Spontaneous reinitiation of atrial fibrillation following transvenous atrial defibrillation

Spontaneous reinitiation of atrial fibrillation (AF) has not been systematically looked at in patients undergoing transvenous AF. This study involved 11 patients, the mean age 60 +/- 8 years, 3 male and 8 female, in whom transvenous atrial defibrillation successfully converted AF to sinus rhythm. Eight patients had paroxysmal AF and three patients had chronic persistent AF for 4 weeks or more. Four patients were taking antiarrhythmic medications at the time of testing. Multipolar transvenous catheters were positioned inside the coronary sinus, right atrium, and the right ventricle. Atrial defibrillation testing was performed using the METRIX atrial defibrillation system in nine patients and the Ventritex HVSO2 in the remaining two patients. A total of 64 therapeutic shocks (range 3-11) were delivered in the 11 patients, and 31 of these successfully converted AF to sinus rhythm. In four patients spontaneous AF was reinitiated following 12 successful transvenous atrial defibrillation episodes. The mean time to reinitiation of AF following shock delivery and restoration of sinus rhythm was 8.26 +/- 5.25 seconds, range 1.8-19.9 seconds. All 12 episodes of spontaneous AF were preceded by a spontaneous premature atrial complex. The coupling interval of the premature atrial complexes was 443 +/- 43 ms, range 390-510 ms. None of the patients taking antiarrhythmic medications or those demonstrating no premature atrial complexes had spontaneous reinitiation of AF. In conclusion, spontaneous reinitiation of AF can occur in a significant proportion of patients with AF undergoing transvenous atrial defibrillation. This phenomenon is preceded by the occurrence of atrial premature complex. Findings of this study may have significant clinical implications.     

Effects of left atrial dilatation on the endocardial atrial defibrillation threshold: a study in an ovine model of pacing induced dilated cardiomyopathy

Left atrial (LA) dilation is a common finding in patients with chronic atrial fibrillation (AF). Progressive dilatation may alter the atrial defibrillation threshold (ADFT). In our study, epicardial electrodes were implanted on the LA free wall and right ventricular apex of eight adult sheep. Large surface area, coiled endocardial electrodes were positioned in the coronary sinus and right atrium (RA). LA dilatation was induced by rapid ventricular pacing (190 beats/min) for 6 weeks and echocardiographically assessed weekly along with the ADFT (under propofol anesthesia). LA effective refractory period (ERP) was measured every 2-3 days using a standard extra stimulus technique and 400 ms drive. The AF cycle length (AFCL) was assessed from LA electrograms. During the 6 weeks of pacing the mean LA area increased from 6.1 +/- 1.5 to 21.3 +/- 2.4 cm2. There were no significant changes in the mean ADFT (122 +/- 15 V), circuit impedance (46 +/- 5 omega), or LA AFCL (136 +/- 23 ms). There was a significant increase in the mean LA ERP (106 +/- 10 ms at day 0, and 120 +/- 13 ms at day 42 of pacing). In this study, using chronically implanted defibrillation leads, the minimal energy requirements for successful AF were not significantly altered by ongoing left atrial dilatation. This finding is a further endorsement of the efficiency of the coronary sinus/RA shock vector. Furthermore, the apparent stability of the AF present may be a further indication of a link between the type of AF and the ADFT.     

Tachycardia-induced change of atrial refractory period in humans: rate dependency and effects of antiarrhythmic drugs

BACKGROUND: Atrial fibrillation (AF) has been shown to shorten the atrial effective refractory period (ERP) and make the atrium more vulnerable to AF. This study investigated the effect of atrial rate and antiarrhythmic drugs on ERP shortening induced by tachycardia. METHODS AND RESULTS: Seventy adult patients without structural heart disease were included. For the first part of the study, right atrial ERP was measured with a drive cycle length of 500 ms before and after 10 minutes of rapid atrial pacing using five pacing cycle lengths (450, 400, 350, 300, and 250 ms) in 10 patients. For the second part of the study, the remaining 60 patients were included to study the effects of antiarrhythmic drugs on changes in atrial ERP induced by AF. Atrial ERP was measured with a drive cycle of 500 ms before and after an episode of pacing-induced AF. After the patients were randomized to receive one of six antiarrhythmic drugs (procainamide, propafenone, propranolol, dl-sotalol, amiodarone, and verapamil), atrial ERP was measured before and after another episode of pacing-induced AF. In the first part of the study, atrial ERP shortened significantly after 10 minutes of rapid atrial pacing, and the degree of shortening was correlated with pacing cycle length. The second part of the study showed that atrial ERP shortened after conversion of AF (172+/-15 versus 202+/-14 ms, P<0.0001) and that ERP shortening was attenuated after verapamil infusion (-4.6+/-1.2% versus -15.1+/-3.4%, P<0.001) but was unchanged after infusion of the other antiarrhythmic drugs. Furthermore, all of these antiarrhythmic drugs could decrease the incidence and duration of secondary AF. CONCLUSIONS: The atrial ERP shortening induced by tachycardia was a rate-dependent response. Verapamil, but not other antiarrhythmic drugs, could markedly attenuate this effect. However, verapamil and the other drugs could decrease the incidence and duration of secondary AF.     

