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Low energy endocardial cardioversion of atrial arrhythmias in humans.

We assessed the feasibility of low energy endocardial defibrillation in patients with atrial fibrillation or atrial flutter who had failed a trial of pharmacological reversion with amiodarone. Low energy endocardial defibrillation under general anesthesia was attempted in 9 patients, 5 with atrial flutter and 4 with atrial fibrillation (median duration of arrhythmia 3.75 months). Two large surface area endocardial leads were introduced percutaneously and sited in the right atrial appendage and at the right ventricular apex. A cutaneous patch electrode was placed on the left thorax. Biphasic shocks synchronized to the ventricular electrogram were used to terminate atrial arrhythmias. Three electrode configurations were evaluated in the following sequence at each energy level: atrial cathode to ventricular anode; ventricular cathode to atrial anode; atrial cathode to a combined ventricular and cutaneous anode. If endocardial defibrillation failed (0.5-10 J), transthoracic defibrillation using 200 joules followed by 360 joules, if required, was performed. Endocardial defibrillation was successful in all five patients with atrial flutter (0.5 J, 1.0 J, 1.0 J, 4.0 J, and 10.0 J) but in only one patient with atrial fibrillation (10 J). On no occasion did successful defibrillation occur with one configuration when it had failed with an alternate configuration at that particular energy level. Ventricular fibrillation did not occur, and there were no other significant complications. Low energy endocardial defibrillation is feasible in patients with atrial flutter using large surface area electrodes. Although the success rate of atrial defibrillation was low, further work is required, particularly in patients with more recent onset of the arrhythmia and using a right to left electrode configuration.

Adult↗

Transthoracic cardioversion of atrial fibrillation and flutter: standard techniques and new advances.

Direct current electric shocks have been used to terminate atrial arrhythmias (cardioversion) in humans since the 1960s. The likelihood of successful cardioversion and maintenance of sinus rhythm is increased if the left atrium is not markedly enlarged and fibrotic, if there is no marked left atrial hypertension (e.g., mitral stenosis), and if the arrhythmia is not long-standing. To minimize the risk of thromboembolic phenomena, therapeutic anticoagulation should be established for at least 3 weeks before and for 4 weeks after cardioversion; coumadin is usually used for this purpose. A more recent approach uses transesophageal echocardiography to demonstrate the absence of thrombi in the left atrium and left atrial appendage. If no thrombi are evident, 48 hours of heparin anticoagulation may be adequate prior to cardioversion. Anticoagulation is still required after cardioversion. Quinidine and digitalis, singly or in combination, are frequently used to achieve and maintain sinus rhythm in association with cardioversion. For the procedure itself, traditional hand-held paddle electrodes or self-adhesive electrode pads may be used; the apex-anterior and anterior-posterior positions are equally effective. Gel couplants and firm pressure should always be used with hand-held paddles to reduce transthoracic impedance and maximize current flow. Electrodes should be widely separated to avoid shunting of current along the chest wall between electrodes. Generally, electrodes should be large in size; small "pediatric" electrodes should only be used in infants < 1 year of age (< 10 kg). Shocks should always be synchronized to the R wave to avoid the vulnerable period and the inadvertent induction of ventricular fibrillation. Initial shocks for atrial fibrillation should begin at 100 J; atrial flutter generally requires a smaller shock (initial shocks at 50 J). Effective anesthesia, not merely sedation, is required to achieve amnesia and avoid pain. Exciting new developments in defibrillation and cardioversion have occurred. It is now understood that excessive energy and current may induce cardiac damage, and recent studies suggest such damage may be mediated in part by free radicals. New shock waveforms, such as biphasic and multiphasic waveforms from multiple encircling electrodes, may be superior to the standard damped sinusoidal waveform.

Animals↗

Clinical and electrophysiologic effects of calcium channel blockers in patients receiving ibutilide.

