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PubMed1999

Transverse conduction capabilities of the crista terminalis in patients with atrial flutter and atrial fibrillation.

OBJECTIVES: In this study, the transverse conduction capabilities of the crista terminalis (CT) were determined during pacing in sinus rhythm in patients with atrial flutter and atrial fibrillation. BACKGROUND: It has been demonstrated that the CT is a barrier to transverse conduction during typical atrial flutter. Mapping studies in animal models provide evidence that this is functional. The influence of transverse conduction capabilities of the CT on the development of atrial flutter remains unclear. METHODS: The CT was identified by intracardiac echocardiography. The atrial activation at the CT was determined during programmed stimulation with one extrastimulus at five pacing sites anteriorly to the CT in 10 patients with atrial flutter and 10 patients with atrial fibrillation before and after intravenous administration of 2 mg/kg disopyramide. Subsequently, atrial arrhythmias were reinduced. RESULTS: At baseline, pacing with longer coupling intervals resulted in a transverse pulse propagation across the CT. During shorter coupling intervals, split electrograms and a marked alteration of the activation sequence of its second component were found, indicating a functional conduction block. In patients with atrial flutter, the longest coupling interval that resulted in a complete transverse conduction block at the CT was significantly longer than that in patients with atrial fibrillation (285 +/- 49 ms vs. 221 +/- 28 ms; p < 0.05). After disopyramide administration, a transverse conduction block occurred at longer coupling intervals as compared with baseline (287 +/- 68 ms vs. 250 +/- 52 ms; p < 0.05). Subsequently, a sustained atrial arrhythmia was inducible in 15 of 20 patients. This was atrial flutter in three patients with previously documented atrial fibrillation and in eight patients with history of atrial flutter. Mapping revealed a conduction block at the CT in all of these patients. CONCLUSIONS: It was found that the CT provides transverse conduction capabilities and that the conduction block during atrial flutter is functional. Limited transverse conduction capabilities of the CT seem to contribute to the development of atrial flutter.

Aged↗
PubMed1999

Electrocardiographic differentiation of atrial flutter from atrial fibrillation by physicians.

The purpose of this study was to determine the ability of physicians to differentiate atrial flutter from atrial fibrillation on a surface electrocardiogram (ECG). A questionnaire containing three 12-lead ECGs was mailed to 689 physicians, with multiple-choice questions asking whether the rhythm on each ECG was atrial flutter or atrial fibrillation. ECG 1 showed atrial fibrillation with prominent atrial activity (>0.2 mV) in lead V1; ECG 2 displayed atrial fibrillation with prominent atrial activity (>0.2 mV) in leads III and V1; and ECG 3 displayed atrial flutter. Overall, ECG1 was correctly identified as atrial fibrillation by 79% of physicians, ECG 2 was correctly identified as atrial fibrillation by 31%, and ECG 3 was correctly identified as atrial flutter by 90%. Cardiology fellows and cardiologists correctly identified ECG 1 more often than house officers and internists (95% vs 63%; P < or = .01). ECG 2 was correctly identified by 26% of cardiology fellows and cardiologists and by 37% of house officers and internists (P = .10). ECG 3 was correctly identified by 91% of cardiology fellows and cardiologists and by 82% of house officers and internists (P = .06). In conclusion, atrial fibrillation is frequently misdiagnosed as atrial flutter. Misdiagnosis of atrial fibrillation occurs more often when atrial activity is prominent on an ECG in more than one lead.

Atrial Fibrillation↗
PubMed2006

Usefulness and limitations of the surface electrocardiogram in the classification of right and left atrial flutter.

Atrial flutter is a common arrhythmia that may cause significant symptoms, including palpitations, dyspnoea, chest pain and even syncope. Frequently, it is possible to diagnose atrial flutter with a 12-lead surface electrocardiogram (ECG), looking for distinctive waves in leads II, III, aVF, aVL, V1 and V2. Puech and Waldo developed the first classification of atrial flutter in the 1970s. These authors divided the dysrhythmia into types I and II. Therefore, in 2001, the European Society of Cardiology and the North American Society of Pacing and Electrophysiology developed a new classification of atrial flutter based not only on the ECG, but also on the electrophysiological mechanism. More recently, Scheinman and colleagues have provided an updated classification and nomenclature. Terms such as common, uncommon, typical, reverse typical or atypical flutter are abandoned, because they may generate confusion. The authors worked out a new terminology, which differentiates atrial flutter only on the basis of electrophysiological mechanism.

