Incessant Atrial Tachycardia Research Articles

PO-04-060 FOUND WITH SOUND: INTRACARDIAC ECHOCARDIOGRAPHY CORRELATED WITH MEDIUM-OUTPUT PACING TO AVOID PHRENIC NERVE INJURY WITH RIGHT ATRIAL ABLATION

Catheter ablation within the right atrium can be limited by proximity to the phrenic nerve and potential for hemi diaphragmatic paralysis. High output pacing is frequently employed to map phrenic position relative to endocardium, particularly in relation to the superior vena cava and the right superior pulmonary vein. The use of intracardiac echocardiography (ICE) in correlation with lower output pacing to rigorously map the course of the right phrenic nerve along the right atrium has not been previously described. We describe a case of incessant right atrial tachycardia successfully mapped and ablated close to the phrenic nerve using a combination of ICE imaging and medium-output pacing to rigorously map the phrenic nerve. n/a An 18-year-old man with incessant atrial tachycardia was referred for repeat ablation following unsuccessful attempt at ablation at an outside institution. Prior ablation was limited by proximity to the phrenic nerve and transient phrenic nerve palsy with cryoablation at the mid crista terminalis. Epicardial access to deflect the phrenic nerve was anticipated. Atrial tachycardia was mapped endocardially prior to obtaining epicardial access. An ICE catheter was advanced to the SVC and used to identify the phrenic nerve. The course of the phrenic nerve was rigorously mapped with ICE and integrated into the CARTO navigational system (Biosense Webster). Pacing along the course of the phrenic nerve was performed at 10 mA to further refine the course of the phrenic nerve within the SVC and right atrium. Regions in close anatomic proximity to the phrenic nerve with loss of pace-capture correlated with sites of physiologic effusion, where pericardial fluid was concentrated and separation of the phrenic nerve from the visceral epicardium was noted. After mapping the phrenic nerve, endocardial ablation of atrial tachycardia was successfully performed in the absence of phrenic nerve injury without the need for epicardial access. Phrenic nerve injury may be prevented by rigorous mapping of the phrenic nerve within the right atrium using intracardiac ultrasound with medium-output pacing.

PO-672-02 TERROR FROM THE DEEP APPENDAGE: INCESSANT LEFT ATRIAL APPENDAGE ATRIAL TACHYCARDIA

Ablation in the left atrial appendage (LAA) is risky due to numerous ridges separated by thin tissue. There are few reported cases of successful ablation of incessant atrial tachycardia (AT) originating within the LAA.

Abstract 11080: A Young Woman with Incessant Left Atrial Tachycardia

Introduction: Left atrial tachycardia (AT) is uncommon and usually does not occur in the absence of congenital heart disease, or prior catheter ablation (CA). Case: A 29-year-old woman with a 2-year history of SVT refractory to metoprolol and no prior CA presented to the emergency department with palpitations. Initial ECG showed a regular, narrow complex, short RP tachycardia, at 180 bpm, insensitive to adenosine and 2 electrical cardioversions. Echocardiogram showed LVEF of 40%. The patient underwent an entirely non-fluoroscopic electrophysiology study using intracardiac echocardiography and electroanatomic mapping (EAM). AT (cycle length 300 ms) was induced by programmed atrial stimulation with isoproterenol infusion. AT was confirmed with ventriculo-atrial dissociation after pacing maneuvers and adenosine administration. Right atrial (RA) activation map revealed early atrial activation in the mid coronary sinus (CS), raising suspicion of a left atrial (LA) origin. LA was accessed via transseptal puncture. The site of earliest atrial activation was in the LA wall inferior to the left inferior pulmonary vein (LIPV) ostium and was successfully terminated with radiofrequency ablation (40 W, 5 to 10 g) (Figure) with no further inducibility. The patient's symptoms resolved after the procedure. Discussion: Left AT usually originates from PVs or the atrial wall. The EAM in this patient showed centrifugal activation consistent with a focal mechanism. Adenosine is generally not helpful in terminating AT but is useful in diagnosis. Rapid conduction across the LA to CS may have given rise to early activation in the mid CS on RA mapping. However, LA mapping revealed that atrial activation was earliest in the LA wall inferior to the LIPV. Conclusion: AT is unusual in young, healthy women. A high index of suspicion to perform transseptal puncture can lead to successful ablation of AT with LA origin. We surmise that the patient’s EF may improve with termination of the tachycardia.

