Distribution of atrial electrogram types during atrial fibrillation: Effect of rapid atrial pacing and intercaval junction ablation

Objectives. This study examined the anatomic distribution types and possible determinant of atrial electrogram types during atrial fibrillation.

Background. Different types of atrial electrograms during atrial fibrillation have been observed and classified, but their anatomic distribution patterns, determinants and potential usefulness in guiding future catheter ablation are unknown.

Methods. Two animal models of atrial fibrillation were used: the sterile pericarditis model (n = 10) and the rapid atrial pacing model (400 beats/min for 6 weeks, N = 6). The atrial electrogram of atrial fibrillation and the atrial effective refractory period were obtained from multiple sites of the right and left atrium. In addition, decremental rapid atrial stimulation was applied to the site of shortest and longest atrial effective refractory periods until atrial fibrillation induction in a subgroup of nine dogs. Ablation of the intereaval junction was performed using the radiofrequency catheter technique in dogs with atrial fibrillation duration > 1 min.

Results. In both models, organized atrial electrograms (type I) were predominantly observed at the left atrial sites and the right atrial appendage, whereas disorganized atrial electrograms (type III) were mainly observed at the right posterolateral atrium. The distribution of the atrial electrogram types closely followed that of the atrial effective refractory period, with the shortest atrial effective refractory period corresponding to organized atrial electrograms (type I) and the longest atrial effective refractory period corresponding to disorganized atrial electrograms (type III). The correlation of atrial electrogram type with the atrial effective refractory period was further demonstrated by the effect of rapid atrial stimulation. When rapid atrial stimulation was applied to the site with the shortest atrial effective refractory period, disorganized atrial electrograms were observed at sites with the longest atrial effective refractory period, whereas 1:1 atrial capture was still present at the stimulation site. Ablation of the intercaval junction made atrial fibrillation noninducible or tended to shorten the atrial fibrillation duration (from 26.4 ± 24.2 to 8.8 ± 22.6 min in the pericarditis group, P = 0.02, and from 33.7 ± 29.2 to 12.1 ± 23.8 min in the rapid pacing group, P = 0.09) bud did not change the atrial electrogram types during atrial fibrillation.

Conclusions. Various types of atrial electrograms are present at different locations during atrial fibrillation. The atrial electrogram characteristics of atrial fibrillation at a specific location are related to the atrial effective refractory period, with short effective refractory periods associated with organized atrial electrograms and long effective refractory periods associated with disorganized electrograms.     

Determinants of the ventricular rate during atrial fibrillation

Determinants of the ventricular cycle length during atrial fibrillation were examined in 52 patients. Thirty-three patients had structural heart disease and none had an accessory atrioventricular (AV) connection. The AV node effective and functional refractory periods, the shortest atrial pacing cycle length associated with 1:1 conduction, the AV node conduction time and indexes of concealed conduction in the AV node were measured in the baseline state (36 patients) and after modification of sympathetic tone by infusion of isoproterenol or propranolol (8 patients each). Atrial fibrillation was then induced with rapid atrial pacing, and the mean, shortest and longest ventricular cycle lengths were measured. Variables that correlated most strongly with the mean RR interval during atrial fibrillation were the AV node effective refractory period (r = 0.93; p less than 0.001), AV node functional refractory period (r = 0.87; p less than 0.001) and shortest atrial pacing cycle length associated with 1:1 conduction (r = 0.91; p less than 0.001). The AH interval during sinus rhythm (r = 0.74; p less than 0.001) and during atrial pacing at the shortest cycle length with 1:1 conduction (r = 0.52; p less than 0.001) had weaker correlations. Measures of concealed conduction did not improve the prediction of the mean or longest ventricular cycle length during atrial fibrillation. In conclusion, the refractory periods and conductivity of the AV node are the best indicators of the potential of the node to transmit atrial impulses to the ventricles during atrial fibrillation. The degree of concealed conduction in the AV node is a less important determinant of the mean ventricular rate during atrial fibrillation.     

