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Previous therapy with amiodarone increases the recurrence rate in successfully ablated patients with isthmus-dependent atrial flutter.

Ablation of isthmus-dependent atrial flutter in patients previously medicated with antiarrhythmic drugs may cause functional isthmus block during ablation, and subsequent discontinuation of therapy may lead to incomplete isthmus block (and recurrence). This may be particularly important if the drugs previously used have long plasma half-lives (and washout periods). The objective of this study was to evaluate whether the recurrence rate of isthmus-dependent atrial flutter was greater in patients previously medicated with antiarrhythmic drugs and whether there were differences in recurrence rate with different types of antiarrhythmic drugs. During a mean follow-up of 20 +/- 7 months, we observed 57 patients with previous successful ablation of isthmus-dependent atrial flutter. This population of patients was divided into three groups according to the type or absence of previous antiarrhythmic drugs: Group 1--n = 18, patients previously medicated with amiodarone; Group 2--n = 27, patients previously medicated with drugs with short plasma half-lives (propafenone; flecainide; beta-blockers); Group 3--patients without previous antiarrhythmic medication. In all 57 patients bidirectional isthmus block was achieved after the ablation procedure; 8 mm non-irrigated tip catheters were used. During follow-up a recurrence rate of 33% was observed in Group 1 (6 recurrences in 18 patients; p < 0.05 in comparison with Groups 2 and 3); 3.7% in Group 2 (1 in 27 patients) and 0% recurrence rate in Group 3. We conclude that in our study the patients previously medicated with amiodarone had a higher recurrence rate of the arrhythmia compared to patients not previously medicated with antiarrhythmic drugs or medicated with antiarrhythmics with short plasma half-lives.

Amiodarone↗

Predictors of atrial flutter with 1:1 conduction in patients treated with class I antiarrhythmic drugs for atrial tachyarrhythmias.

OBJECTIVES: The purpose of the study was to look for the predictor factors of atrial proarrhythmic effects of class I antiarrhythmic drugs. BACKGROUND: Class I antiarrhythmic drugs may induce or exacerbate cardiac arrhythmias. The predictors of ventricular proarrhythmia are known. The predictors of atrial flutter with 1:1 conduction are unknown. METHODS: Clinical history, EGG, signal-averaged EGG (SAECG) and electrophysiologic study were analysed in 24 cases of 1:1 atrial flutter with class I AA drugs and in 100 control patients without history of 1:1 atrial flutter with class I AA drugs. RESULTS: The ages of patients varied from 46 to 78 years. Underlying heart disease was present in nine patients. The surface EGG revealed the presence of a short PR interval (PR<0.13 ms), visible in leads V5, V6 in eight (35%) patients with normal P wave duration; in other patients with prolonged P wave duration, PR seemed normaL On SAECG recording, there was a pseudofusion between P wave and QRS complex. The electrophysiologic study revealed some signs indicating a rapid AV nodal conduction (short AH interval or rate of 2nd degree AV block at atrial pacing >200 beats/mm) in 19 of the 23 studied patients. All patients, except one, had at least one sign indicating a rapid AV nodal conduction (short PR and/or P wave-QRS complex continuity on SAECG). In the control group, seven patients (7%) had a short PR interval (P<0.01) and 11 (11%) had a pseudofusion between P wave and QRS complex on SAECG (P<0.001). The P wave-QRS complex pseudofusion on SAECG had a sensitivity of 100% and a specificity of 89% for the prediction of an atrial proarrhythmic effect with class I antiarrhythmic drug. CONCLUSION: We recommend avoiding class I AA drugs in patients with a short PR interval on surface EGG and to record SAECG in those with apparently normal PR interval to detect a continuity between P wave and QRS complex, which could indicate a rapid AV nodal conduction, predisposing to 1:1 atrial flutter with the drug.

Adult↗

Atrial and ventricular electromechanical function in 1-ventricle hearts: influence of atrial flutter and Fontan procedure.

