The relationship of myocardial contraction and electrical excitation--the correlation between scintigraphic phase image analysis and electrophysiologic mapping.

BACKGROUND: Phase imaging derived from equilibrium radionuclide angiography presents the ventricular contraction sequence. It has been widely but only indirectly correlated with the sequence of electrical myocardial activation. OBJECTIVES: We sought to determine the specific relationship between the sequence of phase progression and the sequence of myocardial activation, contraction and conduction, in order to document a noninvasive method that could monitor both. METHODS: In 7 normal and 9 infarcted dogs, the sequence of phase angle was correlated with the epicardial activation map in 126 episodes of sinus rhythm and pacing from three ventricular sites. RESULTS: In each episode, the site of earliest phase angle was identical to the focus of initial epicardial activation. Similarly, the serial contraction pattern by phase image analysis matched the electrical epicardial activation sequence completely or demonstrated good agreement in approximately 85% of pacing episodes, without differences between normal or infarct groups. CONCLUSIONS: A noninvasive method to accurately determine the sequence of contraction may serve as a surrogate for the associated electrical activation sequence or be applied to identify their differences.

Clinical outcome after radiofrequency catheter ablation of focal atrial fibrillation triggers.

INTRODUCTION: Ablative therapy for atrial fibrillation (AF) by targeting initiating triggers, usually in or around the pulmonary veins, has been reported by several centers. Evidence for an overall improvement in quality of life (QOL) and amelioration of symptoms is lacking. METHODS AND RESULTS: Seventy-one patients undergoing attempted ablation of focal AF were followed for 60+/-33 weeks. QOL and symptom questionnaires were completed 1 month before and 6 months after electrophysiologic study. Twenty-three patients (32%) underwent electrophysiologic mapping but no ablation because of either insufficient or multifocal ectopy; the other 48 patients (68%) underwent attempted ablation. Sixteen of 48 patients (33%) undergoing ablation, or 16 (23%) of 71 on an intention-to-treat basis, were found at last follow-up to have persistent sinus rhythm without antiarrhythmic drugs. Patients who underwent mapping without ablation reported no improvements in any QOL or symptom score, whereas patients who had long-term successful ablation had significant improvements in all six QOL measures. Interestingly, patients who developed AF recurrence after ablation still reported significant improvements in 4 of 6 QOL measures. Four of 48 patients (8.3%) undergoing ablation developed pulmonary vein stenosis. CONCLUSION: Paroxysmal AF can be treated successfully in some patients by ablating initiating triggers in the pulmonary veins; however, in our experience the recurrence rate (32/48 [68%]) and risk of pulmonary vein stenosis (8%) after ablation are high. Patients with recurrent AF after ablation of focal AF triggers have significant improvement in QOL and symptoms compared with before ablation. Patients and their physicians should carefully balance the risks and benefits before considering ablation.

Electrocardiographic analysis of ectopic atrial activity obscured by ventricular repolarization: P wave isolation using an automatic 62-lead QRST subtraction algorithm.

INTRODUCTION: Atrial activity on the surface ECG during premature beats and supraventricular arrhythmias frequently is obscured by the superimposed QRST complex of the previous cardiac cycle. This study examines the performance of a newly developed automatic QRST subtraction algorithm to isolate ectopic P waves from the preceding T-U wave. METHODS AND RESULTS: The 62-lead ECG recordings were obtained during (1) sinus rhythm and programmed right atrial stimulation in 12 patients (group A); and (2) sinus rhythm and atrial premature beats, atrial tachycardia, or paroxysmal atrial fibrillation in 5 patients (group B). Pacing in group A patients was conducted at a slow drive cycle length to generate an ectopic P wave not obscured by the previous QRST complex and by delivering single premature extrastimuli at progressively shorter coupling intervals to produce an ectopic P wave obscured by the upsloping (early T-U wave), peak (middle T-U wave), and downsloping component of the T-U wave (late T-U wave). All ectopic P waves in group B patients were concealed by the preceding T-U wave. Automatic QRST subtraction was attained using an adaptive template constructed from averaged QRST complexes (mean 83 +/- 25 complexes) obtained during sinus rhythm (groups A and B) or atrial overdrive pacing (group A). P wave integral maps subsequently were computed, visually compared, and mathematically correlated. A high correspondence in spatial map pattern was observed between integral maps of "nonobscured" and previously "obscured" paced P waves obtained in group A patients (mean r = 0.88 +/- 0.07) as well as between integral maps of two to three previously obscured P waves with the same atrial arrhythmia morphology obtained in group B patients (mean r = 0.94 +/- 0.05). Improved morphologic P wave replication in group A patients was acquired when concealment occurred in the early (mean r = 0.90 +/- 0.08) or late part of the T-U wave (mean r = 0.90 +/- 0.06) as opposed to the middle T-U wave (mean r = 0.85 +/- 0.07) (P = NS and P < 0.05 for early vs middle and late vs middle T-U wave, respectively). CONCLUSION: This novel automatic 62-lead QRST subtraction algorithm enables discrete isolation of T-U wave obscured ectopic atrial activity on the surface ECG while retaining the intricate spatial detail in P wave morphology. Future clinical application of the algorithm may enable improved ECG localization of focal triggers of paroxysmal atrial fibrillation, atrial tachycardia, and the atrial insertion of accessory pathways.

