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Response to flecainide infusion predicts long-term success of hybrid pharmacologic and ablation therapy in patients with atrial fibrillation.

OBJECTIVES: We tested the hypothesis that the response to flecainide infusion can identify patients with atrial fibrillation (AF) in whom the hybrid pharmacologic and ablation therapy reduces the recurrences of AF. BACKGROUND: Infusion of class IC anti-arrhythmic drugs may promote transformation of AF into atrial flutter. Catheter ablation of atrial flutter has been demonstrated to be highly effective in preventing recurrences of atrial flutter. METHODS: Seventy-one consecutive patients with paroxysmal or chronic AF, in whom flecainide infusion (2 mg/kg body weight, intravenously) determined the transformation of AF into common atrial flutter (positive response), were randomized to receive one of the following treatments: oral pharmacologic treatment with flecainide (group A, n = 23); the hybrid treatment (catheter ablation of the inferior vena cava-tricuspid annulus isthmus, plus oral flecainide) (group B, n = 24); or catheter ablation of the isthmus only (group C, n = 24). Thirty-seven patients with a negative response to flecainide, who chose to be submitted to the hybrid treatment, were selected as the control group (group D). RESULTS: During a mean follow-up period of 24 +/- 7.2 months, the recurrences of AF and atrial flutter in group B (42%) were significantly lower than those in group A (78%, p < 0.001), group C (92%, p < 0.001) and group D (92%, p < 0.001). CONCLUSIONS: The creation of a complete bi-directional conduction block at the inferior vena cava-tricuspid annulus isthmus, plus flecainide administration, reduces the recurrences of both AF and atrial flutter in patients with class IC atrial flutter. Moreover, the early response to flecainide is safe and reliable in identifying patients who may benefit from this therapy.

Administration, Oral↗

[Value and safety of ambulatory electrophysiologic study].

One-hundred-thirty patients underwent 53 electrophysiological studies including programmed atrial and ventricular stimulation and 96 atrial overdrive stimulations on an outpatient basis. The indications for electrophysiological study were disabling palpitation, syncope, or presyncope, intracardiac conduction disturbance, and bradyarrhythmia. In one patient the efficacy of oral antiarrhythmic drug therapy was evaluated by repeat electrophysiological study. Atrial overdrive stimulation was performed in patients with atrial flutter or atrial tachycardia. On the basis of the result of electrophysiological testing, 25 patients were believed not to require any treatment, 16 patients received new drug therapy, 7 patients underwent catheter ablation in a second session, 2 patients had either a pacemaker or an ICD implanted, and 1 patient continued to receive the drug therapy that had been tested. Atrial overdrive stimulation resulted in a regular sinus rhythm in 66 patients (69%). Except for one patient in whom atrial flutter could not be terminated, atrial fibrillation was induced in the remaining 30 patients. After the procedure, patients were monitored for 30 min in case of overdrive stimulation, and for approximately 3 h after electrophysiological study or 6 h if additional coronary angiography had been performed. Severe complications were not observed. In 10 cases minor hematoma occurred at the puncture site without serious sequelae.--Outpatient electrophysiological study as well as atrial overdrive stimulation are feasible and safe in a selected group of patients.

Adult↗

Atrial tachyarrhythmias and permanent pacing after pediatric heart transplantation.

