Ibutilide for Termination of Atrial Fibrillation in the Wolff-Parkinson-White Syndrome

Ibutilide promptly restored sinus rhythm on two occasions in an elderly patient with AF and rapid ventricular response associated with the WPW syndrome. As a selective Class III antiarrhythmic agent that prolongs cardiac refractoriness, ibutilide offers an alternative effective therapy for rapid termination of AF in WPW.     

Atrial Fibrillation in Wolff-Parkinson-White Syndrome: Reversal of Isoproterenol Effects by Sotalol

Sotalol has Class II and III antiarrhythmic effects. Its efficacy and safety as a treatment of atrial fibrillation in patients with the Wolff-Parkinson-White (WPW) syndrome is controversial. We evaluated the effects of isoproterenol and IV sotalol (1.5 mg/kg in 10 minutes) given together versus isoproterenol alone on anterograde conduction through the AV node and accessory pathway. Atrial fibrillation was induced in 22 patients with WPW (13 men, 9 women, 36 ± 16 years old). AV node and accessory pathway conduction were both enhanced by isoproterenol, although the effect was greater on the AV node. The minimum interval between preexcited QRS complexes shortened in all patients. Conversely, sotalol caused a significant prolongation of the shortest preexcited QRS interval as well as of the shortest interval between narrow QRS complexes. In addition, sotalol reversed all the effects of isoproterenol during atrial fibrillation. The percent of preexcited QRS complexes was not significantly modified because variations in ventricular preexcitation results from a balance between the relative effects on refractoriness of the accessory pathway versus of the AV node and in the amount of respective anterograde and- retrograde concealed conduction. There were no serious adverse effects.'Reversion to sinus rhythm was documented in 12 patients (60%). These short-term observations suggest that sotalol may be safe and effective in the treatment of patients with WPW and atrial fibrillation.     

Atrial and Ventricular Vulnerability in a Patient with the Wolff-Parkinson-White Syndrome

An electrophysiologic study was carried out in a patient with the Wolff-Parkinson-White syndrome and a history of spontaneous atrial fibrillation but with no evidence of organic cardiac disease. A single induced premature ventricular depolarization resulted in ventricular tachycardia followed by ventricular fibrillation. Similarly, atrial pacing or premature atrial stimulation resulted in frequent episodes of atrial fibrillation or flutter, The atrial and ventricular effective refractory periods were 180 ms and < 160 ms, respectively, at a driven cycle length of 480 ms. Intravenous administration of procainamide resulted in lengthening of the refractory periods and failure to induce either atriaJ or ventricular arrhythmias with pacing. In most patients with enhanced atrioventricular nodal or accessory atrioventricular nodal bypass, the mechanism of ventricular tachycardia is related to an inordinately rapid ventricular response during supraventricular arrhythmias. In our patient, a unique mechanism was apparent: atrial and ventricular vulnerability to fibrillation was associated with extremely short myocardial effective refractory periods. The relationship of this finding to sudden cardiac death bears further study.     

Electrophysiological Abnormalities of the Atrial Muscle in Patients with Manifest Wolff-Parkinson-White Syndrome Associated with Paroxysmal Atrial Fibrillation