Dependency on atrial electrophysiological properties of appearance of paroxysmal atrial fibrillation in patients with Wolff-Parkinson-White syndrome: evidence from atrial vulnerability before and after radiofrequency catheter ablation and surgical cryoablation

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

Coronary sinus pacing prevents induction of atrial fibrillation

BACKGROUND: Atrial fibrillation (AF) is due to reentry, and its incidence has been shown to decrease after dual-site atrial or biatrial pacing. We investigated whether a simpler pacing approach via the distal coronary sinus (CSd) could eliminate AF inducibility by high right atrial (HRA) extrastimuli (APDs). We based our hypothesis on our previous observation that AF inducibility by HRA APDs was associated with conduction delays to the posterior triangle of Koch, whereas AF was never induced with CSd APDs, which were associated with minimal intra-atrial conduction delays. METHODS AND RESULTS: Programmed electrical stimulation was performed from the high right atrium and CSd, and bipolar recordings were obtained from the high right atrium, His bundle, posterior triangle of Koch, and coronary sinus. In 13 patients (age, 44+/-18 years), AF was reproducibly induced with a critically timed HRA APD (220+/-22 ms) delivered during HRA pacing. AF was not induced in any of the patients when HRA APDs were delivered during CSd pacing at the same critical coupling intervals. Coronary sinus APDs delivered during HRA pacing also were not associated with AF induction. The APD coupling interval measured at the posterior triangle of Koch during CSd pacing was significantly prolonged compared with the one measured during HRA pacing and AF induction (381+/-58 versus 263+/-37 ms; P<.0001). CONCLUSIONS: We propose that CSd pacing suppresses the propensity of HRA APDs to induce AF by limiting their prematurity at the posterior triangle of Koch and not allowing local conduction delay and local reentry to occur.     

Atrial vulnerability in patients with paroxysmal "lone" atrial fibrillation

Little is known about the electrophysiological properties of the atrium predisposing to paroxysmal atrial fibrillation (AF), especially in patients without structural heart disease. This study was conducted to analyze intraatrial conduction, atrial refractoriness, and arrhythmia inducibility in patients with lone paroxysmal AF. An electrophysiological study was performed in 24 patients with a documented history of lone paroxysmal AF but in sinus rhythm at the time of the electrophysiological study. Twelve patients without any history of atrial arrhythmias served as controls. The patients with lone paroxysmal AF showed a significant prolonged local conduction time S1A1 (70 +/- 21 ms vs 36 +/- 12 ms, P < 0.0001), a lack of rate adaptation of the functional refractory period (FRP changes/cycle length changes < 10% in 15 of 24 patients with lone paroxysmal AF vs 1/12 controls, P = 0.002) and a higher incidence of inducible AF with only one extrastimulus (13/24 vs 0/12, P = 0.0014). The total P wave duration in the surface ECG (89 +/- 14 ms vs 83 +/- 8 ms, P = 0.15), the intraatrial conduction time (36 +/- 14 ms vs 28 +/- 8 ms, P = 0.07), the presence of a fragmented atrial electrogram (16/24 vs 7/12, P = 0.62), the absolute value of the effective refractory period (204 +/- 28 ms vs 212 +/- 23 ms, P = 0.42), and the vulnerability index (3.0 +/- 1.5 vs 3.6 +/- 1.5, P = 0.26) were not statistically different between the two groups. The presence of a prolonged (> 50 ms) S1A1 and/or the presence of a lack of rate adaptation of the FRP and/or the presence of inducible AF identified patients with spontaneous lone paroxysmal AF with a sensitivity of 96%, a specificity of 67%, a positive predictive value of 85%, and a negative predictive value of 89%. In patients with lone paroxysmal AF, the electrophysiological study using conventional techniques allows not only to detect AF inducibility using a nonaggressive protocol, but also to reveal several electrophysiological abnormalities related to the atrial substrate itself. This atrial vulnerability may explain the high incidence of recurrences in patients with lone paroxysmal AF.     

