Mechanisms for the genesis of paroxysmal atrial fibrillation in the Wolff--Parkinson--White syndrome: intrinsic atrial muscle vulnerability vs. electrophysiological properties of the accessory pathway

Background: Paroxysmal atrial fibrillation (PAF) develops in up to one-thirdof patients with the Wolff Parkinson–White syndrome (WPW).The reason for this high incidence of PAF in the WPW syndromeis not yet clearly understood. When PAF appears in patientswith WPW syndrome who have anterograde conduction via the accessorypathway (AP), it may be life-threatening if an extremely rapidventricular response develops degenerating into ventricularfibrillation. Methods and results: Several mechanisms responsible for the genesis of PAF in WPWpatients were hypothesized, namely, spontaneous degenerationof atrioventricular reciprocating tachycardia into atrial fibrillation(AF), electrical properties of the APs, effects of APs on atrialarchitecture, and intrinsic atrial muscle vulnerability. Focalactivity, multiple reentrant wavelets, and macroreentry haveall been implicated in AF, perhaps under the further influenceof the autonomic nervous system. AF can also be initiated byectopic beats originating from the pulmonary veins, and elsewhere.Several studies demonstrated a decrease incidence of PAF aftersuccessful elimination of the AP, suggesting that the AP itselfmay play an important role in the initiation of PAF. However,PAF still occurs in some patients with the WPW syndrome evenafter successful elimination of the AP. There is an importantevidence of an underlying atrial disease in patients with theWPW syndrome. Conclusions: Atrial vulnerability has been studied performing an atrial endocardialcatheter mapping and analysing abnormal atrial electrograms.Other studies evaluated atrial refractoriness and intraatrialconduction times, suggesting an intrinsic atrial vulnerabilityas the mechanism of PAF and considering the AP as an innocentbystander. It is our intention to analyse the available dataon this particular and interesting topic since AF has a singularprognostic significance in patients with the WPW syndrome, andits incidence is unusually high in the absence of any clinicalevidence of cardiac organic disease.     

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.     

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.     

Iatrogenic ventricular fibrillation in Wolff-Parkinson-White syndrome

Wolff-Parkinson-White (WPW) syndrome is the most common manifestation of ventricular pre-excitation syndrome and is mostly found in individuals with no structural heart disease. Although the risk of malignant arrhythmias is low, sudden cardiac death (SCD) as the first clinical manifestation of WPW syndrome is well documented, and atrial fibrillation (AF) with a rapid ventricular response is the main mechanism involved. Unfortunately, the signs of pre-excitation and arrhythmias are sometimes under-diagnosed and under-treated. We describe the case of a 31-year-old man who was admitted with an irregular wide complex tachycardia consistent with pre-excited AF, which was not promptly diagnosed, and who developed ventricular fibrillation (VF) after administration of atrioventricular (AV) nodal blockers, as a primary manifestation of WPW syndrome. Blocking the AV node in patients with pre-excited AF may increase the ventricular rate and potentially result in hemodynamic instability. Among patients with WPW syndrome who survive an episode of SCD, catheter ablation of the accessory pathway is the treatment of choice.     

Surgical treatment of cardiac arrhythmias

This report describes 20 consecutive patients who underwent surgical procedures for treatment of cardiac arrhythmias.16 patients have been operated for WPW. syndrome, always using the epicardial approach, without extracorporeal circulation.Three patients underwent surgery for atrio-ventricular nodal reentrant tachycardia, using a discrete perinodal cryotreatment, during normothermic extracorporeal circulation.In one case we used cryoablation of the atrial myocardium below the coronary sinus to treat atrial flutter. This operation was performed under normothermic extracorporeal circulation. In our observations, there was no early or late death; postoperative complications developed in 1 patient (5%) due to pericarditis.Ablation of the AP was completely successful in all the cases (100%) operated for WPW as well as for AVNRT syndromes and atrial flutter.Abbreviations AV atrio-ventricular - AVNRT atrio-ventricular nodal reentrant tachycardia - MSEC millisecond - SD sudden death - VT ventricular tachycardia - WPW Wolff-Parkinson-White     

Atrial fibrillation in the Wolff-Parkinson-White syndrome.

