A comparison of rate control and rhythm control in patients with atrial fibrillation.

BACKGROUND: There are two approaches to the treatment of atrial fibrillation: one is cardioversion and treatment with antiarrhythmic drugs to maintain sinus rhythm, and the other is the use of rate-controlling drugs, allowing atrial fibrillation to persist. In both approaches, the use of anticoagulant drugs is recommended. METHODS: We conducted a randomized, multicenter comparison of these two treatment strategies in patients with atrial fibrillation and a high risk of stroke or death. The primary end point was overall mortality. RESULTS: A total of 4060 patients (mean [+/-SD] age, 69.7+/-9.0 years) were enrolled in the study; 70.8 percent had a history of hypertension, and 38.2 percent had coronary artery disease. Of the 3311 patients with echocardiograms, the left atrium was enlarged in 64.7 percent and left ventricular function was depressed in 26.0 percent. There were 356 deaths among the patients assigned to rhythm-control therapy and 310 deaths among those assigned to rate-control therapy (mortality at five years, 23.8 percent and 21.3 percent, respectively; hazard ratio, 1.15 [95 percent confidence interval, 0.99 to 1.34]; P=0.08). More patients in the rhythm-control group than in the rate-control group were hospitalized, and there were more adverse drug effects in the rhythm-control group as well. In both groups, the majority of strokes occurred after warfarin had been stopped or when the international normalized ratio was subtherapeutic. CONCLUSIONS: Management of atrial fibrillation with the rhythm-control strategy offers no survival advantage over the rate-control strategy, and there are potential advantages, such as a lower risk of adverse drug effects, with the rate-control strategy. Anticoagulation should be continued in this group of high-risk patients.

Role of functional block extension in lesion-related atrial flutter.

BACKGROUND: A line of block in the right atrium (RA) between the venae cavae is necessary to obtain classic atrial flutter (AFL). We tested the hypothesis that the location of that line of block would determine whether the AFL reentrant circuit would be due to single-loop reentry or figure-of-8 reentry. METHODS AND RESULTS: Simultaneous mapping from 392 sites (both atria and the atrial septum) was performed in 13 normal dogs before and after creating a linear lesion on the RA free wall. The lesion was 1 to 1.5 cm anterior and parallel to the crista terminalis (7 dogs) or posterior and close to the crista terminalis region (6 dogs). Sustained AFL (>2 minutes) was then induced. In 4 dogs with an anterior lesion, the AFL reentrant circuit traveled around the lesion (lesion reentry). In 9 dogs (3 with anterior lesions and 6 with posterior lesions), the AFL reentrant circuit included the anterior RA free wall, the atrial septum, and Bachmann's bundle (single-loop reentry). In these 9 dogs, the fixed line of block was extended to the superior and/or inferior vena cava by a functional line of block, thereby preventing lesion reentry. No figure-of-8 reentry was induced. CONCLUSIONS: In this model, the location of a fixed line of block and its functional extension determine the type of AFL reentry. These data provide an explanation for the chronic AFL that occurs in some patients after surgical repair of congenital heart lesions.

Imaging dispersion of myocardial repolarization, I: comparison of body-surface and epicardial measures.