Effects of the novel antiarrhythmic agent azimilide on experimental atrial fibrillation and atrial electrophysiologic properties

OBJECTIVES: This study was designed to evaluate how the atrial electrophysiological and antiarrhythmic effects of azimilide compare with those of the specific rapid delayed rectifier (IKr) blocker dofetilide. BACKGROUND: Azimilide, a new class III drug, was initially believed to be a highly selective blocker of the slow delayed rectifier (IKs), but recent studies suggest that azimilide potently blocks IKr. Thus, it has been suggested that azimilide's in vivo effects may simply be due to IKr blockade. METHODS: Dose regimens producing stable effects over time were developed, and two dose levels of azimilide (10 and then 20 mg/kg) or dofetilide (0.08 and then 0.16 mg/kg) were administered to morphine/chloralose-anesthetized dogs during sustained vagal atrial fibrillation (AF). Epicardial mapping was used to measure conduction velocity and AF cycle length. RESULTS: Azimilide terminated AF in 13/14 dogs (93%), while dofetilide terminated AF in 6/12 (50%, P < 0.05). While dofetilide had strong reverse use-dependent effects on atrial ERP (e.g. at lower doses, dofetilide increased ERP by 51 +/- 3% at a basic cycle length, BCL, of 400 ms and by 17 +/- 3% at a BCL of 200 ms), azimilide's effects on ERP were rate-independent (ERP increased at lower dose by 38 +/- 6%, BCL 400 ms; 35 +/- 10%, BCL 200 ms). Neither drug affected conduction. CONCLUSIONS: Azimilide is effective against experimental AF, and increases ERP with a frequency dependence different from the IKr blocker dofetilide, suggesting that azimilide's actions on atrial tissue cannot be attributed exclusively to IKr block, and that effects on other currents (such as IKs) are likely to be important.     

Atrial mapping and radiofrequency catheter ablation in patients with idiopathic atrial fibrillation. Electrophysiological findings and ablation results

BACKGROUND: Knowledge of the electrophysiological substrates and the cure of atrial fibrillation (AF) is still unsatisfactory. The goal of this study was to evaluate the electrophysiological features of idiopathic AF and their relationship to the results of radiofrequency (RF) catheter ablation of AF and the safety and effectiveness of this procedure. METHODS AND RESULTS: Sixteen patients with idiopathic AF underwent atrial mapping during AF and then RF ablation in the right atrium. The atrial activation was simultaneously recorded in four regions in the right atrium: high lateral wall (HL), low lateral wall (LL), high septum (HS), and low septum (LS) and in the left atrium through the coronary sinus (CS). In these regions, we evaluated the atrial fibrillation intervals (FF) and the morphological features of AF recordings by Wells' classification. No complications occurred during RF ablation. Of the 16 patients, 9 (56%) without AF recurrences during the follow-up (11 +/- 4 months) were considered successfully ablated. These patients showed a significantly shorter mean FF interval in the HS and the LS (122 +/- 32 and 126 +/- 28 ms, respectively), than in the HL and LL (159 +/- 24 and 156 +/- 28 ms, respectively). Moreover, the septum had more irregular electrical activity with greater beat-to-beat changes in FF and a higher prevalence of type III AF than the lateral region. The CS had similar behavior to the septum. Conversely, patients with unsuccessful ablation had an irregular atrial activity in the lateral wall, septum, and CS with no significant differences between the different sites. CONCLUSIONS: Right atrial endocardial catheter ablation of AF is a safe procedure and may be effective in some patients with idiopathic AF. The atrial mapping during AF showed a more disorganized right atrial activation in the septum than in the lateral wall in patients with successful ablation.     