Classification of atrial flutter and regular atrial tachycardia according to electrophysiologic mechanism and anatomic bases: a statement from a joint expert group from the Working Group of Arrhythmias of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology.

Regular atrial tachycardias classically are classified into flutter or tachycardia, depending on the rate and presence of a stable baseline on the ECG. However, current understanding of electrophysiology atrial tachycardias makes this classification obsolete, because it does not correlate with mechanisms. The proposed classification is based on electrophysiologic mechanisms, defined by mapping and entrainment. Radiofrequency ablation of a critical focus or isthmus can afford proof. Focal tachycardias are characterized by radial spread of activation and endocardial activation not covering the whole cycle. Ablation of the focus of origin interrupts the tachycardia. The mechanism of focal firing is difficult to ascertain by clinical methods. Macroreentrant tachycardias are characterized by circular patterns of activation that cover the whole cycle. Fusion can be shown during entrainment on the ECG or by multiple endocardial recordings. Ablation of a critical isthmus interrupts the tachycardia. Macroreentry can occur around normal structures (terminal crest, eustachian ridge) or around atrial lesions. The anatomic bases of these tachycardias must be defined, to guide appropriate treatment. Atrial flutter is a mere description of continuous undulation on the ECG, and only some strictly defined typical flutter patterns correlate with right atrial macroreentry bounded by the tricuspid valve, terminal crest, and caval vein orifices. This classification should be considered open, as some classically described tachycardias, such as reentrant sinus tachycardia, inappropriate sinus tachycardia, and type II atrial flutter, cannot be classified accurately. Furthermore, the possibility of fibrillatory conduction makes the limits with atrial fibrillation still ill defined.

Atypical right atrial flutter patterns.

BACKGROUND: The purpose of our study was to define the incidence and mechanisms of atypical right atrial flutter. METHODS AND RESULTS: A total of 28 (8%) of 372 consecutive patients with atrial flutter (AFL) had 36 episodes of sustained atypical right AFL. Among 24 (67%) of 36 episodes of lower loop reentry (LLR), 13 (54%) of 24 episodes had early breakthrough at the lower lateral tricuspid annulus, whereas 11 (46%) of 24 episodes had early breakthrough at the high lateral tricuspid annulus, and 9 (38%) of 24 episodes showed multiple annular breaks. Bidirectional isthmus block resulted in elimination of LLR. A pattern of posterior breakthrough from the eustachian ridge to the septum was observed in 4 (14%) of 28 patients. Upper loop reentry was observed in 8 (22%) of 36 episodes and was defined as showing a clockwise orientation with early annular break and wave-front collision over the isthmus. Two patients had atypical right AFL around low voltage areas ("scars") in the posterolateral right atrium. CONCLUSIONS: Atypical right AFL is most commonly associated with an isthmus-dependent mechanism (ie, LLR or subeustachian isthmus breaks). Non-isthmus-dependent circuits include upper loop reentry or scar-related circuits.

Central clinical research issues in electrophysiology: report of the NASPE Committee.

This article contains the results of an attempt by appointed members of the North American Society of Pacing and Electrophysiology to define the research frontier in electrophysiology and suggest areas of study as an aid in setting the research agenda.

Empirical pulmonary vein isolation in patients with chronic atrial fibrillation using a three-dimensional nonfluoroscopic mapping system: long-term follow-up.