BACKGROUND: Body-surface ECG measures (QT dispersion [QTd], QRST integrals) have been used as indices of myocardial repolarization abnormalities with the goal of identifying patients at risk of fatal arrhythmias. The clinical utility of these measures has been questioned. We investigate the complex relationship between epicardial and body-surface potentials in the context of regionally abnormal myocardial repolarization. METHODS AND RESULTS: Epicardial potentials were recorded with a 224-electrode sock from an open-chest dog during control, regional epicardial warming, cooling, and adjacent warming and cooling to induce localized alterations in myocardial repolarization and regions of increased repolarization dispersion. Body-surface potentials were generated from these epicardial potentials in a human torso model. Epicardial estimates of repolarization (activation recovery intervals [ARIs] and QRST integrals) were evaluated for their ability to identify regions with increased repolarization dispersion. Body-surface QRST integrals and QTd in 12-lead ECG and 64-lead body-surface potential maps were evaluated for their ability to detect increased dispersion of myocardial repolarization. Epicardial ARI and QRST integral maps successfully located epicardial regions with increased dispersion of repolarization. The increased dispersion was not consistently reflected in the 12-lead or 64-lead ECG QTd or in the body-surface QRST integral maps. CONCLUSIONS: This study demonstrates the inadequacy of body-surface measures that are thought to reflect myocardial dispersion of repolarization. In contrast, measures based on epicardial electrograms (ARI or epicardial QRST integral maps) provide physiologically relevant information about myocardial repolarization and can locate regions of increased dispersion.

Imaging dispersion of myocardial repolarization, II: noninvasive reconstruction of epicardial measures.

BACKGROUND: Dispersion of myocardial repolarization supports the development and maintenance of life-threatening arrhythmias. Current noninvasive approaches for detecting substrates with increased dispersion based on ECG measures (eg, QT dispersion) have shown limited success and inconsistencies. The companion article shows that, in contrast, epicardial potentials and derived measures reflect local dispersion of repolarization. Here, using a recently developed ECG imaging method, we evaluate the feasibility of noninvasive reconstruction of such epicardial measures from body-surface ECG data. METHODS AND RESULTS: Epicardial potentials were recorded with a 224-electrode sock from an open-chest dog during control, regional warming, cooling, and simultaneous adjacent warming and cooling to induce localized changes in myocardial repolarization and regions of increased dispersion. Body-surface potentials were generated from these epicardial potentials in a human torso model. Realistic geometric errors and measurement noise were added to the torso data, which were then used to noninvasively reconstruct epicardial measures of repolarization dispersion (activation recovery intervals [ARIs] and QRST integrals). Repolarization properties were accurately depicted by ECG imaging, including (1) shortened ARIs and increased QRST integrals over the warmed region, (2) prolonged ARIs and decreased QRST integrals over the cooled region, and (3) high gradients of ARIs and QRST integrals over the adjacent warmed and cooled regions. CONCLUSIONS: ECG imaging can reconstruct repolarization properties accurately and localize areas of increased dispersion of repolarization in the heart noninvasively. Its clinical significance lies in the possibility of noninvasive risk stratification and in guidance and evaluation of therapy.

New insights regarding the atrial flutter reentrant circuit : studies in the canine sterile pericarditis model.

Background-We studied atrial activation during induced atrial flutter in the canine sterile pericarditis model to test the hypothesis that the atrial flutter reentrant circuit includes a septal component. Methods and Results-We studied 10 episodes of induced, sustained (>5 minutes) atrial flutter in 9 dogs. In all episodes, the reentrant circuit included a septal component. In 6 episodes, there were 2 reentrant circuits, one in the right atrial free wall and the second involving the atrial septum, Bachmann's bundle, and the right atrial free wall; both circuits shared a pathway in the right atrial free wall (figure-of-eight). The direction (superior or inferior) of the septal wave front of the second circuit correlated with the direction (clockwise or counterclockwise, respectively) of the right atrial free-wall circuit. A line of functional block in the right atrial free wall was part of both reentrant circuits. In the other 4 atrial flutter episodes, only 1 reentrant circuit was present, with activation in an inferior-to-superior direction in the septum and a superior-to-inferior direction in the right atrial free wall in 2 episodes and in the opposite direction in the other 2 episodes. In all atrial flutter episodes, the flutter wave polarity in ECG lead II was determined by the direction of activation in the left atrium; polarity was positive when the direction was superior to inferior and negative when the direction was inferior to superior. Conclusions-In this model of atrial flutter, the reentrant circuit (1) always included a septal component, (2) did not always require a right atrial free-wall reentrant circuit, (3) demonstrated figure-of-eight reentry when a reentrant circuit was present in the right atrial free wall, and (4) was associated with a line of functional block in the right atrial free wall.

