Intra-atrial Reentry Research Articles

Mechanisms of atrial fibrillation and flutter and implications for management

Both electrophysiologic and anatomical substrates are important in the generation and maintenance of atrial fibrillation. This review discusses the nature of re-entrant wavefronts in atrial fibrillation and the importance of anatomical structures, such as the pectinate muscles, in the generation and maintenance of re-entry. The involvement of the pectinate muscle structure on intra-atrial re-entry may have significant implications for both ablation and pharmacologic management of patients with atrial fibrillation.

Electrophysiology and endocardial mapping of induced atrial fibrillation in patients with spontaneous atrial fibrillation

We analyzed the patterns of atrial activation and characterized the electrophysiologic properties of regional atrial sites in the right atrium and left atrium at the onset of atrial fibrillation (AF) induced with programmed right atrial (RA) stimulation. Intraatrial conduction, atrial electrogram return cycle lengths for the first AF cycle, RA and left atrial (LA) activation maps during AF, and the stability and reproducibility of atrial activation sequences at AF onset and maintenance were analyzed in 23 patients with AF. Correlation of intracardiac electrograms with surface electrocardiographic morphology was attempted. Maximum intraatrial conduction delay for high RA premature beats was observed at the coronary sinus ostium (n = 15), His bundle region (n = 13) or interatrial septum (n = 15). The return cycle lengths for the first AF cycle showed increasing conduction delay with increasing prematurity of the last extrastimulus in most patients. Suprisingly, discrete atrial electrograms with regular or irregular cycle lengths were present at the onset of electrocardiographic documented coarse AF in 13 of 15 patients (87%). Fragmented or chaotic atrial activity were present in 2 of 15 patients (13%) in coarse AF but observed at ≥1 atrial sites in 7 of 8 patients (88%) with fine AF (p = 0.001). The atrial activation sequence at the onset of the induced AF elicited by high RA extrastimuli usually showed the earliest activation site at the crista terminalis (9 patients) or interatrial septum (9 patients). In contrast, induced AF elicited from other RA sites usually showed earliest atrial activation at the septum (3 patients) or coronary sinus ostium (3 patients). Atrial activation sequences for the first induced AF cycle were usually reproducible in most patients. Atrial activation patterns during the first 10 cycles for AF were stable in RA and LA regions in 6 of 23 patients (26%) but demonstrated significant change(s) at ≥1 region in 17 of 23 patients (74%) (p <0.05). We conclude that pacing induced AF elicited by RA premature beats commences as a regular or irregular rapid atrial tachycardia consistent with a transitional, but often organized, arrhythmia. The activation sequence and electrophysiologic behavior of the first induced AF cycle is consistent with intraatrial reentry and reproducible in most patients. More than 1 atrial activation sequence can sometimes be observed, emphasizing the dynamic nature of the initial RA reentrant circuits.

Role of pectinate muscle bundles in the generation and maintenance of intra-atrial reentry: potential implications for the mechanism of conversion between atrial fibrillation and atrial flutter.

To determine the role of pectinate muscle (PM) bundles in the formation of intra-atrial reentry, 10 isolated canine right atrial tissues were perfused with Tyrode's solution containing 1 to 2.5 micromol/L acetylcholine (ACh). The endocardium was mapped using 477 bipolar electrodes with 1.6-mm resolution. Reentry was induced by a premature stimulus (S2). Computer simulation studies were used to investigate the importance of regional myocardial thickness in reentry formation. A total of 40 episodes of reentry were induced; 28 episodes were stationary, and the remaining 12 were nonstationary. The stationary reentry was induced either immediately after the S2 stimuli (n=9) or after an initial period of irregular activations that lasted 1460+/-1077 ms (n= 19). Of 28 episodes, 20 were initiated by conduction block along large PM ridges, leading to wave break and the initiation of reentry. The reentrant wave fronts remained stationary and rotated around these ridges as anchoring sites. During the transition from the initial irregular activations to stationary reentry, the electrogram morphology converted from "fibrillation-like" to "flutter-like" activity. In 8 episodes, initially stationary reentry converted to irregular activations because of interference with outside wave fronts (n=5) or spontaneous separation of waves from the ridges (n=3). Compared with stationary reentry, nonstationary reentry always occurred over an area without large PMs, and the mean life span was much shorter (102+/-151 versus 3.8+/-1.1 rotations, P<0.001). Computer simulation studies showed that a critical ridge thickness is needed for reentry to anchor, thereby converting fibrillation to flutter. We conclude that PM ridge forms an area where wave break occurs, allowing the initiation of reentry. It also provides a natural anchor to the reentrant wave front, lengthening the life span of reentry. The attachment and detachment of the reentrant wave front to and from the ridge determine "flutter-like" or "fibrillation-like" activity.