Maturational changes in ventriculoatrial conduction in the intact canine heart

This study reports on the changes in ventriculoatrial (VA) conduction that occur with maturation. Programmed atrial and ventricular premature extra-stimulation (coupled to a fixed paced cycle length) and rapid atrial pacing were performed in three groups of dogs: Group I = 8 neonates aged 5 to 14 days, Group II = 9 young dogs aged 6 to 9 weeks and Group III = 10 adult dogs. High right atrial, His bundle and right ventricular electrograms were recorded. There were no differences in the AH intervals at rest. In all but five animals, atrioventricular conduction was limited by the atrial functional refractory period (Group I, 109 +/- 12 ms; Group II, 152 +/- 22 ms; Group III, 167 +/- 19 ms). As expected, with rapid atrial pacing, Wenckebach conduction developed at a shorter cycle length in the younger animals (Group I, 145 +/- 20 ms; Group II, 153 +/- 15 ms; Group III, 200 +/- 25 ms, p less than 0.01). Ventriculoatrial conduction was documented in 87% of Group I puppies and 100% of Group II, but only 40% of Group III dogs. The effective and functional refractory periods of the VA conduction system were significantly shorter in the more immature groups of dogs (effective/functional: Group I, 124 +/- 27/168 +/- 22 ms; Group II, 139 +/- 23/202 +/- 13 ms; Group III, 270 +/- 28/326 +/- 25 ms; p less than 0.01). Relative to the adult dog, the immature heart showed a greater incidence of VA conduction and shorter VA refractory periods. This enhanced VA conduction may be of physiologic importance in the initiation and perpetuation of certain supraventricular arrhythmias.     

Electrophysiological determinants of atrial fibrillation in sinus node dysfunction despite atrial pacing.

AIMS: The effectiveness of atrial pacing in reducing the incidence of atrial fibrillation in patients with sinus node dysfunction is incomplete, and the correlation between electrophysiological atrial properties and the effect of permanent atrial pacing has been poorly investigated. Accordingly, the aim of the present study was to correlate electrophysiological data, in terms of atrial refractoriness, conduction parameters, and propensity to atrial fibrillation induction, and the likelihood of atrial fibrillation after DDD device implantation. METHODS AND RESULTS: The authors reviewed electrophysiological data of 41 patients with sinus node dysfunction (mean age 70 +/- 8 years, who were investigated free of anti-arrhythmic treatments before pacemaker implantation. At a drive cycle length of 600 ms, effective and functional refractory periods, S1-A1 and S2-A2 latency, A1 and A2 width, and latent vulnerability index (effective refractory period [ERP] A2), were measured. Atrial fibrillation induction was tested with up to three extrastimuli in 34 patients. Induction of sustained atrial fibrillation (> 1 min) was considered as the end-point. P-wave duration on the surface ECG in lead II/V1 was also measured. Minimal atrial rate was programmed between 60 and 75 bpm (mean: 64 +/- 4 bpm). After implantation, the patients were followed-up for 28 +/- 17 months, and ECG-documented occurrence of atrial fibrillation was determined. Electrophysiological characteristics of patients with (n = 12) or without (n = 29) paroxysmal atrial fibrillation before implantation were similar. When comparing patients with (n = 11) or without (n = 30) post-pacing atrial fibrillation occurrence, no differences were found in age, underlying heart disease, left atrial size, minimal pacing rate, and follow-up duration. Additionally, between the two former groups, there was no significant difference in terms of effective refractory periods (233 +/- 47 ms vs 239 +/- 25 ms), functional refractory periods (280 +/- 48 ms vs 272 +/- 21 ms), S1-A1 (44 +/- 20 ms vs 37 +/- 13 ms) and S2-A2 latency (77 +/- 28 ms vs 66 +/- 22 ms), and A1 duration (60 +/- 23 ms vs 53 +/- 16 ms). In contrast, in patients with post-pacing atrial fibrillation occurrence, the P wave was more prolonged (116 +/- 22 ms vs 98 +/- 13 ms; P < 0.01), A2 was longer (116 +/- 41 ms vs 87 +/- 27 ms; P < 0.01), effective refractory periods/A2 was lower (2.1 +/- 0.4 cm vs 3.1 +/- 1.4 cm; P < 0.05), and rate of atrial fibrillation induction was higher (8/11 patients vs 8/23 patients; P < 0.05). Electrophysiological characteristics of patients free of post-pacing atrial fibrillation with associated (n = 6) or unassociated (n = 24) paroxysmal atrial fibrillation history before implantation were quite similar. In patients with post-pacing atrial fibrillation with associated (n = 6) or unassociated atrial fibrillation history (n = 5) before implantation, effective refractory periods was statistically different (207 +/- 23 ms vs 264 +/- 46 ms; P < 0.05). Values of effective refractory periods < 220 ms were significantly more frequent in patients with post-pacing atrial fibrillation than in patients without (4/11 patients vs 2/30 patients; P < 0.05). When comparing patients with post-pacing atrial fibrillation with effective refractory periods > or = 220 ms (n = 7) and < 220 ms (n = 4), A2 duration was remarkably prolonged (145 +/- 42 ms vs 90 +/- 11 ms; P < 0.05) in those with effective refractory periods > or = 220 ms. By contrast, between the two groups, effective refractory periods/A2 were identical (2.08 +/- 0.6 cm vs 2.15 +/- 0.3 cm; P = n.s.). CONCLUSION: Prolonged atrial refractoriness, lesser degrees of conduction disturbance and a lower rate of atrial fibrillation induction seem to be predictive of stable sinus rhythm. In contrast, patients with persistence of atrial fibrillation despite pacing have a more abnormal and inhomogeneous atrial substrate, as well as a higher rate of atrial fibrillation induction. Prolonged P wave, shortened refractoriness, or remarkably abnormal conduction disturbances in the presence of prolonged refractoriness limit the effectiveness of standard atrial pacing in atrial fibrillation prevention. Identification of predictive criteria of failure of single-site atrial pacing may be used to consider dual-site atrial pacing in such patients with sinus node dysfunction.     