The P wave and P-R interval. Effects of the site of origin of atrial depolarization.

The atria of 37 patients were paced from selected sites during cardiac surgery. When the atria were paced from endocardial sites low in the right atrium, the P waves in ECG leads II, III, and aVF were shown to be either negative, biphasic, or positive, depending on the site paced. When the endocardial sites were paced, the P-R intervals were, almost without exception, less than 0.12 sec. When those endocardial sites closest to the A-V junction were paced, the P-R intervals were always less than 0.12 sec. When the atria were paced, from the epicardial sites, the P-R intervals were always greater than 0.12 sec. Negative P waves in ECG leads II, III, and aVF were recorded when the atria were paced from the postero-inferior left atrium and the caudal right atrium. The P-R interval did not always reflect the initial period of atrial activation because an isoelectric interval, generally of 0.01 to 0.025 sec, was frequently present between the onset of atrial stimulation and the first clear evidence of the P wave in the ECG. The implications of these results are discussed.

Importance of atrial flutter isthmus in postoperative intra-atrial reentrant tachycardia.

BACKGROUND: In survivors of congenital heart surgery, intra-atrial reentrant tachycardia (IART) often develops. Previous reports have emphasized the atriotomy scar as the central barrier around which a reentrant circuit may rotate but have not systematically evaluated the atrial flutter isthmus in such patients. We sought to determine the role of the atrial flutter isthmus in supporting IART in a group of postoperative patients with congenital heart disease. METHODS AND RESULTS: Nineteen postoperative patients with IART underwent electrophysiological studies with entrainment mapping of the atrial flutter isthmus for determining postpacing intervals. Radiofrequency ablation was performed at the identified isthmus in an effort to create a complete line of block. Twenty-one IARTs were identified in 19 patients, with a mean tachycardia cycle length of 293+/-73 ms. The atrial flutter isthmus was part of the circuit in 15 of 21 (71. 4%). In the remaining 6 of 21, the ablation target zone was at sites near atrial incisions or suture lines. Ablation was successful in 19 of 21 (90.4%) IARTs and in 14 of 15 (93.3%) cases at the atrial flutter isthmus. CONCLUSIONS: In most of our postoperative patients, the atrial flutter isthmus was part of the reentrant circuit. The fact that the atrial flutter isthmus is vulnerable to ablation suggests that whenever IART occurs late after repair of a congenital heart defect, the atrial flutter isthmus should be evaluated. These data support the theory that some form of conduction block between the vena cava is essential for the establishment of a stable substrate for the atrial flutter reentrant circuit.

Effects of N-acetylprocainamide on experimental atrial flutter and atrial electrophysiologic properties in conscious dogs with sterile pericarditis: comparison with the effects of quinidine.

N-acetylprocainamide (NAPA) is said to have class III antiarrhythmic drug properties. The effects of NAPA (25 mg/kg intravenously) on sustained, stable, reentrant atrial flutter induced in 12 conscious dogs using a sterile pericarditis model were studied and compared with the effects of quinidine (5 mg/kg intravenously) given on a different day in 10 of the same 12 dogs. The effects of these drugs on atrial excitability, the atrial effective refractory period and intraatrial conduction time measured during rapid atrial pacing performed during sinus rhythm were also compared. The mean NAPA and quinidine serum levels were 17.7 and 7.1 micrograms/ml, respectively. Both NAPA and quinidine immediately prolonged the atrial flutter cycle length in all dogs, from 118 +/- 15 to 141 +/- 18 ms and from 119 +/- 17 to 153 +/- 21 ms, respectively (both p less than 0.001), and then terminated atrial flutter in 11 of the 12 NAPA studies and in 6 of the 10 quinidine studies. Neither drug affected atrial excitability. Both NAPA and quinidine increased the atrial effective refractory period significantly, from 138 +/- 17 to 168 +/- 20 ms (p less than 0.001) and from 136 +/- 14 to 148 +/- 16 ms (p less than 0.01), respectively. NAPA did not change intraatrial conduction time measured during atrial pacing at 150 beats/min, but during atrial pacing at 300 beats/min, it prolonged it from 51 +/- 9 to 54 +/- 10 ms (p less than 0.05), and at 400 beats/min, from 52 +/- 10 to 64 +/- 13 ms (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Spontaneous onset of type I atrial flutter in patients.