Electrophysiological properties of the fibrillating atrium: implications for therapy.

1. Atrial fibrillation (AF) is the most commonly occurring cardiac dysrhythmia and remains a challenge to medical therapy. Although the disorder has been recognized for over 100 years, surprisingly very little is understood about its pathophysiology. Over the past decade, a variety of experimental and animal models of AF have been developed and these have provided insights into the mechanism of AF. 2. The pathophysiology of AF is complex. Atrial fibrillation can be caused either by a single source of very rapid impulses or, in the majority of cases, by multiple random re-entering wavelets. The notion that AF may be initiated by a single rapid firing focus and the perpetuation of AF may be partly dependent on macro re-entry around the natural atrial orifices provides a new potential curative therapy for AF by radiofrequency ablation. 3. Shortening of atrial wavelength, either by slow atrial conduction velocities, short atrial refractory periods or both, seems to predispose to development of intra-atrial re-entry and, thus, AF. The functional mechanism by which anti-arrhythmic drugs terminate AF appears to be by prolonging the wavelength and decreasing the number of re-entry wavelets. These understandings are important for the future development of effective anti-arrhythmic agents against AF. 4. The presence of a short and variable excitable gap during AF may be potentially important for termination of AF by pacing. 5. New insights are being gained into the potential role and mechanism of electrical remodelling of the atrium due to AF. Repeated induction of AF by rapid atrial pacing leads to a shortening of atrial refractoriness with loss of rate adaptation, which favours the induction and maintenance of AF. These electrophysiological changes were assumed to occur during repeated AF and to facilitate the generation of multiple re-entrant wavelets. These data suggest that prompt restoration of sinus rhythm and new novel therapy that prevents or diminishes electrical remodelling may promote maintenance of sinus rhythm after successful cardioversion.

Electrical-anatomic correlations between typical atrial flutter and intra-atrial re-entry following atrial surgery

It is well known that in typical (or type I) atrial flutter, conduction proceeds counterclockwise, up the interatrial septum and down the right atrial wall anterior to the crista terminalis (CT). Recent careful mapping studies using entrainment pacing have clearly shown the importance of the CT and the eustachian valve ridge (EVR), which act as fixed barriers to intraatrial conduction and interact with other barriers, including the tricuspid valve, inferior vena cava (IVC), and coronary sinus os, to create a long macroreentrant circuit. Ablative lesions are directed at the isthmus between the tricuspid valve and the IVC or between the tricuspid valve and the EVR. Patients who have had cardiac surgery may have typical atrial flutter, either counterclockwise or clockwise, and prior surgery may act to stabilize the circuit. Such patients may also have atypical flutter, which does not utilize this circuit. Surgical closure of septal defects requires a long anterior oblique atriotomy. Commonly, reentrant circuits are identified that use this barrier, as well as the tricuspid valve and CT, and are confined to the anterior atrial wall and do not involve the typical flutter isthmus. These may be ablated at the lower or the upper end of the atriotomy, extending the block to the tricuspid valve, IVC, or superior vena cava. After the Senning or Mustard procedure, typical flutter is common, and the baffle bisects the isthmus at the site of the EVR, perhaps enforcing block. Anterior atriotomy-mediated reentry also is seen, and both circuits need to be approached in a retrograde manner. After the Fontan atriopulmonary connection, atriotomies and atrial dilation may interact to make reentry more likely. After the “lateral tunnel” Fontan (cavopulmonary connection) suture lines are similar to those of the Senning procedure, but nearly all right atrial anatomy is in the pulmonary venous atrium. Such circuits may need to be approached via an atrial fenestration.

Can intraatrial reentry be prevented by changes in surgical technique?