Effects of atrial pacing site on atrial and atrioventricular nodal function.

The effects of the site used for atrial pacing on atrial and atrioventricular nodal conduction were assesed in 16 patients. In 13 patients, three atrial pacing sites were used: high right atrium, low lateral right atrium, and midcoronary sinus. Two recording sites were used: low septal right atrium, including His electrogram, and high right atrium. Stimulus (S) to high right atrium interval was longest with coronary sinus pacing (76 plus or minus 7 ms) (P less than 0.001), and shortes with high right atrial pacing (41 plus or minus 3 ms) (P less than 0.05). There was no significant difference in stimulus to low septal right atrium from all three pacing sites. Atrial functional and effective refractory periods were not significantly different. Mean low septal right atrium to His was significantly shorter from the coronary sinus (93 plus or minus 8 ms) (P less than 0.001), as compared to high right atrium (139 plus or minus 16 ms), and low lateral right atrium (129 plus or minus 13 ms) pacing. AV nodal functional and effective refractory periods, and the paced rate producing AV nodal Wenckebach were not significantly different when comparing the three sites. Left atrial appendage and high right atrium were similarly compared in three additional patients, and no significant differences were found in conduction times and refractory periods.     

Effects of atrial pacing site on atrial and atrioventricular nodal function.

The effects of the site used for atrial pacing on atrial and atrioventricular nodal conduction were assesed in 16 patients. In 13 patients, three atrial pacing sites were used: high right atrium, low lateral right atrium, and midcoronary sinus. Two recording sites were used: low septal right atrium, including His electrogram, and high right atrium. Stimulus (S) to high right atrium interval was longest with coronary sinus pacing (76 plus or minus 7 ms) (P less than 0.001), and shortes with high right atrial pacing (41 plus or minus 3 ms) (P less than 0.05). There was no significant difference in stimulus to low septal right atrium from all three pacing sites. Atrial functional and effective refractory periods were not significantly different. Mean low septal right atrium to His was significantly shorter from the coronary sinus (93 plus or minus 8 ms) (P less than 0.001), as compared to high right atrium (139 plus or minus 16 ms), and low lateral right atrium (129 plus or minus 13 ms) pacing. AV nodal functional and effective refractory periods, and the paced rate producing AV nodal Wenckebach were not significantly different when comparing the three sites. Left atrial appendage and high right atrium were similarly compared in three additional patients, and no significant differences were found in conduction times and refractory periods.     

Reversal of atrial electrical remodeling following cardioversion of long-standing atrial fibrillation in man.

BACKGROUND: In animal studies, atrial fibrillation has been shown to shorten the atrial refractory period and impair its rate adaptation. However, little is known about the effects of chronic atrial fibrillation on atrial electrophysiology and its recovery course in humans. METHODS AND RESULTS: Nineteen patients, mean age 64 +/- 14 years, with chronic atrial fibrillation of more than six months duration were included in this study. All of them were successfully converted to sinus rhythm with an external defibrillator. Atrial effective refractory periods at right atrial appendage and distal coronary sinus were determined with five pacing cycle lengths (300, 400, 500, 600 and 700 ms) at 30 min after cardioversion and once a day for four days. The atrial conduction properties, including P wave duration of surface ECG, and right and left atrial conduction times, were also measured at the same time interval. Twenty age-matched patients without a history of atrial tachyarrhythmia were evaluated as controls. In comparison with controls, chronic atrial fibrillation significantly shortened the atrial effective refractory period, impaired its rate adaptation response, especially at distal coronary sinus, and depressed the conduction properties of atria. The atrial conduction properties did not change during the four-day follow-up period; however, the atrial effective refractory period was gradually prolonged and its rate adaptation response improved after restoration of sinus rhythm. CONCLUSIONS: In humans, chronic atrial fibrillation significantly shortened the atrial effective refractory period, and impaired its rate adaptation response. Restoration and maintenance of sinus rhythm could reverse these electrophysiological changes.     