BACKGROUND: Ibutilide is indicated for the acute termination of atrial fibrillation and atrial flutter. Recent work concludes that ibutilide activates a late inward sodium current that is blocked by nifedipine. Because calcium channel blockers are commonly used in patients with atrial fibrillation, it is important to exclude an antagonistic effect on ibutilide in the clinical setting. METHODS: We performed a retrospective electrocardiographic (ECG) review of patients enrolled in 3 clinical trials of ibutilide (2 atrial fibrillation conversion protocols and 1 ventricular tachycardia suppression protocol) to determine clinical efficacy and ECG effects of ibutilide in patients receiving and not receiving calcium channel blockers. Calcium channel blockers were administered as clinically indicated. A meta-analysis of the effects of calcium channel blockers on the conversion efficacy of atrial fibrillation and atrial flutter by ibutilide was also performed for studies in the literature. RESULTS: One hundred thirty patients were included in the ECG analysis (106 from atrial fibrillation protocols and 24 from the ventricular tachycardia protocol). Sixty-eight of the 130 patients were taking calcium channel blockers at the time of ibutilide administration. There were no differences in the QT or QTc intervals, conversion rate for atrial fibrillation or atrial flutter, or suppression of ventricular tachycardia between patients taking and not taking calcium channel blockers. In the meta-analysis of 4 studies, there was no difference in the conversion rates between patients taking (52%, n = 221) and not taking (45%, n = 402) calcium channel blockers (P =.09). CONCLUSIONS: In the clinical setting, the concomitant use of calcium channel blockers does not alter the ECG effects or efficacy of ibutilide for the treatment of atrial or ventricular arrhythmias.

Aged↗

Proarrhythmic effects of the new antiarrhythmic agent flecainide acetate.

Flecainide acetate, a new potent class I antiarrhythmic agent, was given to 152 patients (46 orally and 106 intravenously) over a period of 22 months. Seven patients developed proarrhythmic effects. The only conduction abnormalities induced were PR interval prolongation and QRS complex widening, and no patient developed significant sinus bradyarrhythmias; patients with known serious abnormalities of impulse generation or conduction were excluded from this study. Five patients developed ventricular tachycardia or ventricular fibrillation of whom only three had preexisting ventricular arrhythmias. QT and QTc interval prolongation was observed but was due to QRS complex widening rather than to an increase in the JT interval. A patient with the Wolff-Parkinson-White syndrome had an inducible orthodromic atrioventricular (AV) tachycardia prior to flecainide, but only an antidromic tachycardia was induced after the drug. In one patient flecainide administration resulted in an increase of atrial flutter cycle length which resulted in development of 1:1 AV conduction and overall faster ventricular rate. Two patients who developed ventricular arrhythmias were taking other antiarrhythmic agents, and in this series proarrhythmic effects occurred with both normal and high flecainide concentrations.

Administration, Oral↗

Dissimilar atrial rhythms in a patient with the Wolff-Parkinson-White syndrome.

In this report, we present the findings in a patient who had paroxysmal supraventricular tachycardia and atrial flutter associated with the Wolff-Parkinson-White syndrome. During atrial flutter, localized atrial fibrillation was recorded in the coronary sinus (dissimilar atrial rhythms), near the accessory pathway; and during 90 minutes of observation, ventricular activation occurred solely over the normal pathway. We postulate that localized atrial fibrillation repetitively invaded the accessory pathway and rendered it refractory to conduction by flutter impulses.

Atrial Fibrillation↗

Spontaneously terminating apparent ventricular fibrillation during transesophageal electrophysiological testing in infants with Wolff-Parkinson-White syndrome.

This article describes two infants with Wolff-Parkinson-White (WPW) syndrome in whom apparent VF occurred without antecedent AF or atrial flutter during routine transesophageal electrophysiological testing. Remarkably, this arrhythmia terminated spontaneously in both infants. The documentation of self-limited apparent VF, or polymorphic ventricular tachycardia close to VF, in transesophageal testing adds another dimension to the management of WPW.

Electrocardiography↗

[Pre and Postoperative evaluation of the incidence of arrhythmia in patients undergoing corrective intervention for Ebstein anomaly].

