Class IC antiarrhythmic drug induced atrial flutter: electrocardiographic and electrophysiological findings and their importance for long term outcome after right atrial isthmus ablation.
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OBJECTIVE: To describe the electrocardiographic and electrophysiological findings of new atrial flutter developing in patients taking class IC antiarrhythmic drugs for recurrent atrial fibrillation, and to report the long term results of right atrial isthmus ablation in relation to the ECG pattern of spontaneous atrial flutter. DESIGN: Retrospective analysis. SETTING: Tertiary care academic hospital. PATIENTS: 24 consecutive patients with atrial fibrillation (age 54 (12) years; 5 female, 19 male) developing atrial flutter while taking propafenone (n = 12) or flecainide (n = 12). RESULTS: The ECG was classified as typical (n = 13; 54%) or atypical atrial flutter (n = 8) or coarse atrial fibrillation (n = 3). Counterclockwise atrial flutter was the predominant arrhythmia. Acute success after isthmus ablation was similar in patients with typical (12/13) and atypical (8/8) atrial flutter. After long term follow up (13 (6) months, range 6-26 months), continuation of antiarrhythmic drug treatment appeared to result in better control of recurrences of atrial fibrillation in patients with typical atrial flutter (11/13) than in those with atypical atrial flutter (4/8), but the difference was not significant. Ablation for coarse atrial fibrillation was unsuccessful. CONCLUSIONS: New atrial flutter developing in patients taking class IC antiarrhythmic drugs for recurrent atrial fibrillation has either typical or atypical flutter wave morphology on ECG. The endocardial activation pattern and the acute results of ablation suggest that the flutter circuit was located in the right atrium and that the isthmus was involved in the re-entry mechanism. There appeared to be better long term control of recurrent atrial fibrillation in patients with typical (85%) as compared with atypical atrial flutter (50%). Patients developing coarse atrial fibrillation may not be candidates for this strategy. (+info)
Predictors of failure of transoesophageal cardioversion of common atrial flutter.
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BACKGROUND: Common atrial flutter is due to a re-entry circuit in the right atrium. It is possible to entrain and interrupt this arrhythmia with transoesophageal pacing (TEAP) in a substantial percentage of patients. The aim of this study is to evaluate factors associated with failure of transoesophageal cardioversion of common atrial flutter. METHODS: One hundred consecutive patients underwent an attempted transoesophageal cardioversion of their common atrial flutter. In order to detect factors associated with failure of this procedure, the following were considered: (a) age and gender; (b) underlying heart disease; (c) time of onset of the arrhythmia; (d) antiarrhythmic treatment at the time of cardioversion; (e) flutter cycle length, (f) A/V deflection ratio at the site of transoesophageal pacing; and (g) longitudinal and transverse diameters of right and left atrium on the echocardiogram. RESULTS: In 84 of 100 patients, TEAP modified the atrial flutter circuit: in 23 of these, sinus rhythm was restored; in 31 patients, flutter was converted into atrial fibrillation which spontaneously reverted to sinus rhythm; and in remaining 30 patients, persistent atrial fibrillation was obtained. In 16 cases, no modification in atrial flutter circuit was obtained by TEAP (Group 2). Using univariate analysis, this group of patients showed no significant difference in flutter cycle length, a smaller A/V ratio at the site of TEAP, a longer transverse diameter of left atrium and a shorter transverse diameter of right atrium. Analysis of the therapy at cardioversion shows that no Group 2 patients was on intravenous amiodarone, while a greater percentage of patients of the former group was on chronic amiodarone treatment. A logistic regression model applied to the data showed that flutter cycle length, transverse diameter of left atrium and A/V deflection ratio at the site of TEAP were independent variables with influence on the failure rate. CONCLUSION: Transoesophageal pacing is able to modify the circuit of common atrial flutter in a large percentage of patients, and can convert this arrhythmia to sinus rhythm in more than 50% of cases. Failure of this procedure is associated with electrophysiological parameters (flutter cycle length, A/V ratio at the site of TEAP), anatomical factors (left and right atrial diameters) and treatment in use at the time of TEAP. (+info)
Influence of atrial flutter ablation on right to left inter-atrial conduction.