Importance of refractoriness heterogeneity in the enhanced vulnerability to atrial fibrillation induction caused by tachycardia-induced atrial electrical remodeling

BACKGROUND: Rapid atrial activation causes electrical remodeling that promotes the occurrence and the maintenance of atrial fibrillation (AF). Although remodeling has been shown to alter electrophysiological variables, the spatial uniformity of these changes is unknown. METHODS AND RESULTS: Dogs subjected to rapid atrial pacing (400 bpm) for 24 hours (n=12) were compared with sham-operated dogs (instrumented but not paced, n=12). Epicardial mapping (240 bipolar electrodes) and extrastimulation at a large number of sites (mean+/-SEM, 66+/-4 per dog) were used to evaluate atrial activation and the heterogeneity of the effective refractory period (ERP), respectively. Rapid pacing increased both the percentage of sites at which AF could be induced by single premature stimuli (from 2.6+/-0.9% to 11.8+/-2.8%, P=0.007) and AF duration (from 39+/-28 to 146+/-49 seconds, P=0.03). Atrial tachycardia decreased atrial ERP (from 120+/-4 to 103+/-2 ms, P=0.003), increased the coefficient of variation of ERP (from 14.9+/-0.9% to 20.7+/-0.9%, P<0.0001), and accelerated conduction velocity (from 91+/-2 to 108+/-3 cm/s, P=0.0004), with no change in the wavelength. The increase in ERP heterogeneity was due both to interregional differences in the extent of ERP remodeling and to increased intersite variability within regions. Stepwise multilinear regression indicated that ERP heterogeneity was an independent determinant of the inducibility (P<0.0001) and duration (P<0.0001) of AF, whereas ERP per se and wavelength were not significant determinants. Combined mapping of AF induction and atrial ERP showed that premature extrastimuli induced AF at sites with short ERP by causing local conduction slowing and/or block in adjacent zones with longer ERP values. CONCLUSIONS: Atrial tachycardia causes nonuniform remodeling of atrial refractoriness that plays an important role in increasing atrial vulnerability to AF induction and the duration of induced AF.     

Electrophysiological characteristics of the human atria after cardioversion of persistent atrial fibrillation

BACKGROUND: In animal models, induced atrial fibrillation shortens the atrial effective refractory period (ERP) and reverses its physiological adaptation to rate. It is not clear whether this process, known as "electrical remodeling," occurs in humans. METHODS AND RESULTS: We determined the ERPs, at 5 pacing cycle lengths (300 to 700 ms) and in 5 right atrial sites, after internal cardioversion of chronic atrial fibrillation in 25 patients (14 in pharmacological washout and 11 on amiodarone). The ERPs were 195.5+/-18.8 ms in the washout and 206.3+/-17.9 ms in the amiodarone patients (P<0.0001). ERPs were closely correlated with the stimulation rates (r=0.95 in the washout and r=0.94 in the amiodarone group), and slope values indicating a normal (>/=0.07) or nearly normal (0.05 to 0.06) adaptation of ERP to rate were found in 77% of the 84 paced sites. The mean ERP was shorter in the lateral wall (198.1+/-17.9 ms) than in the atrial roof (203.3+/-21.5 ms) and in the septum (210.5+/-20.0 ms) (P<0.03). After 4 weeks of sinus rhythm, the mean ERP, determined again in 8 patients (4 in wash-out and 4 on amiodarone), was significantly increased compared with the basal study (221. 4+/-21.4 versus 197.8+/-18.3 ms, P<0.0001). CONCLUSIONS: After cardioversion of chronic atrial fibrillation, (1) atrial ERP adaptation to rate was normal or nearly normal in the majority of the cases, (2) a significant dispersion of refractoriness between different right atrial sites was present, and (3) ERPs were significantly increased after 4 weeks of sinus rhythm in both washout and amiodarone patients.     

Ventriculophasic modulation of atrioventricular nodal conduction in humans

BACKGROUND: Baroreceptor-mediated phasic changes in vagal tone have been hypothesized to cause ventriculophasic sinus arrhythmia (VPSA). The objectives of this study were to demonstrate ventriculophasic modulation of AV nodal conduction and to substantiate the role of the baroreflex on ventriculophasic AV nodal conduction (VPAVN) by pharmacological perturbation of parasympathetic tone. METHODS AND RESULTS: Twelve patients with infra-Hisian second-degree heart block and VPSA were studied. Incremental atrial pacing was performed until AV nodal Wenckebach block at baseline, after phenylephrine infusion, and after atropine. AV nodal conduction curves were constructed for each phase and compared. At baseline, VPAVN was present in 9 of 12 patients on the steep portion of the AV nodal conduction curves. Phenylephrine increased systolic blood pressure from 149+/-33 to 177+/-22 mmHg (P<0.001) and sinus cycle length from 844+/-169 to 1010+/-190 ms (P<0.001) and shifted the AV nodal conduction curves up and to the right. Phenylephrine induced VPAVN in 2 of 3 patients in whom it was not present at baseline and in 11 of 12 total. Atropine abolished both VPSA and VPAVN in all patients. CONCLUSIONS: VPAVN was demonstrated in patients with infra-Hisian second-degree AV block. It was accentuated by phenylephrine and abolished by atropine, suggesting a baroreflex mechanism for VPSA and VPAVN.     