We investigated the electrophysiological properties of the atrial muscle in 33 patients with manifest Wolff-Parkinson-White syndrome. Group I consisted of 13 patients with paroxysmal atrial fibrillation and group II consisted of 20 patients without paroxysmal atrial fibrillation. The anterograde and retrograde effective refractory periods of the accessory pathway and the inducibility of atrioventricular reciprocating tachycardia were not significantly different between the two groups. Endocardial electrograms, obtained by right atrial catheter mapping, were recorded during sinus rhythm from 12 sites of the right atrium in 12 of the 13 group I patients and in all group II patients. An abnormal atrial electrogram was defined as 100 msec or longer in duration, and/or the occurrence of eight or more deflections. Ten (83%) of the 12 group I patients had abnormal atrial electrograms, while only two (10%) of the 20 group II patients had abnormal atrial electrograms, and the difference was significant (P less than 0.01). Thirty-six (26%) of the total 139 electrograms obtained from 12 group I patients and two (1%) of the total 199 electrograms obtained from 20 group II patients fulfilled the criteria for an abnormal atrial electrogram, and the difference was significant (P less than 0.01). The fragmented atrial activity zone, interatrial conduction delay zone, and repetitive atrial firing zone obtained by right atrial extrastimulation were significantly wider in group I than in group II, respectively. It was concluded that electrical abnormalities of the atrial muscle may play an important role in the occurrence of paroxysmal atrial fibrillation in patients with Wolff-Parkinson-White syndrome.     

Relation between Spontaneous Atrial Fibrillation and Atrial Vulnerability in Patients with Wolff-Parkinson-White Pattern

An intracavitary electrophysiological study was carried out on 103 patients with Wolff-Parkinson-White (WPW), 23 symptomatic patients had documented episodes of atrial fibrillation, 54 symptomatic patients had atrioventricular reentrant tachycardias, and 26 asymptomatic. Patients were examined for the relation between spontaneous atrial fibrillation and atrial vulnerability, defined as the possibility to induce sustained (greater than 1 minute) episodes of atrial fibrillation with a stimulation protocol excluding atrial bursts. Atrail fibrillation induction was attempted by single and double atrial extrastimuli during pacing at two different cycle lengths and incremental atrial pacing. Sustained atrail fibrillation was induced in 65% of the patients with spontaneous atrial fibrillation, and in 13% of the symptomatic patients with documented episodes of atrioventricular reentrant tachycardias and in 15% of the asymptomatic patients (P less than 0.0005). Atrial vulnerability was higher in patients with spontaneous atrial fibrillation than in patients without this arrhythmia. No significant difference was observed between symptomatic without atrial fibrillation and asymptomatic patients.     

Right Atrial Diverticulum Presenting as Wolff-Parkinson-White Syndrome

A 7-year-old male presenting with Wolff-Parkinson-White syndrome and tachycardia was suspected by echocardiographic and magnetic resonance imaging evaluation to have an associated pericardial cyst anterior to the right atrium and ventricle. Electrophysiological evaluation demonstrated short antegrade and retrograde accessory connection refractory periods, with inducible orthodromic atrioventricular reentrant tachycardia. Surgical observation revealed a rare congenital right atrial diverticulum bridging the anterior right atrioventricular groove, with the functional accessory connection lateralized to the medial aspect of this structure. Endocardial and epicardial incisions and cryolesions placed along the anterior right atrioventricular groove initially appeared successful, but preexcitation recurred within 4 weeks postoperatively.     

Adenosine Induced Ventricular Fibrillation in Wolff-Parkinson-White Syndrome

GUPTA, A. K., et al. : Adenosine Induced Ventricular Fibrillation in Wolff-Parkinson-White Syndrome. VF was observed in four patients (group A) with preexcited AF presenting to the emergency department who had been given 12 mg of adenosine. These patients were resuscitated and underwent electrophysiological study and catheter ablation of the accessory pathway (AP). In a control (group B) of five patients with manifest AP, sustained AF was induced by rapid atrial pacing during electrophysiological study and 12 mg of adenosine was administered. The ECG and electrophysiologic features in the two groups were compared. All patients had a single manifest AP. In group A, three patients had a left free-wall AP and one patient had a posteroseptal AP, while in the control group all had left free-wall APs. The antegrade AP effective refractory period (ERP) in groups A and B was  227 ± 29 and 289 ± 37 ms  , respectively (  P < 0.05  ). The atrial ERP was  210 ± 17 versus 219 ± 21 ms  , respectively, in groups A and B (  P > 0.05  ). The shortest R-R interval during AF in group A was  246 ± 51 ms and 301 ± 60 ms  in group B (  P value < 0.05  ). After adenosine, no patient in group B developed VF. Adenosine may cause VF when administered during preexcited AF. This phenomenon is seen in patients having APs with short refractory periods.     

