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PubMed1997

[Can 1/1 atrial flutter be foreseen by class I anti-arrhythmics?].

1/1 atrial tachycardia or "quinidine" flutter under class I antiarrhythmic drugs is a serious complication of these agents which, unfortunately, cannot be anticipated. The aim of this study was to review the cases of 11 patients who had suffered this complication of class I antiarrhythmic therapy to see if it could have been prevented. All drugs of this class were included. The 11 subjects were aged 57 to 78: 7 had no apparent underlying cardiac disease and the others had valvular (n = 1), hypertensive (n = 1) and ischaemic (n = 2) heart disease. They were treated for episodes of paroxysmal atrial fibrillation or tachycardia. In the absence of treatment, 7 patients had a short PR interval on the ECG (PR between 0.11 and 0.14 s). In the other 4, the PR interval was normal (0.16 to 0.20 s), but the P wave was widened with appearances of left atrial hypertrophy or an intra-atrial conduction defect. High amplification ECG performed in 3 patients showed continuity of atrial and ventricular depolarisation. Atrial stimulation showed excellent nodal conduction with a Wenckebach point of 200/min. The authors conclude that a short PR interval is predisposing factor to 1/1 atrial tachycardia with class I antiarrhythmics. High amplification ECG which allows identification of the end of the P wave with respect to the QRS complex could help identify subjects at risk when the P wave is widened and that, consequently, the PR interval appears to be normal.

Aged↗
PubMed1990

Intravenous amiodarone bolus versus oral quinidine for atrial flutter and fibrillation after cardiac operations.

The safety and efficacy of amiodarone and quinidine in reverting atrial tachyarrhythmias after cardiac operations were compared in a randomized cross-over trial. Patients with sustained atrial fibrillation or flutter for more than 2 hours' duration, stable hemodynamic status, and prior digoxin therapy were randomized to receive either intravenous amiodarone, 5 mg/kg over 20 minutes (41 patients), or oral quinidine, 400 mg immediately and 400 mg in 4 hours (39 patients), with cross-over at 8 hours if reversion was not achieved. Thirty-six patients had a coronary artery operation, 35 a valvular operation, five had both, and there were four miscellaneous cases. There was a male:female ratio of 1.5:1 and a mean age of 58 years (range 23 to 75 years). Preoperative atrial fibrillation or flutter was present in nine patients, and four patients had an ejection fraction less than 40%. Twenty-five of 39 patients (64%) given quinidine first reverted to sinus rhythm, compared with 17 of 41 patients (41%) given amiodarone first (2p = 0.04). Side-effects occurred in 18 patients given quinidine and five patients given amiodarone (2p = 0.01). Two patients, both given quinidine, were withdrawn from the study. There was no correlation, with either drug, between serum levels and clinical efficacy. Multivariate analysis identified longer times from arrhythmia to treatment, preoperative atrial fibrillation, mitral valve operations, and concomitant propranolol therapy as factors predictive of failure to revert to sinus rhythm. Oral quinidine was more effective than intravenous amiodarone in reverting postoperative atrial fibrillation and flutter but caused more side-effects.

Administration, Oral↗
PubMed2002

[Pharmacological therapy of atrial fibrillation and atrial flutter].