Intraatrial reentry tachycardias can be prevented by surgical technique. Crucial in prevention is not to create areas of slow conduction. Also, the integrity of the terminal crest appears to be essential for normal impulse propagation; at surgery the crest should preferably be left intact. The number of incisions in the atrium should be kept to an absolute minimum. One single incision is the best. Therefore, it is also better to cannulate the caval veins directly instead of using the right atrial auricle.

Radiofrequency ablation of intraatrial reentrant tachycardia after surgery for congenital heart disease.

Intraatrial reentry tachycardia is a common cause of both morbidity and mortality after surgery for a variety of congenital heart defects. Despite an armamentarium of arrhythmia management tools, including drug therapy, antibradycardia, and antitachycardia pacing, and catheter ablation, management of these arrhythmias remains a challenge. This report briefly reviews the problem, assesses the current successes and failures of radiofrequency catheter ablation for treating it, and discusses a number of ongoing developments that may improve both early and late outcome.

Supraventricular tachycardia. ECG diagnosis and anatomy.

This paper reviews the anatomical substrates responsible for the induction and maintenance of supraventricular tachycardia and discusses the ECG findings associated with these tachycardias. The normal anatomy of the supraventricular conducting system, particularly within the atria, is complex with conduction proceeding along preferential pathway, which are in turn determined in part by the anisotropic properties of the atrial myocardium. There appear to be at least dual inputs to the atrioventricular node, a posteriorly situated slow pathway and an anterior fast pathway. It is sometimes possible to relate ECG findings directly to anatomical substrates; for example, in some cases of atrial tachycardia the site of the atrial focus (left or right, superior or inferior) can be determined by the polarity of the P wave. The anatomical substrates responsible for intra-atrial re-entry, atrial flutter and atrial fibrillation relate to anatomical barriers to impulse propagation and areas of slow conduction. In atrial flutter the crista terminalis, Eustachian valve, inferior vena cava, coronary sinus os, and tricuspid annulus have been identified as anatomical barriers to conduction around which a macro re-entrant circuit within the right atrium may conduct, usually in a counter-clockwise direction. Clockwise direction of conduction, and other mechanisms of tachycardia, occur in some of the less typical forms of atrial fluter. Atrial fibrillation is caused by multiple wavelets which randomly conduct through the atrial myocardium and are responsible for the irregular 'fibrillation waves' on the ECG. Supraventricular tachycardia presents as a narrow complex tachycardia unless pre-existing or rate-related bundle branch block is present. Less common causes for a broad complex tachycardia occurring in supraventricular tachycardia include an accessory atrioventricular or atriofascicular pathway conducting antegradely during tachycardia, or accessory pathway participation as a bystander during supraventricular tachycardia. ECG features which can help to distinguish between atrioventricular nodal re-entrant tachycardia and atrioventricular re-entrant tachycardia include: (1) the presence of a delta wave during sinus rhythm which is highly suggestive of atrioventricular re-entrant tachycardia as the mechanism of supraventricular tachycardia; (2) the finding of a pseudo s (lead II) or pseudo r' (lead V1) during tachycardia in atrioventricular nodal re-entrant tachycardia; (3) lengthening of the tachycardia cycle length in cases of atrioventricular re-entrant tachycardia when bundle branch block occurs ipsilateral to the accessory pathway and (4) the finding of QRS alternans during tachycardia which is suggestive of atrioventricular re-entrant tachycardia. "Long RP' tachycardia may be caused by an atrial tachycardia due to an inferiorly situated area of abnormal automaticity, atypical atrioventricular nodal re-entrant tachycardia with slow retrograde conduction, or atrioventricular re-entrant tachycardia with an accessory pathway conducting slowly from ventricle to atrium during tachycardia.

Mapping reentry around atriotomy scars using double potentials.

Supraventricular arrhythmias, often seen in patients after cardiac surgery, may be associated with scars produced in the atria at the time of surgery. Double potentials, found in the presence of functional or anatomical block, can define the limits and critical regions of a reentrant circuit associated with the atriotomy scars. We describe six patients with seven distinct atrial tachycardias in whom atriotomy scars were successfully mapped during intraatrial reentry utilizing the presence and interelectrogram relationship of observed double potentials. The reentrant circuit was mapped in all patients by following the relationship between double potentials along the surgical scar, assuming that they would be widely split in the middle of the scar and merge into a single continuous fractionated potential at the apex of the scar. At this site, atrial pacing was performed to entrain the tachycardia and confirm the participation of the atriotomy scar in the clinically relevant atrial tachycardia. Radiofrequency ablation was performed from the site of electrogram fusion to the nearest anatomical obstacle. Five of seven atrial tachycardias were successfully ablated utilizing this technique over a mean follow-up of 10 months. We proposed that these double potentials and their interelectrogram relationship are an effective means of mapping atriotomy scars and guiding successful radiofrequency ablation.