Efficacy of Ventricular Rate Stabilization by Right Ventricular Pacing During Atrial Fibrillation

To assess the effect of right ventricular pacing on rate regularity during exercise and daily life activities, 16 patients with sinoatrial disease and chronic atrial fibrillation (AF) were studied. Incremental ventricular pacing was commenced at 40 beats/min until > 95% of ventricular pacing were achieved during supine, sitting, and standing. Thirteen patients also underwent randomized paired submaximal exercise tests in either a fixed rate mode (VVI) or a ventricular rate stabilization (VRS) mode in which the pacingrate was set manually at 10 beats/min above the average AF rate duringthe last minute of each exercise stage. The pacing interval for rate regularization was shortest during standing (692 ± 26 ms) compared with either supine or sitting (757 ± 30 and 705 ± 26 ms, respectively, P < 0.05). During exercise, VRS pacing significantly increased the maximum rate (119 ± 5.2 vs 106 ± 4.2 ms, P < 0.05), percent of ventricular pacing (85%± 5% vs 23%± 7%, P < 0.05), rate regularity index (5.8%± 1.6% vs 13.4%± 1.9%, P < 0.05), and maximum level of oxygen consumption (12.4 ± 0.5 vs 11.3 ± 0.5 ml/kg, P < 0.05) compared with VVI pacing. There was no change in oxygen pulse or difference in symptom scores in this acute study between the two pacing modes. It is concluded that right ventricular pacing may significantly improve rate regularity and cardiopulmonary performance in patients with chronic AF. This may be incorporated in a pacing device for rate regularization of AF using an algorithm that is rate adaptive to postural and exercise stresses.     

Dependency on Atrial Electrophysiological Properties of Appearance of Paroxysmal Atrial Fibrillation in Patients with Wolff-Parkinson-White Syndrome: Evidence from Atrial Vulnerability Before and After Radiofrequency Catheter Ablation and Surgical Cryoablation

The pathogenesis of paroxysmal atrial fibrillation in patients with Wolff-Parkinson-White syndrome and the effects of elimination of accessory pathways on the appearance of atrial fibrillation are still controversial. Fifty-four patients with Wolff-Parkinson-White syndrome were classified into three groups: a No AFgroup (n = 24), patients without paroxysmal atrial fibrillation; an RF-AF Group (n =12), patients with paroxysmal atrial fibrillation whose accessory pathways were eliminated using radiofrequency catheter ablation; and a Cryo-AF Group (n = 18), patients with paroxysmal atrial fibrillation whose accessory pathways were eliminated with surgical Cryoablation. The electrophysiological characteristics of each group were evaluated prior to and following the elimination of their accessory pathways. As indices of atrial vulnerability, the presence of fragmented atrial activity and repetitive atrial firing zones were assessed. Deducibility of atrial fibrillation was significantly reduced following ablation of accessory pathways in the Cryo-AF group (83.3%-5.6%, P < 0.0001), while it was unchanged in the RF-AF group (83.3%-75%). In preablation studies, the effective refractory periods of the atrium in the RF-AF group and the Cryo-AF group were significantly shorter compared with the No AF group (204 ± 18 ms, 197 ± 16 ms vs 246 ± 44 ms, respectively, P < 0.0001). Following ablation, the effective refractory period for patients in the Cryo-AF group was significantly prolonged compared with before ablation (197 ± 16 ms to 232 ± 24 ms, P < 0.0001). As a result of this prolongation of the effective refractory period of the atrium, the fragmented atrial activity and repetitive atrial response zones narrowed following ablation in the Cryo-AF group, but not in the RF-AF group. Therefore, the pathogenesis of atrial fibrillation in patients with Wolff-Parkinson-White syndrome may depend on the refractory period of the atrium rather than on the presence of accessory pathways.     