Atrial fibrillation in patients with Wolff-Parkinson-White (WPW) syndrome may lead to syncope, ventricular fibrillation, and sudden death. In a follow-up study of 241 patients with WPW syndrome in a relatively unselected population, 26 patients had documented atrial fibrillation (11%). These patients were followed up after 1-37 years (median 11 years; mean 15 years). During this period, 2 of 26 died suddenly. These 2 patients had the shortest RR interval during spontaneous atrial fibrillation (less than or equal to 220 msec), greater than or equal to 1 episodes of syncope, and a persistent delta wave in all available electrocardiograms. In comparison, sudden or tachycardia-related death was seen in 4 of the 241 patients. This difference is not statistically significant. Thus, atrial fibrillation of 26 patients with WPW syndrome was surprisingly well tolerated in our follow-up study with only 2 sudden deaths.     

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.     

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.     

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.     

Problems concerning assessment of anatomical site of accessory pathway in Wolff-Parkinson-White syndrome.

Twp patients with type B WPW syndrome and reciprocal tachycardias have been studied using intracardiac electrograms and programmed electrical stimulation of the heart. One patient, who had a right-sided accessory pathway giving the surface electrocardiographic appearances of type B WPW syndrome, was shown to have an additional left-sided accessory pathway as occurs in type A WPW syndrome. This concealed left-sided atrioventricular connexion formed the retrograde pathway during reciprocal tachycardia. In the second patient the appearances of type B WPW syndrome were shown to be caused by an accessory pathway between the atrial septum and the right side of the interventricular septum rather than an accessory pathway in the right atrioventricular groove. The significance of these findings when considering surgical interruption of an accessory atrioventricular conduction pathway is discussed.     

Molecular genetic analysis of PRKAG2 in sporadic Wolff-Parkinson-White syndrome

INTRODUCTION: Mutations in the PRKAG2 gene that encodes the gamma2 regulatory subunit of AMP-activated protein kinase have been shown to cause autosomal dominant Wolff-Parkinson-White (WPW) syndrome associated with hypertrophic cardiomyopathy. Prior studies focused on familial WPW syndrome associated with other heart disease such as hypertrophic cardiomyopathy. However, such disease accounts for only a small fraction of WPW cases, and the contribution of PRKAG2 mutations to sporadic isolated WPW syndrome is unknown. METHODS AND RESULTS: Subjects presented for clinical electrophysiologic evaluation of suspected WPW syndrome. WPW syndrome was diagnosed by ECG findings and/or by clinically indicated electrophysiologic study prior to enrollment. Echocardiography excluded hypertrophic cardiomyopathy. Denaturing high-performance liquid chromatography and automated sequencing were used to search for PRKAG2 mutations. Twenty-six patients without a family history of WPW syndrome were studied. No subject had cardiac hypertrophy, and only one patient had associated congenital heart disease. Accessory pathways were detected at diverse locations within the heart. Two polymorphisms in PRKAG2 were detected. [inv6+36insA] occurred in intron 6 in 4 WPW patients and [inv10+10delT] in intron 10 in 1 WPW patient. Both occurred in normal unrelated chromosomes. No PRKAG2 mutations were detected. CONCLUSION: This study shows that, unlike familial WPW syndrome, constitutional mutation of PRKAG2 is not commonly associated with sporadic WPW syndrome. Although polymorphisms within the PRKAG2 introns were identified, there is no evidence that these polymorphisms predispose to accessory pathway formation because their frequency is similarly high in both WPW patients and normal individuals. Further studies are warranted to identify the molecular basis of common sporadic WPW syndrome.     

