Surgical treatment for ectopic atrial tachycardia (original) (raw)

Atrial Tachycardia: Mechanisms, Diagnosis, and Management

Current Problems in Cardiology, 2005

Atrial tachycardia is an uncommon arrhythmia and may be focal or macroreentrant. This review concentrates on focal atrial tachycardia. Over the last decade there have been a number of advances in delineating the mechanism and anatomic locations of focal atrial tachycardia. The lack of efficacy of antiarrhythmic therapy and the advent of radiofrequency ablation have altered our primary approach to the treatment of focal atrial tachycardia. This review discusses the clinical features, diagnosis, and treatment of focal atrial tachycardia. There is particular focus on the mechanisms, anatomic locations, and P wave morphology, as well as the techniques of mapping and radiofrequency ablation. (Curr Probl Cardiol 2005;30: 529-573.)

Tachycardia Related Cardiomyopathy: Response to Control of the Arrhythmia

Journal of Interventional Cardiology, 1989

To evaluate the clinical response of five children with automatic atrial tachycardia (AA T) and associated cardiomyopathy to arrhythmia control, we compared pretreatment and posttreatment 24hour ECG heart rates, cardiothoracic ratio by chest radiograph, and echocardiographic measures of ventricular ,function. Two children were treated with amiodarone, two with surgical excision and cryoablation of the ectopic focus, and one with digoxin alone. Signijicantly slower mean heart rates were achieved, along with a dominant sinus rhythm and improvement in symptoms. Control of the AAT resulted in improved mean cardiothoracic ratio (0.53 pre vs 0.49 post; P = 0.021, as well as improvement in a number of echocardiographic measurements: mean shorten-ingfraction (20% pre vs 34% post; P = 0.006), mean ejection fraction (36% pre vs 50% post; P < 0.01), mean velocity of' circumferential fiber shortening (0.62 pre vs 1.20 post; P = 0.003). Mean E-point septa1 separation corrected for enddiastolic dimension also showed a trend toward improvement (0.25 pre vs 0.16 post; P = 0.11). Right ventricular endocardial biopsies in four were nonspecific; an atrial biopsy from surgery showed a Purkinje fiber-like tissue in one patient, but was nonspecijic in another. We conclude that cardiomyopathy can be causally linked to automatic atrial tachycardia and that aggressive medical and/or surgical management is warranted in those patients with signs and symptoms of impaired ventricular function. (J Interven Cardiol 1989:2:4)

Atrial Bigeminy With Recurrent Supraventricular Tachycardia

Journal of Cardiovascular Electrophysiology, 2010

A 16-year-old male was referred for recurrent episodes of drug-resistant symptomatic palpitations. He had successful ablation of a concealed para-Hisian accessory pathway (AP) 7 years previously. At baseline, 12-lead ECG showed frequent atrial premature beats (APB) in a bigeminal pattern with inferior axis in the frontal plane and a fixed coupling interval to the preceding QRS complex. There was no evidence of pre-excitation. APBs were conducted to the ventricles with a functional left posterior fascicular delay, causing shift in the frontal QRS axis from +60° to +120°. Nonsustained, narrow complex tachycardia initiated by the APB is shown in Figure 1A. An electrophysiological study was performed, using a deflectable decapolar catheter (Xtrem, ELA Medical, Le-Plessis-Robinson, France) for His bundle recording, a deflectable quadripolar catheter (Xtrem, ELA Medical) at the high right atrium, and a 4-mm nonirrigated tip ablation catheter (Celcius, BiosenseWebster, Diamond Bar, CA, USA). Intracardiac recordings in sinus rhythm showed normal AH (68 ms) and HV (44 ms) intervals. APBs conducted through the atrioventricular (AV) node in a decremental fashion causing an increase in A-H interval to 192 ms. On mapping the APBs, the earliest site of atrial activation was recorded just proximal to the His bundle. The activation of the right atrium and the coronary sinus was concentric during the APB. Intermittently, APBs initiated narrow complex tachycardia with 1:1 AV relationship at a cycle length (CL) of 366 ms (Fig.