OBJECTIVES: This study sought to characterize the spontaneous onset of atrial flutter in patients. BACKGROUND: Temporary epicardial electrodes are routinely placed on the atria of patients at the time of open heart surgery and brought out through the anterior chest wall for potential diagnostic and therapeutic use in the postoperative period. We utilized these electrodes to study the spontaneous onset of type 1 atrial flutter in 16 patients in the postoperative period after open heart surgery. METHODS: Twenty-seven episodes of the spontaneous onset of type I atrial flutter from sinus rhythm were studied in these 16 patients by recording bipolar atrial electrograms simultaneously with at least one electrocardiographic lead during each episode. RESULTS: In all 27 episodes, the onset of type I atrial flutter was through a transitional rhythm of variable duration (mean 9.3 s) precipitated by a premature atrial beat. In 21 episodes, the transitional rhythm was atrial fibrillation; in 3 episodes it was type II atrial flutter that appeared to generate atrial fibrillation; and in 3 episodes it was a brief (3 to 6 beats), rapid, irregular arrhythmia. CONCLUSIONS: Type I atrial flutter does not start immediately after a premature atrial beat. Rather, it starts after a transitional rhythm that is usually atrial fibrillation. Extrapolating from mapping studies of the onset of atrial flutter in the canine pericarditis model, we suggest that a transitional rhythm is required for the initiation of type I atrial flutter because during that rhythm, the requisites for development of the atrial flutter reentry circuit evolve.

Transient entrainment and interruption of atrioventricular node tachycardia.

The possibility of transiently entraining and interrupting the common type of atrioventricular (AV) node tachycardia (anterograde slow, retrograde fast AV node pathway) was studied using atrial and ventricular pacing in 18 patients with paroxysmal AV node tachycardia. Transient entrainment occurred in all patients. During atrial pacing, localized block in the AV node for one beat followed by anterograde conduction over the fast pathway was observed in three patients. During ventricular pacing, localized block for one beat followed by retrograde conduction over the slow pathway was not observed in any patient. Neither atrial nor ventricular fusion beats were observed during entrainment. These observations indicate in a way not previously shown that reentry involving two functionally dissociated pathways in the AV node is the underlying mechanism of paroxysmal AV node tachycardia. The inability to demonstrate atrial or ventricular fusion beats during entrainment suggests a true intranodal location of the reentrant circuit. Finally, the ability to transiently entrain intranodal tachycardia demonstrates that this electrophysiologic phenomenon is not exclusively limited to macroreentrant circuits.

Onset of induced atrial flutter in the canine pericarditis model.