Atrial Flutter↗
PubMed1998

Pathophysiology of atrial flutter.

Atrial flutter is a macroreentrant tachyarrhythmia most often contained within the right atrium. Typical atrial flutter is defined on an electrocardiogram by the classic "sawtooth" pattern of flutter waves with negative polarity in leads II, III, and aVF. In contrast to atrial fibrillation, which is sustained by multiple reentrant wavelets defined by anatomic and/or functional barriers, typical atrial flutter is sustained by a single reentrant circuit defined by anatomical barriers. The isthmus of atrial tissue bordered by the inferior vena cava and the tricuspid annulus forms a critical zone of slow conduction in the reentry circuit of atrial flutter. The goal of radiofrequency catheter ablation is to create a line of conduction block across this isthmus. This line of block interrupts the flutter circuit and often provides long-term freedom from recurrence.

Atrial Fibrillation↗
PubMed1998

[Pathophysiologic mechanisms of atrial rhythm disorders. II. Atrial flutter].

Atrial flutter is a common cardiac dysrhythmia which responds for half of the supraventricular tachycardias with exception of atrial fibrillation. Activation and entrainment mapping studies in man and in animals confirmed the reentry mechanism of atrial flutter and demonstrated that the reentry circuit is located in the right atrium. The most important anatomical structures which enable the occurrence of atrial flutter are crista terminalis, Eustachian valve/ridge and tricuspid annulus. In typical atrial flutter the impulse rotates "counterclockwise". According to the present knowledge the reentry circuit surrounds a central obstacle made by the orifices of the superior and inferior vena cava linked by a line of functional block in the region of crista terminalis. The anterior barrier is created by tricuspid annulus. The anterolateral wall of the right atrium is activated craniocaudally. Crista terminalis and tricuspid annulus form a funnel which leads the impulse into the isthmus with slow conduction located between the vena cava orifice and tricuspid annulus. Septal activation is ascending and the activation wave considerably widens and becomes irregular. The upper link of the circuit is located above and anteriorly to the superior vena cava. The left atrium is activated passively and does not play an important role in the reentrant circuit. Reverse flutter has the same substrate as typical flutter but rotates in an opposite "clockwise" manner.

Animals↗
PubMed2000

[Theory and practical approaches in catheter ablation of atrial flutter].

Atrial flutter can be understood as atrial tachycardia due to a single intraatrial macroreentrant circuit that is determined by fixed or functional boundaries. In various types of atrial flutter, radiofrequency ablation became an established curative therapy. During the course of an ablation procedure, initially, the reentrant circuit has to be determined, e.g. by activation and entrainment mapping. Subsequently, the boundaries have to be identified. By connecting two appropriate boundaries with a linear lesion, the intraatrial reentrant circuit can be inhibited. Finally, it should be proven that the linear lesion results in a complete line of conduction block. Doing so, the acute and long-term results of atrial flutter ablation are comparable to those of other supraventricular tachycardias.

Atrial Flutter↗
PubMed1998

Atrial flutter.

Atrial flutter is a specific electrical entity. It has a now well-established mechanism involving a single macro-re-entrant circuit. Whilst many patients with atrial flutter may develop atrial fibrillation, atrial flutter deserves its own recognition and requires specific management. Acute termination by drugs is possible, although adding pacing improves efficacy. Ibutilide is a new intravenous therapy with considerable efficacy by with a risk of torsade de pointes. For long-term control, radiofrequency ablation is gradually supplanting chronic oral antiarrhythmic strategies.

Anti-Arrhythmia Agents↗
PubMed1996

Comparative efficacy of intravenous ibutilide versus procainamide for enhancing termination of atrial flutter by atrial overdrive pacing.