BACKGROUND: Patients with Ebstein's anomaly frequently have troublesome cardiac arrhythmias. In particular, this malformation is the most common congenital defect associated with the Wolff-Parkinson-White syndrome. The aim of this study was to investigate the postoperative evolution of arrhythmias without the aid of any surgical techniques for arrhythmia. METHODS: Between 1980 and 1999, 48 patients (22 males, 26 females), with a preoperatively documented arrhythmia, underwent an operation for the correction of Ebstein's anomaly at the Hôpital Broussais. Of these, 24 had paroxysmal supraventricular tachycardia, 12 had atrial fibrillation or flutter, 8 had Wolff-Parkinson-White syndrome, 1 had non-sustained ventricular tachycardia, and the remaining 3 patients had atrioventricular block. RESULTS: The operative mortality was 8% (4/48). After operation 46% (20/44) of the patients regained permanent sinus rhythm (20/44 vs 2/48, p < 0.01), supraventricular tachyarrhythmia occurred in 16% of the patients (7/44), 8 patients (18%) had atrial fibrillation, and ventricular preexcitation syndrome was present in 3 patients (7%). The incidence of pacemaker implantation for complete heart block was 11% (5/44). Follow-up was achieved in 95% of patients (40/44) who survived the operation and the perioperative period. The mean follow-up was 63 +/- 54 months (range 4-226 months). During this time there were 6 additional deaths. Eight patients continued to have symptomatic arrhythmias (2 had paroxysmal supraventricular tachycardia, 6 had atrial fibrillation), but 55% of patients (20/36) reported no symptoms of arrhythmia (20/36 vs 2/48, p < 0.01). CONCLUSIONS: Surgical repair improves the quality of life of these patients by reducing the incidence of arrhythmias, in fact less than one sixth of patients continued to have postoperative symptomatic arrhythmias. This can be explained by the interruption of accessory pathways that seem to be a major cause of arrhythmia in Ebstein's anomaly.

Adolescent↗

[Pharmacology of modern anti-arrhythmia drugs in therapy of supraventricular tachycardia].

Prevention of recurrences of atrial fibrillation, slowing the ventricular rate during atrial fibrillation, and the acute management of atrioventricular junctional reentrant supraventricular tachycardia (paroxysmal supraventricular tachycardia) often require treatment with antiarrhythmic drugs. These drugs comprise a pharmacodynamically and pharmacokinetically heterogeneous group of agents whose individual properties determine correct use, contraindications and side effects. Stabilisation of sinus rhythm can be achieved with class IA and class IC sodium channel blocking drugs as well as with the class III agents amiodarone or sotalol. Verapamil, diltiazem, cardioselective beta-adrenoceptor-blocking drugs or cardiac glycosides can be used to slow the ventricular rate during atrial fibrillation. Rapid termination of paroxysmal supraventricular tachycardia is achieved with i.v. administration of adenosine, verapamil, ajmaline, diltiazem, propafenone, or flecainide. If atrial flutter complicates the preexcitation syndrome, this type of supraventricular tachycardia must not be treated with calcium antagonists, cardiac glycosides or lidocaine, since these agents decrease refractoriness of the accessory pathway which may precipitate fatal ventricular fibrillation.

Anti-Arrhythmia Agents↗

Role of electrophysiological study and ablation in the management of recurrent atrial flutter associated with haemodynamic compromise in a critically ill patient.

Atrial flutter is a common arrhythmia. In the critical care setting, the arrhythmia may present in any patient, but it is most commonly seen in patients with impaired ventricular function, valvular disease, atrial dilatation or after cardiac surgery. We present a 68-year-old lady with recurrent poorly tolerated atrial flutter that was resistant to multiple pharmacological interventions and complicated by cardiogenic shock following direct current cardioversion. The flutter was successfully cured with radiofrequency ablation and was followed by an immediate improvement in her haemodynamic status. We review the management of acute atrial flutter and discuss the role of electrophysiologically guided ablation.