BACKGROUND: Despite the increasing availability of nonpharmacological treatment options for atrial fibrillation, drug therapy targeted at restoration and maintenance of sinus rhythm, or aimed at symptomatic ventricular rate control remains the mainstay of therapy for the majority of patients. METHOD: Available data suggest that these two treatment approaches yield similar responder rates with regard to symptomatic improvement. RESULTS: Detailed results from major prospective studies investigating the prognostic effects of different atrial fibrillation treatment modalities are expected to become available soon. At present, however, the choice of the primary treatment strategy, i.e. rate control or rhythm control, still remains upon the clinical decision and expertise of the treating physician. Cardioversion by means of external biphasic shock delivery has shown to effectively convert atrial fibrillation to sinus rhythm in more than 90% of patients. Pharmacological cardioversion, in contrast, has a far lower success rate and may be followed by severe complications mandating in-hospital administration with the majority of drug regimens. For the maintenance of sinus rhythm, the proarrhythmic side effects of Class I antiarrhythmic drugs currently limit their use to those patients without any structural heart disease. Clinical investigation of newer "pure" Class III drugs have shown to excite considerable prolongation of ventricular repolarization duration resulting in a significant risk for torsade-de-pointes tachycardia. Betablockers are beneficial in many clinical situations associated with the occurrence of atrial fibrillation, such as heart failure, arterial hypertension and coronary artery disease. These substances, however, do not seem to improve cardioversion rates and their effect in maintaining sinus rhythm is only moderate. Patients with structural heart disease in whom maintenance of sinus rhythm is strongly desired, therefore, are left to amiodarone therapy. The cardiac safety profile as well as the proven effectiveness are unsurpassed by any other available drug at present. This paper reviews major studies published during the last decade implementing recent guidelines regarding pharmacological rate control, cardioversion and maintenance of sinus rhythm and the approach towards patients suffering from paroxysmal atrial fibrillation.

Anti-Arrhythmia Agents↗
PubMed1998

Long-term outcome of patients with drug-refractory atrial flutter and fibrillation after single- and dual-site right atrial pacing for arrhythmia prevention.

OBJECTIVES: An initial crossover study comparing dual- and single-site right atrial pacing was performed followed by a long-term efficacy and safety evaluation of dual-site right atrial pacing in patients with drug-refractory atrial fibrillation (AF). Also examined was the efficacy of two single-site right atrial pacing modes (high right atrium and coronary sinus ostium) and the long-term need for cardioversion, antithrombotic and antiarrhythmic drug therapies during dual-site atrial pacing. METHODS: Thirty consecutive patients with drug-refractory symptomatic AF and documented primary or drug-induced bradycardia were implanted with a dual chamber rate-responsive pacemaker and two atrial leads. Single-site atrial pacing was performed at the high right atrium or the coronary sinus ostium. Continuous atrial pacing was maintained. RESULTS: Mean arrhythmia-free intervals increased from 9+/-10 days in the control period preceding implant to 143+/-110 days (p < 0.0001) in single-site right atrial pacing and 195+/-96 days in dual-site right atrial pacing (p < 0.005 versus single-site pacing and p < 0.0001 versus control). Dual-site right atrial pacing significantly increased the proportion of patients free of AF recurrence (89%) as compared to single-site right atrial pacing (62%, p = 0.02). High right atrial pacing and coronary sinus ostial pacing had similar efficacy for AF prevention. Effective rhythm control was achieved in 86% of patients during dual right atrial pacing. Seventy-eight percent of patients at 1 year and 56% at 3 years remained free of symptomatic AF. The need for cardioversion was reduced after pacemaker implant (p < 0.05) and antithrombotic therapy was reduced (p < 0.06) without any thromboembolic event. Coronary sinus ostial lead dislodgement was not observed after discharge. CONCLUSIONS: Atrial pacing in combination with antiarrhythmic drugs eliminates or markedly reduces recurrent AF. Prevention of AF is enhanced by dual-site right atrial pacing. High right atrial and coronary sinus ostial pacing do not differ in efficacy. Dual-site right atrial pacing is safe, achieves long-term rhythm control in most patients, decreases the need for cardioversion, and antithrombotic therapy can be selectively reduced.

Aged↗
PubMed2002

[Radiofrequency ablation of periatriotomy atrial flutter after interatrial defect surgical repair].

We report a successful ablation of reentrant atrial tachycardia complicating atrial septal defect repair. This tachyarrhythmia was poorly tolerated hemodynamically and difficult to control with antiarrhythmic drug therapy and atrial pacing. Ablation therapy has focused on extending a line of block from the surgical incision to the inferior veno cava. Immediate success was achieved and the patient is free of arrhythmia after 4 months of Follow-up.

Atrial Flutter↗
PubMed1991

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.

Actuarial Analysis↗