BACKGROUND: Atrial tachyarrhythmias have been reported in as high as 50% of adult heart recipients. Limited information is available on arrhythmias in pediatric transplant patients. Our objective was to determine the prevalence and significance of atrial tachyarrhythmias and permanent pacing following pediatric heart transplantation. METHODS: A retrospective review of the medical records, electrocardiograms, and Holter recordings of all consecutive patients following heart transplantation at Children's Hospital, Boston (n = 104) and Lucile Packard Children's Hospital, Stanford (n = 123) was performed. The study group consisted of 227 patients with a median age at transplant of 10.2 yrs (1 day-23.3 yrs). RESULTS: Atrial tachyarrhythmias occurred in 32 patients (14%) at a median of 15 days post-transplant (1 day-9.2 yrs) and included atrial flutter (n = 13), atrial fibrillation (n = 7), ectopic atrial tachycardia (n = 5), atrioventricular reciprocating tachycardia or atrioventricular node reentry (n = 5), and other (n = 2). Atrial flutter was the only tachyarrhythmia associated with allograft rejection (6/13 atrial flutter vs. 0/7 atrial fibrillation vs. 0/5 ectopic atrial tachycardia, p = 0.03). Patients with atrial fibrillation had a 2.5 fold (95%CI 1.7-3.5) higher risk of death or retransplant compared to patients without atrial fibrillation. Ectopic atrial tachycardia tended to occur in younger recipients compared to atrial fibrillation and flutter (2.7 yrs vs 18.6 yrs and 8.5 yrs respectively, p = 0.06) and was associated with a benign clinical course. There was no association between atrial tachyarrhythmias and graft ischemic time, surgical technique, or coronary artery disease. Pacemakers were required in 12 patients (5.2%), 7 with sinus node dysfunction and 5 for intermittent complete atrioventricular block. There was no consistent association between the need for permanent pacing and coronary artery disease, rejection, or surgical technique. CONCLUSIONS: Atrial tachyarrhythmias and permanent pacing were uncommon in this cohort of pediatric heart transplant recipients. Association with cardiac rejection, clinical course, and mortality varied depending on the tachyarrhythmia mechanism.

Atrial Fibrillation↗

The role of catheter ablation in atrial tachycardia, flutter, and fibrillation.

The first experiences of nonpharmacological treatment of ectopic atrial tachycardia (EAT), common atrial flutter (AFl), and atrial fibrillation (AF) were performed by surgical techniques. Many studies reported a very high success rate on the use of catheter ablation with radiofrequency current for the treatment of supraventricular arrhythmias; and recently, various preliminary reports are dedicated to the treatment of EAT, AFl, and AF with that source of energy. To our knowledge 108 cases of EAT treated by catheter ablation of the ectopic focus are reported in the literature with a success rate superior to 90%. On the basis of our personal experience regarding 11 cases (4 of right atrium EAT and 7 of left) we discuss here the essential role of unipolar leads derived from the mapping catheter to select the target for radiofrequency applications. Two hundred and one cases of AFl tested by catheter ablation were previously reported. The majority of them (> 80%) were successfully treated with radiofrequency. Some working groups performed the procedure as the basis of electrophysiological findings, while others preferred an anatomical approach applying radiofrequency energy at the isthmus lying between the coronary sinus ostium and the tricuspid ring, near the vena cava orifice. On the basis of these assumptions, we obtained 83% of final success in 12 cases of AFl treated by radiofrequency. Finally, we discuss the problem related to the modulation of atrioventricular (AV) nodal conduction during AF. In our laboratory, five cases with chronic AF and very fast ventricular response were treated with radiofrequency with a posterior septal approach. In all patients, we obtained very encouraging results with a constant decrease of ventricular rate (from 137 +/- 33 to 69 +/- 14 beats per minute). All cases treated by modulation of AV nodal conduction demonstrated an appropriate chronotropic response to the variations of the functional state that persists during the follow-up. More experience with longer follow-up and accurate pre- and postprocedure evaluations are needed to finalize the most appropriate technique of radiofrequency applications in these cases.

Adult↗

[Electrotherapy of supraventricular tachycardia (atrial fibrillation/atrial flutter)].