Aged↗

Hemodynamic consequences of supraventricular tachycardias and their antiarrhythmic treatment.

Complex adjustments in contractility, resistance, stroke volume and atrio-ventricular contraction relationships underlie the optimization of cardiac output during variations in sinus rate. In patients with intra AV nodal re-entry tachycardia and accessory pathway tachycardias, rate and loss of appropriately timed atrial transport reduce cardiac efficiency, but this is serious only when heart rates are very high. True atrial tachycardia, atrial fibrillation, and atrial flutter are often associated with cardiovascular disease. In atrial fibrillation and flutter, loss of atrial transport may be less important than the hemodynamic consequences of irregularity of ventricular systole. Antiarrhythmic management may ameliorate the consequences of the arrhythmia by reducing heart rate, restoring sinus rhythm or more controversially by regularizing ventricular contraction. Digoxin and antiarrhythmic surgery have little negative inotropic potential but most other antiarrhythmic drugs and ablation procedures depress myocardial function. Antitachycardia pacemakers may produce acute adverse hemodynamic effects depending upon the type of pulse trains delivered to terminate the tachycardia.

Anti-Arrhythmia Agents↗

Amplitude of atrial electrical activity during sinus rhythm and during atrial flutter-fibrillation.

The onset of atrial flutter or fibrillation in a patient with a DDD pacemaker may result in sensing of the atrial arrhythmia and an inappropriate ventricular pacing response. In order to assess the potential of this problem, we evaluated the amplitude of atrial electrograms recorded from the right atrial appendage during sinus rhythm and during atrial flutter or fibrillation during 19 episodes in 18 patients. In 11 episodes of fibrillation and eight episodes of flutter, there was no difference in amplitude of either unipolar or bipolar atrial electrograms compared to that recorded during sinus rhythm (p greater than 0.05). In 14 of 19 episodes, the direction of depolarization of the bipolar electrogram did not change appreciably between sinus rhythm and the atrial arrhythmia. In summary, there is insufficient difference between amplitude of atrial depolarizations recorded during sinus rhythm and atrial flutter or fibrillation to be differentiated reliably by DDD pacemakers.

Adult↗

The Multicentre European Radiofrequency Survey (MERFS): complications of radiofrequency catheter ablation of arrhythmias. The Multicentre European Radiofrequency Survey (MERFS) investigators of the Working Group on Arrhythmias of the European Society of Cardiology.

Radiofrequency (RF) catheter ablation has developed into a new non-pharmacological therapy for the definitive treatment of patients with cardiac arrhythmias. Although an increasing number of recent reports have indicated the widespread use of the procedure, no data are available to estimate the number of procedures performed in Europe. Furthermore, currently no data on a large series of patients are available that provide information on the risk of procedure-related complications. This report presents the results of the Multicentre European Radiofrequency Survey (MERFS) that was conducted by the Working Group on Arrhythmias of the European Society of Cardiology. The objectives of this voluntary retrospective survey were to assess the number of radiofrequency catheter ablation procedures performed in 86 European institutions from January 1987 until March 1992 and the incidence of procedure-related complications with respect to the different types of ablative procedures. A total of 4398 patients were reported on from 68 out of 86 institutions (79%) from 15 European countries that agreed to participate in MERFS. From 1987 to 1991, the number of patients who underwent RF ablation per year increased from 45 to 2000. In the first 3 months of 1992, a total of 1640 patients were reported on. The number of patients reported on in relation to the different types of ablative procedures were: ablation of atrial tachycardialatrial flutter: n = 141 (3.2%); ablation of the atrioventricular junction: n = 900 (20.5%); modification of the atrioventricular junction in atrioventricular nodal reentrant tachycardia: n = 815 (18.5%); ablation of accessory pathway: n = 2222 (50.5%); ablation of ventricular tachycardia: n = 320 (7.3%). Procedure-related complications occurred in 223 patients (5.1%). The incidence of complications in relation to the ablative procedure was: ablation of atrial tachycardia/atrial flutter: 5.0%; ablation of the atrioventricular junction: 3.2%; modification of the atrioventricular junction in atrioventricular nodal reentrant tachycardia: 8.0%; ablation of accessory pathway: 4.4%; ablation of ventricular tachycardia: 7.5%. Complications occurred significantly more often in patients who underwent modification of the atrioventricular junction in atrioventricular nodal reentrant tachycardia, when compared to ablation of the atrioventricular junction (P < 0.001) or ablation of accessory pathway (P < 0.001), and in patients who underwent ablation of ventricular tachycardia, when compared to ablation of the atrioventricular junction (P < 0.002) or ablation of accessory pathway (P < 0.02). The highest incidence of complications was reported after modification of the atrioventricular junction in atrioventricular nodal reentrant tachycardia.(ABSTRACT TRUNCATED AT 400 WORDS)