Wolff-Parkinson-White syndrome and atrial fibrillation: Relation between refractory period of accessory pathway and ventricular rate during atrial fibrillation

To assess the relation between the length of the effective refractory period of the accessory pathway and the ventricular rate during atrial fibrillation, we studied two groups of patients with the Wolff-Parkinson-White syndrome: Group I, 17 patients with electrocardiographlcally documented episodes of atrial fibrillation, and Group II, 9 patients without this arrhythmia. In 17 of these 26 patients the effective refractory period of the accessory pathway could be determined by the single test stimulus method during atrial pacing.

After measurement of the refractory period, atrial fibrillation was induced by rapid atrial pacing (400 to 500/min). The duration of the effective refractory period of the accessory pathway was found to correlate with the shortest R-R interval and the mean ventricular rate during documented or induced atrial fibrillation. In nine patients the effective refractory period of the accessory pathway could not be determined because the atrium became refractory while atrioventricular (A-V) conduction was still occurring over this pathway. In these patients the right atrium was regularly paced at rates of up to 280/min. All nine patients had 1:1 A-V conduction over the accessory pathway up to driving rates of 240/min. In five patients conduction still manifested a 1:1 ratio at pacing rates of 280/min. During atrial fibrillation all nine patients had a mean ventricular rate greater than 200/min.

Although factors other than the effective refractory period of the accessory pathway affect ventricular rate during atrial fibrillation in patients with the Wolff-Parkinson-White syndrome, the duration of this period is of value in identifying patients at risk of having life-threatening high ventricular rates when atrial fibrillation occurs.     

Prolonged fractionation of paced right atrial electrograms in patients with atrial flutter and fibrillation

OBJECTIVES: This study investigated the extent of fractionation of paced right atrial electrograms in patients with and without paroxysmal atrial flutter (AFL) or atrial fibrillation (AF). BACKGROUND: Slow conduction through nonuniform anisotropic atrial muscles, represented by fractionated electrograms, may favor the generation of atrial tachyarrhythmias. METHODS: This study included 10 control patients (Group 1), 8 patients with documented paroxysmal AFL (Group 2) and 10 patients with documented paroxysmal AF (Group 3). Five electrode catheters were placed in the different sites of the right atrium and one catheter was positioned at the coronary sinus ostium. Atrial pacing from one site was done by a constant drive train with an extrastimulus inserted every fourth beat while recording at the other five sites was performed. The delay of each fractionated potential in the high-pass filtered atrial electrogram in response to extrastimulation was determined and used to construct conduction curves of delay versus the S1S2 interval. RESULTS: The mean increase in electrogram duration between a coupling interval of 350 ms and 10 ms above atrial refractoriness was significantly greater in Groups 2 and 3 compared with that in Group 1 (8.5 +/- 2.5 vs. 11.0 +/- 2.7 vs. 5.9 +/- 2.3 ms, respectively, p < 0.001). The mean S1S2 interval at which delay increased suddenly was also longer in Groups 2 and 3 compared with Group 1 (326 +/- 9 vs. 343 +/- 12 vs. 307 +/- 17 ms, respectively, p < 0.001). CONCLUSIONS: Increased delays in the individual potential of the fractionated atrial electrograms may be related to the development of AFL and AF.     

Effect of phenylephrine infusion on atrial electrophysiological properties.

