Repetitive Atrial Tachycardia Research Articles

PO-01-011 EFFECT OF TRANSVENOUS SYSTEMIC RIGHT VENTRICULAR PACING FOR HEART FAILURE IN ADDITION TO MANAGING ARRHYTHMIAS IN THE PATIENT WITH UNREPAIRED D-TGA

Survival of dextro-transposition of the great arteries (d-TGA) patients is dismal without a surgical repair. Even after the repair, arrhythmias and heart failure (HF) are common in adult patients with a systemic right ventricle (S-RV). N/A N/A Case: A 60-year-old woman with an unrepaired d-TGA, atrial septal defect (ASD), and partial anomalous pulmonary venous return was admitted to our institute due to syncope and heart failure (HF) caused by repetitive atrial tachycardia (AT) recurrences after radiofrequency catheter ablation (RFCA). In a previous session, while the clinical AT was successfully ablated in the right atrium (RA), multiple ATs were still inducible, and it was difficult to control all ATs by RFCA. Further, sinus node dysfunction was observed. Therefore, a pacemaker implantation (PMI) and antiarrhythmic drug therapy were considered the better choice. An epicardial lead was considered to avoid thromboembolic events due to a bidirectional shunt via the ASD. However, her complex hemodynamics concomitant with severe S-RV dysfunction and tricuspid regurgitation (TR) were intolerable for a surgical approach. Therefore, a transvenous PMI was chosen after receiving informed consent. Before the implantation, a pacing study was performed. The ECG at the baseline had a wide QRS duration (QRSD=170ms) with right bundle branch block. Left ventricular (LV) septal pacing using an electrode catheter via the ASD increased the QRSD (180ms) and caused significant S-RV dyssynchrony and worsening TR. Contrarily, S-RV pacing decreased the QRSD (120ms) and preserved the S-RV contraction synchrony suggesting it was the appropriate pacing site. A transvenous DDD PMI was performed under local anesthesia and systemic sedation. A stylet-driven lead could not be inserted into the S-RV because of a huge RA. After all, a thin lumenless lead (SelectSecureR) was implanted on the S-RV septum using a guiding sheath. The stroke volume measured by non-invasive electrical cardiometry (AesculonR) was the best during S-RV paced fusion beats with a 220ms atrioventricular delay. No S-RV dyssynchrony was observed, and the systolic function improved. The ATs were suppressed after amiodarone. She had no syncope, and her HF improved (NYHA class IV→II) after discharge. No thromboembolic events occurred after taking apixaban. S-RV endocardial pacing in an unrepaired d-TGA patient was effective for re-synchronization and improved the HF in addition to managing arrhythmias.

Idiopathic left ventricular tachycardia following atrioventricular conduction block by rapid atrial tachycardia

Key Clinical MessageThe present case demonstrated a rare situation alternating between a repetitive atrial tachycardia (AT) and ventricular tachycardia (VT). A unique induction mechanism was noted in which the VT was induced after Wenckebach AV node conduction block following the repetitive rapid AT.

A Reappraisal on Lidocaine-Sensitive Repetitive, Uniform Atrial Tachycardia

Lidocaine sensitive, repetitive atrial tachycardia is an unusual arrhythmia whose electrophysiologic substrate remains undefined. We aimed to analyze the electropharmacologic characteristics of this arrhythmia with emphasis on its cellular substrate and response to drug challenges. We retrospectively analyzed a series of 18 patients from an electrocardiographic and electrophysiologic perspective and the response to pharmacological challenge. There was no evidence of structural heart disease in 12 patients, 4 patients presented with systemic hypertension; one patient had a prior myocardial infarction and one a mitral valve prolapse. The arrhythmia depicted a consistent pattern in nine patients. The first initiating ectopic beat showed a long coupling interval, the cycle length of the second atrial ectopic beat presented the shortest cycle length and a further prolongation was apparent towards the end of the atrial salvos. Conversely, in the other nine cases, the atrial tachycardia cycle length was erratic. The arrhythmia was suppressed by asynchronous atrial pacing at cycle lengths longer than those of the atrial tachycardia. Intravenous lidocaine eliminated the arrhythmia in all patients, but intravenous verapamil suppressed the atrial tachycardia in only two patients while adenosine caused a transient disappearance in 2/8 patients. Only one patient responded to all the three agents. Radiofrequency ablation was successfully performed in 10 patients. Repetitive uniform atrial tachycardia can be sensitive to lidocaine. In few cases, this rare focal arrhythmia may be also suppressed by adenosine and/or verapamil, which suggests a diversity of electrophysiologic substrates that deserve to be accurately identified.