Catheter ablation of clinical intraatrial reentrant tachycardias resulting from previous atrial surgery: Localizing and transecting the critical isthmus

We sought to evaluate the efficacy of anatomically based radiofrequency catheter ablation for the treatment of intraatrial reentrant tachycardia in patients with previous atrial surgery. Intraatrial reentrant tachycardias, a common late complication of atrial surgery, are often refractory to standard medical management. Data from experimental animals and from humans indicate that anatomic barriers resulting from residual atrial scars provide a substrate for intraatrial reentry. We speculated that these tachycardias require a narrow isthmus of tissue between surgical scars and native nonconductive boundaries and that transection of this isthmus with radiofrequency ablation would therefore constitute an effective treatment. Fourteen patients with a history of atrial surgery and clinical intraatrial reentrant tachycardia underwent electrophysiologic testing. From activation mapping, putative surgical scars and patches that served as boundaries of reentrant circuits were identified. Radiofrequency lesions were then placed to transect the narrowest isthmus of conducting tissue between a surgical scar and an anatomic barrier. Catheter ablation was attempted only for tachycardias consistent with the patient's clinical arrhythmias. Radiofrequency catheter ablation was attempted for 17 (55%) of 31 tachycardias identified; it successfully terminated tachycardias in 13 (93%) of 14 patients (95% confidence interval [CI] 79% to 99%). There were clinical recurrences in six patients (46%, 95% CI 19% to 73%), each of whom underwent a repeat ablation that was successful. Twelve (86%) of 14 patients (95% CI 67% to 99%) have remained free of intraatrial reentrant tachycardia for a mean of 7.5 +/- 5.3 months. Anatomically guided radiofrequency catheter ablation is an effective technique for definitive management of intraatrial reentrant tachycardia in patients with previous atrial surgery.

Unravelling the electrical mysteries of atrial fibrillation.

Animal experiments have confirmed that a short but variable excitable gap is present during induced atrial fibrillation. The existence of this gap allows atrial fibrillation to be locally captured by rapid pacing. An area of up to 4 cm in diameter can be activated by uniform wave fronts propagating away from the site of stimulation, although the size of this area may be limited by intra-atrial conduction block or by collision with fibrillation waves. Rapid pacing can accelerate atrial fibrillation by inducing local re-entry circuits with a cycle length shorter than the pacing interval. During pacing-induced atrial fibrillation in patients undergoing surgery for Wolff-Parkinson-White syndrome, three types of atrial activation have been identified, which vary in their degree of complexity and in the length of their fibrillation intervals. It appears that the spectrum of varying cycle lengths during atrial fibrillation might be explained by a mixture of different sorts of atrial re-entry patterns, comprising purely functional intra-atrial re-entry, random re-entry, anatomical re-entry, and nodal re-entry.

Effect of intraatrial reentry on initiation of atrioventricular reentrant tachycardia.

We studied the effect of intraatrial reentry (IAR) on initiation of orthodromic reentrant tachycardia (ORT) in 150 patients with Wolff-Parkinson-White syndrome using His-bundle recording and the atrial extrastimulus technique. IAR was initiated by premature atrial stimulation in 44 patients (29%), and it was followed by ORT in 16 patients (11%). In 8 patients (5%), IAR promoted the initiation of ORT, whereas in 5 patients (3%), IAR inhibited the initiation of ORT. These findings suggest that ORT is frequently induced following IAR. IAR, which was frequently observed during electrophysiological studies, seems to play an important role in the initiation of ORT.

The use of radiofrequency energy in pediatric cardiology.

