Wolff-Parkinson-White syndrome presenting in atrial fibrillation

A case of atrial fibrillation in a patient with Wolff-Parkinson-White (WPW) syndrome is presented. In this case, the patient's ECG initially was misread as ventricular tachycardia. The therapy was appropriate for the actual condition, although electrical cardioversion and defibrillation eventually were required. The treatment of WPW with atrial fibrillation in this case consisted of lidocaine and procainamide. Verapamil, propranolol, and digoxin, which normally are indicated for WPW with tachyarrhythmias, are contraindicated for WPW with atrial fibrillation.     

Encainide for atrial fibrillation associated with Wolff-Parkinson-White syndrome

Thirty-six patients with a history of atrial fibrillation and Wolff-Parkinson-White syndrome were treated with oral encainide, 175 ± 44 ing/day, after undergoing baseline drug-free electrophysiologic studies. The mean age was 38 ± 15 years, with structural heart disease present in only 3 patients. Nine patients had only paroxysmal atrial fibrillation and 27 patients had both atrial fibrillation and atrioventricular reciprocating tachycardia (AVRT). Symptoms were present for a mean of 195 ± 168 months and were treated with an average of 2.7 ± 1.6 drugs before encainide. Anterograde block in the accessory pathway occurred in 12 of 30 patients (40%) and retrograde block accessory pathway occurred in 10 of 24 patients in whom comparison could be made. AVRT was initiated in 29 of 36 patients during the control study and could be initiated in 19 of 29 patients while receiving encainide.

Drug efficacy was determined by the clinical response judged completely effective, partially effective or ineffective. During a mean follow-up of 30.1 ± 25 months, 24 patients (67%) continued to take encainide. Encainide was completely effective in 14 of 24 patients and partially effective in another 7 patients. Noncardiac side effects were mild and generally resolved, and required discontinuance in only 1 patient. More frequent AVRT occurred in 2 patients, but was managed with dose reduction and the addition of a β blocker. Three patients had ventricular tachycardia requiring discontinuance; however 2 of 3 patients had a history of ventricular tachycardia before receiving encainide. Encainide is an effective and safe agent for treating atrial fibrillation in patients with Wolff-Parkinson-White syndrome.     

Lidocaine in Wolff-Parkinson-White syndrome with atrial fibrillation.

Atrial fibrillation in the Wolff-Parkinson-White syndrome may be life-threatening because of the extremely rapid ventricular rates that can occur over the accessory pathway. An 18-year-old man with Wolff-Parkinson-White (type B) syndrome developed episodes of syncope due to atrial fibrillation. In studies during hospitalization the administration of lidocaine immediately slowed the ventricular response by abolishing antegrade conduction over the accessory pathway. The role of lidocaine and other antiarrhythmic drugs in the management of arrhythmias in the Wolff-Parkinson-White syndrome is discussed.     

Fatal ventricular fibrillation following verapamil in Wolff-Parkinson-White syndrome with atrial fibrillation

A 29-year-old man with Wolff-Parkinson-White syndrome and atrial fibrillation developed fatal ventricular fibrillation shortly after receiving intravenous verapamil. The patient presented with an irregular pulse of 190. A total of 23 mg of verapamil was administered in small intravenous doses over 35 minutes. The ventricular rate accelerated as verapamil was administered, and fatal ventricular fibrillation followed. Three theoretical mechanisms by which verapamil may enhance conduction of atrial fibrillation in Wolff-Parkinson-White syndrome, predisposing to ventricular fibrillation, are mentioned.     