Contrary to patients with the WPW-syndrome and AV nodal reentry in whom radiofrequency catheter ablation is the therapy of first choice for cure from these arrhythmias instead of life-long medical therapy, pharmacologic therapy of atrial fibrillation and atrial flutter remains the treatment of choice in these patients. If, however, atrial fibrillation with rapid atrioventricular conduction is medically intractable and associated with severe haemodynamic impairment, these patients may be offered catheter ablation of AV conduction by radiofrequency energy. Compared to DC ablation, this approach is associated by an acceptable complication rate. Including the left ventricular approach in cases where it is not possible to ablate AV conduction using the venous approach, the success rate to achieve third degree AV block approaches 100%. With the development of temperature-controlled radiofrequency catheter ablation, a further reduction of side effects is anticipated. A disadvantage of this approach is the need for permanent pacemaker implantation (usually rate-adaptive VVI stimulation) after induction of complete AV block. Therefore, the advantage of normalization of ventricular rate by ablation of AV conduction has to be weighed against the risk of life-long pacemaker treatment for complete AV block in every patient. Patients with medically intractable typical atrial flutter may be offered the following alternative modes of electric treatment: selective ablation of the area of slow conduction sustaining circus movement in the right atrium underlying atrial flutter, by radiofrequency energy without interrupting AV conduction, implantation of a permanent antitachycardia pacemaker with electrodes positioned in the right atrium, radiofrequency catheter ablation of AV conduction.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Fibrillation↗

Results of sotalol (Darob) therapy in supraventricular tachyarrhythmias.

UNLABELLED: The benefit of sotalol therapy in atrial flutter and in atrial fibrillation was considered, aiming as well the suppression of paroxysmal episodes and the prevention of their recurrencies and the control of the ventricular rhythm in chronic cases. The prospective study comprises 60 patients institutionalized in the Cardiology Clinic in which the supraventricular tachyarrhythmia range included: atrial flutter (20 cases) and atrial fibrillation (40 cases), from which atrial fibrillation of recent onset (20 cases) and chronic atrial fibrillation with fast ventricular response (20 cases). Sotalol was administered orally in doses of 80 to 320 mg daily, b.i.d. The conversion to sinus rhythm was obtained in 45% of cases of atrial fibrillation of recent onset and in 30% of cases of atrial flutter. The prophylactic administration of sotalol on long term (6 months), in medium dose of 160 mg daily, may protect against the recurrence of the supraventricular arrhythmias (63.85%). As adverse effect, a case of "torsade des pointes" was recorded. IN CONCLUSION: 1) a greater benefit was noticed by using sotalol prophylactically for the recurrence of the supraventricular arrhythmias (63.85%) compared to the positive results in the therapy of acute cases (37.5%); 2) the maximal efficiency in the prevention of arrhythmia recurrencies can be observed in patients that present underlying compensated ischemic cardiopathy; 3) a decrease of 30% of the ventricular rhythm in patients with atrial fibrillation was obtained.

Anti-Arrhythmia Agents↗

Prevention of unbalanced lung perfusion and atrial arrhythmias after the lateral tunnel operation.

BACKGROUND: The lateral tunnel operation has become increasingly popular with pediatric cardiac surgeons, as it is technically reproducible, is relatively easy to perform, and can be used in a variety of patients with single-ventricle physiology. The main drawbacks of the original operation are uneven blood flow distribution to the lungs and increasing incidence of supraventricular arrhythmias over time. METHODS: In 1988, we modified this technique by avoiding narrowing of the tunnel at the superior vena cava-atrial junction, avoiding incorporation of the crista terminalis in the baffle suture line, and minimizing damage to the sinoatrial node. Between 1988 and 1995, 19 patients underwent this operation at Marie-Lannelongue Hospital in Paris. RESULTS: There was one early death and no late deaths. At a mean follow-up of 5.2 years, all survivors are in New York Heart Association class I. Early atrial flutter, related to atrial scarring secondary to multiple previous surgical procedures, developed in 1 patient, and late atrial flutter developed in 1 patient who had a previous Blalock-Hanlon atrial septectomy. All patients are currently in sinus rhythm. Atrial flutter did not occur in 17 patients who had had no previous atrial wall surgical procedure. CONCLUSIONS: We believe that the good long-term clinical results are directly attributable to our modifications, which ensure optimal hemodynamics and absence of rhythm disturbances. All patients who had not previously undergone operation on the atrial wall were free from supraventricular tachyarrhythmias at a mean follow-up of 5.2 years. This is a consequence of protecting the sinus node, crista terminalis, and Bachmann's bundle.