The purpose of this study was to assess the feasibility and long-term results of empirical isolation of both superior pulmonary veins in patients with chronic AF. Although localizing and ablating the focal triggers of AF has been proven an effective approach, this strategy is time consuming, often requires multiple procedures, and carries the risk of pulmonary vein stenosis. Whether ostial electrical isolation of the superior pulmonary veins, without initial detailed mapping, is a more efficient approach is not known. The study included 71 consecutive patients who had chronic AF. Using a nonfluoroscopic electroanatomic mapping system, the left and right superior pulmonary veins were ablated circumferentially at the venoatrial junction, with the aim of achieving electrical isolation of the veins. Following ablation, if frequent atrial ectopies were present, mapping and ablation were considered. The patients were periodically followed with 48-hour Holter and loop recorder monitoring. After the ablation of the right and left superior pulmonary veins 59 (83%) of 71 patients maintained sinus rhythm without premature atrial beats. The remaining 12 patients underwent further mapping and ablation including 5 patients who required isolation of the left inferior pulmonary veins. True electrical isolation could be achieved only in 45 (31%) of the 147 targeted veins. At the latest follow-up (mean 29 +/- 8 months), 80% of the patients with upper vein isolation remained in sinus rhythm off medications, 62% of the patients maintained sinus rhythm on previously ineffective medications, and 17% continued to be in AF. Fourteen (20%) patients developed intermittent episodes of left atrial flutter, and mapping in these patients revealed large electrically silent areas in the left atrium. Empirical isolation of pulmonary veins appeared to be an effective approach to help maintain sinus rhythm in patients with chronic AF. True electrical isolation of the pulmonary veins was associated with a higher likelihood of long-term success. Left atrial flutter was seen in a significant number of patients at long-term follow-up.

First human experience with pulmonary vein isolation using a through-the-balloon circumferential ultrasound ablation system for recurrent atrial fibrillation.

BACKGROUND: Standard mapping and ablation of focal sources of atrial fibrillation are associated with very long procedure times and low efficacy. An anatomic approach to complete pulmonary vein isolation could overcome these limitations. METHODS AND RESULTS: Fifteen patients with atrial fibrillation refractory to medication underwent circumferential isolation of the pulmonary veins by using a novel catheter, with an ultrasound transducer (8-MHz) mounted near the tip, in a saline-filled balloon. Twelve atrial foci and/or atrial fibrillation triggers were identified in 9 patients (pulmonary vein locations: left upper, 3; right upper, 6; right middle, 1; right lower, 1; and left inferior, 1). In 5 patients, lesions were placed in the absence of any mapped triggers. Irrespective of trigger mapping, circumferential isolation of both upper pulmonary veins was attempted in all patients. The lower pulmonary veins were ablated when sinus rhythm activation mapping revealed evidence of a sleeve of atrial muscle in the vein. The median number of lesions per patient required to isolate 1 pulmonary vein was 4 (range, 1 to 29). After ablation, no evidence of narrowing was seen with repeat venography or follow-up computed tomography scan. After a mean follow-up of 35+/-6 weeks, 5 patients had recurrence of atrial fibrillation. Three responded to drugs that were previously ineffective, and 2 remained in atrial fibrillation. CONCLUSIONS: This novel ultrasound ablation system can successfully isolate multiple pulmonary veins. At early follow-up, this approach seems to be effective in preventing recurrent atrial fibrillation in a significant number of patients.

The role of the crista terminalis in atrial flutter and fibrillation: a computer modeling study.

Although atrial fibrillation is a common arrhythmia, the underlying mechanisms are incompletely understood. Recent studies have determined the role of the crista terminalis in the mechanisms of a simpler arrhythmia, atrial flutter. We hypothesize that as transverse coupling across the crista terminalis increases, the activation pattern that results is less like typical atrial flutter and more like atrial fibrillation. 6480 Van Capelle elements were coupled in an icosahedron, simulating the right atrium. Atrial simulations were created which incorporated no heterogeneity, heterogeneous coupling, heterogeneous effective refractory periods, and both heterogeneous coupling and effective refractory periods. When the entire crista terminalis was uncoupled, typical atrial flutter occurred. When transverse coupling allowed activation to propagate across the crista terminalis, the flutter cycle length decreased (p<0.0001). In addition, when heterogeneity was present, both the coefficient of variation of cycle length and the number of activation wavelets increased (p<0.0001). Thus, a more rapid reentrant circuit in the superior right atrium drove fibrillatory activity in the remainder of the atrium, as predicted by the "mother wavelet hypothesis." While awaiting in vivo validation, our study indicates that transverse coupling along the crista terminalis may play an important role in the development of atrial fibrillation from atrial flutter.