Radiofrequency catheter ablation of atrlal tachycardia due to myocarditis six months after a viper bite

The present report describes a 20-year old man who developed an incessant atrial tachycardia several days after snakebite. Antiarrhythmic treatment was ineffective and six months later radiofrequency ablation of atrial tachycardia was successfully performed. A chronic arrythmia was considered as manifestation of toxic-allergic myocarditis. The possible mechanisms leading to myocarditis are discussed.

Arrhythmogenic right ventricular cardiomyopathy associated with arrhythmia-induced cardiomyopathy: A case report

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a kind of inherited cardio-myopathy, which is characterized by fibro-fatty replacement of right ventricular myocardium, leading to ventricular arrhythmia. However, rapid atrial arrhythmias are also common, including atrial fibrillation, atrial flutter and atrial tachycardia. Long term rapid atrial arrhythmia can lead to further deterioration of cardiac function. This case is a 51-year-old male. He was admitted to Department of Cardiology, Peking University Third Hospital with palpitation and fatigue after exercise. Electrocardiogram showed incessant atrial tachycardia. Echocardiography revealed dilation of all his four chambers, especially the right ventricle, with the left ventricular ejection fraction of 40% and the right ventricular hypokinesis. Cardiac magnetic resonance imaging found that the right ventricle was significantly enlarged, and the right ventricular aneurysm had formed; the right ventricular ejection fraction was as low as 8%, and the left ventricular ejection fraction was 35%. The patients met the diagnostic criteria of ARVC, and both left and right ventricles were involved. His physical activities were restricted, and metoprolol, digoxin, spironolactone and ramipril were given. Rivaroxaban was also given because atrial tachycardia could cause left atrial thrombosis and embolism. His atrial tachycardia converted spontaneously to normal sinus rhythm after these treatments. Since the patient had severe right ventricular dysfunction, frequent premature ventricular beats and non-sustained ventricular tachycardia on Holter monitoring, indicating a high risk of sudden death, implantable cardioverter defibrillator (ICD) was implanted. After discharge from hospital, physical activity restriction and the above medicines were continued. As rapid atrial arrhythmia could lead to inappropriate ICD shocks, amiodarone was added to prevent the recurrence of atrial tachycardia, and also control ventricular arrhythmia. After 6 months, echocardiography was repeated and showed that the left ventricle diameter was reduced significantly, and the left ventricular ejection fraction increased to 60%, while the size of right ventricle and right atrium decreased slightly. According to the clinical manifestations and outcomes, he was diagnosed with ARVC associated with arrhythmia induced cardiomyopathy. According to the results of his cardiac magnetic resonance imaging, the patient had left ventricular involvement caused by ARVC, and the persistent atrial tachycardia led to left ventricular systolic dysfunction.

Incessant Atrial Tachycardia: Problem Solving With Minimally Invasive Surgery

A 35-year-old female with sarcoidosis sought medical attention due to palpitations. The ECG showed an atrial tachycardia (AT), apparently originating in the left atrium. A 24-hour Holter monitoring revealed AT to be present during the entire day. Cardiac magnetic resonance exhibited no cardiac involvement by sarcoidosis but registered a mildly depressed left ventricular ejection fraction (LVEF). Atrial electroanatomical mapping showed the earliest activation zone on the distal portion of the left atrial appendage (LAA). Considering the high risk for perforation with catheter ablation in this region, she was sent to thoracoscopic surgical LAA exclusion with a clip device; it was possible to witness the termination of the arrhythmia during the procedure. She was safely discharged two days after surgery and has completed a one-year follow-up without recurrence of AT or symptoms, and with normalization of LVEF.