OBJECTIVE: To determine the effect of changes in autonomic tone induced by phenylephrine infusion on atrial refractoriness and conduction. DESIGN: Left and right atrial electrophysiological properties were measured before and after a constant phenylephrine infusion designed to increase sinus cycle length by 25%. SUBJECTS: 20 patients, aged 53 (SD 6) years, undergoing electrophysiological study for investigation of idiopathic paroxysmal atrial fibrillation (seven patients) or for routine follow up after successful catheter ablation of supraventricular tachycardia (13 patients). MAIN OUTCOME MEASURES: Changes in left and right atrial effective refractory periods, atrial activation times, and frequency of induction of atrial fibrillation. RESULTS: Phenylephrine (mean dose 69 (SD 18) mg/min) increased mean blood pressure by 22 (12) mm Hg (range 7 to 44) and lengthened sinus cycle length by 223 (94) ms (20 to 430). Left atrial effective refractory period lengthened following phenylephrine infusion from 250 (25) to 264 (21) ms (P < 0.001) but there was no significant change in right atrial effective refractory period: 200 (20) v 206 (29), P = 0.11. There was a significant relation between the effect of phenylephrine on sinus cycle length and on right atrial refractoriness (r = 0.6, P = 0.005) with shortening of right atrial refractoriness in patients with the greatest prolongation in sinus cycle length. During phenylephrine infusion, the right atrial stimulus to left atrial activation time at the basic pacing cycle length of 600 ms was unchanged, at 130 (18) v 131 (17) ms, but activation delay with a premature extrastimulus increased: 212 (28) v 227 (38) ms, P = 0.002. Atrial fibrillation was induced by two of 58 refractory period measurements at baseline and by 12 of 61 measurements during phenylephrine infusion (P < 0.01). Phenylephrine increased the difference between left and right atrial refractory periods by 22.8 (19.4) ms in the five patients with induced atrial fibrillation after phenylephrine compared to 0.9 (16.2) ms in the 13 patients without induced atrial fibrillation after phenylephrine infusion (P = 0.02). CONCLUSIONS: Phenylephrine infusion increased left atrial refractoriness and intra-atrial conduction delay following a premature right atrial extrastimulus. Induction of atrial fibrillation during phenylephrine infusion was associated with non-uniform changes in atrial refractoriness. These data support the concept that changes in autonomic tone may precipitate atrial fibrillation in susceptible individuals.     

Electrophysiology of the chemically sympathectomised dog

The contribution of the sympathetic nervous system in the definition of various electrophysiological variables was studied in chemically sympathectomised dogs. Chemical sympathectomy was obtained following intravenous injection of 50 mg X kg-1 of 6-hydroxydopamine. Sympathectomised dogs presented significant increases in: basic sinus period, sino-atrial conduction time (SACT), AH and HV intervals of the His bundle electrogram, atrial functional (AFRP) and effective (AERP) refractory periods, atrio-ventricular node functional (AVNFRP) and effective (AVNERP) refractory periods, ventricular functional (VFRP) and effective (EVRP) refractory periods and atrial (AMAP) and ventricular (VMAP) monophasic action potential durations. Corrected sinus recovery time (CSRT) was not affected by chemical sympathectomy. Neither was the atrial ERP/MAP duration ratio. This new form of sympathectomy affects all the levels of the cardiac conduction system. Such results are in accordance with those obtained with surgical sympathectomy or the use of beta-blocking agents.     

Multisite pacing for prevention of atrial tachyarrhythmias: potential mechanisms

OBJECTIVES

To determine the effects of single-, dual-, triple- and quadruple-site atrial pacing on atrial activation and refractoriness in normal canine hearts.

BACKGROUND

Multisite pacing has been suggested to be superior to single-site pacing for prevention of atrial tachyarrhythmias. However, the underlying electrophysiological mechanisms are undetermined at the moment, as is the rationale for the selection of pacing locations and the number of pacing sites.

METHODS

In 13 normal beagle dogs, an epicardial multielectrode (128 bipoles) and a multiplexer mapping system were used to reconstruct epicardial atrial activation patterns obtained during simultaneous stimulation from up to four electrodes located in the high and low right and left atrium, respectively. For all pacing modes (single-, dual-, triple- and quadruple-site pacing), total activation times and local effective refractory periods at eight randomly selected sites as well as local recovery intervals were determined. In a subgroup of five dogs, total epicardial activation times were also obtained during single-site septal stimulation (septal group).

RESULTS

Activation times and local recovery intervals were minimized by triple-site stimulation, whereas a fourth site did not produce further shortening. Septal stimulation produced epicardial activation times comparable to quadruple-site stimulation. Local refractory periods and their dispersion always remained unaffected. Functional conduction blocks apparent during single-site were found to resolve during multisite stimulation.

CONCLUSIONS

Multisite pacing can prevent functional conduction blocks by multidirectional excitation and a reduction in total activation time. Triple-site and, possibly, septal pacing modes are expected to be most efficient because both minimize total activation times and maximize the multidirectionality of excitation. In spite of unaffected local refractory periods, the shortening of local recovery intervals might homogenize atrial repolarization and, thus, contribute to the preventive effects of multisite pacing.     

Quantification of human atrioventricular nodal concealed conduction utilizing S1S2S3 stimulation.