The consequences of anterior femoral notching in total knee arthroplasty. A biomechanical study.

BACKGROUND: Notching of the anterior femoral cortex during total knee arthroplasty has been implicated as a cause of subsequent periprosthetic supracondylar femoral fracture. However, other than observational clinical data, no reliable association between these events has been established, to our knowledge. The purpose of the present study was to investigate the biomechanical effects of notching of the anterior femoral cortex. METHODS: The femoral component of a total knee replacement was implanted in twelve matched pairs of human cadaveric femora; one specimen in each pair had preservation of the anterior femoral cortex, and the other had a full-thickness cortical defect created just proximal to the anterior flange of the femoral component. The pairs were then subjected to either bending or torsional loading to failure. Both the fracture pattern and the quantitative load to failure were analyzed. Two matched pairs were excluded from the analysis because of inadvertent fracture during placement of the component. RESULTS: Following the application of a bending load, femora with notching of the anterior femoral cortex sustained a short oblique fracture that originated at the cortical defect proximal to the femoral component and femora without notching had a midshaft fracture. In contrast, notching of the anterior femoral cortex had no effect on the fracture pattern that was observed after the application of a torsional load. The mean load to failure was significantly reduced by notching in both testing modes. Notching decreased bending strength from 11,813 to 9690 newtons (18 percent; p = 0.0034), and it decreased torsional strength from 134.7 to 81.8 newton-meters (39.2 percent; p = 0.01). CONCLUSIONS: Biomechanical testing demonstrated that notching of the anterior femoral cortex significantly lessens the load to failure following total knee arthroplasty and influences the subsequent fracture pattern. These effects are manifested in different ways under the two loading conditions: the fracture pattern is altered under bending load, and there is a greater quantitative decrease in load to failure with torsional loading. CLINICAL RELEVANCE: Weakening of the femur by notching of the anterior cortex after total knee arthroplasty may warrant alteration in the customary postoperative regimen for these patients. Manipulation of a total knee replacement with a notched anterior femoral cortex should probably be avoided.

Prevalence of the Brugada sign in idiopathic ventricular fibrillation and healthy controls.

OBJECTIVE: To determine the prevalence of the Brugada sign (right bundle branch block with ST elevation in V1-V3) in idiopathic ventricular fibrillation and in an age matched healthy population. DESIGN: ECGs from 39 consecutive patients with idiopathic ventricular fibrillation and 592 healthy controls were reviewed. They were classified as definite, questionable, and no Brugada sign (according to predetermined criteria) by four investigators blinded to the subjects' status. RESULTS: Eight patients (21%) with idiopathic ventricular fibrillation but none of the 592 controls had a definite Brugada sign (p < 0.005). Thus the estimated 95% confidence limits for the prevalence of a definite Brugada sign among healthy controls was less than 0.5%. A questionable Brugada sign was seen in two patients with idiopathic ventricular fibrillation (5%) but also in five controls (1%) (p < 0.05). Normal ECGs were found following resuscitation and during long term follow up in 31 patients with idiopathic ventricular fibrillation (79%). Patients with idiopathic ventricular fibrillation and a normal ECG and those with the Brugada syndrome were of similar age and had similar spontaneous and inducible arrhythmias. However, the two groups differed in terms of sex, family history, and the incidence of sleep related ventricular fibrillation. CONCLUSIONS: A definite Brugada sign is a specific marker of arrhythmic risk. However, less than obvious ECG abnormalities have little diagnostic value, as a "questionable" Brugada sign was observed in 1% of healthy controls. In this series of consecutive patients with idiopathic ventricular fibrillation, most had normal ECGs.

Body surface mapping of counterclockwise and clockwise typical atrial flutter: a comparative analysis with endocardial activation sequence mapping.