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AIMS: Ablation of the atrial isthmus between the tricuspid annulus and the inferior vena cava changes P-wave morphology during low lateral right atrial pacing. For better understanding of the mechanism of this alteration, the sequence of activation of the inter-atrial septum and the left atrium were compared before and after ablation of the isthmus between the inferior vena cava and the tricuspid annulus. METHODS AND RESULTS: In 13 patients, left atrial mapping was performed using a duodecapolar electrode catheter advanced to the far distal coronary sinus. The inter-atrial septum was mapped using a right atrial duodecapolar electrode catheter. Conduction times were measured during low lateral right atrial pacing from the pacing artefact and during sinus rhythm from the earliest right atrial electrogram to every intra-cardiac electrogram before and after the ablation. During low lateral right atrial pacing, isthmus ablation resulted in a significant delay in every left atrial lead. Changes were maximal at the posterior aspect of the left atrium and minimal at its anterior aspect. No significant change was discernible on the inter-atrial septum. During sinus rhythm, atrial activations remained unchanged. CONCLUSION: Electrocardiographic changes of P-wave morphology result from alteration in the sequence of left atrial activation rather than that of the inter-atrial septum. (+info)
The N + 1 difference: a new measure for entrainment mapping.
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OBJECTIVES: The purpose of this study was to develop and test a new entrainment mapping measurement, the N + 1 difference. BACKGROUND: Entrainment mapping is useful for identifying re-entry circuit sites but is often limited by difficulty in assessing: 1) changes in QRS complexes or P-waves that indicate fusion, and 2) the postpacing interval (PPI) recorded directly from the stimulation site. METHODS: In computer simulations of re-entry circuits, the interval from a stimulus that reset tachycardia to a timing reference during the second beat after the stimulus was compared with the timing of local activation at the site during tachycardia to define an interval designated the N + 1 difference. The N + 1 difference was compared with the PPI-tachycardia cycle length (TCL) difference in simulations and at 65 sites in 10 consecutive patients with ventricular tachycardia (VT) after myocardial infarction and at 45 sites in 10 consecutive patients with atrial flutter. RESULTS: In simulations, the N + 1 difference was equal to the PPI-TCL difference. During mapping of VT and atrial flutter, the N + 1 difference correlated well with the PPI-TCL difference (r > or = 0.91, p < 0.0001), identifying re-entry circuit sites with sensitivity of > or = 86% and specificity of > or = 90%. Accuracy was similar using either the surface electrocardiogram or an intracardiac electrogram (Eg) as the timing reference. CONCLUSIONS: The N + 1 difference allows entrainment mapping to be used to identify re-entry circuit sites when it is difficult to evaluate Egs at the mapping site or fusion in the surface electrocardiogram. (+info)
Electroanatomic mapping of entrained and exit zones in patients with repaired congenital heart disease and intra-atrial reentrant tachycardia.
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BACKGROUND: Characterization of reentrant circuits and targeting ablation sites remains difficult for intra-atrial reentrant tachycardias (IART) in congenital heart disease (CHD). METHODS AND RESULTS: Electroanatomic mapping and entrainment pacing were performed before successful ablation of 18 IART circuits in 15 patients with CHD. Principal features of IART circuits were atrial septal defect (4 patients), atriotomy (3 patients), other atrial scar (3 patients), crista terminalis (3 patients), and right atrioventricular valve (5 patients). A median of 176 sites (range, 96 to 317 sites) was mapped for activation and 13 sites (range, 9 to 28 sites) for entrainment response. Postpacing intervals within 20 ms of tachycardia cycle length and stimulus-to-P-wave intervals of 0 to 90 ms (exit zones) were mapped to atrial surfaces generated by electroanatomic mapping. Criteria for entrainment were met over a median of 21 cm2 of atrial surface (range, 2 to 75 cm2), 19% (range, 1% to 81%) of total area tested. Using integrated data, relations between activation sequence and protected corridor of conduction could be inferred for 16 of 17 LARTs. Successful ablation was achieved at a site distant from the putative protected corridor in 9 of 18 (50%) circuits. CONCLUSIONS: The right atrium in CHD supports a variety of IART mechanisms. Fusion of activation and entrainment data provided insight into specific IART mechanisms relevant to ablation. (+info)
Response to flecainide infusion predicts long-term success of hybrid pharmacologic and ablation therapy in patients with atrial fibrillation.