To test the hypothesis that induced atrial flutter evolves from a transitional rhythm, the onset of 99 episodes of induced atrial flutter (mean cycle length 135 +/- 18 ms) lasting greater than 5 min in 40 dogs with sterile pericarditis was first characterized. In 85 (86%) of the 99 episodes, atrial flutter was preceded by a brief period (mean 1.4 +/- 0.9 s, range 0.4 to 42) of atrial fibrillation. Then, in 11 open chest studies, atrial electrograms were recorded simultaneously from 95 pairs of right atrial electrodes during the onset of 18 episodes of induced atrial flutter (mean cycle length 136 +/- 16 ms). Atrial flutter was induced by a train of eight paced atrial beats, followed by one or two premature atrial beats (7 episodes) or rapid atrial pacing (11 episodes). A short period of atrial fibrillation (mean cycle length 110 +/- 7 ms) induced by atrial pacing activated the right atrium through wave fronts, which produced a localized area of slow conduction. Then unidirectional conduction block of the wave front occurred for one beat in all or a portion of the area of slow conduction. This permitted the unblocked wave front to turn around an area of functional block and return through the area of slow conduction that had developed the unidirectional conduction block, thereby initiating the reentrant circuit. The location of the unidirectional block relative to the direction of the circulating wave fronts determined whether the circus movement was clockwise or counterclockwise. The area of slow conduction and unidirectional conduction block occurred where the wave front crossed perpendicular to the orientation of the atrial muscle fibers, suggesting a role for anisotropic conduction. These areas included the high right atrial portion of the sulcus terminalis (10 episodes), the low right atrial portion of the sulcus terminalis (4 episodes) and the pectinate muscle region (4 episodes). It is concluded that the development of a localized area of slow conduction in the right atrium followed by unidirectional conduction block in this area produced during a short period of atrial fibrillation or rapid atrial pacing is necessary for atrial flutter to occur in this model.

Characterization of double potentials in a functionally determined reentrant circuit. Multiplexing studies during interruption of atrial flutter in the canine pericarditis model.

OBJECTIVES: We tested the hypothesis that double potentials recorded during atrial flutter in a functionally determined reentrant circuit reflect activation of the reentrant wave front around an area of functional conduction block. BACKGROUND: The center of the atrial flutter reentrant circuit in the sterile pericarditis canine model is characterized by double potentials. METHODS: We studied 11 episodes of atrial flutter in eight dogs during interruption of atrial flutter while pacing the atria. A multielectrode mapping system was used to record simultaneously from 190 electrodes on the right atrium (location of reentry). RESULTS: Interruption of atrial flutter occurred when the orthodromic wave front from the pacing impulse blocked in an area of slow conduction in the reentrant circuit. The response of the double potential with interruption of atrial flutter depended on the location of the recording site relative to this area of block. Two types of response were seen. When the double potential was recorded orthodromically distal to this area of block, interruption of atrial flutter was associated with disappearance of the second deflection, and continued pacing after interruption of atrial flutter was not associated with reappearance of the second potential. When the double potential was recorded at a site orthodromically proximal to the area of block, interruption of atrial flutter was not associated with disappearance of the second potential, and when rapid atrial pacing was continued, the double potential remained despite disappearance of the atrial flutter reentrant circuit. CONCLUSIONS: Double potentials represent functional conduction block in the center of the reentrant circuit, with each deflection of the double potential reflecting activation on either side of the area of functional block. The data also demonstrate that double potentials are not limited to a reentrant circuit, as they were recorded on either side of an area of block in the absence of such a circuit.

Demonstration of an area of slow conduction in human atrial flutter.

Ten patients with chronic atrial flutter were studied prospectively using electrophysiologic mapping and pacing techniques to assess the mechanism of atrial flutter and the presence of an area of slow conduction in the atria. Electrograms recorded from greater than or equal to 30 right atrial sites for each patient during atrial flutter demonstrated that right atrial free wall activation was craniocaudal and that the interatrial septum activation was caudocranial, consistent with a reentrant circuit involving the right atrium. In six patients, slow conduction occurred during atrial flutter in the inferior right atrium and was spatially associated with fractionated electrographic recordings. In the other four patients, a "missing" interval of electrical activity occurred in the inferior right atrium for an average of 40% of the atrial flutter cycle. Transient entrainment criteria were demonstrated in each patient during rapid high right atrial pacing. The mean activation time from the high right atrial pacing site to the coronary sinus (inferior left atrial) recording site was long (228 ms) and consistent with activation through an area of slow conduction. During rapid pacing of atrial flutter from the coronary sinus site, no transient entrainment criteria could be demonstrated. The mean activation time from the coronary sinus pacing site to the high right atrial recording site was relatively short (134 ms) and consistent with orthodromic activation of the high right atrium not through an area of slow conduction. High right atrial pacing during sinus rhythm at rates similar to atrial flutter demonstrated a short activation time to the coronary sinus and low right atrial sites (mean 169 and 88 ms, respectively), indicating activation that did not traverse an area of slow conduction. Coronary sinus pacing during sinus rhythm demonstrated the same phenomena. Low right atrial electrograms recorded during sinus rhythm and during rapid pacing of sinus rhythm were not fractionated, although they were during atrial flutter. Thus, atrial mapping and pacing data were complementary, indicating that human atrial flutter in the patients studied was generated by a reentrant circuit in the right atrium, with an area of slow conduction in the low right atrium present only during atrial flutter.