Mechanisms for atrial fibrillation in patients with Wolff-Parkinson-White syndrome

INTRODUCTION: Paroxysmal atrial fibrillation (PAF) frequently occurs in patients with Wolff-Parkinson-White (WPW) syndrome. To elucidate the mechanisms for PAF, we performed electrophysiologic studies (EPS) before and after ablation of accessory pathways (APs). METHODS AND RESULTS: We investigated 24 patients with WPW syndrome who had AV reciprocating tachycardia and prior PAF and had undergone successful ablation of APs. Patients in whom atrial fibrillation (AF) was induced by EPS at day 7 after ablation were considered the inducible AF group (n = 14), and patients in whom AF was not induced by EPS at day 7 after ablation were considered the noninducible AF group (n = 10). Fifteen patients with AV nodal reentrant tachycardia (AVNRT) but without PAF who underwent ablation of the slow AV nodal pathways served as the control group (AVNRT group). Maximal atrial conduction delay and conduction delay zone, which are indices of atrial vulnerability, were measured before and after ablation. Before ablation, maximal atrial conduction delay and conduction delay zone were significantly greater (P < 0.0001 and P < 0.0001, respectively) in the two WPW syndrome groups than in the AVNRT group, indicating increased atrial vulnerability in WPW syndrome with PAF. After ablation, these parameters did not change in the inducible AF group, whereas they were significantly (P < 0.0001) decreased in the noninducible AF group and were not different from those in the AVNRT group, indicating normalized atrial vulnerability in the noninducible AF group after ablation. The prospective study demonstrated that PAF recurred only in the inducible AF group during long-term follow-up (17+/-7 months). CONCLUSION: The findings of this study suggest that there are two mechanisms of PAF in patients with WPW syndrome: one mechanism is reversible and AP-dependent atrial vulnerability, and the other is intrinsic and AP-independent atrial vulnerability.     

Treatment of atrial fibrillation with mexiletine in Wolff-Parkinson-White syndrome

It is reported on 6 patients with Wolff-Parkinson-White syndrome in whom spontaneously appeared auricular fibrillation with high ventricular frequency. By the intravenous administration of mexiletine in three patients the sinus rhythm could be restored. In two patients at first only a reduction of the tachycardia and a disappearing of the QRS-broadening took place; the additional administration of quinidine then led to the return of the sinus rhythm. In one patient, despite combined treatment, the return of sinus rhythm could not be achieved, mexiletine, however, led at once to the decrease of the ventricular rate, to the normalisation of the QRS-duration and to the disappearance of all signs of congestive heart failure. The therapeutic mechanism of mexiletine in the Wolff-Parkinson-White syndrome is discussed and it administration for the treatment of the cases complicated by auricular fibrillation is recommended.     

Sinus bradycardia and atrial fibrillation associated with the Wolff-Parkinson-White syndrome

Thirty-three patients with atrial fibrillation associated with the Wolff-Parkinson-White (WPW) syndrome were studied to determine the relation of sinus bradycardia and atrial fibrillation. In seven patients the sinus rate was less than 40 beats/min and sinus nodal disease was considered a cause of the periods of bradycardia. Ventricular fibrillation or functional cardiac arrest was documented in four instances. Twenty-six patients demonstrated a type A and seven a type B WPW pattern during periods of sinus rhythm. Male patients predominated. The average age was 38.5 years among patients with a type A pattern compared with 25.3 years among those with a type B pattern. The shortest R-R cycle length in this group was 130 msec during a period of atrial fibrillation. Five thousand serial microscopic sections were studied in one patient who demonstrated ventricular fibrillation. Three anomalous pathways were located in this patient with the widest tract, 380 μ, containing about 400 muscle cells. Most of the sinoatrial node was replaced by collagen elastic fibers, and there was widespread destruction of the atria with a marked increase in fibrous connective tissue.Ventricular fibrillation or functional cardiac arrest is not a rare arrhythmia in patients with atrial fibrillation associated with the WPW syndrome and may be responsible for sudden death in patients with these arrhythmias. Hence, precise electrophysiologic studies and pharmacologic or surgical management, or both, are suggested to prevent sudden death in patients with short refractory periods associated with atrial fibrillation and the WPW syndrome.     