相同基因型而不同表现型的PRKAG2基因突变一家系报道

目的 位于7号染色体上的腺苷一磷酸激活的蛋白激酶γ^2调节亚单位基因（PRKAG2基因）调节代谢通路。报道一个具有PRKAG2基因突变而临床表现型不同的家系。方法 使用DNA直接测序法,对一个具有多种形式心律失常的患者家系（13例患者）进行PRKAG2外显子及外显子和内含子拼接部位序列筛查寻找基因突变。结果 心电图显示患者家系存在窦性心动过缓、短PR间期、完全性右束支传导阻滞、房室传导阻滞和房性心动过速。其中3例患者在年轻时发生猝死,没有1例有预激综合征（预激）表现,只有1例有心肌肥厚。DNA测序结果显示,该家系所有患者皆有一个PRKAG2错义突变（R302Q）。这个基因突变以前曾描述并与预激和左室肥厚有关。结论 PRKAG2基因突变不仅导致预激而且与多种临床表现型有关。完全性右束支传导阻滞、窦性心动过缓、短PR间期应该高度怀疑有PRKAG2基因突变的可能。     

Should the Isuprel test be performed systematically in Wolff-Parkinson-White syndrome?

The isoprenaline (Is) test was designed by Wellens et al. in 1982 to evaluate the effect of catecholamines on the effective refractory period (ERP) of Kent's bundle (K). The purpose of our study was to assess the value of this test in the prognosis of Wolff-Parkinson-White syndrome (WPW), to define its criteria of severity and to determine the usefulness of the test. Out of 33 patients with WPW syndrome, 10 (group I) had a clinical history of severe arrhythmia and 23 (group II) were asymptomatic or had paroxysmal nodal tachycardia. The prognosis of WPW syndrome was evaluated by measuring Kent's bundle ERP under coupled atrial stimulation (S1 S2) and the shortest cycle conducted by K during induced atrial fibrillation (AF) and atrial pacing (AP) both in the basal state (B) and under a 20-30 micrograms Is infusion. (table; see text). Analysis of the results showed constant shortening of ERP in group I and reproduction of the clinical tachycardia in 6 cases. In group II patients isoprenaline unmasked the WPW syndrome in 3 cases and reproduced the clinical tachycardia in 5 cases. The ERP of Kent's bundle evaluated by S1 S2 became smaller or equal to 220 ms in 70 p. 100 of the cases, and this shortening was not specific. The shortest cycle in AF or AP became inferior of equal to 220 ms in only 6 cases, the history being concordant with clinical findings in 4 of them. Altogether, the most reliable and simplest way of evaluating the severity of WPW syndrome is the highest frequency conducted by Kent's bundle in atrial pacing during the Is test which should be performed in all patients in view of its specificity, simplicity and safety.     

Prediction of a fatal atrial fibrillation in patients with asymptomatic Wolff-Parkinson-White pattern

Paroxysmal atrial fibrillation (PAF) in patients with manifest WPW syndrome can be a life-threatening arrhythmia by deterioration into ventricular fibrillation. In patients with asymptomatic WPW pattern, the first PAF may lead to ventricular fibrillation or sudden death. Therefore, the purpose of this study was to predict a fatal PAF in patients with asymptomatic WPW pattern. The patient population was divided into two groups: (1) 145 patients with manifest WPW syndrome, excluding intermittent ones (32 with an episode of PAF, 49 with AV reciprocating tachycardia alone, and 64 without any episode of paroxysmal tachyarrhythmia), and (2) mixed group of patients with and without WPW syndrome (36 with an episode of PAF and 66 without PAF). The results were as follows: (1) (a) out of 32 patients with WPW syndrome and PAF, 8 patients were observed to have both the shortest preexcited R-R interval of less than 200 msec during PAF and the shortest antegrade effective refractory period of the accessory pathway (ERP-AP) of less than 250 msec, 7 of whom had dizziness or syncope during PAF and 2 died suddenly during the follow-up period; (b) 21 (32.8%) out of 64 patients with asymptomatic WPW pattern showed the shortest antegrade ERP-AP less than 250 msec; (2) patients with PAF had a higher tendency to develop repetitive atrial firing (RAF), as well as fragmented atrial activity (FAA), which were induced using programmed atrial stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Usefulness of invasive and non-invasive electrophysiologic studies in the selection of antiarrhythmic drugs for the patients with paroxysmal supraventricular tachyarrhythmia