Atrial Flutter↗

Supraventricular tachycardia. ECG diagnosis and anatomy.

This paper reviews the anatomical substrates responsible for the induction and maintenance of supraventricular tachycardia and discusses the ECG findings associated with these tachycardias. The normal anatomy of the supraventricular conducting system, particularly within the atria, is complex with conduction proceeding along preferential pathway, which are in turn determined in part by the anisotropic properties of the atrial myocardium. There appear to be at least dual inputs to the atrioventricular node, a posteriorly situated slow pathway and an anterior fast pathway. It is sometimes possible to relate ECG findings directly to anatomical substrates; for example, in some cases of atrial tachycardia the site of the atrial focus (left or right, superior or inferior) can be determined by the polarity of the P wave. The anatomical substrates responsible for intra-atrial re-entry, atrial flutter and atrial fibrillation relate to anatomical barriers to impulse propagation and areas of slow conduction. In atrial flutter the crista terminalis, Eustachian valve, inferior vena cava, coronary sinus os, and tricuspid annulus have been identified as anatomical barriers to conduction around which a macro re-entrant circuit within the right atrium may conduct, usually in a counter-clockwise direction. Clockwise direction of conduction, and other mechanisms of tachycardia, occur in some of the less typical forms of atrial fluter. Atrial fibrillation is caused by multiple wavelets which randomly conduct through the atrial myocardium and are responsible for the irregular 'fibrillation waves' on the ECG. Supraventricular tachycardia presents as a narrow complex tachycardia unless pre-existing or rate-related bundle branch block is present. Less common causes for a broad complex tachycardia occurring in supraventricular tachycardia include an accessory atrioventricular or atriofascicular pathway conducting antegradely during tachycardia, or accessory pathway participation as a bystander during supraventricular tachycardia. ECG features which can help to distinguish between atrioventricular nodal re-entrant tachycardia and atrioventricular re-entrant tachycardia include: (1) the presence of a delta wave during sinus rhythm which is highly suggestive of atrioventricular re-entrant tachycardia as the mechanism of supraventricular tachycardia; (2) the finding of a pseudo s (lead II) or pseudo r' (lead V1) during tachycardia in atrioventricular nodal re-entrant tachycardia; (3) lengthening of the tachycardia cycle length in cases of atrioventricular re-entrant tachycardia when bundle branch block occurs ipsilateral to the accessory pathway and (4) the finding of QRS alternans during tachycardia which is suggestive of atrioventricular re-entrant tachycardia. "Long RP' tachycardia may be caused by an atrial tachycardia due to an inferiorly situated area of abnormal automaticity, atypical atrioventricular nodal re-entrant tachycardia with slow retrograde conduction, or atrioventricular re-entrant tachycardia with an accessory pathway conducting slowly from ventricle to atrium during tachycardia.

Atrioventricular Node↗

Length of excitation wave and susceptibility to reentrant atrial arrhythmias in normal conscious dogs.

We calculated the wavelength of the atrial impulse in chronically instrumented conscious dogs by measuring both conduction velocity and refractory period: wavelength = refractory period X conduction velocity. Implantation of multiple stimulating and recording electrodes allowed wavelength determination at four different areas: the right and left parts of Bachmann's bundle and the free walls of the right and left atria. During programmed electrical stimulation, three types of arrhythmias were observed: rapid repetitive responses, atrial flutter, and atrial fibrillation. During normal rhythm, the wavelength of the atrial impulse varied between 14 and 18 cm. Premature beats had a shorter wavelength, depending on the degree of prematurity. Premature beats that evoked rapid repetitive responses showed a critical shortening of the wavelength below 12.3 cm. Episodes of atrial flutter were induced at a wavelength below 9.7 cm, while fibrillation occurred at wavelengths shorter than 7.8 cm. We correlated the induction of these arrhythmias with the values of refractory period, conduction velocity, and wavelength during control and during administration of several drugs. Intravenous administration of acetylcholine shortened the wavelength by 30-40%, mainly because of refractory period shortening. Both propafenone and lidocaine had strong but opposite effects on refractoriness and conduction and, consequently, little effect on the wavelength. Quinidine markedly prolonged the refractory period, but prolongation of wavelength was less because of a simultaneous decrease in conduction velocity. d-Sotalol also increased refractory period, but because it had no appreciable effect on conduction velocity, this drug was the most effective in prolongation of wavelength. Linear discriminant analysis of the data showed that the refractory period and the conduction velocity each were poor parameters to predict the occurrence of the different arrhythmias (predictive value 48% and 38%, respectively). The combination of both properties, however, as expressed in the wavelength, was a more reliable index that predicted the induction of the different arrhythmias correctly in 75% of the cases. We conclude that the wavelength is a useful parameter for evaluating antiarrhythmic drugs.

