flutter after successful electrical cardioversion. The rationale for serial treatment is that the arrhythmogenic mechanism may vary between patients, leading to different responses to 1 specific drug. To investigate this issue prospectively, 127 patients having chronic fibrillation or flutter exclusively, underwent serial drug treatment with flecainide (stage I) followed by sotalol or, if contraindicated, quinidine (stage II) and eventually amiodarone (stage III). Stages II and III were entered after electrical recardioversion for a recurrence during stages I or II, respectively. Calculated on an actuarial basis, the 2-year cumulative percentage of patients free of the arrhythmia increased from 31% after stage I to 63% at the end of serial treatment. To reach this result, a mean of 1.8 +/- 0.8 cardioversions per patient were needed, with 53 patients progressing to stage II and 34 to stage III. Sixteen patients stopped serial treatment prematurely and 15 patients were considered to have intractable atrial fibrillation at the end of stage III. Incidence of proarrhythmia was low. Multivariate analysis disclosed that an older age, in combination with a large number of previous episodes of arrhythmia, a long previous duration of arrhythmia and presence of mitral valve disease, were predictive for medical refractoriness during serial treatment. It is concluded that serial treatment may improve arrhythmia prognosis in atrial fibrillation or flutter, with an acceptable incidence of proarrhythmic events.     

Role of prophylactic anticoagulation for direct current cardioversion in patients with atrial fibrillation or atrial flutter.

The need for prophylactic anticoagulation to prevent embolism before direct current cardioversion is performed for atrial fibrillation or atrial flutter is controversial. To examine this issue further, a retrospective review was undertaken to assess the incidence of embolic complications after cardioversion. The review involved 454 elective direct current cardioversions performed for atrial fibrillation or atrial flutter over a 7 year period. The incidence rate of embolic complications was 1.32% (six patients); the complications ranged from minor visual disturbances to a fatal cerebrovascular event. All six patients had atrial fibrillation, and none had been on anticoagulant therapy (p = 0.026). The duration of atrial fibrillation was less than 1 week in five of the six patients who had embolic complications. Baseline characteristics of patients with a postcardioversion embolic event are compared with those of patients who did not have an embolic event. There was no difference in the prevalence of hypertension, diabetes mellitus or prior stroke between the two groups, and there was no difference in the number of patients who were postoperative or had poor left ventricular function. Left atrial size was similar between the two groups. No patient in the embolic group had valvular disease. No patient with atrial flutter had an embolic event regardless of anticoagulant status; therefore, anticoagulation is not recommended for patients with atrial flutter undergoing cardioversion. Prophylactic anticoagulation is pivotal in patients undergoing elective direct current cardioversion for atrial fibrillation, even those with atrial fibrillation of less than 1 week's duration.     

Pre-treatment with Irbesartan attenuates left atrial stunning after electrical cardioversion of atrial fibrillation.

AIMS: Left atrial (LA) stunning, the transient impairment of LA function, is responsible for an increased thrombo-embolic risk after cardioversion of atrial fibrillation (AF). Angiotensin receptor blockers (ARBs) attenuate atrial remodelling in AF and could theoretically influence LA stunning. We studied the effect of Irbesartan on LA stunning. METHODS AND RESULTS: We prospectively assigned 50 patients from the outpatient clinic undergoing electrical cardioversion for AF with duration of >4 weeks, into two matched groups: 25 patients were treated with Irbesartan (228+/-93 mg/day) for at least 2 weeks prior to cardioversion (Irbesartan group); 25 patients did not receive ARBs (control group). The groups did not differ concerning age (64+/-13 vs. 63+/-13 years, respectively), AF duration (20+/-18 vs. 20+/-19 weeks), underlying disease, LA diameter (46+/-7 vs. 47+/-9 mm), left ventricular dimensions, and ejection fraction (47.7+/-11.6 vs. 49.7+/-14.5%). We assessed LA appendage emptying velocities (LAAEV) and LA spontaneous echo contrast (LASEC) by transoesophageal echocardiography before and after cardioversion and at 2 weeks, and the A-wave by transthoracic echocardiography after cardioversion, at 2 and at 4 weeks. LA stunning was significantly attenuated in the Irbesartan group. The reduction of LAAEV immediately after cardioversion was significantly less in the Irbesartan group (LAAEV reduction of 9+/-49% from 28+/-9 cm/s before cardioversion to 25+/-13 cm/s immediately afterwards) than in the control group (reduction of 48+/-20% from 34+/-15 cm/s before cardioversion to 16+/-6 cm/s afterwards) (P = 0.048). New or increased LASEC occurred in eight patients (32%) in the Irbesartan vs. 16 patients (64%) in the control group (P = 0.046). CONCLUSION: Irbesartan significantly attenuates LA stunning after electrical cardioversion of AF. Therefore, ARBs may represent an important pharmacological supplementation in patients being prepared for cardioversion.     