Effect of flecainide on atrial and ventricular refractoriness and conduction in patients with normal left ventricle. Implications for possible antiarrhythmic and proarrhythmic mechanisms

We studied the effects of intravenous flecainide (2 mg.kg-1) on atrial and ventricular refractoriness and conduction during sinus rhythm, induced atrial fibrillation and atrial pacing at rates of 100, 120 and 150 ppm, in 14 patients with normal left ventricle. Flecainide caused a significant increase in QRS duration during sinus rhythm (mean +/- SD: 87.2 +/- 8.4 ms vs 102.8 +/- 9.1 ms, P < 0.001), atrial fibrillation (87.8 +/- 10.0 ms vs 108.8 +/- 13.7 ms, P < 0.001) and at all paced rates. The duration of the atrial electrogram was significantly increased during sinus rhythm (54.9 +/- 13.2 ms vs 64.8 +/- 16.6 ms, P = 0.003) and at all pacing rates. The PA interval was also significantly prolonged, as was the pacing stimulus-to-atrial-electrogram interval at all pacing rates. There was increased QRS duration and atrial electrogram prolongation at higher pacing rates. Atrial refractoriness was prolonged during sinus rhythm (216.4 +/- 28.2 vs 228.6 +/- 36.1, P = 0.02), but not during atrial pacing at any rate. The QT interval, but not the JT interval or ventricular refractoriness, was significantly prolonged during sinus rhythm and at all pacing rates. Flecainide slows atrial conduction in a use dependent manner and increases atrial refractoriness during sinus rhythm but not during faster atrial pacing, thus not displaying a use-dependent effect. QRS duration is prolonged in a use-dependent manner without a commensurate increase in ventricular refractoriness. In the presence of rapidly conducted atrial fibrillation, which was not found to be slowed by flecainide, this effect may constitute a proarrhythmic mechanism even in patients with no apparent myocardial abnormality.     

Favorable effects of flecainide in transvenous internal cardioversion of atrial fibrillation

OBJECTIVES: The aim of the study was to evaluate the effects of intravenous (IV) flecainide on defibrillation energy requirements in patients treated with low-energy internal atrial cardioversion. BACKGROUND: Internal cardioversion of atrial fibrillation is becoming a more widely accepted therapy for acute episode termination and for implantable atrial defibrillators. METHODS: Twenty-four patients with atrial fibrillation (19 persistent, 5 paroxysmal) underwent elective transvenous cardioversion according to a step-up protocol. After successful conversion in a drug-free state, atrial fibrillation was induced by atrial pacing; IV flecainide (2 mg/kg) was administered and a second threshold was determined. In patients in whom cardioversion in a drug-free state failed notwithstanding a 400- to 550-V shock, a threshold determination was attempted after flecainide. RESULTS: Chronic persistent atrial fibrillation was converted in 13/19 (68%) patients at baseline and in 16/19 (84%) patients after flecainide. Paroxysmal atrial fibrillation was successfully cardioverted in all the patients. A favorable effect of flecainide was observed either in chronic persistent atrial fibrillation (13 patients) or in paroxysmal atrial fibrillation (5 patients) with significant reductions in energy requirements for effective defibrillation (persistent atrial fibrillation: 4.42+/-1.37 to 3.50+/-1.51 J, p < 0.005; paroxysmal atrial fibrillation: 1.68+/-0.29 to 0.84+/-0.26 J, p < 0.01). In 14 patients not requiring sedation, the favorable effects of flecainide on defibrillation threshold resulted in a significant reduction in the scores of shock-induced discomfort (3.71+/-0.83 vs. 4.29+/-0.61, p < 0.005). No ventricular proarrhythmia was observed for any shock. CONCLUSIONS: Intravenous flecainide reduces atrial defibrillation threshold in patients treated with low-energy internal atrial cardioversion. This reduction in threshold results in lower shock-induced discomfort. Additionally, flecainide may increase the procedure success rate in patients with chronic persistent atrial fibrillation.     