Acetylcholine↗

[Diagnosis and clinical aspects of supraventricular tachycardia].

Supraventricular tachycardias are the most frequently occurring manifestations of arrhythmia. They make very high demands on the physician in respect of differential diagnosis and clinical assessment. Atrial tachycardias, atrial flutter and atrial fibrillation are mainly associated with an underlying cardiac disease. The isolated forms of atrial flutter and fibrillation without any detectable cardiac disease are a diagnostic challenge and are associated with a relatively high rate of complications. AV node reentry and AV tachycardias with accessory path are not associated with cardiac disease; they occur in 0.8% of the population and can be assessed with satisfactory accuracy in respect of mechanism and risk by means of the 12-lead ECG alone.

Atrioventricular Node↗

Differentiation of atrial rhythms from the electrocardiogram with coherence spectra.

Automated electrocardiogram (ECG) interpretation systems fail to reliably discriminate atrial fibrillation from sinus rhythm and other more regular atrial arrhythmias. Previously, magnitude-squared coherence (MSC), a frequency domain measure of the linear phase relation between 2 signals, has been shown to be a reliable discriminator of fibrillatory and nonfibrillatory cardiac rhythms when applied to intracardiac electrograms. This study determines whether MSC, when applied to the surface electrocardiogram, would discriminate between atrial fibrillation and nonfibrillatory atrial rhythms. MSC was analyzed by using 2 surface leads of a 10-second ECG. For 68 ECG recordings (23 sinus rhythm, 22 atrial flutter, and 23 atrial fibrillation), MSC was computed between leads II and V1 and the mean MSC in several frequency bands was examined. The performance of MSC was compared to previously published measures of ventricular irregularity and percent power in discriminating atrial fibrillation from nonfibrillatory rhythms. As hypothesized, atrial fibrillation exhibited low coherence in the 2 to 9 Hz band while nonfibrillatory atrial rhythms exhibited relatively moderate to high levels of coherence in the same frequency band. Mean MSC in the 2 to 9 Hz band was significantly lower for atrial fibrillation (range, 0.04 to 0.48; mean +/- SD: 0.15 +/- 0.11) than for sinus rhythm (range, 0.18 to 0.81; 0.47 +/- 0.17) (P <.0005) and atrial flutter (range, 0.06 to 0.80; 0.44 +/- 0.21) (P <.0005). Mean MSC in the 2 to 9 Hz band showed less overlap between atrial fibrillation and atrial flutter than R-R variability and percent power. However, R-R variability showed less overlap between atrial fibrillation and sinus rhythm than mean MSC and percent power. Thus, MSC and RRV both discriminate atrial fibrillation from more organized atrial rhythms. Conversely, percent power was highly variable for both atrial fibrillation and organized atrial rhythms. Results suggest that MSC applied to surface ECG may be used to quantify rhythm organization.

Adult↗

Cardioversion of atrial arrhythmias: audit of anticoagulation management.