Atrial pacing for cardioversion of atrial flutter in digitalized patients

To test the safety and reliability of atrial pacing as a conversion technique in patients with atrial flutter who are receiving digitalis therapy, atrial pacing conversion was attempted for 49 episodes of atrial flutter in 32 consecutive patients. All patients except one were receiving digitalis. To control ventricular rates most patients had received larger than usual therapeutic doses of digitalis glycoside before pacing. Fourteen of the 25 patients whose serum levels were measured had glycoside concentrations greater than 2 ng/ml. Before atrial pacing the mean atrial and ventricular rates were, respectively, 290 +/- 20.6 and 134 +/- 27.9/min (mean +/- standard deviation). Successful rhythm conversion was achieved on 48 occasions (98%) in 31 patients. One patient required transthoracic direct current synchronized countershock cardioversion. With atrial pacing, the atrial flutter rhythm reverted immediately to sinus mechanism in 23 instances, and there were 25 episodes of atrial fibrillation. Among those who experienced atrial fibrillation, the rhythm spontaneously reverted to sinus mechanism within 24 hours on 14 occasions; on 11 occasions; the rhythm reverted to atrial flutter and repeat pacing was required. Sinus mechanism was eventually established in all 31 patients.     

Prevalence of atrial thrombi in patients with atrial fibrillation/flutter and subtherapeutic anticoagulation prior to cardioversion.

AIMS: Thromboembolism may complicate electrical cardioversion (ECV) of atrial fibrillation/flutter (AF). The use of 3 weeks of warfarin before ECV results in a substantial reduction of thromboembolic complications. Nevertheless, in patients scheduled for ECV subtherapeutic INR levels are common. We sought to assess the prevalence and the predictors of atrial thrombi in patients affected with sustained AF in whom subtherapeutic INR values were detected in the 3 weeks preceding scheduled ECV. METHODS AND RESULTS: Forty-one patients with persistent AF and > or =3 weeks warfarin anticoagulation who exhibited subtherapeutic INR values in the last 3 weeks underwent a transoesophageal echocardiogram (TOE) before a scheduled ECV. A left atrial appendage (LAA) thrombus was diagnosed on TOE in four patients (9.8%). Patients with thrombus had lower INR values (1.45+/-0.09 vs 1.72+/-0.20; p=0.0068), lower LAA emptying velocities (13.75+/-4.5 vs 25.86+/-12.4 cm/s; p=0.0313) and higher prevalence of atrial smoke (100 vs 37.8%,p=0.03). CONCLUSIONS: Subtherapeutic levels of anticoagulation before elective ECV of AF may expose patients to post-ECV thromboembolic sequelae, especially in patients with lowest INR values. Current recommendations of a full course of therapeutic anticoagulation before ECV of persistent AF should be firmly observed.     

Plasma levels of NT-pro-BNP in patients with atrial fibrillation before and after electrical cardioversion

