© 2005 The European Society of Cardiology. Published by Elsevier Ltd. All rights reserved.
CASE REPORT
Atrial fibrillation triggered by postinfarction ventricular premature beats in a patient with Wolff–Parkinson–White syndrome
Unidad de Arritmias y Electrofisiología, Hospital Universitario "La Paz", Universidad Autónoma Madrid, Spain
Manuscript submitted 5 September 2004. Accepted after revision 5 December 2004.
*Corresponding author. Unidad de Arritmias, U.M.Q. de Cardiología, Hospital Universitario "La Paz", Paseo de la Castellana 261, 28046 Madrid, Spain. Tel./fax: +34 91 727 7564. E-mail address: rpeinado{at}secardiologia.es (R. Peinado).
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Abstract |
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The mechanism by which atrial fibrillation is initiated in patients with accessory pathways is not fully understood. Retrograde conduction of ventricular premature beats to the atrium, causing the arrhythmia, is a very rare cause. We report a patient with Wolff–Parkinson–White syndrome (WPW), without previous tachycardias, who presented multiple episodes of paroxysmal atrial fibrillation after having a myocardial infarction. During the electrophysiological (EP) study the patient presented two spontaneous episodes of atrial fibrillation initiated by ventricular premature beats conducted to the atria through the accessory pathway. After successful catheter ablation of the accessory pathway the patient did not present arrhythmia recurrences.
Key Words: Wolff–Parkinson–White syndrome, atrial fibrillation, ventricular premature beats, catheter ablation
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Introduction |
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Paroxysmal atrial fibrillation (AF) is a common arrhythmia in patients with accessory pathways (AP) and is observed in up to one-third of these patients [1]
. However, the mechanism by which AF is initiated in these patients is not fully understood. Although several causes have been proposed [2–5], the role of ventricular premature complexes (PVCs) in initiating AF has not been well investigated. We report on a patient with an AP in whom we observed that the episodes of AF were triggered by PVCs conducted to the atria through the AP.
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A 53-year-old male with AF and Wolff–Parkinson–White (WPW) syndrome was referred to our unit for radiofrequency (RF) ablation. Four years prior to referral he had suffered acute myocardial infarction which was treated with thrombolysis. After hospital discharge the patient was in functional class I (NYHA) without angina episodes. Left ventricular ejection fraction, determined by echocardiogram, was 54% and an exercise test was negative for inducible ischaemia. Several weeks after the myocardial infarction the patient presented episodes of sudden onset palpitations and mild chest pain. Episode duration ranged between 1 and 5 h. ECGs taken in the emergency room on several occasions showed AF without preexcitation. The ECG during sinus rhythm showed intermittent antegrade preexcitation (Fig. 1A). Sotalol 80 mg twice daily was started but was unable to prevent arrhythmia recurrences. An electrophysiological (EP) study was recommended for this reason.
EP was performed in the fasting state after informed consent. Antiarrhythmic drugs had been discontinued five days before the procedure. Three tetrapolar and one decapolar electrode catheters were positioned in the high right atrium, right ventricular apex, His bundle area and coronary sinus. At baseline, sinus rhythm without preexcitation was observed. Baseline conduction intervals were: AH 77 ms, and HV 48 ms, PA interval: 48 ms, PA-distal coronary sinus: 76 ms. Incremental ventricular pacing demonstrated retrograde AV conduction through the AV node and intermittent conduction through the AP. Maximal atrial conduction delay was 60 ms [6]. The earliest retrograde atrial activation during AP conduction was recorded in the posterior region of the left AV junction. Incremental atrial pacing showed the absence of antegrade conduction through the AP. On two occasions a spontaneous PVC, conducted to the atria through the AP, induced AF (Fig. 1B). The earliest activation site at the onset of AF was located near the atrial insertion of the AP (Fig. 2). After isoprenaline infusion, persistent bidirectional conduction through the AP was observed. The minimum 1:1 antegrade and retrograde conduction rate through the AP were 620 and 440 ms, respectively. Antegrade and retrograde effective refractory period (ERP) of the AP were 510 and 350 ms, respectively. Atrial and ventricular stimulation failed to induce tachycardia. RF catheter ablation was performed using a retrograde aortic approach, with bidirectional conduction being abolished after two RF applications at the ventricular insertion of the AP. After two years' follow-up, the patient is asymptomatic, with no recurrence of tachycardia or preexcitation despite the persistence of frequent PVCs on Holter monitoring.