We studied antegrade concealed conduction of atrial extrastimuli (A2) that blocked in the atrioventricular (AV) node in eight subjects, using a third extrastimulus (A3), coupled at decreasing coupling intervals to A2. Three A1-A2 intervals were tested in each subject: late (just shorter than AV nodal effective refractory period), intermediate, and early (just longer than atrial functional refractory period). The curves relating the following variables were constructed for each A2: A1-A3, H1-H3 and A2-A3, A3-H3. The former was compared to the control A1-A2, H1-H2 curve. Concealment of A2 was demonstrated in all eight subjects at the three tested values of A1-A2. The A2-A3, A3-H3 curve allowed analysis of AV nodal conduction time (A3-H3) and AV nodal recovery time (defined as the shortest A2-A3 at which the impulse conducted to the His bundle) at identical values of A2-A3. In all subjects the timing of blocked A2 had minimal effect on both AV nodal conduction time and recovery time. In five of the eight subjects a late A2 sporadically conducted to the His bundle. Conduction of A2 to the His bundle resulted in marked lengthening of both AV nodal conduction and recovery times. Concealed conduction of A2 was always demonstrated, but the degree of concealment was relatively fixed, whether A2 was an early, intermediate, or late blocked premature beat. Slow conduction of A2 had a much greater effect than concealment of A2 on subsequent impulse conduction.     

Local effects of electrical and mechanical stimulation on the recovery properties of the canine ventricle

The effects of electrical stimulation on local recovery properties of the canine ventricle were studied. Ventricular excitability was examined by an analysis of unipolar or bipolar strength-interval curves, and the effective refractory period was derived from the steep portion of the curve. Conduction times of all propagated responses to testing stimuli were recorded. When ventricular driving and testing sites were the same, effective refractory periods were significantly shorter (probability [p] < 0.001), conduction times longer (p < 0.001) and anodal dip thresholds lower (p < 0.001) than during atrial drive. However, as ventricular driving and testing sites were separated, effective refractory periods increased and conduction times shortened. At interelectrode distances of greater than 15 mm, both effective refractory periods and conduction times remained constant and similar to those observed during atrial drive. Effective refractory periods measured at the ventricular drive electrode shortened by 8.2 percent (p < 0.001) when the driving stimulus was twice threshold and by 15.4 percent (p < 0.001) when 10 times threshold. At a distance of 15 mm from the driving sites, the effective refractory period was not significantly shortened when testing stimuli of twice threshold intensity were used and was reduced by only 8.1 percent (p < 0.002) when stimuli 10 times threshold were used. Shortening of the effective refractory period near the ventricular driving site was accentuated by short coupling intervals. When ventricular drive was accomplished using mechanical impulses delivered to the epicardium, effective refractory periods during atrial and ventricular drive were virtually the same, regardless of the proximity of ventricular driving and testing sites.Thus, shortening of the effective refractory period and prolonged conduction in the vicinity of the driving electrode are a function of stimulus intensity, distance from the driving site and time. These local alterations in the recovery properties of the ventricle provide conditions that may be favorable for the induction of reentrant arrhythmias.     

Transesophageal versus intracardiac atrial stimulation in assessing anterograde conduction properties of the accessory pathway in Wolff-Parkinson-White syndrome

Electrophysiologic intracardiac and noninvasive transesophageal testing, used to evaluate parameters of anterograde conduction across the accessory pathway, the refractory period and shortest atrial cycle length with 1:1 conduction over the pathway, were compared to assess the reliability of the noninvasive technique in identifying patients with Wolff-Parkinson-White syndrome, at risk of rapid ventricular response during atrial fibrillation when this arrhythmia is not inducible. Sixteen patients with Wolff-Parkinson-White syndrome were submitted both to invasive and transesophageal atrial stimulation. We evaluated both the functional and effective refractory periods of the accessory pathway, using the same drive cycle length, and the shortest cycle length with 1:1 atrioventricular conduction over the accessory pathway. There were no differences between the parameters obtained by intracardiac atrial stimulation and by transesophageal atrial stimulation. The two approaches correlated well: mean functional refractory periods of the accessory pathway were 285 +/- 42 msec and 289 +/- 32 msec, respectively (NS, r = 0.88); mean effective refractory periods of the accessory pathway were 267 +/- 41 msec and 271 +/- 32 msec, respectively (NS, r = 0.89); mean shortest cycle lengths with 1:1 conduction over the accessory pathway were 255 +/- 48 msec and 255 +/- 44 msec, respectively (NS, r = 0.94). These data demonstrate the reliability of transesophageal atrial stimulation in estimating the parameters for anterograde conduction across an accessory pathway. These results, and the already documented ability of transesophageal atrial stimulation to induce atrial fibrillation, suggest this noninvasive technique should be taken as a first approach in screening patients with Wolff-Parkinson-White syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)     