Distinct Pharmacologic Substrate in Lidocaine-Sensitive, Repetitive Atrial Tachycardia

Lidocaine-sensitive, repetitive atrial tachycardia is an uncommon arrhythmia. The electrophysiologic substrate is still unknown, and the pharmacologic responses have not been fully explored. The aim of this study was to investigate the effects of intravenous adenosine and verapamil in patients with lidocaine-sensitive atrial tachycardia. In 9 patients with repetitive uniform atrial tachycardia, the response to intravenous adenosine (12 mg), lidocaine (1 mg/kg body weight), and verapamil (10 mg) were sequentially investigated. Simultaneous 12-lead electrocardiogram (ECG) was recorded at baseline and continuously monitored thereafter. Tracings were obtained at regularly timed intervals right after the administration of each drug to evaluate changes in the arrhythmia characteristics. Repetitive atrial tachycardia was abolished by intravenous lidocaine in the 9 patients within the first 2 minutes after the end of injection. Adenosine suppressed the arrhythmia in 2 patients and shortened the runs of atrial ectopic activity in 1 patient, while verapamil was effective in 2 patients, 1 of them insensitive to adenosine and the other 1 sensitive to this agent. In 5 patients, the arrhythmia was abolished by radiofrequency ablation at different sites of the right atrium. Lidocaine-sensitive atrial tachycardia may eventually be also suppressed by adenosine and/or verapamil. This suggests that this enigmatic arrhythmia may be caused by different underlying electrophysiologic substrates and that at least in some cases, delayed afterdepolarizations seem to play a determining role.

Bi‐focal Atrial Tachycardia Mimicking Atrial Fibrillation: Fusion and Interference Between Two Distinct Tachycardias

Irregular tachycardias mimicking atrial fibrillation (AF) have previously been described. We report a case of a 60-year-old man with an antiarrhythmic drug-resistant atrial tachycardia (AT) mimicking AF. The tachycardia consisted of two distinct ATs with interference of one repetitive AT with another sustained AT. Radiofrequency (RF) ablation of two distinct right atrial foci eliminated the irregular tachycardia. Although catheter-based pulmonary vein isolation has become a popular therapeutic approach for patients with symptomatic AF, careful evaluation of the intracardiac recordings in the patients undergoing RF ablation for AF is important.

Complete pulmonary vein isolation guided by three-dimensional electroanatomical mapping for the treatment of paroxysmal atrial fibrillation in patients with hypertrophic obstructive cardiomyopathy

Evaluation of the clinical outcome of patients with hypertrophic obstructive cardiomyopathy (HOCM) and paroxysmal atrial fibrillation (AF) treated with complete pulmonary vein (PV) isolation guided by three-dimensional (3-D) electroanatomical (EA) mapping. Circumferential radiofrequency (RF) ablation and continuous circular lesions (CCLs) around the left and right-sided PVs were performed in 4 highly symptomatic patients (2 males; age 57.5 +/- 8.3 years) with HOCM and anti-arrhythmic drug (AAD) refractory paroxysmal AF. Ablation was guided by 3-D EA mapping combined with conventional circumferential PV mapping. The endpoints of the ablation were defined as: (1) absence of all PV spikes documented with the two Lasso catheters within the ipsilateral PVs; and (2) no recurrence of the PV spikes within all PVs following intravenous administration of adenosine. The ablation endpoints were achieved in all patients. A repeat ablation was performed in one patient due to repetitive atrial tachycardia, 1 month after the initial procedure. During a follow-up of 5.8 +/- 2.7 months, all patients are free of AF recurrence. Short episodes of symptomatic AT were documented after the repeat procedure, and were well controlled with oral amiodarone in the patient. No procedure-related complications were observed. The present study demonstrates that complete isolation of ipsilateral PVs guided by 3-D EA mapping is potentially effective for the treatment of highly symptomatic, drug refractory paroxysmal AF in patients with HOCM.