Characterization of double potentials in human atrial flutter: studies during transient entrainment.

Double potentials, defined as atrial electrograms with two discrete deflections per beat separated by an isoelectric interval or a low amplitude baseline, have been observed during right atrial endocardial mapping of human atrial flutter. In this study, bipolar atrial electrograms were recorded during atrial flutter (mean cycle length 235 +/- 27 ms [+/- SEM]) from the high right atrium, the His bundle region, the coronary sinus and at least 30 right atrial endocardial mapping sites in 10 patients. Double potentials were recorded from the right atrium in all patients during atrial flutter. Double potentials were evaluated during transient entrainment of atrial flutter by rapid high right atrial pacing in 5 of the 10 patients. In four of these five patients during such transient entrainment 1) one deflection of the double potential was captured with a relatively short activation time (mean interval 89 +/- 45 ms) and the other deflection was captured with a relatively long activation time (mean interval 233 +/- 24 ms), producing a paradoxical decrease in the short interdeflection interval from a mean of 75 +/- 20 ms to a mean of 59 +/- 24 ms; and 2) the configuration of the double potential remained similar to that observed during spontaneous atrial flutter. On pacing termination 1) the two double potential deflections were found to be associated with two different atrial flutter complexes in the electrocardiogram (ECG); 2) the previous double potential deflection relation resumed; and 3) when sinus rhythm was present, the double potentials were replaced by a broad, low amplitude electrogram recording at the same site.(ABSTRACT TRUNCATED AT 250 WORDS)

A new animal model of atrial flutter.

A new, simple and reliable model of atrial flutter utilizing postpericardiotomy pericarditis was developed in the dog. Using a sterile technique, the pericardium was opened by way of a right thoracotomy, Teflon-coated, stainless steel wire electrodes were fixed to three selected sites on the atria and exteriorized, the atrial surfaces were generously dusted with talcum powder and a single layer of gauze was placed on the free left and right atrial walls. The dogs were allowed to recover. Subsequently, the inducibility of atrial flutter and selected electrophysiologic properties of the atria were determined by daily programmed atrial stimulation studies with the dogs in the conscious, nonsedated state. Atrial flutter could be induced in 23 of 25 dogs initially studied. It was sustained (that is, lasting greater than or equal to 5 min) in 17 of the 23. Neither atrial excitability, intraatrial conduction time nor atrial refractoriness determined by pacing and recording from the three fixed sites predicted the inducibility of atrial flutter. One hundred thirty-nine episodes of atrial flutter induced in these 23 dogs were analyzed. The mean sustained atrial flutter cycle length was 131 +/- 20 ms (mean +/- SD) (range 100 to 170); the atrial flutter cycle length was 150 ms or more in 23 episodes, between 120 and 150 ms in 64 episodes and 120 ms or less in 52 episodes. In five dogs, the stability of the atrial flutter cycle length during sustained atrial flutter was studied and shown to be remarkably stable in all five until interrupted by rapid atrial pacing 35 to 95 minutes after its induction.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial activation sequence during atrial flutter in the canine pericarditis model and its effects on the polarity of the flutter wave in the electrocardiogram.