Atrial Electrophysiological Features in Patients with Wolff-Parkinson-White and Atrial Fibrillation: Absence of Rate Adaptation of Intraatrial Conduction Time Parameters

Clinical electrophysiology has not yet clearly defined atrial features that can predict spontaneous occurrence of atrial fibrillation (AF). The aim of this work was to identify atrial electrophysiological features that can distinguish Wolff-Parkinson-White patients with spontaneous AF from those without this arrhythmia. Sixty-nine patients with Wolff-Parkinson-White were divided into three groups: group I (16 patients) with spontaneous AF; group II (35 patients) with reciprocating tachycardia but not AF; and group III (18 patients) asymptomatic without documented arrhythmias. Atrial effective refractory periods (ERPs) and intraatrial conduction times in response to premature extrastimuli were analyzed. The latter were evaluated as the A₁A₂ interval minus the correspondent S₁S₂ interval (A₁A₂-S₁S₂), S₂A₂ and the interval A₁A₂ following the shortest S₁S₂ producing atrial activation (FRP'). All the parameters have been evaluated in two atrial sites and at two atrial pacing cycle lengths (600 and 400 ms). For all the parameters, the difference (“gradient”) was calculated between the values of the same parameter measured at the atrial pacing cycle length of 600 ms and that found at the atrial pacing cycle length of 400 ms in the same recording site in each patient was calculated. Atrial FRP did not differ significantly in the three groups. Intraatrial conduction parameters, evaluated in the high right atrium (HRA), were longer when measured at an atrial pacing of 400 ms and showed a lack of rate adaptation in patients with spontaneous AF. In group I patients in particular, FRP’became longer with the increase of atrial rate, while in groups 2 and 3, it usually shortened. The mean gradient of HRA FRP’was -15.0 ± 19 ms in group I as compared to 5.7 ±13 ms in group II and 6.4± 13 ms in group III (P < 0.001); sensitivity. specificity, and negative predictive value of a negative gradient in the identification of patients with spontaneous AF, were, respectively, 83%, 75%, and 93%. Patients from groups 2 and 3 did not differ in any of the analyzed parameters. Patients with Wolff-Parkinson-White and spontaneous AF showed prolonged intraatrial conduction times and a different behavior in response to modification of heart rate. (PACE 1997;20[Pt. I]:1318-1327)     

Patterns of Atrioventricular Conduction During Postexercise Recovery in Patients with Atrial Fibrillation and Wolff-Parkinson-White Syndrome