A comparison of the effects of several antiarrhythmic agents was made in a study of 70 patients - 15 with manifest Wolff-Parkinson-White (WPW) syndrome, 17 with concealed WPW syndrome, 18 with AV nodal re-entrant tachycardia, 14 with paroxysmal atrial fibrillation and 6 with paroxysmal atrial flutter - employing intracardiac stimulation and esophageal pacing. For the termination of paroxysmal supraventricular tachycardia, intravenous administration of verapamil or aprindine was more effective than that of disopyramide or procainamide. In AV nodal re-entrant tachycardia, verapamil was the most effective for termination. In the manifest WPW syndrome, disopyramide or aprindine was indicated especially for patients with the accessory pathways of the short antegrade refractory period, because these drugs lengthened the refractory period of the accessory pathways. For the purpose of converting atrial fibrillation or flutter to the sinus rhythm, type IA drugs such as disopyramide were indicated. However, verapamil was effective for slowing down the ventricular rate in atrial fibrillation or flutter except in cases of manifest WPW syndrome. A 6-month follow-up study showed that oral administration of verapamil was also useful for putting a stop to the attacks in 24 out of 32 patients with paroxysmal supraventricular tachycardia, while oral disopyramide prevented the recurrence of atrial fibrillation in only 4 of 10 patients.     

Flecainide acetate in the treatment of supraventricular tachycardias: value of programmed electrical stimulation for long-term prognosis

Twenty patients with recurrent symptomatic supraventricular tachycardia were studied to estimate the efficacy of flecainide in the long-term treatment of these arrhythmias and to evaluate the prognostic value of programmed electrophysiologic stimulation. All patients had their arrhythmia inducible at baseline evaluation. Nine patients had a Wolff-Parkinson-White (WPW) syndrome, five had a concealed bypass tract, and two had dual atrioventricular (AV) nodal pathways. In the remaining patients there was an intraatrial reentry circuit. Previous medication was no to five antiarrhythmic drugs (mean 2.4 drugs). At baseline, a circus movement tachycardia was induced in 12, AV nodal tachycardia was induced in two, atrial tachycardia was induced in three, atrial fibrillation was induced in five, and a flutter was induced in two patients. After flecainide, 2 mg/kg intravenously in 10 minutes, six patients no longer had their arrhythmia inducible. In the WPW patients, atrial fibrillation was no more inducible. In 65% of the patients there was no recurrence during a follow-up period of 11 +/- 10 months. None of the six patients who no longer had their arrhythmia inducible had a recurrence of the tachycardia over a period of up to 3 years. Seven of the other 14 patients (who still had their arrhythmia inducible) had a recurrence of the tachycardia. Positive and negative predictive values are 50% and 100%, respectively. We conclude that flecainide prevents recurrences of supraventricular tachycardias in 65% of patients with inducible supraventricular tachycardias during a mean follow-up of 11 months. Programmed electrical stimulation has a high negative predictive value in this setting. Flecainide is especially effective in preventing atrial fibrillation in patients with WPW syndrome.     

Perception and Documentation of Arrhythmias after Successful Radiofrequency Catheter Ablation of Accessory Pathways