Arrhythmias, Cardiac↗

Effectiveness of oral sotalol for treatment of pediatric arrhythmias.

Sotalol is a beta blocker with class III activity. Few investigators have reported its use in pediatric patients. From August 1985 to May 1990, 66 patients (mean age 8.7 years; range 9 days to 24 years), including 14 infants aged less than 3 months, were treated with oral sotalol alone (n = 46) or in association with digoxin (n = 20). Supraventricular reentrant tachycardia was present in 38 patients (20 with documented preexcitation), atrial flutter in 10 and atrial ectopic tachycardia in 7. Three patients had other types of supraventricular tachycardia. Tachycardia was of ventricular origin in 6 patients and both of supraventricular and ventricular origin in the remaining 2. Mean dose of oral sotalol was 135 mg/m2/day given in 2 doses. Congenital heart disease was present in 28 patients, 14 with previous cardiac surgery, mostly at the atrial level. Prior treatment with 1 or more antiarrhythmic agent had been unsuccessful in 83% of patients. Mean duration of treatment was 13.3 months (range 2 months to 5 years). Overall, treatment was successful in 79% of cases. Highest rate of success was observed in patients with supraventricular reentrant tachycardia with or without preexcitation (89%) and in those with atrial ectopic tachycardia (85.5%). Atrial flutter could be controlled in 60% of cases. Sotalol seemed less effective in ventricular tachycardia with a complete control of the arrhythmia being achieved in only 17%; however, it decreased the number of runs of ventricular tachycardia and the number of ventricular premature complexes in 50% of patients. There were no adverse effects in 89% of patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

Electrophysiology and indications for pacing in the '80's.

Newer electrophysiological studies have improved our understanding of the pathogenesis of cardiac arrhythmias. Bradycardias originate either from a dysfunction of impulse formation in the sinoatrial node or from a disturbed conduction of the impulse. Different pathogenetic mechanisms are discussed as causes of tachyarrhythmias: circus movement (re-entry) is primarily due to pathological changes in conduction and refractoriness. Focal impulse formation results from local disturbances of depolarization and repolarization of the cell membrane: increased automaticity, abnormal automaticity, triggered activity. Symptomatic bradycardias still represent the standard indication for cardiac pacing particularly with implantable pacemakers. Based on clinical electrophysiology, various types of pacemakers are available at present: atrial triggered and atrial pacing pacemakers, AV-sequential pacemakers, ventricular demand-pacemakers, stand-by pacemakers, and fixed rate pacemakers. The multiprogrammability of newer pacemaker devices is a very useful tool in avoiding secondary interventions. For antitachycardia pacemaker therapy there are essentially three methods in use: 1. overdrive pacing to prevent re-entry phenomena and automaticity and also to suppress tachyarrhythmias based on increased or abnormal automaticity; 2. competitive stimulation for termination of tachycardias by means of single impulses; and 3. rapid atrial stimulation to convert atrial flutter into atrial fibrillation and consequently to normal sinus rhythm. In very rare cases rapid ventricular stimulation is mandatory. The positive results achieved with temporary stimulation methods have led to the development of permanent (implantable) antitachycardia pacemakers for long-term therapy, which have proven to be a low-risk alternative in drug-resistant tachyarrhythmias.