OBJECTIVES: This study was directed at developing spatial 62-lead electrocardiogram (ECG) criteria for classification of counterclockwise (CCW) and clockwise (CW) typical atrial flutter (Fl) in patients with and without structural heart disease. BACKGROUND: Electrocardiographic classification of CCW and CW typical atrial Fl is frequently hampered by inaccurate and inconclusive scalar waveform analysis of the 12-lead ECG. METHODS: Electrocardiogram signals from 62 torso sites and multisite endocardial recordings were obtained during CCW typical atrial Fl (12 patients), CW typical Fl (3 patients), both forms of typical Fl (4 patients) and CCW typical and atypical atrial Fl (1 patient). All the Fl wave episodes were divided into two or three successive time periods showing stable potential distributions from which integral maps were computed. RESULTS: The initial, intermediate and terminal CCW Fl wave map patterns coincided with: 1) caudocranial activation of the right atrial septum and proximal-to-distal coronary sinus activation, 2) craniocaudal activation of the right atrial free wall, and 3) activation of the lateral part of the subeustachian isthmus, respectively. The initial, intermediate and terminal CW Fl wave map patterns corresponded with : 1) craniocaudal right atrial septal activation, 2) activation of the subeustachian isthmus and proximal-to-distal coronary sinus activation, and 3) caudocranial right atrial free wall activation, respectively. A reference set of typical CCW and CW mean integral maps of the three successive Fl wave periods was computed after establishing a high degree of quantitative interpatient integral map pattern correspondence irrespective of the presence or absence of organic heart disease. CONCLUSIONS: The 62-lead ECG of CCW and CW typical atrial Fl in man is characterized by a stereotypical spatial voltage distribution that can be directly related to the underlying activation sequence and is highly specific to the direction of Fl wave rotation. The mean CCW and CW Fl wave integral maps present a unique reference set for improved clinical detection and classification of typical atrial Fl.

Heterogeneous sympathetic innervation influences local myocardial repolarization in normally perfused rabbit hearts.

BACKGROUND: Heterogeneity of sympathetic innervation is thought to contribute to the potential for fatal arrhythmia. However, little is known about the effects of heterogeneous innervation on repolarization. METHODS AND RESULTS: To assess this relationship, we measured activation recovery intervals (ARIs) from 64 epicardial sites in 11 rabbits studied 2 weeks after regional denervation produced by phenol and 4 sham-operated rabbits. ARI results were compared with the distribution of sympathetic innervation measured from 3D reconstructions of serial autoradiographs of [(125)I]metaiodobenzylguanidine and (99m)Tc-sestamibi. ARIs were recorded during baseline sinus rhythm, norepinephrine (NE) infusion (0.1 microg. kg(-1). min(-1)), and left stellate ganglion stimulation (SS). NE shortened ARI in 98% of electrodes in the denervated region. The degree of ARI shortening and dispersion increased (P<0.001 and P<0.01, respectively) as denervation became more severe. SS shortened ARI in 30% of electrodes in the denervated area, with increased shortening and dispersion related to increased severity of denervation (P<0.01). SS prolonged ARI in 70% of electrodes in the denervated area, with no correlation with severity of denervation. CONCLUSIONS: The magnitude and dispersion of local repolarization responses are related to the severity of denervation, as well as the type of stimulation: neural (SS) versus humoral (NE). The differences may relate to the concentration of NE released.

Derivation of an optimal lead set for measuring ectopic atrial activation from the pulmonary veins by using body surface mapping.

Atrial fibrillation is often initiated by atrial premature beats originating in the pulmonary veins. Non-invasive localization of these ectopic beats would be of significant value in guiding therapy. Body surface potential mapping was performed in nine patients undergoing invasive electrophysiologic study. Signals were recorded from 62 electrodes during pace mapping from each of the pulmonary veins. Optimal electrodes for localizing pulmonary vein activation were sequentially chosen. Seven optimal electrodes (6 anterior, 1 posterior) for recording ectopic atrial activation originating in the pulmonary veins were selected. The seven optimal electrode set performed better than the standard 9 electrode ECG at estimating the full body surface map (correlation 97 vs. 95.7%; p < 0.05). Seven optimally selected electrodes can estimate the body surface potential distribution during ectopic atrial activation orignating from the pulmonary veins. The ability of this electrode configuration to discriminate the site of origin of ectopic atrial beats requires prospective evaluation.

An anatomic approach to prevention of atrial fibrillation: pulmonary vein isolation with through-the-balloon ultrasound ablation (TTB-USA).