The effects of the postexercise recovery phase on the functional anterograde conduction properties of the accessory pathway (AP) were evaluated. Twenty-nine patients with Wolff-Parkinson-White (WPW) syndrome were submitted to supine maximal bicycle exercise testing. In seven patients (group I), in whom sustained atrial fibrillation (AF) could be induced by transesophageal pacing (TP), mean ventricular rate (MVR), the shortest R-R interval (SRR) between preexcited beats, and the observed percentage of preexcited beats were evaluated at rest, after each step of exercise and 2 minutes after the end of exercise. In 22 patients (group II), in whom sustained AF could not be induced, decremental TP was performed to evaluate the shortest atrial cycle length (SCL) with 1:1 conduction over AP at rest, after each step of exercise, and 2 minutes after the end of exercise. In four patients in group I, the protocol was repealed with atropine injected during the last minute of exercise. In 12 patients (three from group I and nine from group II), catecholamine plasma levels were measured at rest, at peak exercise, and during recovery. MVR was 144 ± 20 beats/min at rest, 186 ± 21 beats/min at peak exercise (P < 0.001 vs rest), and 179 ± 21 beats/min during recovery (P < 0,001 vs rest; P < 0.05 vs peak exercise). SRR was 289 ± 73 msec at rest, 223 ± 25 msec at peak exercise (P < 0.05 vs rest), and 227 ± 29 msec during recovery. Preexcited beat percentage was 95.4 ± 12 at rest, 35.2 ± 24.2 at peak exercise (P < 0.001 vs rest), and 85.1 ± 22.5 during recovery fP < 0.01 vs peak exercise and n.s. vs rest). In patients in whom atropine was injected MVR was 139 ± 17 beafs/min at rest, 184 ± 19 beats/min at peak exercise (P < 0.05 vs rest), and 172 ± 16 beats/min during recovery (P < 0.05 vs peak exercise, P < 0.05 vs rest); SRR was 320 ± 71 msec at rest, 225 ± 25 msec at peak exercise, and 232 ± 3 inset; during recovery; preexcited beat percentage was 99 ± 1 at rest, 26 ± 18 at peak exercise (P < 0.01 vs rest), and 28 ± 20 during recovery (NS vs peak exercise, P < 0.01 vsrest). In group II. mean sinus rate was 84 ± 12 beats/min at rest, 151 ± 15 beats/min at peak exercise, and 117 ± 21 beats/min 2 minutes after the end of exercise; mean SCL was 328 ± 75 msec at rest, 273 ± 76 msec at peak exercise (P < 0.0001 vs rest), and 280 ± 79 msec during recovery (P < 0.0001 vs rest and NS vs peak exercise). Mean epinephrineand norepinephrine plasma levels (12 patients from groups I and II) were; 4 7.9 ± 76.6 and 355.5 ± 185.1 pg/mL at rest; 193.0 ± 88.0 and 823.9 ± 390.3 pg/mL at peak exercise (P < 0.0001 vsrest); 148.5 ± 94.5 and 672.7 ± 272.3 during recovery (P < 0.001 vs rest; P < 0.01 vs peak exercise). Thus, during early recovery versus peak exercise: SCL and SRR are still lower and confirm the persistence of increased AP conductivity; in patients with atrial fibrillation preexcited beat percentage is markedly enhanced while the duration of preexcited complexes is increased and MVR is still high. The poslexercise recovery phase in patients with WPWand atrial fibrillation determines a higher ventricular response rate with major preexcitation than does rest and peak exercise. The fact that atropine prevents increases in preexcited beats percentage demonstrates that the underlying electrophysiological basis is a discordance of autonomic effects on the conduction properties of the two afrioventricular pathways.     

The Use of Atrial Pacing to Evaluate Patients with Definite or Suspected Wolff-Parkinson-White Syndrome

Four patients with definite or suspected WPW syndrome are presented in order to show that valuable clinical information can be obtained via simple atrial pacing. In three cases with a questionable resting ECG, atrial pacing produced pathognomonic changes in the QRS complex, establishing the diagnosis of WPW syndrome. In the fourth case, atrial pacing provoked the associated tachyarrhythmia, which had not previously been documented. In all four cases, functional properties of the accessory pathway could be assessed, and in three cases, the induction of atrial fibrillation allowed estimation of the risk of ventricular fibrillation. For evaluating patients with definite or suspected WPW syndrome, the technique of atrial pacing is recommended as an alternative to sophisticated electrophysiological studies which are costly and require special expertise and equipment. Atrial pacing is easier, cheaper, and less traumatic, and for many patients will provide most, if not all, the necessary information.     

Concealed Antidromic Re-entrance During Rapid Atrial Pacing in the Wolff-Parkinson-White Syndrome

In a patient with Wolff-Parkinson-White syndrome, rapid atrial pacing up to rates of 140/min resulted in A-H prolongation; increases in rate up to 200/min, however, failed to lengthen A-H further. The delta-H interval increased as rate rose to 120/min, but remained stable thereafter. These and other findings suggest retrograde activation of the His bundle via the accessory pathway at rates greater than 140/min. Such a phenomenon: 1) prevents initiation of PSVT with atrial pacing; 2) prevents one from determining the anterograde block rate of the AV node; 3) represents concealed antidromic re-entrance, which may theoretically lead to antidromic re-entrant PSVT.     