This study compares the influence of intravenous ibutilide, a class III antiarrhythmic agent, with procainamide, a class IA antiarrhythmic agent, and with placebo on its ability to terminate atrial flutter using rapid atrial pacing. Fifty-nine episodes of atrial flutter in 54 patients who failed to terminate with an intravenous infusion of ibutilide, procainamide, or placebo alone underwent attempts at pacing termination using a standard protocol of burst atrial overdrive pacing. Atrial flutter cycle length and atrial monophasic action potential duration recorded from the right atrium during atrial flutter were measured at baseline and following infusion of ibutilide, procainamide, or placebo. Both ibutilide and procainamide significantly enhanced (p <0.001) pacing-induced termination of atrial flutter compared with placebo. Pacing converted 2 of 11 patients (18%) who received placebo, 13 of 15 patients (87%) who received ibutilide, and 29 of 33 patients (88%) who received procainamide to sinus rhythm. Ibutilide and procainamide compared with placebo markedly reduced (p <0.001) the incidence of pacing-induced atrial fibrillation. The atrial flutter cycle length was prolonged significantly less (p <0.001), and the atrial monophasic action potential duration was increased significantly more (p <0.001) by ibutilide than by procainamide. Although the electrophysiologic changes induced by these antiarrhythmic agents contributed to facilitating pacing-induced termination, neither tachycardia cycle length nor action potential duration were useful predictors of the ability of pacing to terminate atrial flutter. In conclusion, despite differing electrophysiologic effects, the use of intravenous ibutilide or procainamide enhances the termination of atrial flutter by atrial overdrive pacing.

Aged↗
PubMed1996

Pharmacologic therapy of atrial flutter.

Atrial flutter is a relatively rare but nonetheless important arrhythmia. Its mechanism and anatomy have been defined as right atrial macroreentry. It responds to treatment with a variety of antiarrhythmic agents but, in general, drug efficacy for acute termination is low. The addition of pacing to drug therapy markedly improves the success rate for restoration of sinus rhythm. Useful antiarrhythmic agents include amiodarone, sotalol, disopyramide, flecainide, and propafenone, but definitive efficacy studies have not been performed. The risk of provoking 1:1 AV conduction and a marked increase in ventricular response rate is always present. AV nodal blocking drugs (digoxin and verapamil) probably offer protection from this unwanted effect, but the prevalence of 1:1 conduction and the efficacy of AV nodal blockade remain to be established. When drug management fails, there is a place for radiofrequency ablation. Little is known about the thromboembolic risk of atrial flutter. As a consequence, the role of prophylactic anticoagulation is uncertain. Current interest in atrial flutter will ensure that these and other clinical questions are answered in the near future.

Animals↗
PubMed1996

Primary ablation of atrial flutter and atrial fibrillation.

Direct treatment of atrial flutter and atrial fibrillation--that is, attempting to prevent arrhythmia recurrences by ablating atrial tissue--has been a challenge because of uncertainty about the location of optimal target tissues as well as the amount of atrial tissue requiring destruction to effect cure. Advances have yielded success rates for ablation of the common form of atrial flutter comparable to those for other types of supraventricular tachycardia and provide reason for optimism about the use of catheter techniques, to treat atrial fibrillation definitively. This article discusses some of these advances as well as the current status of catheter ablation for atrial flutter and atrial fibrillation and, finally, what the future may bring.

Animals↗
PubMed1977

Entrainment and interruption of atrial flutter with atrial pacing: studies in man following open heart surgery.

To examine the question of why the pacing rate and duration of atrial pacing are crucial factors in the successful interruption of atrial flutter, studies were performed on 30 patients in the period following open heart surgery. In each patient the diagnosis of atrial flutter was made using a pair of wire electrodes placed on the right atrial epicardium at the time of operation and brought out through the anterior chest wall. The same electrodes were used for atrial pacing. Pacing faster than the spontaneous rate of the atrial flutter which failed to interrupt the atrial flutter was associated with transient entrainment of the atrial flutter up to the atrial pacing rate. Atrial flutter was interrupted successfully when the atria were paced at a rate which was too fast for the atrial flutter to follow. This was heralded by the conversion of previously negative flutter waves to positive atrial complexes in ECG lead II. When pacing the atria at a constant rate, 2-22 seconds with a mean of 10 seconds were required to interrupt the atrial flutter.

Adult↗
PubMed2001

Mechanism of spontaneous transition from typical atrial flutter to atrial fibrillation: role of ectopic atrial fibrillation foci.