Anti-Arrhythmia Agents↗

["Arrhythmica" or: history, extent and practical consequences of pro-arrhythmia effects].

It has been known for many years that antiarrhythmic drugs may have a potential proarrhythmic effect. But it was not until two very important prospective studies were published, of Velebit et al. (1982) and in particular the CAST study (1989), that the extent and potentially deleterious consequences of the proarrhythmic effect were realized. This review attempts to lessen some doubts that have emerged in the management of antiarrhythmic therapy and the prophylaxis of cardiac arrhythmias, in particular for general practitioners and specialists in internal medicine. First, it is pointed out that the diagnosis "healthy heart" is only permissible after careful clinical investigation and in some cases special studies (e.g. echocardiogram). Reasonable therapy (or non-therapy) is then proposed for the current arrhythmias having regard to left (or right) ventricular function, the patient's age, the implicated disease and the individual circumstances. Electrotherapy (catheter ablation and implantation of a cardioverter-defibrillator) is mentioned as being superior to drug therapy in some patients with supraventricular and ventricular arrhythmias.

Aged↗

[Left ventricular-right atrial communication. Diagnostic and therapeutic aspects: report of 16 cases (author's transl)].

16 cases of left ventricular-right atrial communication are reported. The most consistent clinical features, suggestive of this condition, were: auscultatory findings of V.S.D., electrocardiographic patterns of right atrial enlargement and biventricular hypertrophy, considerable right atrial enlargement coexisting with signs of left-sided cardiac enlargement and increased polmonary vascularity to Xray examination, echocardiographic fluttering of the tricuspid valve. Cardiac catheterization revealed an increased oxygen content in the right atrial or ventricular blood without the passage of the catheter through an A.S.D. The definitive diagnosis was established by left ventricular angiocardiography which demonstrated immediate opacification of a dilated right atrium through a septal defect; the location of the septal defect in the cardiac septum was attempted. In patients who suffered from a large left to right shunt were recommended for surgical treatment also in view of the relatively bad tolerance of this defect and low operative risk. There were two deaths: one baby died of early congestive failure. 9 cases were operated upon with one immediate postoperative death. The remaining, controlled by clinic follow-up, had good results.

Adult↗

Incidence and clinical relevance of supraventricular tachyarrhythmias in pulmonary hypertension.

BACKGROUND: In patients with severe pulmonary hypertension (PH), right ventricular function is a main determinant of clinical stability and outcome. Supraventricular tachyarrhythmias (SVTs) may compromise cardiac function and threaten prognosis in patients with PH, but the incidence and clinical relevance of SVTs in PH and chronic right ventricular failure have not been evaluated. METHODS: In a 6-year retrospective single-center analysis, 231 consecutive patients followed for pulmonary arterial hypertension, or inoperable chronic thromboembolic PH were studied for SVTs. Analysis included incidence, clinical consequences, treatment, and outcome. RESULTS: Thirty-one episodes of SVT were observed in 27 of 231 patients (cumulative incidence 11.7%, annual risk 2.8% per patient), including atrial flutter (n = 15), atrial fibrillation (n = 13), and AV nodal reentry tachycardia (n = 3). Supraventricular tachyarrhythmia onset was almost invariably associated with marked clinical deterioration and right ventricular failure (84% of SVT episodes). Outcome was strongly associated with the type of SVT and restoration of sinus rhythm. During follow-up, cumulative mortality was low (6.3%, follow-up 26 +/- 23 months) when sinus rhythm was restored (all cases of AV nodal reentry tachycardia and atrial flutter). In contrast, 9 of 11 patients with sustained atrial fibrillation died from right ventricular failure (cumulative mortality 82%, follow-up 11 +/- 8 months). CONCLUSIONS: In patients with PH, SVTs constitute a relevant problem, often resulting in clinical deterioration. Sustained atrial fibrillation may be associated with a high risk of death from right ventricular failure.

Adult↗