The Induction of Atrial Flutter and Fibrillation and the Termination of Atrial Flutter by Esophageal Pacing

In patients with Wolff-Parkinson-White syndrome (WPW), it is important to assess the ventricular response during atrial flutter or fibrillation since conduction across the accessory pathway during these atrial rhythms may cause hemodynamic impairment or life-threatening ventricular arrhythmias. We have recently reported the effective use of an esophageal electrode in pacing the atrium. In this study we praspectively assessed the ability to induce atrial flutter and fibrillation by esophageal pacing in 23 patients with WPW or other electrophysiological abnormalities. An esophageal bipolar electrode with 29 mm interelectrode distance was positioned in the esophagus to record the most rapid and largest esophageal electrogram (mean distance of 36.6 ± 2.9 cm (SD) from the nares). Pacing was performed at cycle lengths of 40–340 ms (mean 166 ± 72), pulse durations of 7.0–9.9 ms, and currents of 10–25 mA. Atrial flutter alone was induced in 6 patients, fibrillation alone in 11 patients, and both arrhythmias in 5 patients, In one patient neither flutter nor fibrillation was induced by esophugeal pacing, and fibrillation was induced only with difficulty using intracavitary pacing. Of the 11 patients with flutter, the arrhythmia was terminated in 8 by esophageal pacing at cycle lengths of 160–220 ms fmean 176 ± 18 ms). All patients tolerated the procedure well with only mild to moderate discomfort. Therefore, esophageal pacing appears to offer an effective, well tolerated method of initiating atrial fibrillation and flutter and terminating atrial flutter and offers a potentially useful noninvasive method of following patients serially.     

Effect of Digoxin on the Ventricular Rate Variability During Paroxysmal Atrial Fibrillation

This study investigated whether the, irregularity of ventricular cycle length during atriai fibrillation (AF) is affected by digoxin. Patients (n = 41) with paroxysmal AF enrolled in a randomized crossover comparison of digoxin and placebo underwent 24-hour ambulatory monitoring during each treatment. Tapes containing AF episodes lasting at least 2 minutes were selected (24 recordings on placebo and 17 on digoxin). The mean (mRR) and standard deviation (SDRR) of RR intervals was calculated for each 30-second segment of AF. The resulting SDRR values were clustered according to bins of mRR values ranging from 350–650 ms in 25-ms steps. In each bin, the SDRR values of all placebo and all digoxin recordings were statistically compared for the top 5, 10, and 15 percentiles of each bin which represented the extremes of ventricular cycle length irregularity during AF. There were no significant differences between the total data of SDRR values in individual bins of mRR. However, the top 5, 10, and 15 percentiles of SDRR values corresponding to mRR values from 350–550 ms were significantly reduced by digoxin (P < 0,0001). The study concludes that although digoxin does not influence the mean variability of RR cycles during AF paroxysms, it suppresses episodes in which a fast ventricular response is associated with extreme variability of RR periods.     

Comparison of Isoproterenol and Exercise Tests in Asymptomatic Subjects with Wolff-Parkinson-White Syndrome