Stable atrial flutter induced in both conscious and open chest states was studied in 30 mongrel dogs after production of sterile pericarditis. During the conscious state studies, induced atrial flutter (mean cycle length 128 +/- 15 ms) was always sustained greater than 15 min and was stable. Three types of flutter wave polarity were noted in electrocardiogram (ECG) lead II: positive in 16 dogs, negative in 3 and flat or slightly positive in 11. Sequential site atrial mapping during atrial flutter (mean cycle length 133 +/- 18 ms) in the open chest state showed either clockwise (18 dogs) or counterclockwise (12 dogs) circus movement in the right atrium. In 19 of 30 dogs, the circus movement clearly did not require any naturally existing anatomic obstacle; in 11, the orifice of the superior vena cava probably was also involved. Double potentials were recorded from the center of the reentrant circuit during atrial flutter, and fractionated electrograms were recorded from a pivot point of the reentrant wave front. A positive flutter wave in ECG lead II (12 dogs with counterclockwise circus movement) was associated with early activation of the Bachmann's bundle region compared with the posteroinferior left atrium and activation of the left atrium mainly in a superoinferior direction. A negative flutter was associated with the early activation of the posteroinferior left atrium compared with Bachmann's bundle and activation of a considerable portion of the left atrium in an inferosuperior direction. A flat or slightly positive flutter wave (14 of 18 with clockwise circus movement) was associated with activation of the left atrium almost simultaneously by two wave fronts coming from both these sites. In conclusion, atrial flutter in this dog model is due to circus movement in the right atrium, the center of which does not necessarily require an anatomic obstacle. Although atrial flutter is generated by circus movement in the right atrium, the flutter wave polarity in the ECG is determined primarily by the activation sequence of the left atrium.

Single site radiofrequency catheter ablation of atrial fibrillation: studies guided by simultaneous multisite mapping in the canine sterile pericarditis model.

OBJECTIVES: To test the hypothesis that when activation of Bachmann's bundle (BB) is critical to the unstable reentrant circuits that maintain atrial fibrillation (AF) in the sterile pericarditis canine model, a lesion in BB would prevent induction of stable AF. BACKGROUND: One mechanism of induced AF in this model is multiple unstable reentrant circuits, which frequently include BB as part of the reentrant pathway. METHODS: Simultaneous multisite mapping studies during AF and after ablation of BB were performed by recording (384 to 396 electrodes) from both atria and the atrial septum during six induced AF episodes in six dogs with sterile pericarditis. Activation maps of AF (mean duration, 24 +/- 28 min) during 12 consecutive 100-ms windows were analyzed. RESULTS: During AF, multiple unstable reentrant circuits (mean, 1.2 +/- 0.2 per window; range, 1 to 4) were observed, 68% involving BB. Nonactivation zones (mean duration, 57 +/- 16 ms in the right atrium and 53 +/- 23 ms in the left atrium) observed during AF were reactivated by a wave front most often coming from the atrial septum via BB (right atrium, 62%; left atrium, 67%). After successful radiofrequency catheter ablation of the midportion of BB, AF >5 s was not induced in all dogs. Mapping studies of transient AF (< or =5 s) induced after ablation showed neither reentrant circuits nor wave fronts activating the right atrium via BB. CONCLUSIONS: In this AF model, catheter ablation of BB terminates and prevents the induction of AF by preventing 1) formation of unstable reentrant circuits that involve BB, and 2) activation of the atrial-free walls after a nonactivation period.

Insights into the Electrophysiology Study Versus Electrocardiographic Monitoring Trial: its programmed stimulation protocol may introduce bias when assessing long-term antiarrhythmic drug therapy.