Lidocaine-sensitive atrial tachycardia: Lidocaine-sensitive, rate-related, repetitive atrial tachycardia: a new arrhythmogenic syndrome

OBJECTIVESThe goal of this study was to report a variety of atrial tachycardia that might be caused by an unusual electrophysiologic substrate.BACKGROUNDThe mechanism of atrial tachycardias is attributed to re-entry, abnormal automaticity or triggered activity, based on their electropharmacological responses. A rate-related and lidocaine-sensitive atrial tachycardia has not been reported.METHODSEight patients (3 women and 5 men, aged 14 to 60 years) with repetitive, uniform atrial tachycardias were studied. In six patients the arrhythmia had been refractory to at least three antiarrhythmic agents (class 1A and C sodium channel blockers, amiodarone, beta-adrenergic blocking agents, verapamil, digoxin). Conventional electrocardiograms, Holter recordings and B mode echocardiograms were performed in each patient. Intravenous lidocaine and verapamil were tested in the eight patients. Six patients underwent an electrophysiologic study.RESULTSThe baseline electrocardiogram showed nearly incessant runs of atrial tachycardia in all patients. The mean atrial ectopic cycle length ranged from 376 to 502 ms. In seven patients a progressive prolongation of the cycle length from the beginning to the end of the salvos was documented. The arrhythmia was suppressed by increments of sinus node rate and by atrial pacing at cycle lengths longer than that of the atrial tachycardia. In all patients the arrhythmia was abolished by intravenous lidocaine, whereas intravenous verapamil was ineffective. Four symptomatic patients were successfully treated with radiofrequency ablation of the ectopic focus, and two patients were treated with oral mexiletine.CONCLUSIONSThe peculiar electropharmacological responses of this arrhythmia suggest an uncommon underlying mechanism that remains to be elucidated.

Paroxysmal atrial fibrillation with and without primary atrial vulnerability: Clinical and electrophysiological differences

Primary atrial vulnerability defined as induction of repetitive atrial firing by a single atrial extrastimulus cannot always be demonstrated in patients with paroxysmal atrial fibrillation. The authors studied the electrophysiological differences between paroxysmal atrial fibrillation with and without primary atrial vulnerability. In 14 of 31 patients with documented history of atrial fibrillation, single extrastimulation at the high right atrium initiated repetitive atrial firing defined as rapid disorganized atrial activity continuing longer than 1 second. In the 14 patients with vulnerable atrium, the atrial effective and functional refractory were periods significantly shorter and the duration of the local atrial electrogram of the premature beat was longer and was fractionated. The % sinus node recovery time was longer in patients without vulnerability. Nine of the 17 patients without atrial vulnerability had sinus node dysfunction, and 4 of the remaining 8 patients had a repetitive type of atrial automatic tachycardia. In contrast, only 3 (21%) of the 14 patients with vulnerability had sinus node dysfunction, and none showed repetitive atrial tachycardia. The high prevalence of sinus node dysfunction or repetitive type of atrial automatic tachycardia in patients without primary atrial vulnerability suggests that these transient electrophysiological modifications which are not dealt with in the basic conditions may have a role in the enhancement of atrial vulnerability.

Successful treatment of drug-resistant atrial tachycardia and intractable congestive heart failure with permanent coupled atrial pacing

Temporary coupled atrial stimulation slowed the ventricular rate by nearly 50 percent in an adolescent patient with intractable congestive heart failure and focal repetitive atrial tachycardia that was resistant to drug treatment. Because of the success with the temporary pacemaker, a specially designed permanent pacemaker was implanted to provide coupled atrial stimulation. The necessary electrophysiologic conditions for ventricular slowing by coupled atrial pacing are: (1) an atrial effective refractory period shorter than that of the atrioventricular junction, and (2) depolarization of the ectopic atrial pacemaker by the responses to coupled atrial stimulation. During a 4 year follow-up period the treatment resulted in elimination of the tachycardia, followed by return of the heart size to normal and complete clinical recovery. Coupled atrial stimulation can provide effective treatment in selected patients with disabling drug-resistant atrial tachycardia in whom this mode of therapy is shown to be effective by careful electrophysiologic studies.