Risk factors of atrial fibrillation in patients with Wolff-Parkinson-White syndrome

BACKGROUND: Atrial fibrillation (AF) in patients with WPW syndrome may be a life-threatening arrhythmia. AIM: To identify risk factors of AF and their prognostic significance in patients with WPW syndrome. METHODS: Clinical and electrophysiological parameters of 239 patients with WPW syndrome, who underwent successful RF ablation, were analysed using logistic regression and multivariate analysis. One hundred eight patients had no history of AF whereas the remaining 81 patients had previous spontaneous AF episodes. Long-term follow-up data (mean 29+/-23 months, range 1-99 months) were available in 136 patients (87 without AF and 49 with AF). RESULTS: Patients with AF were significantly older, more frequently of male gender and had more often a history of syncope than patients without AF. There were two peaks of AF occurrence - in the third and in the fifth decade of life. Fourteen patients had a history of ventricular fibrillation - 11 patients with AF vs 3 patients without AF (p=0.0016). Patients with a history of AF were more prone to AF induced during electrophysiological study and had less frequently concealed accessory pathways. CONCLUSIONS: Age, gender and a history of syncope are the independent risk factors of AF in patients with WPW syndrome. Anterograde conduction via accessory pathway is of major importance in the development of AF. RF ablation of an accessory pathway should be performed early because the risk of the procedure is small and there is an increasing risk of AF with ageing.     

Atrial fibrillation and atrial vulnerability in the Wolff-Parkinson-White syndrome

To explore the etiology of paroxysmal atrial fibrillation (AF) in the Wolff-Parkinson-White (WPW) syndrome, we examined the rates of AF episodes and performed electrophysiologic studies in 58 patients with WPW syndrome. They were classified into three patient groups depending on the property of antegrade conduction over accessory pathways: manifest WPW, intermittent WPW, and concealed WPW. Atrial vulnerability was defined as the inducibility of AF or repetitive atrial responses. The three groups were: 24 patients in manifest WPW, aged 42 +/- 15 yrs, 38% with AF; 12 patients in intermittent WPW, aged 40 +/- 15 yrs, 25% with AF; 22 patients in concealed WPW, aged 44 +/- 16 yrs, 9% with AF. There were no significant differences in the mean age between the groups. The incidences of atrial vulnerability detected in electrophysiologic studies in each group were 54%, 42%, and 27% respectively. The incidence of AF was well correlated with that of atrial vulnerability (p less than 0.01). The effective refractory periods (ERP) of the atrium and the retrograde ERP of the accessory pathway did not differ significantly between the three groups. Atrial conduction delay was more prominent in manifest WPW than in concealed WPW. The incidence of AF and atrial vulnerability was highest in the manifest WPW group, intermediate in the intermittent WPW group, and lowest in those patients with concealed WPW. The difference in incidence between the manifest WPW group and the concealed WPW group was significant (p less than 0.05). Therefore, the property of antegrade conduction over accessory pathways may be related to the genesis of AF in the WPW syndrome.     

Wolff-Parkinson-White syndrome: atrial fibrillation as the presenting arrhythmia

Atrial fibrillation was identified as the initial arrhythmia complicating the Wolff-Parkinson-White syndrome in ten (9%) of 108 patients. Despite initially rapid ventricular responses in seven, long term survival and control of arrhythmia were excellent on medical treatment. Whereas symptom free patients with the pre-excitation syndrome who have additional underlying disease predisposing to atrial fibrillation may need detailed electrophysiological study, a more conservative approach is suitable for the typical symptom free individual.     

心房颤动伴预激综合征1例

患者,男,41岁,因持续心悸伴心动过速就诊。心电图示P波消失,心室率193次/min;QRS波的形态基本一致,但时限宽窄不一,可见最短的RR间距200ms。结合后期记录的窦性心电图及其QRS波起始部形态一致的特点,不难做出预激综合征合并心房颤动的诊断。     

Wolff-Parkinson-White syndrome: atrial fibrillation as the presenting arrhythmia.