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Discussion |
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AF is a common finding in the WPW syndrome. In the absence of other structural heart disease and atrial enlargement, several potential causative factors have been advocated: spontaneous degeneration of atrioventricular reciprocating tachycardia [2,7–9]
9], increased atrial vulnerability related to the AP [4,10], or intrinsic atrial abnormality [5].
Reciprocating atrioventricular tachycardia is a clearly documented AF initiating factor in some patients. Fujimura et al. [2] observed that reciprocating tachycardia preceded AF in 33 of 95 episodes during electrophysiological studies. It occurred either spontaneously during tachycardia or after atrial or ventricular extrastimuli introduced in an attempt to terminate AV reciprocating tachycardia. The latter may be a natural "trigger" in susceptible patients. In addition, paroxysmal supraventricular tachycardia-induced haemodynamic changes and atrial stretch may be responsible for electrophysiological and/or anatomical remodelling and increased atrial vulnerability [11]. However, our patient had neither previous documented clinical episodes of reciprocating tachycardia nor episodes induced during EP study. In addition, the AP conduction properties did not support this possibility.
Several authors have found that some patients with WPW and AF have different atrial properties than those without AF, including longer intraatrial conduction times, shorter atrial functional refractory periods and a higher incidence of intrinsic atrial vulnerability [5]. This could be a predisposing factor in our patient taking into account the presence of a previous myocardial infarction that could impair the diastolic left ventricular function and modify the electrophysiological properties of the atria because of an increase in atrial pressure and atrial stretch. However, the fact that the patient did not have AF episodes after catheter ablation of the AP is against this mechanism being the only element responsible for the arrhythmia episodes.
The AP itself may be important in the occurrence of AF. Jackman et al. [10] postulated that microreentry within the framework of the AP contributed to atrial fibrillation, and Iesaka et al. [4] demonstrated that the existence of retrograde multiple or multifibre APs in patients with WPW syndrome is associated with a higher incidence of clinical and induced AF. Hamada et al. [5] recently demonstrated that, in some patients with WPW syndrome, there is a reversible and AP-dependent atrial electrical remodelling that results in increased atrial vulnerability. In these patients AF may no longer occur if APs are ablated and they have no intrinsic atrial abnormality. The fact that there was no atrial conduction delay in our patient makes this mechanism improbable, although this could not be totally excluded as we did not study any other indices of atrial vulnerability.
The retrograde conduction of PVCs to the atrium causing the arrhythmia is a very rare finding, and the frequency with which this mode of onset occurs in WPW remains to be determined. Della Bella et al. [9] reported AF resulting from retrograde conduction of ventricular extrastimuli in five patients during EP study, but no spontaneous induction by PVCs was seen. Shen and Sung [12] reported on the initiation of AF by spontaneous PVCs in a patient with concealed AP. In our patient, on two occasions during the EP study we observed spontaneous PVCs conducted to the atria through the AP which initiated AF. We hypothesize that these premature complexes with a short coupling interval resulted in VA conduction to the atria and activated the left atrium during the atrial vulnerable phase, thereby precipitating the onset of AF. This hypothesis is supported by two facts: first, the patient began experiencing AF episodes after myocardial infarction. This could be related to a possible increase in the appearance of PVCs with different origins and coupling intervals. Second, the patient did not present new AF episodes after AP ablation despite the fact that Holter monitoring performed after ablation demonstrated the presence of frequent polymorphic PVCs.
A limitation of our case is that we cannot be sure that clinical episodes had the same mechanism as that found during the EP study, because Holter monitoring was not performed prior to RF ablation. However, the reproducibility found during EP study and the absence of AF recurrences after RF ablation support this possibility.
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The authors wish to thank Martin Hadley-Adams for his assistance with the English language.
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References |
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