Frequency of recurrent atrial fibrillation after catheter ablation of overt accessory pathways

Haı̈ssaguerre, Michel; Fischer, Bruno; Labbé, Thierry; Lemétayer, P; Montserrat, P; d'Ivernois, C; Dartigues, Jean‐François; Warin, J F

doi:10.1016/0002-9149(92)90992-8

Cited by 100 publications

(63 citation statements)

References 25 publications

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“…Up to 30% of patients with accessory pathways can have atrial fibrillation (AF), whereas the incidence of AF is only 3% to 4% in the general population. [9][10][11][12] If AF is rapidly conducted down the accessory pathway, it can lead to ventricular fibrillation (VF). Thus, the speed of conduction in the accessory pathway is critical.…”

Section: Ablation Of Accessory Pathway To Prevent Scdmentioning

confidence: 99%

Radiofrequency Ablation to Prevent Sudden Cardiac Death

Atoui¹,

Gunda²,

Lakkireddy³

et al. 2015

Methodist DeBakey Cardiovascular Journal

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Section: Ablation Of Accessory Pathway To Prevent Scdmentioning

confidence: 99%

Radiofrequency Ablation to Prevent Sudden Cardiac Death

Atoui¹,

Gunda²,

Lakkireddy³

et al. 2015

Methodist DeBakey Cardiovascular Journal

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“…The incidence of AF in patients with WPW syndrome is reported to be 10-30% [3][4][5]. No relationship between the onset of AF and localization of accessory pathways has been reported [6], and successful ablation of the accessory pathway prevents the recurrence of AF in the majority of patients.…”

Section: Explanations Of the Arrhythmiamentioning

confidence: 99%

Irregular wide QRS complex tachycardia without structural heart disease

Kobayashi

Ikeda

2012

Journal of Arrhythmia

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Case presentationA 64-year-old female presented to the emergency room with persistent dizziness that began early that morning. She had a 30-year history of palpitations and known electrocardiogram (ECG) abnormalities. Her pulse was irregular at 130-270 min À 1 and blood pressure was 90/40 mmHg. There were no other abnormalities on physical examination. A chest X-ray was normal and without cardiomegaly. Echocardiography revealed normal left ventricular contraction without structural abnormalities. Blood chemistry evaluation, including electrolytes and cardiac enzymes, was within normal limits. Twelve-lead ECG showed irregular wide QRS tachycardia of various configurations (Fig. 1).How would you diagnose her tachycardia? CommentaryThe patient's ECG shows wide QRS tachycardia with a rate from 150 to 300 beats/min. The RR intervals are irregularly irregular and no P wave preceding QRS was confirmed. The QRS complex has beat-beat variations in morphology. At this point, some of the arrhythmias that should be considered are: (1) irregular ventricular tachycardia (such as torsades des pointes or polymorphic ventricular tachycardia); (2) atrial fibrillation (AF) with bundle branch block; (3) AF in Wolff-Parkinson-White (WPW) syndrome (pseudo-ventricular tachycardia). The QRS complex shows right axis deviation during tachycardia with no progressive change in cardiac axis, thus polymorphic ventricular tachycardia and torsades des pointes associated with QT prolongation are excluded. Polymorphic ventricular tachycardia associated electrolyte abnormality and myocardial ischemia could not be totally excluded by this ECG, however laboratory examination did not indicate myocardial ischemia or an electrolyte abnormality.The representative arrhythmia of the patient's irregular heart rate is AF, which is the most common cardiac arrhythmia. When the ventricular rate is slow, AF can be easily diagnosed. However if the ventricular rate is rapid, AF is difficult to appreciate because QRS complexes are clustered together and fibrillatory waves become more difficult to evaluate. The QRS complexes during AF with bundle branch block usually do not have beat-beat variation, and both an Rr 0 pattern in lead V 1 and R oS amplitude in V 6 are uncommon for the ECG of right bundle branch block. On the other hand, the QRS complexes during AF in WPW syndrome are extremely bizarre and broad because the QRS complex reflects varying degrees of fusion of ventricular activation via the atrioventricular (AV) node and accessory pathways.To terminate AF and block the accessory pathway, procainamide was given intravenously at a dose of 400 mg over 30 min. It is important to note that AV nodal blocking agents are contraindicated in treatment of AF in patients with WPW syndrome. AV nodal blocking agents, for example verapamil and digoxin, decrease the number of impulses conducted through the His-Purkinje system and enhance conduction across accessory pathways, thus increasing the ventricular rate during AF. If the patient is hemodynamically unstable, elect...

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“…The recurrence rate of spontaneous AF after successful ablation of the AP is reported to be in the range of 6% to 10%. [11][12][13] However, Hamada et al made a very interesting observation in this respect. They observed that clinical episodes of AF recurred in 71% of their patients whose AF remained inducible immediately postablation, however, in none of the patients who remained uninducible postablation .…”

Section: Electrophysiological Properties Of the Accessory Pathway In mentioning

confidence: 99%

“…Ablation of the AP is very effective in the abolition of conduction through the AP, and it has been shown that recurrences of AF after succesful AP ablation occur at a low incidence. Haissaguerre et al 12 have documented a reduction in AF inducibility following catheter ablation in patients with WPW syndrome. Sharma et al 11 found a reduction in AF inducibility following elimination of AP by surgical ablation.…”

Section: Intrinsic Atrial Muscle Vulnerability In the Wpw Syndromementioning

confidence: 99%