Patients undergoing cardioversion for chronic atrial fibrillation should receive anticoagulation for three weeks before and four weeks after the procedure. Patients with atrial flutter and acute atrial fibrillation are also at risk of thromboembolic complications, so they too should be anticoagulated for cardioversion. Of the 36 acutely admitted patients who were cardioverted, 18 were in atrial fibrillation and 18 in atrial flutter. All except three of those in fibrillation were anticoagulated with heparin before cardioversion, but only seven received warfarin after cardioversion. Of those in flutter, 10 received heparin and eight received no anticoagulation before cardioversion. One patient underwent transoesophageal echocardiography before cardioversion to exclude atrial thrombi. Only two patients received warfarin for a month after cardioversion. Of the 20 elective cardioversions, 10 were in atrial fibrillation and 10 in atrial flutter. Five of those in fibrillation had received at least three weeks' treatment with warfarin before cardioversion and two underwent transoesophageal echocardiography; the other three received either up to two hours of heparin or no anticoagulation before cardioversion. Only five patients received warfarin for a month after cardioversion. Nine of those in flutter received a few hours of heparin before cardioversion and one was not anticoagulated; none underwent transoesophageal echocardiography or received warfarin after cardioversion. The results of this audit demonstrate that anticoagulation for atrial arrhythmias was inconsistent and often inadequate. A formal anticoagulation policy for cardioversion has now been adopted.

Anticoagulants↗

Ventricular performance and quality of life in patients who underwent radiofrequency AV junction ablation and permanent pacemaker implantation due to medically refractory atrial tachyarrhythmias.

UNLABELLED: In patients with drug refractory atrial tachyarrhythmias and previous failed attempts of ablation of the arrhythmia substrate, radiofrequency (RF) modulation or ablation of the atrioventricular (AV) junction is an alternative procedure. AIM: Of this study was to assess the efficacy and long term results of RF AV junction ablation in conjunction with permanent pacemaker implantation, in the management of patients with drug resistant atrial tachyarrhythmias. METHODS: Between 4/92 and 1/97, 46 patients (30 male, 16 female, 67 +/- 12 years) underwent RF AV junction ablation because of paroxysmal atrial fibrillation (24 patients), chronic atrial fibrillation (13 patients), atrial flutter (5 patients) and atrial tachycardia (4 patients). The underlying heart disease was dilated cardiomyopathy (16), ischemic heart disease (9), hypertensive heart disease (6), hypertrophic cardiomyopathy (3), atrial septal defect (2) and non structural heart disease (10). The duration of symptoms was 6.4 +/- 3.5 years at a maximal heart rate 169 +/- 24 bpm. The hospital admissions in the last 12 months were 8.2 +/- 3 per patient. The failed antiarrhythmic drugs were 3.5 +/- 2.1. The functional NYHA class was 2.7 +/- 0.6. Patients with atrial flutter and atrial tachycardia had previous failed attempts of RF ablation of the arrhythmia substrate. Thirty patients had a compromised left ventricular systolic function with LVEF below 50% (mean 34 +/- 9%). AV junction ablation was achieved in all patients after 4 +/- 2.5 RF applications. Post ablation, the selected pacing mode was DDD-R for the 33 patients with paroxysmal atrial tachyarrhythmias and VVI-R for the 13 pts with chronic atrial fibrillation. The dual chamber pacemakers implanted had the option of automatic mode switch. RESULTS: During the follow-up period of 28 +/- 13 months (6-47), AV conduction recovered in 1 patient. Antiarrhythmic treatment was necessary in only 7 patients. Post ablation the new functional NYHA class was 1.4 +/- 0.8 (p < 0.001). Post ablation hospital admissions, including ordinary pacemaker follow-up visits, were 4 +/- 1 per patient per year (p < 0.001). Six months after the procedure the LVEF of the study population was increased from 42 +/- 16% to 50 +/- 14% (p = NS). In the 30 patients with heart failure the LVEF was significantly increased to 46 +/- 8% (p < 0.05). Symptomatic relief or significant improvement was observed in all patients as showed by the answers given in a customized questionnaire before and after the procedure. CONCLUSIONS: In patients with drug refractory atrial tachyarrhythmias, RF AV junction ablation and permanent pacemaker implantation is an alternative therapy with excellent long term results in terms of arrhythmia control, ventricular performance and quality of life.