Background: Some patients continue to have palpitations in spite of successful ablation of Wolff‐Parkinson‐White (WPW) syndrome. Recurrence of accessory pathways as well as unrelated arrhythmias may explain the symptoms. Methods: We followed 194 consecutive patients after successful radiofrequency catheter ablation of overt (147) or concealed (47) WPW syndrome. The mean duration of symptoms was 16 ±; 13 years. Atrial fibrillation was documented in 54 patients (24%) prior to ablation. 185 patients responded to a questionnaire 24 ±; 12 months after ablation. Results: The physical well‐being was improved in 94%, unchanged in 5%, and deteriorated in 1%. However, 76 patients (39%) reported arrhythmia symptoms, in 40 patients causing pharmacological treatment (14 patients) and/or continued contact with their doctor. The underlying arrhythmias were orthodromic tachycardia (10), atrial fibrillation (12), premature beats (12), atrial flutter (1), and ventricular tachycardia (1), while in four patients no explanation was found. Minor symptoms in the other 36 patients were explained by premature beats in 29, while unexplained in 7. All patients with atrial fibrillation after ablation had atrial fibrillation before ablation. Ten relapses of WPW syndrome occurred: eight were known before the time of the questionnaire, two were confirmed at transesophageal atrial stimulation. Conclusion: 94% patients with a long history of tachyarrhythmias due to the WPW syndrome reported improved physical well‐being after ablation, but palpitations were common during a 2‐year follow‐up period; 8% continued to use pharmacological antiarrhythmic treatment. Five percent had symptomatic relapses and in 6% atrial fibrillation episodes reoccurred, i.e., in half of those who had atrial fibrillation before ablation. A.N.E. 2001; 6(3):216–221     

Effects of disopyramide on electrophysiological properties of specialized conduction system in man and on accessory atrioventricular pathway in Wolff-Parkinson-White syndrome.

Seven patients with normal specialized conduction system and three patients with the Wolff-Parkinson-White (WPW) syndrome were studied using programmed stimulation of the heart before and after the administration of intravenous disopyramide. The principal effect of this drug was to prolong the effective refractory period of the atria and ventricles, and to prolong the effective refractory period of the anomalous pathway in the WPW syndrome. In addition, it prolonged the conduction time in the anomalous pathway in the WPW syndrome. These findings suggest that disopyramide would be a useful and safe drug in the management of certain atrial and ventricular arrhythmias and in the management of the Wolff-Parkinson-White syndrome with atrial fibrillation.     

Double Atrial Potentials Recorded in the Coronary Sinus in Patients with Wolff-Parkinson-White Syndrome: A Possible Mechanism of Induced Atrial Fibrillation

BACKGROUND: Double atrial potentials recorded in the coronary sinus are not an unusual phenomenon in patients with supraventricular tachyarrhythmias. They have been demonstrated to potentiate the occurrence of atrial tachyarrhythmias. METHODS: Two hundred and forty-eight patients were included for investigating the presence of double atrial potentials on the coronary sinus recordings during electrophysiologic study. Group 1 consisted of 136 patients with WPW syndrome and group 2 consisted of 112 patients with atrioventricular nodal reentrant tachycardia (AVNRT). Group 1 patients had a higher incidence of induced atrial fibrillation (AF) (27% vs. 15%, P = 0.045) than group 2 patients. In addition, the incidence of double atrial potentials was significantly higher in group 1 than in group 2 patients (14% vs. 2%, P = 0.001). In group 1, 19 patients with double atrial potentials had a significantly higher incidence of left lateral bypass tracts (79% vs. 39%, P = 0.001) and induced AF (47% vs. 22%, P = 0.01) than 117 patients without double atrial potentials. CONCLUSIONS: WPW syndrome, especially with a left lateral bypass tract, had a higher incidence of double atrial potentials and induced AF than AVNRT. WPW patients with double atrial potentials had a higher incidence of induced AF than those without double atrial potentials. These findings may contribute to understanding the mechanism of induced AF in WPW syndrome.     

Effects of disopyramide on electrophysiological properties of specialized conduction system in man and on accessory atrioventricular pathway in Wolff-Parkinson-White syndrome.

Seven patients with normal specialized conduction system and three patients with the Wolff-Parkinson-White (WPW) syndrome were studied using programmed stimulation of the heart before and after the administration of intravenous disopyramide. The principal effect of this drug was to prolong the effective refractory period of the atria and ventricles, and to prolong the effective refractory period of the anomalous pathway in the WPW syndrome. In addition, it prolonged the conduction time in the anomalous pathway in the WPW syndrome. These findings suggest that disopyramide would be a useful and safe drug in the management of certain atrial and ventricular arrhythmias and in the management of the Wolff-Parkinson-White syndrome with atrial fibrillation.