Role of autonomic reflexes in syncope associated with paroxysmal atrial fibrillation

OBJECTIVES: The purpose of this study was to evaluate the role of autonomic reflexes in the genesis of syncope associated with the onset of paroxysmal atrial fibrillation. BACKGROUND: Syncope associated with paroxysmal atrial fibrillation has been interpreted as an ominous finding predictive of rapid ventricular rates. However, various mechanisms may be involved when heart rate is not particularly high. METHODS: Forty patients (age 60 +/- 14 years, 20 men, 20 women) with syncope and atrial fibrillation were compared with atrial fibrillation without syncope. Carotid sinus massage and head-up tilt testing (at 60 degrees for 60 min at baseline and during isoproterenol infusion) were performed during sinus rhythm. A positive response was defined as the induction of syncope. Atrial fibrillation was also induced on a tilt table at 60 degrees by means of short bursts of atrial pacing. RESULTS: Results of carotid sinus massage were positive in 15 (37%) of 40 patients but in no control subjects (p = 0.002). Head-up tilt test findings were positive in 25 (66%) of 38 patients and in 2 (12%) of 16 control subjects (p = 0.0004). The induction of atrial fibrillation in the upright position elicited syncope in 16 (42%) of 38 patients but in none of 16 control subjects (p = 0.001). At the beginning of atrial fibrillation, systolic blood pressure was lower in patients than in control subjects (88 +/- 32 vs. 127 +/- 32 mm Hg), whereas mean heart rate was similar (142 +/- 35 vs. 134 +/- 25 beats/min). The correlation between heart rate and systolic blood pressure was weak (r = 0.35), and in five patients syncope occurred at a heart rate < or = 130 beats/min. At the time of syncope, heart rate decreased (-12 +/- 21 beats/min) in patients with induced syncope, whereas it remained unchanged in patients without induced syncope (+1 +/- 17 beats/min, p = 0.04) or slightly increased in control subjects (+9 +/- 21 beats/min, p = 0.009). CONCLUSIONS: Patients with syncope associated with paroxysmal atrial fibrillation are predisposed to an abnormal neural response during both sinus rhythm and arrhythmia. In some patients the onset of atrial fibrillation triggers vasovagal syncope.     

Radiofrequency catheter ablation in type I atrial flutter: preliminary experience of 10 cases

Common atrial flutter results from macroreentry in the right atrium. Catheter ablation of slow conduction, between tricuspid annulus and inferior vena cava (TA-IVC) or tricuspid annulus and coronary sinus ostium (TA-CS os) has been reported to terminate and prevent recurrence of this arrhythmia. We reported 10 consecutive patients, 7 men and 3 women, who underwent radiofrequency catheter ablation of common atrial flutter. The mean age was 59.4 +/- 11.2 years (range 42-82 years). During the paroxysmal atrial flutter, all patients had palpitation, 4 had dyspnea on exertion, 3 patients had syncope and 1 patient had presyncope. The mean duration of symptoms was 5.7 +/- 4.9 years (range 0.5-13 years). Two patients had dilated cardiomyopathy, 1 Ebstein's anomaly and 1 chronic obstructive pulmonary disease. Four patients (40%) had history of atrial fibrillation (AF) before ablation. The mean cycle length of atrial rhythm was 257.2 +/- 36.6 ms. Ablation was done by anatomical approach and could terminate arrhythmia in 9 patients (90%), 7 from TA-IVC, 2 from TA-CS os without major complication. The mean number of applications was 20.4 +/- 16.9 and turned atrial flutter to normal sinus rhythm in 13.5 +/- 10.7 seconds. Fluoroscopic and procedure times were 38.4 +/- 31.4 and 157.2 +/- 68.8 minutes, respectively. During the follow-up period of 24.0 +/- 28.7 weeks, 2 patients had recurrent atrial arrhythmia, 1 atrial fibrillation and 1 atrial flutter type I, giving the final success rate of 70 per cent. All patients who had recurrence or failure had a history of paroxysmal AF before ablation. In conclusion, radiofrequency catheter ablation in atrial flutter type I, using anatomical approach, is an effective treatment to terminate and prevent this arrhythmia in short term follow-up. It may be considered as an alternative treatment in patients with atrial flutter who were refractory to antiarrhythmic agents.     