OBJECTIVES: We hypothesized that if the Electrophysiology Study Versus Electrocardiographic Monitoring (ESVEM) trial programmed stimulation protocol misclassified some drug trials as effective, then the misclassification rate would be proportionally greater for drugs other than sotalol. BACKGROUND: In the ESVEM trial, patients treated with sotalol had fewer arrhythmic recurrences than those treated with other antiarrhythmic drugs despite similar efficacy predictions during electrophysiologic testing. METHODS: We retrospectively compared the standard programmed stimulation protocol used at Case Western Reserve University, which used three extrastimuli during all follow-up studies, with the ESVEM protocol in 176 antiarrhythmic drug trials: sotalol (n = 54), procainamide (n = 73) and quinidine/mexiletine (n = 49). RESULTS: Predictions of efficacy were higher in the sotalol trials (14 of 54 standard, 20 of 54 ESVEM) than in procainamide trials (7 of 73 standard, 14 of 73 ESVEM) or quinidine/mexiletine trials (1 of 49 standard, 7 of 49 ESVEM). Thus, the two protocols classified 19 of 176 trials differently: not effective by the standard protocol but effective by the ESVEM trial. Discordant predictions of drug efficacy constituted a smaller proportion of ESVEM protocol efficacy predictions for sotalol (6 [30%] of 20) than for the other drugs (13 [62%] of 21, p < or = 0.05). CONCLUSIONS: In the present study, the ESVEM programmed stimulation protocol predicted efficacy more often than the standard protocol. Discordant predictions represented a smaller portion of efficacy predictions for sotalol than for the other drugs. Thus, in the ESVEM trial, the superior long-term follow-up observed in patients assigned to sotalol may have been an artifact of the stimulation protocol utilized by the ESVEM investigators.

Demonstration of the mechanism of transient entrainment and interruption of ventricular tachycardia with rapid atrial pacing.

An unusual case is presented in which ventricular tachycardia at a rate of 141 beats/min was transiently entrained by rapid atrial pacing at rates of 150, 155 and 160 beats/min, and was interrupted by rapid atrial pacing at a rate of 165 beats/min. During each period of transient entrainment, constant ventricular fusion beats were present except for the last entrained beat, and progressive ventricular fusion (different fusion QRS complexes) was demonstrated when comparing QRS complex configurations during transient entrainment at each pacing rate. Interruption of the ventricular tachycardia was associated with localized conduction block to the right ventricular recording site, followed by activation of that site from a different direction and with a shorter conduction time by the subsequent pacing impulse. These data clearly distinguish transient entrainment of a tachycardia from overdrive suppression of a tachycardia, and strongly suggest that reentry was the underlying mechanism of the ventricular tachycardia.

Use of procainamide with rapid atrial pacing for successful conversion of atrial flutter to sinus rhythm.

Rapid atrial pacing is a useful technique and often the therapy of choice to terminate atrial flutter in patients. However, interruption of atrial flutter by rapid atrial pacing may not always produce sinus rhythm, but rather may result in atrial fibrillation. Twelve patients with spontaneous atrial flutter that had been present for greater than 24 h were studied to assess the efficacy of atrial pacing, alone and in combination with procainamide, to convert atrial flutter to normal sinus rhythm. Rapid atrial pacing for greater than or equal to 15 s from selected atrial sites at selected pacing rates were performed during atrial flutter. The initial pacing rate was always at a cycle length 10 ms shorter than the atrial flutter cycle length. If atrial flutter persisted after cessation of pacing, it was repeated at progressively shorter cycle lengths until either a rate of 400 beats/min was achieved or atrial fibrillation was induced. In two patients, atrial flutter was converted to sinus rhythm with pacing alone. Three patients developed sustained atrial fibrillation as a result of the rapid atrial pacing, this rhythm ultimately reverting back to atrial flutter in two. Ten patients received procainamide and 9 of the 10 had lengthening of the atrial flutter cycle length by a mean of 68 ms (1 patient continued to have atrial fibrillation). Then, using the same atrial pacing protocol, high right atrial pacing alone at a mean cycle length of 227 ms interrupted atrial flutter in all these patients, returning their rhythm to sinus rhythm. It is concluded that intravenous procainamide effectively augments the efficacy of rapid atrial pacing to convert atrial flutter to sinus rhythm.