Summary Objective Plasma levels of brain natriuretic peptide (BNP) have been examined in studies on patients with persistent atrial fibrillation, both before and after electrical cardioversion. Studied patients often showed a comorbidity with congestive heart failure, which complicates interpretation of measured BNP values as a natriuretic peptide. The aim of this study was to examine plasma levels of N-terminal fragment pro-brain natriuretic peptide (NT-pro-BNP), which is the more stable but inactive cleavage product of pro-BNP in patients with atrial fibrillation, but normal left ventricular ejection fraction, before and after electrical cardioversion. Patients and methods NT-pro-BNP plasma levels of 34 consecutive patients were measured before, shortly after and 11 days after electrical cardioversion. All patients showed a normal ejection fraction after echocardiographic or laevocardiographic criteria. Results At baseline, all patients showed elevated NT-pro-BNP compared to a healthy control group (1086 vs. 66.9 pg/ml, p<0.001). After a mean follow-up time of 11 days in patients with persistent restored sinusrhythm, NT-pro-BNP decreased from 1071 pg/ml at baseline to 300 pg/ml (p<0.001). In contrast, patients with recurrence of atrial fibrillation showed increased levels from 1570.5 pg/ml at baseline to 1991 pg/ml (p=0.13; n.s.). Recurrence of atrial fibrillation was independent from height of NT-pro-BNP levels at baseline (p=0.23). Conclusions Atrial fibrillation in patients with a normal left ventricular ejection fraction is associated with elevated NT-pro-BNP plasma levels, which decrease when a persistent sinus-rhythm can be restored by electrical cardioversion. On the other hand, NT-pro-BNP seems to increase (n.s.) when recurrence of atrial fibrillation occurs. Finally, NT-pro-BNP is no valid predictor for long-term success of sinus-rhythm restoration by electrical cardioversion.      

Positive atrial inotropic effect of dofetilide after cardioversion of atrial fibrillation or flutter

The pure class III agent dofetilide was evaluated to determine its effect on atrial function after cardioversion of atrial fibrillation or flutter. Compared with placebo, dofetilide-treated patients had evidence of better atrial function after cardioversion, indicating that this agent has a positive atrial inotropic effect during the period of postcardioversion atrial stunning.     

Systolic blood pressure increases in patients with atrial fibrillation regaining sinus rhythm after electrical cardioversion

Direct current (DC) cardioversion is used to convert persistent atrial fibrillation (AF) to sinus rhythm (SR), but there is limited knowledge about how blood pressure (BP) is affected by conversion to SR. We sought to evaluate how BP changed in AF patients who converted to SR, compared to patients still in AF. In this retrospective registry analysis, we included a total of 487 patients, treated with DC cardioversion for persistent AF. We obtained data regarding medical history, medication, BP, and electrocardiogram the day before and 7 days after cardioversion. Systolic BP increased by 9 (±16) mm Hg (P < 0.01) and diastolic BP decreased by 3 (±9) mm Hg (P < 0.01) after conversion to SR. In the group of patients with restored SR, there was a 40% increase in the proportion of patients with a hypertensive BP level (≥140/90 mm Hg) after DC cardioversion compared to before. Patients still in AF had no significant change in BP. Systolic BP increases and diastolic BP slightly decreases when persistent AF is converted to SR. The underlying mechanisms explaining these findings are not known, but may involve either hemodynamic changes that occur when SR is restored, an underestimation of systolic BP in AF, or a combination of both. Our findings suggest that an increased attention to BP levels after a successful cardioversion is warranted.     

Chemical cardioversion of atrial fibrillation or flutter with ibutilide in patients receiving amiodarone therapy

BACKGROUND: Ibutilide is a class III drug that is used for the cardioversion of atrial arrhythmias, but it can cause torsade de pointes. Amiodarone also prolongs the QT interval but rarely causes torsade de pointes. There are no studies in which the concomitant use of the 2 agents was examined. The purpose of the present study was to assess the efficacy and safety of cardioversion with combination therapy in patients with atrial fibrillation or flutter. METHODS AND RESULTS: The study included 70 patients who were treated with long-term oral amiodarone and were referred for elective cardioversion of atrial fibrillation (57 of 70, 81%) or flutter (13 of 70, 19%). Patients were taking amiodarone (153+/-259 days, mean+/-SD) and were administered 2 mg intravenous ibutilide. Left ventricular ejection fraction was measured with echocardiography. The QT intervals were measured on 12-lead ECG. Fifty-five patients (79%) had structural heart disease. Patients were in arrhythmia for 196+/-508 days before cardioversion, with a left ventricular ejection fraction of 50+/-11%. In patients with atrial fibrillation, 22 (39%) of 57 and 7 (54%) of 13 patients with flutter converted within 30 minutes of infusion. Thirty-nine patients who did not convert after ibutilide were treated with electrical cardioversion, and 35 (90%) of 39 patients were successfully converted. The QT intervals were further prolonged after ibutilide for the group from 371+/-61 to 479+/-92 ms (P:<0.001). There was 1 episode of nonsustained torsade de pointes (1 of 70, 1.4%) after ibutilide. CONCLUSIONS: The use of ibutilide converted 54% of patients with atrial flutter and 39% of patients with atrial fibrillation who were treated with long-term amiodarone. Despite QT-interval prolongation after ibutilide, only 1 episode of torsade de pointes occurred. Our observations suggest that combination therapy may be a useful cardioversion method for chronic atrial fibrillation or flutter.     