Role of the Electrophysiologist in the Treatment of Tachycardia-Induced Cardiomyopathy

The Role of the Clinical Cardiac Electrophysiologist in the Management of Congestive Heart Failure, 2017

Tachycardia-induced cardiomyopathy is a systolic cardiac dysfunction given by prolonged elevated heart rates in patients with incessant or frequent tachyarrhythmias. Arrhythmias associated with tachycardiomyopathy can be either supraventricular (atrial tachycardia, atrial flutter, atrial fibrillation, AVNRT, permanent junctional reciprocating tachycardia, high rates of atrial pacing) or ventricular (frequent premature ventricular complexes, right ventricular outflow tract tachycardia, LVOT, left ventricular fascicular tachycardia, bundle-branch reentry or high rate of ventricular pacing). Electrophysiological study confirms the clinical diagnosis of tachycardia-induced cardiomyopathy, reveals the arrhythmia mechanism and facilitates catheter ablation that results in complete recovery of ventricular function. This chapter has two parts: 1. Theoretical insight into the pathogenesis of tachycardia-induced cardiomyopathy, clinical manifestations and therapy. 2. Practical issues: we describe our EP lab's experience on electrophysiological study and ablation in patients with tachycardia-induced cardiomyopathy. We will present five cases of ablation: PVCs >30,000/24 h, antidromic tachycardia, 2:1 atrial flutter, persistent atrial fibrillation and RVOT PVCs with nonsustained VT.

A Case of Long-RP Tachycardia: What is the Mechanism?

Journal of Cardiovascular Electrophysiology, 2009

A 33-year-old woman with a 12-year history of paroxysmal palpitations that were not responding to medical treatment was referred for EP study. Baseline 12-lead ECG was normal. A 12-lead ECG of her tachycardia showed narrow QRS tachycardia with an RP interval that was longer than the PR interval. P waves were inverted in inferior leads. .

A Hidden Recess of Atrial Tachycardia

The Journal of Innovations in Cardiac Rhythm Management, 2021

We present a case of regular narrow complex tachycardia in a 59-year-old woman with frequent paroxysmal palpitations, a normal electrocardiogram (ECG) in sinus rhythm, and a structurally normal heart. During electrophysiology study, a long R–P tachycardia was present at baseline, with P-waves superimposed on the T-waves and appearing to be positive in the inferior leads. Intracardiac recordings showed the atrial activation to be early in the para-Hisian region. The diagnosis of atrial tachycardia was confirmed by ventricular overdrive pacing, which showed ventriculoatrial dissociation without perturbing the atrial rate. The precise P-wave morphology was brought out in the pause, which followed rapidly delivered ventricular extrastimuli during tachycardia. Based on this information, activation mapping was conducted in the para-Hisian region, high atrial septal regions on the right and left sides, and aortic sinuses. Tachycardia was successfully ablated at one of these sites.

Uncommon presentation of a common tachycardia

Indian Pacing and Electrophysiology Journal, 2010

We describe a patient with an implanted pacemaker for impaired AV conduction who presented with an incessant tachycardia. EP study showed that the tachycardia was atrioventricular nodal reentrant tachycardia (AVNRT) with repeated spontaneous initiation because of poor or absent antegrade fast pathway conduction. Slow pathway ablation was successful in terminating the tachycardia and making it non-inducible.

Introduction to Supraventricular Tachycardia

Cardiac Electrophysiology Clinics, 2010

Paroxysmal supraventricular tachycardia (PSVT) is a clinical syndrome characterized by a rapid tachycardia with an abrupt onset and termination. These arrhythmias are frequently encountered in otherwise healthy patients without structural heart disease. Symptoms vary from palpitations and dyspnea to tachycardia-induced cardiomyopathy. The three most common causes of PSVT are atrioventricular nodal reentrant tachycardia (AVNRT) (50%-60%), atrioventricular reentrant tachycardia (AVRT) in patients with Wolff-Parkinson-White syndrome (25%-30%), and atrial tachycardia (10%). Rare causes of PSVT include focal junctional tachycardia, atriofascicular tachycardia, permanent reciprocating junctional tachycardia, and nodoventricular/nodofascicular tachycardia. This section, based on challenging PSVT cases, is a guide for clinicians dealing with diagnostic or therapeutic dilemmas in the electrophysiology laboratory.