Aged↗

Plasma atrial natriuretic polypeptide concentrations during and after reversion of paroxysmal supraventricular tachycardias.

Plasma concentrations of immunoreactive atrial natriuretic polypeptide were raised in 22 of 23 patients with paroxysmal supraventricular tachycardia and in all seven patients with atrial flutter. Plasma concentrations of atrial natriuretic polypeptide rose soon after the onset of supraventricular tachycardia. A sample taken 30 minutes after reversion to sinus rhythm (pharmacological or non-pharmacological) showed a significant fall in 19 of the 23 patients with paroxysmal supraventricular tachycardia and all seven patients with atrial flutter. Because atrial natriuretic polypeptide has powerful natriuretic and diuretic properties, an increase may contribute considerably to the polyuria that is often associated with episodes of supraventricular tachycardia.

Adolescent↗

The use of drugs for cardioversion of recent onset atrial fibrillation and flutter. Focus on ibutilide.

Atrial fibrillation (AF) is the most common sustained arrhythmia, particularly in the elderly population. It is well recognised that AF is a major cause of stroke, even in the absence of underlying heart disease. Although AF and atrial flutter share many causes and may be seen in the same patient, there are differences between these arrhythmias: atrial flutter is less common, and the risk of stroke associated with it is less than that with AF. In addition to stroke, both AF and atrial flutter may cause cardiomyopathy, which may be fully reversible with effective treatment of the arrhythmia. Both AF and atrial flutter can result in severe symptoms and may precipitate heart failure, ischaemia and syncope. Recent research indicates that AF is a self-perpetuating arrhythmia, and that the longer it is left untreated the less likely it is that effective cardioversion will be possible. Drugs are an attractive option for the cardioversion of AF and atrial flutter because their use does not require anaesthesia. Antiarrhythmic drugs in class III of the Vaughan-Williams classification are effective in the treatment of AF, but they have adverse effects; several new 'pure' class III agents are under development. The first of these to be made available is ibutilide, a methanesulphonamide derivative. Initial results are encouraging, particularly for atrial flutter. However, the drug has the potential for proarrhythmic effects and physicians who use it will need to be aware of these.

Anti-Arrhythmia Agents↗

Ablation of focal atrial arrhythmia in patients with congenital heart defects after surgery: role of circumscribed areas with heterogeneous conduction.

BACKGROUND: In patients late after surgical repair of congenital heart disease (CHD), areas with abnormal electrophysiologic properties may serve as slow conducting pathways within a macroreentrant circuit or may be the source of focal atrial tachycardia. OBJECTIVES: The purpose of this study was to evaluate the role of abnormal areas during focal atrial tachycardia prior to ablation. METHODS: Electroanatomic activation mapping of 62 atrial tachycardias was performed in 43 consecutive patients (37 +/- 12 years) after surgical repair of CHD. The mechanism of atrial tachycardia was scar related intra-atrial reentry (n = 27), cavotricuspid-related atrial flutter (n = 21), atrial fibrillation (n = 2), or focal atrial tachycardia (n = 10). During intra-atrial reentry, channels of slow conduction could be identified in all patients. Subsequent ablation was directed toward connecting two nonconductive borders. The site of origin during focal atrial tachycardia showed fractionated potentials and/or continuous electrical activity. RESULTS: Ablation directed at isolating the source area resulted in termination of focal atrial tachycardia in all cases. In two patients, ablation of an area showing continuous electrical activity giving rise to fibrillatory conduction resulted in termination of atrial fibrillation. Ablation of intra-atrial reentry was successful in 70%. Atrial flutter and focal atrial tachycardia were successfully ablated in all patients. No complications were observed. CONCLUSION: In patients with surgically corrected CHD, atrial tachycardia most often is caused by a macroreentrant mechanism but in some is the result of a focal mechanism. Areas of abnormal conduction may serve not only as a zone of slow conduction within a macroreentrant circuit but also as the site of origin of a focal atrial arrhythmia. Catheter ablation directed at "source isolation" is effective in eliminating focal atrial tachycardia in patients with CHD.

Adolescent↗