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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. (+info)
Prolonged fractionation of paced right atrial electrograms in patients with atrial flutter and fibrillation.
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OBJECTIVES: This study investigated the extent of fractionation of paced right atrial electrograms in patients with and without paroxysmal atrial flutter (AFL) or atrial fibrillation (AF). BACKGROUND: Slow conduction through nonuniform anisotropic atrial muscles, represented by fractionated electrograms, may favor the generation of atrial tachyarrhythmias. METHODS: This study included 10 control patients (Group 1), 8 patients with documented paroxysmal AFL (Group 2) and 10 patients with documented paroxysmal AF (Group 3). Five electrode catheters were placed in the different sites of the right atrium and one catheter was positioned at the coronary sinus ostium. Atrial pacing from one site was done by a constant drive train with an extrastimulus inserted every fourth beat while recording at the other five sites was performed. The delay of each fractionated potential in the high-pass filtered atrial electrogram in response to extrastimulation was determined and used to construct conduction curves of delay versus the S1S2 interval. RESULTS: The mean increase in electrogram duration between a coupling interval of 350 ms and 10 ms above atrial refractoriness was significantly greater in Groups 2 and 3 compared with that in Group 1 (8.5 +/- 2.5 vs. 11.0 +/- 2.7 vs. 5.9 +/- 2.3 ms, respectively, p < 0.001). The mean S1S2 interval at which delay increased suddenly was also longer in Groups 2 and 3 compared with Group 1 (326 +/- 9 vs. 343 +/- 12 vs. 307 +/- 17 ms, respectively, p < 0.001). CONCLUSIONS: Increased delays in the individual potential of the fractionated atrial electrograms may be related to the development of AFL and AF. (+info)
Impact of pulmonary valve replacement on arrhythmia propensity late after repair of tetralogy of Fallot.
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BACKGROUND: Chronic pulmonary regurgitation after repair of tetralogy of Fallot (TOF) may lead to right ventricular dilatation, which may be accompanied by ventricular tachycardia and sudden death. We aimed to examine the effects of pulmonary valve replacement (PVR) on (1) certain electrocardiographic markers predictive of monomorphic ventricular arrhythmia and sudden death and (2) sustained atrial flutter/fibrillation and monomorphic ventricular tachycardia. METHODS AND RESULTS: We studied 70 patients who underwent PVR for pulmonary regurgitation and/or right ventricular outflow tract obstruction late after repair of TOF. Maximum QRS duration and QT dispersion were measured from standard ECGs before PVR and at the latest follow-up. Arrhythmia was defined as sustained atrial flutter/fibrillation or sustained monomorphic ventricular tachycardia. Concomitant intraoperative electrophysiological mapping and/or cryoablation were performed in 9 patients (60%) with preexisting ventricular tachycardia and 6 patients (50%) with preexisting atrial flutter. QRS duration remained unchanged in the study group (P=0.46), but it was significantly prolonged (P<0.001) in a comparable group of patients with repaired TOF who did not undergo PVR. At a mean follow-up of 4.7 years, the incidence of ventricular tachycardia diminished from 22% to 9% (P<0.001), and atrial flutter/fibrillation decreased from 17% to 12% (P=0.32). Intraoperative ablation prevented recurrence of preexisting tachyarrhythmia (0 of 15 patients). CONCLUSIONS: PVR in patients with previous TOF repair and chronic pulmonary regurgitation leads to stabilization of QRS duration and, in conjunction with intraoperative cryoablation, to a decrease in the incidence of preexisting atrial and ventricular tachyarrhythmia. When applicable, this combined approach should be used in patients late after repair of TOF. (+info)