Electrophysiologic consequences of the arterial switch repair of d-transposition of the great arteries

Electrophysiologic studies were performed at 12.7 +/- 4 months postoperatively in 20 patients who had the arterial switch repair at 1 to 120 days (mean 13 +/- 26 [SD]) for d-transposition of the great arteries. Preoperative electrocardiograms (ECGs) at rest revealed an ectopic atrial rhythm in one patient. Postoperative rest ECGs revealed transient postoperative ectopic atrial or junctional rhythms in two patients, intermittent ectopic atrial rhythms in two and right bundle branch block in nine with a normal QRS axis. In addition, ambulatory monitor recordings revealed infrequent premature ventricular complexes in five patients. Catheter endocardial mapping revealed sinus rhythm in 18 patients and ectopic atrial rhythm in 1 patient. Atrial activation after the switch repair was comparable with normal atrial activation. Activation of all low atrial sites was significantly earlier after the switch repair than after the Mustard repair. Mild abnormalities of sinus node function were present and consisted of slight prolongation of corrected sinus node recovery time in six patients and slightly increased sinoatrial conduction time in four. The ratio of sinus node recovery time to sinus cycle length was normal in all 20 patients. Atrial effective and functional refractory periods were normal in all patients and no atrial arrhythmias could be induced by programmed stimulation. Atrioventricular (AV) node conduction was excellent with normal AV node effective and functional refractory periods. The only electrophysiologic abnormality of His-Purkinje function was distal right bundle branch block in nine patients. Programmed stimulation of the ventricle produced repetitive ventricular responses in four patients: bundle branch reentry in three and intraventricular reentry in one.(ABSTRACT TRUNCATED AT 250 WORDS)     

Prolonged and fractionated right atrial electrograms during sinus rhythm in patients with paroxysmal atrial fibrillation and sick sinus node syndrome

Intraatrial catheter mapping of the right atrium was performed during sinus rhythm in 92 patients: Group I = 43 control patients without paroxysmal atrial fibrillation or sick sinus node syndrome; Group II = 31 patients with paroxysmal atrial fibrillation but without sick sinus node syndrome; and Group III = 18 patients with both paroxysmal atrial fibrillation and sick sinus node syndrome. Atrial electrograms were recorded at 12 sites in the right atrium. The duration and number of fragmented deflections of the atrial electrograms were quantitatively measured. The mean duration and number of fragmented deflections of the 516 atrial electrograms in Group I were 74 +/- 11 ms and 3.9 +/- 1.3, respectively. The criteria for an abnormal atrial electrogram were defined as a duration of greater than or equal to 100 ms or eight or more fragmented deflections, or both. Abnormal atrial electrograms were observed in 10 patients (23.3%) in Group I, 21 patients (67.7%) in Group II and 15 patients (83.3%) in Group III (Group II versus Group I, p less than 0.001; Group III versus Group I, p less than 0.001). The mean number of abnormal electrograms per patient with an abnormal electrogram was 1.3 +/- 0.7 in Group I, 2.5 +/- 1.9 in Group II and 3.5 +/- 2.5 in Group III (Group I versus Group II, p less than 0.01; Group II versus Group III, p less than 0.05). A prolonged and fractionated atrial electrogram characteristic of paroxysmal atrial fibrillation can be closely related to the vulnerability of the atrial muscle.(ABSTRACT TRUNCATED AT 250 WORDS)     

Importance of retrograde atrial activation in atrial fibrillation genesis in the initiation of atrial fibrillation in Wolff-Parkinson-White syndrome. Comparison of atrial electrophysiologic parameters between patients with different atrial fibrillation genesis (initiation sites) in atria.