The use of radiofrequency energy for the treatment of supraventricular tachycardia in pediatric patients has gained widespread acceptance, especially for tachyarrhythmias associated with palpitations, dizziness, presyncope or syncope, cardiomyopathy, and cardiac arrest. Ablation of the substrate supporting atrioventricular reentry, atrioventricular node reentry, and automatic atrial tachycardia yields a 90%-98% success rate with low incidence (< 1%) of complications and adverse side-effects. Ablation of intra-atrial reentry, including atrial flutter and fibrillation, appears to be promising and would be a significant advance in the management of patients following extensive atrial surgery for congenital heart disease. Radiofrequency energy is also used to treat various forms of idiopathic ventricular tachycardia. Finally, radiofrequency energy has been extended to control the ventricular rate associated with malignant atrial tachycardia by either modification or ablation of the atrioventricular node, and subsequent pacemaker implant. Long-term outcome of radiofrequency ablation is unknown, but the short-to-intermediate (1-5 yrs) outcome is excellent, with low recurrence rate of the tachycardia, no proarrhythmic effect, and excellent clinical state.

901-58 Slow Fragmented Intraatrial Conduction Post Maze Procedure: A Substrate for Intraatrial Reentrant Tachycardia and Marker for Effective Radiofrequency Ablation

The maze procedure is a surgical alternative for treating drug refractory atrial fibrillation. Although post-maze atrial fibrillation has been noted, slow intraatrial tachycardias have not been reported. Of 31 maze patients with a mean follow-up of 22 ± 9 months, 6 underwent electro physiologic (EP) testing (9 ± 6 months post-op) for symptoms suggestive of recurrent arrhythmia. Conduction was significantly prolonged through the right compared to the left atrium (167 ± 44 vs 57 ± 10 ms, p &lt; 0.01). However, right atrial effective refractory periods were normal (237 ± 29 ms). Programmed atrial stimulation induced sustained slow intraatrial reentry in two patients (cycle lengths of 420 and 520 ms) and atrial flutter (cycle length 190 ms) in one patient. The slow reentrant tachycardias were successfully ablated with radiofrequency energy in both patients. Neither patient has experienced a clinical recurrence after 14 and 9 months. Electrograms at successful ablation sites were markedly fragmented during sinus rhythm, with an apparent reversal of near/far-field activation during tachycardia (see figure). Slow intraatrial tachycardias may be observed in symptomatic post-maze patients. Our findings are consistent with slow conduction and reentry along a line of conduction block. Radiofrequency catheter ablation can be curative for these tachycardias.

Follow-up of radiofrequency catheter ablation in children: Results in 100 consecutive patients

Objectives. The purpose of this study was to determine the outcome of a group of closely followed-up pediatric patients who had undergone radiofrequency ablation for cardiac arrhythmias.Background. Although radiofrequency ablation in children has been shows to be effective and safe in the short term, results of longer term follow-up of these children must he considered when determining the place of radiofrequency ablation in the management of pediatric arrhythmias.Methods. One hundred children aged 2 months to 17 years underwent a total of 119 radiofrequency ablation procedures for cure of tachycardia. Follow-up clinical data, electrocardiograms and 24-h Holter monitors were obtained and analyzed.Results. All patients were alive, and none were lost to follow-up after a mean follow-up of 21.5 months (range 6 to 50). Success at last follow-up included accessory pathways in 66 (89%) of 74 patients, atrioventricular (AV) node reentry in 15 (88%) of 17, intraatrial reentry in 2 (67%) of 3, atrial flutter in 3 (100%) of 3, atrial ectopic tachycardia in 2 (67%) of 3, junctional ectopic tachycardia in 1 (100%) of 1 and ventricular tachycardia in 2 (100%) of 2 (overall success, 90 [90%] of 100). All recurrences were observed within 6 months of ablation. Major and minor complicatons (7%) included chest burn (one patient), foot microembolus (two patients), hematoma without pulse loss (four patients), femoral arteriovenous fistula requiring repair (one patient) and transient Mobitz I AV block (one patient). Immediate success, recurrence and complication rates were similar in the ≥12-year old versus the < 12-year old group. Echocardiograms, available in 109 (92%) of 119 patients, showed possible procedure-related abnormalities in 2 (mitral regurgitation in 1, tricuspid regurgitation in 1, both mild), with no aortic insufficiency after 30 left-sided ablations performed by the retrograde approach. Follow-up Holter monitors, available in 77 (77%) of 100 patients, showed possible procedurerelated abnormalities in 5 (frequent atrial ectopic tachycardia in 2, atrial flutter in 1, accelerated ventricular rhythm in 2). There were no early or late deaths.Conclusions. In children, the risks of radiofrequency ablation are low at follow-up evaluation. Longer-term follow-up of children undergoing radiofrequency ablation will be necessary to determine whether coronary abnormalities or serious new arrhythmias will develop.