OBJECTIVE: Echocardiography was used to study electromechanical atrial and ventricular function in adult patients with a 1-ventricle heart who were in sinus rhythm to better understand the recurrence of atrial flutter in these conditions. Patients who had recent atrial flutter, with and without the Fontan procedure, were compared with those who had no arrhythmia. METHODS: This was a prospective study that used M-mode and 2-dimensional Doppler echocardiography and electrocardiography. Conventional measurements were used to evaluate ventricular long-axis function. Basic data were drawn from case notes. The setting was a designated quaternary service for grown-up congenital heart patients (GUCH) in a tertiary referral center for cardiology and cardiac surgery. From January 1997 to February 1998, 26 consecutive adult patients (aged >16 years) with a heart with one functioning ventricle and a history of atrial flutter were studied: group 1, with non-Fontan palliative surgery or no surgery (10 patients), and group 2, with Fontan-type repair (16 patients). Also studied were 20 patients with a 1-ventricle heart but no history of atrial flutter. These 20 patients were divided into 2 groups: control 1, which comprised 14 patients with previous shunts or no surgery, and control 2, which consisted of 6 patients with Fontan repair. RESULTS: P-wave duration on the electrocardiogram was similar in the 4 patient groups, but the amplitude was reduced in group 2 and control 2 (patients with Fontan surgery) (P <.016). Bifid P wave was seen in 5 (50%) of 10 patients in group 1 and in 6 (43%) of 14 patients in control 1, but it was not seen in patients with Fontan (P <.01). Ventricular systolic and diastolic dimensions and fractional shortening were not different between patients and controls. Right atrial transverse dimensions were greater in group 2 patients compared with those in controls. Significant atrioventricular valve regurgitation was seen in 9 of 10 group 1 patients but in none of the others. Right-sided total long-axis excursion and atrial A-wave amplitude were depressed in group 2 patients compared with the values in the others. The onset of right atrial shortening was delayed by 50 ms in group 2 compared with control 2, whereas the left atrial shortening was delayed by 30 ms in group 1 compared with control 1. This particular disturbance remained 6 months after cardioversion. CONCLUSION: In 1-ventricle hearts, significant atrioventricular valve regurgitation is commonly associated with atrial flutter in patients who did not undergo the Fontan procedure, and with electromechanical disturbances in those who did. Recognition of disturbances in ventricular long-axis function may thus assist in the identification of patients with a 1-ventricle heart who are prone to atrial flutter.

Adolescent↗

Mitral valve closure in atrial flutter.

12 patients who had atrial flutter without clinical, echocardiographic or angiographic evidence of aortic insufficiency were studied with simultaneous echo- and phonocardiograms. In patients with high-grade atrioventricular (AV) block, the mitral valve opened and closed with each flutter wave. Of seven patients, two had persistent and five had intermittent early mitral valve closure before QRS inscription. In five patients (three with 2:1 AV block) the mitral valve closed on time. In one patient with a mitral valve prosthesis, echocardiography and cinefluorography demonstrated closure during mid-diastole, with reopening in late diastole after a flutter wave. Final valve closure occurred before the onset of the QRS, and each closure was associated with a click. Simultaneous phonocardiographic analysis in these patients demonstrated that the first heart sound intensity was inversely related to the degree of mitral valve preclosure. This relationship was independent of the length of the RR interval. Thus, atrial flutter independent of any other cause of abnormal hemodynamics may produce early mitral valve closure. The echocardiographic finding of premature mitral arrhythmias, may not have the same diagnostic or prognostic significance previously described in patients with sinus rhythm and normal AV conduction.

Adult↗

The effects of class IA antiarrhythmic drug on the common type of atrial flutter in combination with pacing therapy.