Paroxysmal AF has been known to be initiated by ectopic beats, especially in the pulmonary veins (PVs), and radiofrequency catheter ablation could cure it. We considered that the spontaneous transition from typical atrial flutter to AF also could be initiated by ectopic beats. Twenty patients (18 men, mean age 66 +/- 14 years) with episodes of spontaneous transition from typical atrial flutter to AF were included in this study. They underwent detailed mapping of both atria. All the patients had spontaneous AF initiated by ectopic beats, and all of them had typical atrial flutter and spontaneous transition from typical atrial flutter (12 patients with counterclockwise atrial flutter and 8 patients with clockwise atrial flutter) to AF. The transition was initiated by ectopic beats from the PVs (17 foci, 85%), crista terminalis (2 foci, 10%), and superior vena cava (1 focus, 5%). After successful ablation of AF foci, typical atrial flutter was induced again, but no spontaneous transition was found after at least 10 minutes of observation. We concluded that paroxysmal AF and spontaneous transition from typical atrial flutter to AF were initiated by ectopic beats, and successful catheter ablation of the ectopic foci can eliminate paroxysmal AF and spontaneous transition from typical atrial flutter to AF.

Aged↗
PubMed1997

Effects of high-frequency atrial pacing in atypical atrial flutter and atrial fibrillation.

Atypical atrial flutter has, hitherto, been relatively refractory to termination by rapid atrial pacing. High-frequency pacing (HFP) in the atrium, for termination of atrial flutter or atrial fibrillation (AF), and the electrophysiologic effects related to it have not been examined. We examined the clinical efficacy, safety, and electrophysiologic mechanisms of HFP using 50-Hz bursts at 10 mA applied at the high right atrium in patients with atypical atrial flutter (group 1) or AF (group 2), using a prospective randomized study protocol. Four burst durations (500, 1000, 2000, and 4000 ms) were applied at the high right atrium repetitively in random sequence in 22 patients with spontaneous atrial flutter or AF. Local and distant right and left atrial electrogram recordings were analyzed during and after HFP. HFP resulted in local and distant right and left atrial electrogram acceleration in 8 of 10 patients (80%) in group 1 but caused less frequent local atrial electrogram acceleration (6 of 12 patients) and no distant atrial electrogram effects in group 2 (p < .05 versus group 1). The HFP protocol was effective in arrhythmia termination in 6 of 10 patients in group 1 but in no patient in group 2 (p < .05 versus group 1). Standard HFP protocol applied at the high right atrium can frequently alter atrial activation in both atria and can terminate atypical atrial flutter. Efficacy in AF is limited, probably due to limited electrophysiologic actions beyond the local pacing site.

Adult↗
PubMed2000

Radiofrequency ablation of atrial tachycardia and atrial flutter.

Atrial endocardial mapping defines the activation pattern during regular atrial arrhythmias. The response to pacing (entrainment mapping) yields additional information about the mechanism and location of the circuit. Regarding radiofrequency ablation, the regular atrial tachycardias may be classified in two broad patterns: 1) macroreentrant tachycardias, characterized by circular activation, including typical atrial flutter and reentry around scars, and 2) focal tachycardias, characterized by radial activation from a small myocardial area. Catheter ablation of right atrial macroreentrant circuits and focal tachycardias are now standard procedures. The target for ablation of focal tachycardia is the point of earliest activation, and single application is effective in most cases. Ablation of macroreentrant tachycardias requires identifying a narrow isthmus inside the circuit, and linear ablation is needed in most cases. The goal of radiofrequency ablation for typical atrial flutter is to interrupt conduction across the inferior vena cavatricuspid valve isthmus. The procedure is highly effective and safe, although recurrences of the arrhythmia are not rare. Incisional macroreentrant tachycardias after surgical correction of congenital heart diseases and primary cardiac tumors may also be ablated identifying critical isthmuses in the circuit by a combination of mapping and entrainment techniques. Left atrial macroreentry is much less known and at present more information is needed before catheter ablation becomes a standard procedure.

Adult↗
PubMed2004

[New concepts in the diagnosis and treatment of atrial flutter].

Atrial flutter may now be very frequently and definitely cured in a single session of radiofrequency ablation. However, the very name of atrial flutter gives rise to a certain confusion. Clinical experience from everyday activity in ablation laboratories, especially since the introduction of new mapping techniques, has shown that this entity is in fact multiple. Flutters may be classified by their electrocardiographic appearance and/or their electrophysiological mechanism with as many prognostic as therapeutic implications. This article reviews diagnostic features of typical and atypical flutter and the different treatments which may be proposed in different clinical situations.