Mechanism-specific effects of adenosine on atrial tachycardia.

Recent reports suggest that adenosine, in addition to terminating supraventricular tachycardia involving the atrioventricular (AV) node, may have antiarrhythmic effects on atrial tachycardia. The electrophysiological effects of adenosine on supraventricular tissue include shortening of action potential duration in atrial myocytes mediated by the potassium current, IKACh,Ado; shortening of action potential duration and hyperpolarization in sinus node cells; and anti-adrenergic electrophysiological effects resulting from inhibition of adenylyl cyclase. We therefore hypothesized that the response of atrial tachycardia to adenosine would be mechanism specific, with termination of atrial tachycardia due to sinus node reentry or cAMP-mediated triggered activity, transient suppression of automatic atrial tachycardia, and an absence of antiarrhythmic effect on tachycardia due to intraatrial reentry. Adenosine (mean +/- SD, 143 +/- 54 micrograms/kg IV) was administered to 27 patients (55 +/- 19 years) in atrial tachycardia whose mechanism was confirmed by electrophysiological study. Adenosine terminated sinus node reentrant tachycardia in 6 of 6 patients and terminated atrial tachycardia due to triggered activity in the 1 patient in whom it was identified. Adenosine transiently suppressed automatic atrial tachycardia in 7 of 7 patients and had no effect in 13 patients with intra-atrial reentrant tachycardia, including 8 patients with atrial flutter. These findings demonstrate that adenosine's effects on atrial tachycardia are mechanism specific and can be used to differentiate between reentrant tachycardia confined to the region of the sinus node or atria and between nonreentrant atrial tachycardia due to either triggered activity or automaticity.

Regional entrainment of atrial fibrillation studied by high-resolution mapping in open-chest dogs.

It recently has been demonstrated that during atrial fibrillation, a short and variable excitable gap exists, allowing regional control of atrial fibrillation by local stimulation. In the present study, we visualized the process of excitation during regional entrainment of atrial fibrillation by rapid pacing. In six open-chest dogs, the excitation of the left atrial free wall was mapped using a spoon-shaped mapping electrode (248 points). Episodes of atrial fibrillation were induced by burst pacing (50 Hz, 2 seconds). During atrial fibrillation, the electrograms showed rapid irregular activity with a median cycle length of 98 +/- 16 ms (mean +/- SD, n = 6). Rapid pacing in the center of the mapping electrode at intervals slightly shorter or longer than the median atrial fibrillation interval resulted in regional capture of atrial fibrillation. The window of entrainment was 16 +/- 5 ms. Mapping of atrial fibrillation showed that the left atrium was activated by fibrillatory wavelets coming from different directions. During entrainment, a relatively large area with a diameter of about 4 cm was activated by uniform wave fronts propagating away from the site of stimulation. The area of entrainment was limited by intra-atrial conduction block and by collision with fibrillation waves. Regional control of atrial fibrillation was lost by pacing either too slowly or too rapidly. In the first case, retrograde invasion of the area of entrainment by fibrillatory waves resulted in depolarization of the pacing site prior to the stimulus. Pacing too rapidly caused acceleration of atrial fibrillation by induction of local intra-atrial reentry circuits with a revolution time shorter than the pacing interval. During atrial fibrillation, an area with a diameter of about 4 cm can be entrained by local pacing. The resulting reduction in fibrillating tissue mass was not sufficient to terminate atrial fibrillation. Extension of the area of entrainment was limited by intra-atrial conduction block, whereas entrainment at a too high rate resulted in acceleration of atrial fibrillation by induction of local microreentry.