Our current understanding is that atrial fibrillation (AF) is initiated most often by a focal trigger from the orifice of or within one of the pulmonary veins. Though mapping and ablation of these triggers appears to be curative in most patients with paroxysmal AF, there are a number of limitations to ablating focal triggers via mapping and ablating the earliest site of activation with a "point" radiofrequency lesion. One way to circumvent thesen limitations is an anatomically-guided ablative approach. By electrically isolating one or more pulmonary veins from the left atrium with a circumferential lesion, firing from within those veins would be unable to reach the body of the atrium, and thus could not trigger atrial fibrillation. We have developed a novel over-the-wire catheter design which integrates a cylindrical ultrasound transducer within a saline filled balloon, termed TTB-USA (through-the-balloon ultrasound ablation) in order to produce narrow circumferential zones of hyperthermic tissue death at the pulmonary vein ostia. Animal studies show great promise, and clinical trials will begin soon.

Use of electroanatomic mapping to delineate transseptal atrial conduction in humans.

BACKGROUND: Interaction between wave fronts in the right and left atrium may be important for maintenance of atrial fibrillation, but little is known about electrophysiological properties and preferential routes of transseptal conduction. METHODS AND RESULTS: Eighteen patients (age 44+/-12 years) without structural heart disease underwent right atrial electroanatomic mapping during pacing from the distal coronary sinus (CS) or the posterior left atrium. During distal CS pacing, 9 patients demonstrated a single transseptal breakthrough near the CS os, 1 patient in the high right atrium near the presumed insertion of Bachmann's bundle and 1 patient near the fossa ovalis. The mean activation time from stimulus to CS os was 48+/-15 ms compared with 86+/-15 ms to Bachmann's bundle insertion (P<0.01) and 59+/-23 ms to the fossa ovalis (P=NS and P<0.01, respectively). During left atrial pacing, the earliest right atrial activation was near Bachmann's bundle in 5 and near the fossa ovalis in 4 patients. The activation time from stimulus to CS os was 70+/-15 ms compared with 47+/-16 ms to Bachmann's bundle (P<0.01) and 59+/-25 ms to the fossa ovalis (P=NS). Whereas the total septal activation time was not significantly different during CS pacing compared with left atrial pacing (41+/-16 versus 33+/-17 ms), the total right atrial activation time was longer during CS pacing (117+/-49 versus 79+/-15 ms; P<0.05). CONCLUSIONS: Three distinct sites of early right atrial activation may be demonstrated during left atrial pacing. These sites are in accord with anatomic muscle bundles and may have relevance for maintenance of atrial flutter or fibrillation.

The spatial dispersion of atrial refractoriness and atrial fibrillation vulnerability.

The local dispersion of conduction and refractoriness has been considered essential for induction of atrial arrhythmias. This study sought to determine whether a difference of refractoriness and vulnerability for induction of atrial fibrillation between trabeculated and smooth as well as high and low right atrium may contribute to initiation of atrial fibrillation in dogs. In 14 healthy mongrel dogs weighing 22.4 +/- 1 kg, closed-chest endocardial programmed stimulation was performed from four distinct right atrial sites. Atrial refractory periods and vulnerability for induction of atrial fibrillation or premature atrial complexes were determined during a basic cycle length of 400 and 300 ms and an increasing pacing current strength. For a pacing cycle length of 300 ms, atrial refractory periods were longer on the smooth, as compared to the trabeculated right atrium (102 +/- 25 vs. 97 +/- 17 ms, p < 0.05), whereas for a pacing cycle length of 400 ms, there was no significant difference. The duration of the vulnerability zone for induction of atrial fibrillation was longer on the smooth right atrium, for a cycle length of both 400 ms (40 +/- 30 vs. 31 +/- 22 ms; p < 0.05) and 300 ms (33 +/- 25 vs. 23 +/- 21 ms; p < 0. 01). When comparing high and low right atrium, refractory periods were longer on the the low right atrium, for a cycle length of both 400 ms (111 +/- 23 vs. 94 +/- 24 ms; p < 0.01) and 300 ms (104 +/- 20 vs. 96 +/- 23 ms; p < 0.01). For a pacing cycle length of 300 ms, the duration of the atrial fibrillation vulnerability zone was longer for the high, as compared to the low right atrium (34 +/- 22 vs. 22 +/- 22, p < 0.01). Seven dogs with easily inducible episodes of atrial fibrillation demonstrated significantly shorter refractory periods as compared to 7 non-vulnerable dogs, regardless of pacing site and current strength. In conclusion, significant differences in refractoriness and vulnerability for induction of atrial fibrillation can be observed in the area of the crista terminalis in healthy dogs. Thus, local anatomic factors may play a role in the initiation of atrial fibrillation.