B-PO01-108 ATRIAL TACHYCARDIA ABLATION AT THE PULMONIC VALVE IN A PATIENT WITH CONGENITALLY CORRECTED TRANSPOSITION OF GREAT ARTERIES

Patients with congenitally-corrected transposition of great arteries (ccTGA) have anatomical differences with clinical ramifications for catheter ablation. To review the relevant anatomical structures in patients with ccTGA for atrial tachycardia (AT) ablation. N/A A 50 year old man with ccTGA with palpitations, refractory to medical management, presented for catheter ablation. Baseline ECG demonstrated AT with biphasic narrow P-waves in V1, suggestive of a para-Hisian origin. During electrophysiologic study, overdrive pacing at various cycle lengths yielded a fixed return cycle length favoring a micro-reentrant tachycardia. Right and left atrial mapping demonstrated early activation along the right atrial (RA) septum, 40 msec preceding the surface P-wave. Ablation at this site resulted in 2:1 exit block, with subsequent return of AT. Mapping of the mitral annulus and pulmonic outflow tract delineated the His-Purkinje system (Figure). Using intracardiac echocardiography, the pulmonic valve was visualized directly opposite to the earliest activation site in the RA (pulmonic and aortic valve locations are reversed in ccTGA). Mapping inside the pulmonic valve demonstrated a double-potential preceding the surface P-wave by 120 msec. Ablation resulted in immediate termination of AT, with no recurrence despite aggressive programmed stimulation, burst pacing, and isoproterenol infusion. We demonstrated the anatomic mapping and ablation of incessant AT in a patient with ccTGA. It is important to appreciate the anatomic relationship between the RA, pulmonic outflow tract, and conduction system to avoid inadvertent injury.

Epicardial ablation of incessant left atrial appendage tachycardia in a case with tachycardiomyopathy

Atrial tachycardias originated at the left atrial appendage (LAA) are uncommon; often they are incessant and might induce tachycardiomyopathy, as discussed by Hillock et al. (Heart Rhythm;3(4):467-469, 2006). A case of a 21-year-old woman with incessant atrial tachycardia is presented, refractory to medical therapy, echocardiography showed global dilation with LV ejection fraction of 20%. After two failed endocardial ablations, an epicardial access was attempted. The earliest activation site was located at the tip of the epicardial aspect of the LAA. RFCA was successful at this site. The patient remains asymptomatic during a follow-up of 10months; the ventricular function was completely recovered after 6months (LVEF of 50%).

Incessant Automatic Atrial Tachycardia in a Neonate Successfully Treated with Nadolol and Closely Spaced Doses of Flecainide: A Case Report

Supraventricular tachyarrhythmia (SVT) is the most common type of arrhythmia in childhood. Management can be challenging with an associated risk of mortality. A female neonate was diagnosed with episodes of SVT, controlled antenatally with digoxin. Flecainide was commenced prophylactically at birth. Despite treatment, the infant developed a narrow complex tachycardia at 5 days of age. The electrocardiogram features were suggestive of either re-entry tachycardia or of automatic atrial tachycardia (AAT). Following several unsuccessful treatments, a wide complex tachycardia developed. A transesophageal electrophysiological study led to a diagnosis of AAT. Stable sinus rhythm was finally achieved through increasing daily administrations of flecainide up to six times a day, in association with nadolol. The shortening of intervals to this extent has never been reported before and supports the evidence of a personal, age-specific variability in pharmacokinetics of flecainide. Larger studies are needed to better define the appropriate dose and timing of administration.

Incidence of drug-induced torsades de pointes with intravenous amiodarone

AimTo define the incidence, presentation, and outcomes of drug-induced Torsades de Pointes (TdP) with intravenous (IV) amiodarone. MethodsFrom January 2014 to August 2016 a total of 268 patients received IV amiodarone, 142 for ventricular tachycardia, 104 for atrial flutter/fibrillation, and 22 for incessant atrial tachycardia. A uniform dosing of amiodarone to yield 1gm/day was used in all patients. ResultsFour of the 268 patients (M:F 1:3) with mean age of 51.25+9.17years developed pause dependent TdP degenerating to VF, after a mean dose of 690+176.63mg, infused over 12+5.88h. The QTc that was 505+9.02ms at the time of TdP normalized to 433.75+6.13ms 48–72h after stopping amiodarone. There was no immediate or late mortality, and patients are well at 5–10 months of follow-up. None of the patients tested positive for LQTS genes. ConclusionThe incidence of drug-induced TdP with IV amiodarone is about 1.5%. Risk factors include female sex, left ventricular dysfunction, electrolyte abnormalities, baseline prolonged QTc, concomitant beta-blocker, and digoxin therapy. Amiodarone induced TdP has favorable prognosis if recognized and treated promptly, and these patients should not receive amiodarone by any route in future.