In 11 patients with common type of atrial flutter (common AF), rapid atrial pacing from the high right atrium was performed before and/or after class Ia antiarrhythmic drug administration, confirming transient entrainment by decreasing the pacing cycle length by 10 ms. In 10 patients before the drug administration, common AF was not interrupted although the pacing cycle length was decreased to 200 ms in 5 patients, accelerated atrial flutter or atrial fibrillation was induced in 4 patients, and common AF was converted into sinus rhythm in only 1 patient. After the drug administration common AF was converted into sinus rhythm in 5 out of 6 patients. The class Ia antiarrhythmic drug prolonged the common AF cycle length (255 +/- 12 ms vs. 298 +/- 37 ms, p less than 0.005) and widened the entrainment zone (64 +/- 7 ms vs. 90 +/- 20 ms, p less than 0.05). The widening of the entrainment zone and the prolongation of the common AF cycle length facilitate the successful conversion of common AF at a longer pacing cycle length, which would not precipitate atrial fibrillation or accelerated atrial flutter. The combination therapy of rapid atrial pacing and the class Ia antiarrhythmic drug is thought to be useful in the therapy of common AF.

Adult↗

Validation of double-spike electrograms as markers of conduction delay or block in atrial flutter.

Recent mapping studies of atrial flutter have shown that fragmented electrograms can be found in most cases from the posterior, posteroseptal and posterolateral walls of the right atrium. The fragmentation pattern most often consists of a double spike. To further assess double-spike electrograms as a possible marker of conduction delay, bipolar electrograms were continuously recorded during atrial overdrive pacing of common flutter from the right atrium (7 patients) and from the proximal coronary sinus (5). Baseline double-spike separation of 50 to 130 ms was unchanged in 1 patient and slightly increased (5 to 25 ms) in 4 by coronary sinus pacing. The electrogram sequence was unchanged and the surface morphology was similar to that of basal flutter. Right atrial pacing decreased double-spike separation by 25 to 85 ms from basal values of 45 to 175 ms (23 to 83%), suggesting fusion in the area of fragmented electrograms. These findings suggest that double-spike electrograms represent activation on both sides of a conduction delay zone. The changes induced in these electrograms by pacing from the anterior right atrium and the coronary sinus are consistent with flutter circuits rotating counterclockwise (frontal plane) in the posterior right atrial wall in common atrial flutter.

Atrial Flutter↗

Altered dystrophin expression in the right atrium of a patient after Fontan procedure with atrial flutter.

Underlying mechanisms in the development of atrial flutter or intra-atrial re-entry tachycardia in patients with structural cardiac abnormalities remain poorly defined. The right atrial myocardium from two patients with congenital heart disease was evaluated, of whom one presented with severe right atrial dilation and arrhythmia and the other with a normal right atrium, to assess whether increased right atrial pressure and volume overload give rise to sarcolemmal alteration. N-terminus dystrophin staining in the atrium from the patient who had undergone a Fontan procedure showed a normally distributed but significantly reduced staining signal compared with the second patient. This is the first report that patients with severe right atrial dilation and atrial flutter have marked reduction in atrial dystrophin expression.

Atrial Flutter↗

Conduction barriers in human atrial flutter: correlation of electrophysiology and anatomy.

Animal models of atrial flutter and early mapping studies of human atrial flutter have suggested the importance of barriers in this reentrant arrhythmia. The consistency of rate and morphology of typical atrial flutter suggest a common anatomic substrate for this arrhythmia. The unique endocardial architecture of the right atrium provides anatomic barriers around which reentry occurs. In typical human atrial flutter, the crista terminalis, eustachian ridge, and tricuspid annulus have been identified as barriers to conduction. The importance of conduction barriers, methodology for defining barriers, the anatomic substrate for these barriers, and the role of these barriers in other atrial arrhythmias are discussed.

Animals↗

Incidence and clinical significance of transformation of atrial fibrillation to atrial flutter in patients undergoing long-term antiarrhythmic drug treatment.