Electrocardiographic and clinical predictors of torsades de pointes induced by almokalant infusion in patients with chronic atrial fibrillation or flutter: a prospective study

The aim of this study was to identify predictors of torsades de pointes (TdP) in patients with atrial fibrillation (AF) or flutter exposed to the Class III antiarrhythmic drug almokalant. TdP can be caused by drugs that prolong myocardial repolarization. One hundred patients received almokalant infusion during AF (infusion 1) and 62 of the patients during sinus rhythm (SR) on the following day (infusion 2). Thirty-two patients converted to SR. Six patients developed TdP. During AF, T wave alternans was more common prior to infusion (baseline) in patients developing TdP (50% vs 4%, P < 0.01). After 30 minutes of infusion 1, the TdP patients exhibited a longer QT interval (493 +/- 114 vs 443 +/- 54 ms [mean +/- SD], P < 0.01), a larger precordial QT dispersion (50 +/- 74 vs 27 +/- 26 ms, P < 0.05), and a lower T wave amplitude (0.12 +/- 0.21 vs 0.24 +/- 0.16 mV, P < 0.01). After 30 minutes of infusion 2, they exhibited a longer QT interval (672 +/- 26 vs 489 +/- 74 ms, P < 0.001), a larger QT dispersion in precordial (82 +/- 7 vs 54 +/- 52 ms, P < 0.01) and extremity leads (163 +/- 0 vs 40 +/- 34 ms, P < 0.001), and T wave alternans was more common (100% vs 0%, P < 0.001). Risk factors for development of TdP were at baseline: female gender, ventricular extrasystoles, and treatment with diuretics; and, after 30 minutes of infusion: sequential bilateral bundle branch block, ventricular extrasystoles in bigeminy, and a biphasic T wave. Patients developing TdP exhibited early during almokalant infusion a pronounced QT prolongation, increased QT dispersion, and marked morphological T wave changes.     

The influence of organic myocardial damage on parameters of signal-averaged electrocardiogram in patients with electrically-induced atrial fibrillation

The aim of this study was to assess the effects of myocardium organic damage on time-domain parameters of atrial signal-averaged ECG (ASAECG) in patients with electrically induced paroxysmal atrial fibrillation (PAF). The investigation was done in 120 patients with subjective symptoms of cardiac rhythm disorders suggesting atrial fibrillation and for further analysis were selected 51 patients in whom atrial PAF was induced during transoesophageal pacing (TEP). Patients were divided according to organic damage of myocardium-38 pts (24 male and 14 female, mean age 52.1 +/- 11.6-group I) and without-13 pts (9 male and 4 female, mean age 35.4 +/- 9.9 -group II). In all two dimensional echocardiographic examination, 24-hours Holter monitoring, exercise testing and TEP were made. Recording of ASAECG was done with a commercially available system HIPEC-200 HA Aerotel. The following time-domain parameters of ASAECG were calculated: the root mean square voltage of the terminal 10, 20, 30 ms of the filtered P-wave (RMS 10, 20, 30) and time duration of filtered P-wave (PWD) and also time duration of P-wave from Frank's leads X, Y, Z (XP, YP, ZP). Atrial late potentials (ALP) were defined as the presence of two parameters: RMS 10 < 4 microV and PWD > 123 ms. If we compared time-domain parameters of ASAECG between examined groups it occurred that only the values of PWD attained statistically significant differences, respectively 123.3 +/- 15.4 ms vs 115 +/- 11.2 ms, p < 0.05. In 14 (36.8%) patients from first group and in 2 (15.4%) patients from second ALP were confirmed. We concluded that presence of myocardium organic damage have essentially influenced on time duration of filtered P-wave.     

The role of an electropharmacological transesophageal test in the prevention of paroxysmal atrial fibrillation. Experience with flecainide