A case of decompensated heart failure with dermatomyositis dramatically improved by catheter ablation for incessant atrial tachycardia

A case of decompensated heart failure with dermatomyositis dramatically improved by catheter ablation for incessant atrial tachycardia

The Small Cardiac Vein as an Unrecognized Substrate for Atrial Tachycardia.

A 29-year-old Chinese male with palpitations was referred to our hospital. The 12-lead electrocardiography demonstrated incessant atrial tachycardia with negative P waves in leads V1 to V2 ([Figure 1A][1]). The patient had twice undergone unsuccessful attempts at ablation of right atrial appendage

Incessant atrial tachycardia: Cause or consequence of heart failure, and the role of radiofrequency ablation

Incessant atrial tachycardia: Cause or consequence of heart failure, and the role of radiofrequency ablation

INTRAVENOUS SOTALOL FOR INCESSANT TACHYARRHYTHMIAS IN CHILDREN

ObjectivesTo investigate the effects and safety of intravenous sotalol to treat paediatric incessant tachyarrhythmias with normal cardiac function.Methods19 children (age 2.0±2.3 years) presenting incessant tachyarrhythmias were treated with intravenous sotalol...

Atrial tachycardia caused by a superior vena cava fibrillation with conduction block

AT caused by SVC fibrillationHere, we report a case of a 62-year-old man with a history of incessant atrial tachycardia (AT) for several years. An electrophysiological study revealed rapid and irregular activity in the superior vena cava (SVC), but the surface 12-lead electrocardiogram (ECG) exhibited a relatively regular AT (atrial cycle length=240ms). CARTO mapping of the right atrium (RA) demonstrated that the earliest atrial activation occurred at the posterior septum of the upper RA (the SVC–RA junction). Intravenous administration of 20mg adenosine triphosphate (ATP) led to an acceleration of the SVC–RA conduction up to 1:1 conduction, and the atrial cycle length decreased, consequently converting the AT to transient atrial fibrillation (AF). Application of single radiofrequency energy at the earliest atrial activation site during tachycardia terminated the AT and achieved isolation of the SVC from the RA, despite the continued presence of fibrillation in the SVC. We speculated that SVC fibrillation with spontaneous conduction block at the SVC–RA junction was the cause of this AT.

Successful catheter ablation of incessant atrial tachycardia in pregnancy using three‐dimensional electroanatomical mapping with minimal radiation

Arrhythmias during pregnancy are not an infrequent problem and present a difficult therapeutic challenge to physicians. Anti-arrhythmic medication is used with some trepidation given concerns for the unborn foetus. Catheter ablation is typically avoided due to concerns regarding foetal exposure to radiation and delayed until the post-partum period. With the availability of three-dimensional mapping systems, catheter ablation may be performed with minimal radiation. We report a pregnant woman who underwent successful ablation of focal atrial tachycardia using three-dimensional electroanatomical mapping with minimal radiation exposure.

Taquicardiomiopatía, causa reversible de insuficiencia cardiaca: caso clínico

Tachycardiomyopathy is a potentially reversible cause of heart failure. It can be induced by supraventricular or ventricular arrhythmias. When these are treated, systolic function improves or normalizes. We report a 20 year-old male with deterioration of left ventricular function and dilated cardiomyopathy secondary to an incessant atrial tachycardia that was treated with radiofrequency catheter ablation. After the procedure, the patient experienced a significant improvement of his ventricular function.