Vulnerability of rabbit atrium to reentry by hypoxia. Role of inhomogeneity in conduction and wavelength

In isolated superfused left atria of the rabbit, the inducibility of tachyarrhythmias by single early premature stimuli was highly increased by hypoxia. High-resolution mapping showed that these arrhythmias were caused by circus movement around a functional arc of conduction block (leading circle reentry). To determine the electrophysiological changes by hypoxia responsible for the higher vulnerability to intra-atrial reentry, the wavelength of the atrial impulse and spatial inhomogeneities in refractory periods and local conduction delays were measured. Hypoxia caused a transient increase in refractory periods during the first 10-15 min of hypoxia. After this period, refractory periods shortened again to values slightly lower than during control. During the whole period of hypoxia, local differences in refractory periods were enlarged. Conduction velocity was significantly depressed by hypoxia. As a result, the wavelength of the atrial impulse gradually shortened during hypoxia to approximately 80% of control. Inhomogeneity in conduction was quantified by phase maps in which the maximal local delays in conduction are plotted. Hypoxia caused a marked increase in inhomogeneity in conduction both during slow rhythm (inhomogeneity index increased from 2.3 to 3.4) and premature activation (from 3.1 to 4.7). We conclude that the higher vulnerability of the atrium for reentrant arrhythmias by hypoxia is based on a combination of a moderate shortening of the wavelength and an increase in inhomogeneity in conduction of premature wavefronts.

Antitachycardia Pacemaker Treatment of Postoperative Arrhythmias in Pediatric Patients

An automatic antitachycardia pulse generator (Intertach 262-12) was implanted in each of six pediatric patients (mean age, 10 years) with drug-resistant and persistent postoperative supraventricular arrhythmias. Four had bradycardia-tachycardia syndrome, two after a Mustard procedure for transposition of the great arteries, one after a Senning procedure for the same anomaly, and one after a Fontan procedure for univentricular heart with transposition of the great arteries. Of the two remaining patients, one had atrial flutter after a modified Fontan procedure for univentricular heart and one had intra-atrial reentry tachycardia after a modified Fontan procedure for double-outlet right ventricle with pulmonary stenosis. During a mean follow-up interval of 31 months after implantation, pacemakers were activated on multiple occasions and functioned appropriately in all six patients. Complications necessitated six invasive interventions in three patients: erosion or infection of the system, adaptor fracture, and connector block fracture on one occasion each and lead dislodgment on three occasions. Four of the six patients continued to take drugs at the end of this study; however, all patients had their drug therapy reduced and one was taking digoxin only. The number of hospital admissions decreased after implantation. Despite a number of technical challenges, this newer multiprogrammable antitachycardia pacemaker appears to be a valuable addition to the treatment of refractory postoperative supraventricular tachyarrhythmias in pediatric patients.

Electrophysiologic findings after Fontan repair of functional single ventricle

Cardiac arrhythmias are well recognized sequelae of the Fontan operation for complex congenital anomalies. In this study the electrophysiologic effects of the Fontan procedure were evaluated in 30 patients who underwent cardiac catheterization with electrophysiologic study 1.9 ± 1.3 years (mean ± SD) after modified Fontan repair for functional single ventricle. Abnormalities of sinus node or ectopic pacemaker automaticity were detected in 50% (15 patients) by determination of a prolonged corrected sinus node or pacemaker recovery time. Total sinoatrial conduction time was prolonged in 50% of the patients with normal sinus rhythm. Sinus noue or ectopic atrial pacemaker function was entirely normal in only 43% of patients. The predominant atrial rhythm was normal sinus in 70% and ectopic atrial or junctional in 30%. Abnormalities of atrial effective and functional refractory periods were noted in 43% of patients and were most pronounced at faster paced cycle lengths. Atrial endocardial catheter mapping revealed intraatrial conduction delays between adjacent sites in 76% of the patients tested and in eight of nine patients with inducible intraatrial reentry.Programmed atrial simulation induced nonsustained supraventricular arrhythmias in 10% of the 30 patients and sustained arrhythmias in 27%. Intraatrial reentry was the most common inducible arrhythmia and was present in seven of the eight patients with sustained and two of the three patients with nonsustained atrial arrhythmias. Atrioventricular conduction abnormalities were noted in 10% (three patients). No patient had inducible ventricular arrhythmias with programmed ventricular stimulation.The electrophysiologic findings after Fontan repair include abnormal sinus node function, prolonged atrial refractoriness, delayed intraatrial conduction and inducible atrial arrhythmias. The predictive value of electrophysiologic testing in this group of patients is unknown. Further study and continued clinical follow-up are essential to determine which patients will be at risk for the development of late life-threatening arrhythmias.