The changes in the duration of atrial electrograms during different atrial activation sequences from a sinus rhythm were evaluated to test the hypothesis that the prolongation of atrial electrogram duration caused by the different atrial activation sequence is more prominent at the site of atrial fibrillation (Afib) genesis (initiation site) than other areas. In 39 patients with single retrograde left-sided accessory connection who had inducible transient atrial fibrillation during an electrophysiologic study, the site of Afib genesis was determined and classified into three groups, i.e., 1) high right atrial genesis (HRA), 2) low right atrial genesis (LRA), and 3) left atrial genesis (LA). Single premature extrastimuli after 8 basic drive trains (600 ms) were delivered at the HRA and the right ventricular apex. Three atrial electrophysiologic parameters were evaluated at three atrial sites, i.e., 1) HRA, 2) LRA, and 3) coronary sinus. The atrial vulnerability parameters were as follows; 1) %A2/A1: % prolongation of atrial electrogram duration during premature beat (A2) in comparison with basic drive (A1), 2) wavelength index (WLI): calculated as [effective refractory period]/[A2], and 3) retrograde activation index (RAI): calculated as [A1 during retrograde activation; i.e., RVA pacing/[A1 during antegrade activation, i.e., HRA pacing], shown as a percentage. The Afib genesis was HRA in 20, LRA in 12 and LA in 7 patients. At the HRA recording site, %A2/A1 and RAI were the largest and WLI the shortest in the HRA genesis group in comparison with the other two groups. Similarly, at the LRA and LA recording sites, %A2/A1 and RAI were the largest and WLI the shortest in the groups with Afib genesis at these recording sites. In patients with inducible Afib, %A2/A1 and RAI were the highest and WLI the shortest at the atrial recording site close to the site of Afib genesis. Atrial wave prolongation during retrograde atrial activation, possibly the anisotropic conduction, was considered to play a role in initiating Afib as well as a conduction delay during the atrial premature beat.     

Atrial electrophysiological properties evaluated by right and left atrial pacing in patients with or without atrial fibrillation

Coronary sinus (CS) pacing has been shown to prevent induction of atrial fibrillation (AF) by suppression of the propensity of atrial premature beats at high right atrium (HRA) to induce local conduction delay at the posterior triangle of Koch. However, other mechanisms of CS pacing in preventing induction of AF have not been explored. This study investigated whether a differential conduction delay exists between the HRA and distal CS pacing in patients with paroxysmal AF but not in patients without AF. Nine patients with atrioventricular reentrant tachycardia utilizing a left accessory pathway undergoing catheter ablation were included in this study. Group 1 consisted of 5 patients with clinically documented paroxysmal AF and group 2 4 patients without a history of AF. The effective refractory periods (ERPs) of HRA, distal CS, and four different left atrial sites were determined. The interatrial conduction time and conduction delay between the HRA and distal CS during HRA or distal CS pacing were measured. The interatrial conduction delay (ICD) from the HRA to the distal CS during HRA pacing was significantly longer than that from the distal CS to the HRA during distal CS pacing in patients of group 1. However, the ICD from the HRA to the distal CS during HRA pacing was not significantly longer than that from the distal CS to the HRA during distal CS pacing in group 2 patients. A differential conduction delay between the HRA and the distal CS pacing is present in this specific population of patients with paroxysmal AF but not in patients without AF. The shorter conduction delay during DCS pacing may contribute to the prevention of induction of AF.     

Effect of radiofrequency ablation on atrial myocardium

Objectives Successful RF ablation of atrial fibrillation supposedly requires the creation of continuous linear lesions. This study aimed to determine the potential role of functional modifications of atrial myocardium in the vicinity of anatomic RF lesions. Methods In 10 normal beagles (group A), a multiplexer mapping system and an epicardial multi-electrode were used to reconstruct atrial activation patterns during pacing at two cycle lengths before and after attempts to induce two linear right atrial lesions with a standard ablation catheter, respectively. An intercaval “drawback” was repeated 3 times over 5 min at a set temperature of 70 °C, followed by a transversal “point-by-point” ablation from the interatrial septum to the right-lateral tricuspid annulus at 70 °C/60 s each. Induction of atrial flutter was attempted before and after each ablation. In another 6 beagles (group B), a high-resolution multi-electrode was used to study epicardial functional effects resulting from single endocardial RF lesions on the free right atrial wall. Using three energy settings (60 °C/30 s, 60 °C/60 s, 70 °C/60 s), activation patterns were analyzed at two cycle lengths and local effective refractory periods were measured across the lesion. Results The lesions induced in group A only marginally affected atrial activation patterns and total activation times. However, as shown in dogs with atrial flutter, regional slow conduction was enhanced and functional conduction blocks were facilitated at high atrial rates, resulting in a significant prolongation in the revolution time of respective reentrant circuits. Apart from inducing anatomic lesions, single endocardial RF lesions (group B) were shown to delay epicardial conduction in adjacent myocardium in an energy- and rate-dependent way. Furthermore, an energy-dependent prolongation of effective refractory periods by far exceeding the size of anatomic lesions was observed. Conclusions Continuous linear atrial lesions are hard to achieve with conventional ablation techniques. However, RF lesions induce changes in conduction and refractoriness around the anatomic lesion, which are likely to contribute to the overall effect of respective therapeutic interventions. Received: 17 October 2000, Returned for revision: 4 December 2000, Revision received: 1 February 2001, Accepted: 20 February 2001