AIMS: To investigate the rate of transformation of atrial fibrillation to atrial flutter in patients taking antiarrhythmic drugs for the prophylaxis of atrial fibrillation, we retrospectively analysed data from 305 consecutive patients with paroxysmal atrial fibrillation (155 male; mean age 63 +/- 11 years) treated with ventricular rate controlling drugs, antiarrhythmic drugs, or without drugs. METHODS AND RESULTS: At a mean follow-up of 9 months (range 1-24) all patients experienced recurrence of arrhythmia: 48 (14.6%, Group A) suffered Type 1 atrial flutter, and 257 (85.4%, Group B) atrial fibrillation. The relative rate of recurrence of atrial flutter vs atrial fibrillation was similar in patients without treatment or with ventricular rate controlling drugs (from 6.8% to 14.6%, P=ns). However, recurrence was higher (25%) in patients administered antiarrhythmic drug therapy. The relative risk in these patients was 3.02 times greater, compared with patients without treatment, or treated with rate controlling drugs (P<0.001). There were no differences between groups concerning the baseline clinical characteristics and the clinical consequences of the recurrence; patients with atrial flutter had a lower rate of conversion to sinus rhythm (42% vs 64%) and a higher rate of hospital admission (69% vs 36%) compared with those with atrial fibrillation. Six patients (8.5%) experienced 1:1 atrioventricular conduction during atrial flutter with a ventricular rate of 240-280 beats x min(-1). CONCLUSION: Our data suggest that the use of antiarrhythmic drugs for the prophylaxis of atrial fibrillation is associated with a threefold increase in the probability of Type 1 atrial flutter recurrence, as opposed to atrial fibrillation, which may have important clinical consequences, but which did not in our study.

Aged↗

Catheter ablation of atrial flutter using radiofrequency current: cumulative experience in 61 patients.

UNLABELLED: We present our experience with radiofrequency catheter ablation of common atrial flutter. METHODS: Radiofrequency ablation of atrial flutter was performed utilizing percutaneous techniques and the anatomic approach under conscious sedation or general anesthesia. RESULTS: Sixty-one consecutive patients (51 men, and 10 women) aged 59 +/- 12 years with medically refractory atrial flutter underwent catheter ablation. Thirty-eight patients (62%) had structural heart disease, including complex congenital anomalies in one patient. Atrial flutter ablation was successfully accomplished in 55 patients (90%) in one session. There were no complications, and all patients were discharged within 24-hours of the procedure. During a mean follow-up of 10 +/- 9 months, recurrent atrial flutter occurred in 11 patients (18%), eight of which successfully underwent repeat atrial flutter ablation. CONCLUSIONS: Catheter ablation of atrial flutter using radiofrequency current is safe and has a high success rate. This nonpharmacologic approach should be considered as the first line of therapy for common atrial flutter prior to the institution of antiarrhythmic drugs.

Adolescent↗

Characterization of double potentials in a functionally determined reentrant circuit. Multiplexing studies during interruption of atrial flutter in the canine pericarditis model.

OBJECTIVES: We tested the hypothesis that double potentials recorded during atrial flutter in a functionally determined reentrant circuit reflect activation of the reentrant wave front around an area of functional conduction block. BACKGROUND: The center of the atrial flutter reentrant circuit in the sterile pericarditis canine model is characterized by double potentials. METHODS: We studied 11 episodes of atrial flutter in eight dogs during interruption of atrial flutter while pacing the atria. A multielectrode mapping system was used to record simultaneously from 190 electrodes on the right atrium (location of reentry). RESULTS: Interruption of atrial flutter occurred when the orthodromic wave front from the pacing impulse blocked in an area of slow conduction in the reentrant circuit. The response of the double potential with interruption of atrial flutter depended on the location of the recording site relative to this area of block. Two types of response were seen. When the double potential was recorded orthodromically distal to this area of block, interruption of atrial flutter was associated with disappearance of the second deflection, and continued pacing after interruption of atrial flutter was not associated with reappearance of the second potential. When the double potential was recorded at a site orthodromically proximal to the area of block, interruption of atrial flutter was not associated with disappearance of the second potential, and when rapid atrial pacing was continued, the double potential remained despite disappearance of the atrial flutter reentrant circuit. CONCLUSIONS: Double potentials represent functional conduction block in the center of the reentrant circuit, with each deflection of the double potential reflecting activation on either side of the area of functional block. The data also demonstrate that double potentials are not limited to a reentrant circuit, as they were recorded on either side of an area of block in the absence of such a circuit.