Atrial fibrillation was identified as the initial arrhythmia complicating the Wolff-Parkinson-White syndrome in ten (9%) of 108 patients. Despite initially rapid ventricular responses in seven, long term survival and control of arrhythmia were excellent on medical treatment. Whereas symptom free patients with the pre-excitation syndrome who have additional underlying disease predisposing to atrial fibrillation may need detailed electrophysiological study, a more conservative approach is suitable for the typical symptom free individual.     

Atrial electrophysiologic abnormalities in patients with Wolff-Parkinson-White syndrome but without paroxysmal atrial fibrillation

BACKGROUND: Paroxysmal atrial fibrillation (PAF) frequently occurs in patients with Wolff-Parkinson-White (WPW) syndrome. HYPOTHESIS: The purpose of this study was to analyze the atrial electrophysiologic abnormalities and vulnerability to develop atrial fibrillation (AF) in patients with WPW syndrome but with no previous history of PAF. METHODS: We investigated atrial electrophysiologic abnormalities and vulnerability to AF in patients with WPW syndrome but without PAF. An electrophysiologic study was performed in 28 patients with WPW syndrome, 23 with atrioventricular nodal reentrant tachycardia (AVNRT) and 25 with other arrhythmias (control), all of whom had no history of PAF. The following atrial excitability parameters were assessed: effective refractory period (ERP), spontaneous or paced (A1) and extrastimulated (A2) atrial electrogram widths, percent maximum atrial fragmentation (%MAF; A2/A1 x 100), wavelength index (WLI; ERP/A2), and inducibility of AF. RESULTS: The ERP tended to be shorter in patients with WPW syndrome and in those with AVNRT than in the control group. The %MAF increased (154 +/- 33 vs. 137 +/- 23%, p < 0.05) and WLI decreased (2.7 +/- 0.8 vs. 3.4 +/- 1.0, p < 0.05) significantly in patients with WPW syndrome compared with the control group; however, these parameters in patients with AVNRT showed intermediate values. Atrial fibrillation was more inducible in patients with WPW syndrome (4/28 [14.3%]) than in those with AVNRT (4.3% [1/23]) and the control group (0/25 [0%]). With respect to patients with WPW syndrome and with and without inducible AF, the %MAF increased (195 +/- 23 vs. 148 +/- 30%, p < 0.01) and the WLI decreased (2.2 +/- 0.3 vs. 2.9 +/- 0.9, p < 0.05) in subjects with inducible AF. CONCLUSIONS: Atrial electrophysiologic abnormalities, especially atrial conduction delays, are more prominent in patients with WPW syndrome, even if they had no previous history of PAF. These abnormalities may play an important role in determining the vulnerability to AF.     

预激综合征患者发生阵发性心房颤动机制的探讨

目的通过分析预激综合征患者旁道的电生理特性以及消融旁道后P波离散度(Pd)的计算,探讨预激综合征发生阵发性心房颤动(简称房颤)的机制。方法分析预激综合征合并旁道介导的阵发性心动过速患者127例。根据既往有无阵发性房颤(PAF)发作将患者分为PAF组(23例)和无PAF组(NPAF,104例)2组进行分析。电生理检查测定旁道的前传和逆传不应期。消融成功术后24h描记12导联心电图测量P波最大时限(Pmax)、P波最小时限(Pmin),计算Pd。结果消融前PAF组旁道前传和逆传不应期较NPAF组短(前传:265.3±42.5msvs331.4±38.7ms;逆传:255.8±46.7msvs317.5±31.7ms;P均<0.05)。消融术后心电图Pmax和PdPAF组显著长于NPAF组(Pmax:135.2±12.5msvs120.4±8.7ms;Pd:51.6±10.3msvs32.7±6.7ms;P均<0.05)。结论旁道有效不应期缩短和窦性激动在心房内的非均质传导在预激综合征患者房颤发生中可能起重要作用。