Interatrial Electrical Dissociation After Catheter-Based Ablation for Atrial Fibrillation and Flutter

A 58-year-old man with hypertension and diabetes with recurrent persistent symptomatic atrial fibrillation resistant to sotalol-facilitated cardioversions was referred for ablation. Catheter-based radiofrequency ablation for persistent atrial fibrillation was performed, which consisted of isolation of all 4 pulmonic veins; linear ablations along the left atrial roof; an ablation line from the lateral mitral annulus to the left inferior vein; and ablation of areas with complex fractionated atrial electrograms along the posterior mitral annulus, anterior septum, and base of left atrial appendage. After these ablation lesions, the atrial fibrillation converted to a focal right atrial tachycardia, which was terminated by ablation in the inferior crista terminalis. The patient remained in sinus rhythm after the procedure for 2 weeks but returned with an incessant atrial tachycardia requiring repeat electrophysiological study. Electroanatomic mapping revealed earliest atrial activation in the proximal coronary sinus. Entrainment from the cavotricuspid isthmus returned long postpacing intervals. Postpacing interval identical to tachycardia cycle length was obtained with entrainment from the ostium of the coronary sinus. A linear ablation from the ostium of the coronary sinus to the inferior vena cava terminated tachycardia and rendered the patient noninducible for atrial arrhythmias. Atrial tachycardia recurred after 3 weeks. The patient's antiarrhythmic medication was switched from sotalol to …

Restoration of Sinus Rhythm by Incarceration, not Elimination, of Focal Atrial Tachycardia in Left Atrial Substrate Post Atrial Fibrillation Ablation

While diseased regions of the atrial body commonly behave as a substrate maintaining atrial fibrillation (AF), these areas can uncommonly behave as trigger foci for atrial tachycardia (AT),1 particularly after previous ablation. Unlike venous triggers, the goal of ablation for these focal ATs is normally elimination of the tachycardia source, rather than complete isolation. We present a case of a difficult to ablate post–AF-ablation AT from the anterior left atrium (LA), in which sinus rhythm was restored by incarcerating the ongoing AT within a small, isolated region of LA myocardium. A 67-year-old man who underwent pulmonary vein isolation, electrogram-based LA ablation, and roof, left mitral and cavotricuspid isthmus ablation for permanent AF in 2002 and repeat ablation of recurrent paroxysmal AF in 2009 (details unavailable), was referred for a third ablation procedure for rate-controlled incessant AT (Figure 1A). Figure 1B shows intracardiac recordings on decapolar catheter in the coronary sinus and 3.5-mm externally irrigated tip ablation catheter in the LA during baseline AT (cycle length, 308 ms). Activation and entrainment mapping2 established the diagnosis of focal source AT arising from the ostium of the left atrial appendage (LAA) where ablation led to cycle length variation of >25% (range, 276 to 402 ms) – unstable AT (Figure 1C). Focal ablation at another site with substantial temporal gradient between the proximal and distal bipoles of the ablation catheter …

Haemodynamic bradycardia in tachycardiomyopathy

A 44-year-old man presented with a 6-month history of progressive dyspnoea (NYHA class III). The electrocardiogram showed sinus rhythm with continuous short runs of atrial tachycardia resulting in a heart rate of 200 beats/min (Fig. 1a). An echocardiogram demonstrated left ventricular dilatation and a reduced ejection fraction of 15–25%. During runs of atrial tachycardia, the mitral valve failed to open due to high end-diastolic pressures, resulting in impaired filling of the left ventricle (Fig. 1b). As a consequence there was a virtual absence of blood flow through the aortic valve during tachycardic runs (Fig. 1c). Effective cardiac output was only seen during sinus beats, which came at a rate of 25–30 beats per minute. The patient was diagnosed with tachycardiomyopathy due to incessant atrial tachycardia. Cryoablation of the atrial focus eliminated the tachycardia. Three months later, tachycardias were still absent and the patient’s left ventricular systolic function and clinical condition had markedly improved. Fig. 1 a Rhythm strip demonstrating sinus rhythm and episodes of atrial tachycardia. b and c) Echocardiogram with apical views demonstrating absence of flow through the mitral valve and aortic valve during a run of atrial tachycardia Tachycardiomyopathy is an abnormality of systolic and/or diastolic function of the heart, resulting in atrial and ventricular dilatation and ultimately development of heart failure symptoms. Tachycardiomyopathy is usually caused by atrial arrhythmias that results in a high and/or irregular ventricular rate. Myocardial dysfunction is completely or partially reversible after normalisation of heart rate and/or rhythm irregularity [1]. The mechanisms responsible for the contractile dysfunction and structural changes in tachycardiomyopathy are not yet fully understood. This case illustrates the direct effect of tachyarrhythmia on cardiac function and its haemodynamic consequences in a patient with tachycardiomyopathy.