Action Potentials↗

Catheter ablation for atrial flutter and fibrillation. An effective alternative to medical therapy.

Atrial flutter and atrial fibrillation are common arrhythmias that can be difficult to manage clinically. In many patients, these conditions are refractory to pharmacologic therapy because of drug failure or intolerance. Radiofrequency catheter ablation may be a reasonable alternative in patients with typical atrial flutter. The procedure has a high initial success rate and a low complication rate. However, recurrence after ablation is common, and a second treatment session may be needed. In selected patients with atrial fibrillation, radiofrequency ablation can be useful for rate control. However, its use in curing chronic fibrillation is still experimental. The procedure involves insertion of a pacemaker, anticoagulation therapy is still needed in most patients, and the need for antiarrhythmic medication may not be obviated.

Atrial Fibrillation↗

Radiofrequency ablation of atrial flutter: a randomized controlled study of two anatomic approaches.

Atrial flutter often results from a macroreentrant circuit that uses anatomic structures within the right atrium as its borders. RF ablation at the site of an obligatory isthmus can eliminate the atrial flutter circuit. The aim of this study was to compare two approaches to atrial flutter ablation: the septal (septal aspect of the tricuspid valve annulus to coronary sinus ostium and Eustachian ridge) approach versus the posterior (inferior vena cava to tricuspid valve annulus) approach. Twenty patients were randomized to either the "septal" or "posterior" approach. Entrainment mapping and/or confirmation of bidirectional isthmus conduction at baseline were performed in those patients in atrial flutter and normal sinus rhythm, respectively. RF ablation was performed with standard catheters and techniques. Crossover was permitted after two lines of RF lesions. Endpoints included acute success rates and fluoroscopy times. There was no statistically significant difference in the success rate between the two approaches using intention-to-treat analysis. Fluoroscopy times in the septal versus posterior approaches were 58.4 +/- 30.3 versus 70.8 +/- 31.1 minutes, respectively (P = 0.7). There was more frequent crossover in patients assigned to the septal approach and the one major complication, atrioventricular block, also occurred using this approach. There was no statistically significant difference in the success rate or fluoroscopy times between the septal and posterior approaches to atrial flutter ablation. However, given the risk of atrioventricular block with the septal approach, the posterior approach should be the preferred initial choice.

Atrial Flutter↗

Uncommon atrial flutter: characteristics, mechanisms, and results of ablative therapy.

Thirty-seven patients with atrial flutter were studied with catheter mapping and radiofrequency ablation. Uncommon atrial flutter occurred in 20 out of 37 (54%) patients. Atrial endocardial mapping showed two types of uncommon atrial flutter. In 15 patients (group I) it was characterized by a single clockwise circuit whereas in 5 patients (Group II) it was characterized by the presence of more than one circuit and/or localized atrial fibrillation. RFA ablation was acutely successful in 14 out of 15 patients (93%) in Group I and in 2 out of 5 (40%) patients in Group II. On long-term follow-up a significantly larger number of patients in Group I versus Group II (86% vs 20%) remained free of atrial flutter recurrence. We conclude that uncommon atrial flutter is a heterogeneous entity involving one or more reentrant circuits. Uncommon atrial flutter with multiple circuits may not be suitable for RFA.

Adult↗

Onset of induced atrial flutter in the canine pericarditis model.