Transient atrial mechanical dysfunction (stunning) after cardioversion of atrial fibrillation and flutter

Background Conversion of atrial fibrillation (AFib) and flutter (AFlt) to sinus rhythm results in a transient mechanical dysfunction of atria (atrial stunning). Methods used as a means of assessing atrial stunning, atrial stunning after conversion of atrial fibrillation/flutter, and the cause, mechanisms, determinants of the extent, and drugs affecting atrial stunning were examined. Methods Studies on the subject, identified through a comprehensive literature search, were thoroughly evaluated. Results and Conclusions Left atrial (LA) stunning has been reported with all modes of conversion of AFib/AFlt to sinus rhythm. The incidence of LA stunning is 38% to 80%. Spontaneous echocardiographic contrast, LA appendage (LAA) flow velocities and emptying fraction, transmitral inflow velocity of atrial wave (A-wave), time-velocity integral of A-wave, and atrial filling fraction have been used as means of assessing LA stunning. The data on right atrial (RA) stunning are limited, but parallel findings have been reported in the right atrium. Atrial stunning does not develop after the unsuccessful attempts of cardioversion or on delivery of electric current to the heart without AFib/AFlt, and it is a function of the underlying AFib/AFlt manifesting at the restoration of sinus rhythm. Tachycardia-induced atrial myopathy and chronic atrial hibernation are suggested mechanisms. Duration of preceding AFib/AFlt, atrial size, and underlying heart disease are determinants of the extent of atrial stunning. Verapamil, dofetilide, and acetylstrophenathidine have been shown to attenuate or protect from atrial stunning in animal or small human studies. A comprehensive knowledge of atrial stunning would be helpful in selecting the patients for, and the duration of, anticoagulation therapy after cardioversion. (Am Heart J 2002;144:11-22.)     

Use of ibutilide in cardioversion of patients with atrial fibrillation or atrial flutter treated with class IC agents

OBJECTIVES: We sought to assess the efficacy and safety of ibutilide cardioversion for those with atrial fibrillation (AF) or atrial flutter (AFL) receiving long-term treatmentwith class IC agents. BACKGROUND: Attenuation of ibutilide-induced QT prolongation has been observed in a small number of patients pretreated with class IC agents. The clinical significance of the interaction between ibutilide and class IC agents is unknown. METHODS: Seventy-one patients with AF (n = 48) or AFL (n = 23), receiving propafenone 300 to 900 mg/day (n = 46) or flecainide 100 to 300 mg/day (n = 25), presented for ibutilide (2.0 mg) cardioversion. RESULTS: The mean durations of arrhythmia episode and arrhythmia history were 25 +/- 48 days and 4.4 +/- 6.4 years, respectively. Sixty-five patients (91.5%) had normal left ventricular systolic function. Twenty-three of 48 patients (47.9%; 95% confidence interval, 33.3% to 62.8%) with AF and 17 of 23 patients (73.9%; 95% confidence interval, 51.6% to 89.8%) with AFL converted with mean conversion times of 25 +/- 14 min and 20 +/- 12 min, respectively. There was a small increase in corrected QT interval after ibutilide (from442 +/- 61 ms to 462 +/- 59 ms, p = 0.006). One patient developed non-sustained polymorphous ventricular tachycardia and responded to intravenous magnesium. Another developed sustained torsade de pointes and was treated effectively with direct-current shock and intravenous dopamine. CONCLUSIONS: Our observations suggest that the use of ibutilide in patients receiving class IC agents is as successful in restoring sinus rhythm and has a similar incidence of adverse effects as the use of ibutilide alone.