Atrial Flutter↗
PubMed1999

Effect of radiofrequency ablation on atrial mechanical function in patients with atrial flutter.

Atrial stunning, as assessed by left atrial appendage emptying and increased spontaneous echo contrast, is known to occur following direct-current cardioversion of atrial fibrillation (AF) and atrial flutter (AFI). Little is known on atrial mechanical function and the time course of atrial recovery following radiofrequency ablation of AFI. Fourteen patients undergoing radiofrequency ablation of persistent typical counterclockwise AFI were enrolled. Two-dimensional and pulse Doppler transesophageal echocardiography (TEE) were performed before ablation and immediately following restoration of sinus rhythm. Left atrial spontaneous echo contrast grades, left atrial appendage emptying fractions, and peak left atrial appendage emptying velocities were measured. Transthoracic echocardiography (TTE) was performed immediately after ablation, then repeated after 1 day, 1 week, and 6 weeks to measure peak transmitral velocities and percent atrial contribution to ventricular filling. Left atrial appendage emptying velocities decreased significantly following AFI termination (44 +/- 23 cm/s before ablation vs 25 +/- 14 cm/s after ablation, p = 0.01). Left atrial appendage emptying fractions also decreased significantly (0.48 +/- 0.1 preablation vs 0.34 +/- 0.17 postablation, p = 0.02). New spontaneous echo contrast developed in 4 patients (29%) after ablation. Four patients had complete atrial standstill after ablation, and 1 patient developed a new left atrial appendage thrombus. The percent atrial contribution to ventricular filling recovered progressively over 6 weeks with significant improvement in peak transmitral velocities at day 7. Thus, atrial stunning occurs after catheter ablation of AFI and may lead to rapid formation of thrombus in the left atrial appendage. Significant improvement in left atrial function occurs in 7 days.

Aged↗
PubMedDate not supplied

Atrial flutter.

Atrial flutter is a supraventricular tachydysrhythmia believed to arise from electrophysiologic disturbances in the atria. It tends to be an unstable rhythm and is usually associated with intrinsic cardiac or pulmonary disease or adverse extrinsic influences on the heart. It is due to either a reentry mechanism or an increased atrial automaticity. Atrial depolarization is regular at a rate of 260 to 340 beats per minute. With a normal atrioventricular (AV) node there is usually a physiologic second-degree block with resultant 2:1 conduction. Higher degrees of AV block can occur in patients with AV nodal disease, increased vagal tone, or when certain drugs are in use. One-to-one conduction may occur in patients with accessory AV nodal pathways. In this situation, serious adverse effects are often seen, including palpitations, dizziness, syncope, angina, and dyspnea. Electrical cardioversion is the safest and most reliable way of terminating atrial flutter and its use should not be delayed in an unstable patient. In the nonemergent situation a variety of medications alone or in combination can be used to convert the rhythm or slow ventricular response.

Atrial Flutter↗
PubMed1993

[Non-drug treatment of atrial flutter].

Atrial flutter is a relatively rare type of cardiac arrhythmia. The clinical tolerability of such attacks may be poor and the efficacy of antiarrhythmic drugs is limited, both in terminating the flutter and in preventing its recurrence. Non-drug treatment is particularly important in this domain. Stopping the flutter is now given top priority and is achieved by rapid atrial stimulation, which is usually delivered by the trans-oesophageal route. This results in restoration of sinus rhythm in between 60 and 90% of cases. External electrical shocks are used only in forms involving poor hemodynamic safety or if the transesophageal approach has failed. It is nearly always successful with low energy levels of 50 to 100 J. Several options can be considered for the etiological treatment. One is the implantation of an anti-tachycardic pacemaker, which is based on the principle of interrupting the flutter by rapid atrial stimulation, the treatment being triggered either manually or automatically. The outcome is disappointing. In disorders of the atrium, atrial flutter can be abolished by suppressing the episodes of bradycardia. Electrical interruption of the bundle of His by catheterization is indicated for the treatment of severe, refractory forms. It is combined with the insertion of a cardiac stimulator, generally VVIR. The functional improvement obtained is remarkable. It has also been suggested that flutter can be dealt with by a direct approach to the right atrium by means of either surgery or catheterization. Experience with endocardial treatment by a radiofrequency current is still limited, but initial results are encouraging.

Atrial Flutter↗