To test the hypothesis that induced atrial flutter evolves from a transitional rhythm, the onset of 99 episodes of induced atrial flutter (mean cycle length 135 +/- 18 ms) lasting greater than 5 min in 40 dogs with sterile pericarditis was first characterized. In 85 (86%) of the 99 episodes, atrial flutter was preceded by a brief period (mean 1.4 +/- 0.9 s, range 0.4 to 42) of atrial fibrillation. Then, in 11 open chest studies, atrial electrograms were recorded simultaneously from 95 pairs of right atrial electrodes during the onset of 18 episodes of induced atrial flutter (mean cycle length 136 +/- 16 ms). Atrial flutter was induced by a train of eight paced atrial beats, followed by one or two premature atrial beats (7 episodes) or rapid atrial pacing (11 episodes). A short period of atrial fibrillation (mean cycle length 110 +/- 7 ms) induced by atrial pacing activated the right atrium through wave fronts, which produced a localized area of slow conduction. Then unidirectional conduction block of the wave front occurred for one beat in all or a portion of the area of slow conduction. This permitted the unblocked wave front to turn around an area of functional block and return through the area of slow conduction that had developed the unidirectional conduction block, thereby initiating the reentrant circuit. The location of the unidirectional block relative to the direction of the circulating wave fronts determined whether the circus movement was clockwise or counterclockwise. The area of slow conduction and unidirectional conduction block occurred where the wave front crossed perpendicular to the orientation of the atrial muscle fibers, suggesting a role for anisotropic conduction. These areas included the high right atrial portion of the sulcus terminalis (10 episodes), the low right atrial portion of the sulcus terminalis (4 episodes) and the pectinate muscle region (4 episodes). It is concluded that the development of a localized area of slow conduction in the right atrium followed by unidirectional conduction block in this area produced during a short period of atrial fibrillation or rapid atrial pacing is necessary for atrial flutter to occur in this model.

Animals↗

Electrophysiological determinant for induction of isthmus dependent counterclockwise and clockwise atrial flutter in humans.

OBJECTIVE: To investigate the electrophysiological determinant underlying the electrical induction of counterclockwise and clockwise isthmus dependent atrial flutter. PATIENTS AND METHODS: The isthmus bordered by the inferior vena caval orifice-tricuspid annulus-coronary sinus ostium (IVCO-TA-CSO) has been assumed to be the site of both slow conduction and unidirectional block critical to the initiation of atrial flutter. Trans-isthmus and the global atrial conduction were studied in 25 patients with isthmus dependent atrial flutter (group A) and in 21 patients without atrial flutter (group B), by pacing at the coronary sinus ostium and the low lateral right atrium (LLRA) and mapping with a 20 pole Halo catheter in the right atrium. RESULTS: Mean (SD) fluoroscopic isthmus length between the coronary sinus ostium and LLRA sites was 28.1 (4.0) mm in group A and 28.0 (3.9) mm in group B (p = 0.95), but the trans-isthmus conduction velocity of both directions at various pacing cycle lengths was nearly halved in group A compared with group B (mean 0.39-0.46 m/s v 0.83-0.89 m/s, p < 0.0001). Pacing at coronary sinus ostium directly induced counterclockwise atrial flutter in 14 patients and pacing at LLRA induced clockwise atrial flutter in 11 patients, following abrupt unidirectional trans-isthmus block. Transient atrial tachyarrhythmias preceded the onset of atrial flutter in 10 counterclockwise and six clockwise cases of atrial flutter. None of the group B patients had inducible atrial flutter even in the presence of trans-isthmus block. The intra- and interatrial conduction times, as well as the conduction velocities at the right atrial free wall and the septum, were similar and largely within the normal range in both groups. CONCLUSIONS: Critical slowing of the trans-IVCO-TA-CSO isthmus conduction, but not the unidirectional block or the global atrial performance, is the electrophysiological determinant of the induction of counterclockwise and clockwise isthmus dependent atrial flutter in man.

Adult↗