In order to evaluate the effects of increases of sympathetic tone in ventricular response during atrial fibrillation and in the relationship between the accessory pathway effective refractory period (ERP) and ventricular rate during atrial fibrillation, 20 male subjects, aged 19 +/- 6 years, were studied electrophysiologically in basal conditions, after isoproterenol infusion (2-4 micrograms/min) and during submaximal bicycle exercise test, at a constant workload equal to that which increases the sinus rate to the same extent (140 beats/min) induced by isoproterenol infusion. Accessory pathway ERP was evaluated at the same driven rate (150 beats/min) in both instances. In the control study as during both tests atrial fibrillation paroxysms were induced by burst stimulation. In control conditions the rate increase from 100 to 150 beats/min induced a reduction of accessory pathway ERP from 266 +/- 27 msec to 244 +/- 22 msec (P less than 0.005). At the same driven rate of 150 beats/min, isoproterenol infusion and exercise test induced a more marked shortening of accessory pathway ERP to 211 +/- 28 msec (P less than 0.005) and to 214 +/- 29 msec (P less than 0.005), respectively. Atrial fibrillation paroxysms lasting more than 10 seconds were induced in 20/20 cases in the control study, in 15/20 during isoproterenol infusion and in 13/19 cases during exercise test. The shortest cycle length during atrial fibrillation was reduced from a basal value of 253 +/- 72 msec to 204 +/- 27 msec (P less than 0.05) during isoproterenol infusion and to 236 +/- 32 msec (NS) during exercise test.(ABSTRACT TRUNCATED AT 250 WORDS)     

Rate Stabilization by Right Ventricular Pacing in Patients with Atrial Fibrillation

A recent study of de Jongste has demonstrated the lengthening of short R-R intervals in patients with atrial fibrillation by right ventricular pacing. We have further analyzed the data from this study and specifically looked at the effect of right ventricular pacing on the R-R interval instability and heart rate. At the cost of only a slight increase in mean heart rate, a major reduction of the R-R interval instability can be obtained by right ventricular pacing. Based on these findings, we have developed and evaluated an automatic pacing rate algorithm, which continuously varies the stimulation rate in order to stabilize the otherwise irregular rhythm in patients with atrial fibrillation.     

Wolff-Parkinson-White syndrome concomitant with asymptomatic Brugada syndrome

A 29-year-old man was referred for electrophysiological testing and radiofrequency ablation because of repeated episodes of palpitation over 2 years. A 12-lead electrocardiogram during sinus rhythm showed manifest Wolff-Parkinson-White syndrome and during palpitation showed narrow QRS tachycardia at a rate of 213 beats/min. Following successful radiofrequency ablation of the left anterolateral accessory pathway, sustained atrial fibrillation was induced by atrial extrastimulation. Cibenzoline (2 mg/kg body weight) was injected to terminate atrial fibrillation. ST-T segment elevation in the right precordial leads was observed following cibenzoline administration. Ventricular fibrillation was reproducibly induced by ventricular extrastimuli (S1: 600 ms, S2: 220 ms, S3: 210 ms).     

Role of the Atrial Rate as a Factor Modulating Ventricular Response during Atrial Fibrillation

Background: During atrial fibrillation (AF), RR interval histograms show different populations of predominant RR (pRR) intervals. These pRR intervals have been suggested to be multiples of the refractory period of the atrioventricular (AV) node or caused by the existence of a dual AV node physiology. In this study, the hypothesis that pRR intervals are related to the dominant atrial fibrillatory rate is tested. Methods: In this study, Holter electrocardiogram signals from 55 patients with persistent AF were analyzed. Number and position of pRR intervals were detected and compared with mean and standard deviation of the dominant atrial cycle length (DACL). In addition, effects of an enhancement of vagal activity and rate‐control treatments (β‐blockers and verapamil) were evaluated. Results: In all patients with more than one pRR interval and in 47% with one pRR interval, RR interval populations were statistically related with multiples of the DACL. During night activities and during β‐blockers treatment, mean ventricular rate was decreased (P < 0.01). This change was associated with a variation in the percentage of occurrences of each pRR (P < 0.01), whereas no statistical differences were present in the mean DACL or in the position of pRR intervals. A variation of the DACL due to verapamil was associated with a consistent modification in the position of the pRR intervals. Conclusion: The relation between pRR and multiples of the DACL during AF suggests that more probable RR intervals are caused by different conduction ratios of the atrial rate. (PACE 2010; 33:1510–1517)