BACKGROUND: The management of patients with paroxysmal atrial fibrillation (AF) is unsuccessful, because AF recurs in about 50% of patients despite an antiarrhythmic treatment. Usefulness of non-pharmacological strategies is available in a limited subset of patients and it does not present a global solution to the problem. At present, treatment with antiarrhythmic agents is the only available tool in patients with AF recurrence. The aim of this study was to assess the predictive value of the electropharmacological transesophageal (TE) test in the management of patients with paroxysmal AF treated by flecainide. METHODS: In 32 patients, ranging in age from 38 to 70 years (mean: 59 +/- 12 years), with documented episodes of paroxysmal AF (mean: 5.6 +/- 3.7 episodes/last year), we performed an electrophysiological transesophageal (TE) test following pharmacological wash-out. An aggressive protocol was used: step A: 10 sec atrial burst at Wenckebach point + 10 bpm, 200 and 250 bpm; step B: 10 sec atrial bursts at 300, 400, 500 and 600 bpm; step C: 8 sec increasing rate burst from 200 to 800 bpm. Induction of sustained AF (> 1 min) was considered the end-point. Patients were treated with flecainide 100 mg bid and a second TE test was performed at the steady-state, with an identical induction protocol and end-point. Based on the response of the second test, patients were divided into responders (R Group: non-inducible AF) and non-responders (NR Group: inducible, sustained AF). Patients were followed-up by periodical controls and contacted by telephone to confirm their clinical status. RESULTS: Sustained AF was induced in 30 patients (94%) at the first TE study. Eight of them dropped-out at the time of the second TE test (6 patients for lack of consent, 1 patient for side-effects and another one for proarrhythmic effects). In the mean follow-up of 15 +/- 6 months, among patients who underwent a second TE test, AF recurrence was documented in 2 out of 14 patients from the R Group and in 7 out of 10 patients from the NR Group (p < 0.01). There were 4 AF episodes in the R Group and 19 in the NR Group (p < 0.001). We did not find significant statistical differences between the two groups in terms of age, sex, body weight, AF episodes/past year, P-wave duration, left atrial dimension, structural heart disease, AF duration at the first TE test and follow-up duration. In five patients from the NR Group with induced AF lasting > 5 min, the percentage of recurrence was 100% and there were 16 AF episodes. Global percentage of patients with recurrence was 37%. CONCLUSIONS: Flecainide is effective in reducing the incidence of AF and results are similar to other antiarrhythmic agents generally used. The electropharmacological TE test might be a useful tool to predict the response to an antiarrhythmic treatment.     

Interference of mitral valve stenosis with left ventricular diastole and left atrial appendage flow

Atrial fibrillation (AF) has been reported as an independent risk factor of systemic thromboembolism. Almost half of the left atrial thrombi are located in the left atrial appendage (LAA). LAA function, reflected by LAA flow, thus has an influence on the potential of distal embolic complications. To identify factors other than atrial contraction that influence LAA flow during AF, transthoracic and transesophageal echocardiographic studies were performed on 130 patients. Seventy patients with nonrheumatic AF were divided into two groups with higher peak LAA outflow velocity (group 1) and lower peak LAA outflow velocity (group 2) at the ventricular systolic phase. Sixty patients with rheumatic AF were classified as group 3. Group 1 had a higher peak LAA outflow velocity than group 2 at both the ventricular systolic and diastolic phases. Group 2 had a higher peak LAA outflow at the ventricular diastolic phase than group 3 (18.9 +/- 8.0 vs. 11.8 +/- 7.5 cm/s, p < 0.001), whereas there was no significant difference in the peak LAA outflow at the ventricular systolic phase between the two groups (9.6 +/- 4.0 vs. 10.8 +/- 6.8 cm/s, p = NS). Group 3 was subdivided according to mitral valve area. Patients with severe mitral stenosis (mitral valve area < 1 cm2) had a significantly lower diastolic augmentation of LAA outflow velocity (difference of LAA outflow velocity between ventricle systole and diastole) than patients with mild to moderate stenosis (0.5 +/- 3.2 vs. 2.6 +/- 4.9 cm/s, p < 0.05). In conclusion, patients with rheumatic AF, especially those with severe mitral stenosis, have a lower diastolic augmentation of LAA outflow velocity. The lower diastolic augmentation of the LAA outflow velocity at the ventricular diastolic phase might result from interference with the suction effect of the left ventricular diastole by the stenotic mitral valve.     

Effects of procainamide on the excitable gap composition in common human atrial flutter

The composition of the excitable gap (EG) in common atrial flutter (AF1) was determined before and during infusion of procainamide (PA) in 9 patients (6 men and 3 women; age 70 +/- 7 years). The EG was determined by introducing a premature stimulus after every 20th AF1 complex detected using a quadripolar electrode catheter placed just above the tricuspid valve. Diastole was scanned in 2- to 4-ms decrements to the atrial effective refractory period (ERP). The relationship between the coupling interval and the return cycle length (CL) determined a reset-response curve (RRC), which described the EG. PA (15 mg/kg) was administered during AF1 over 30 minutes and RRC was repeated at maximum AF1 CL. PA prolonged AF1 CL from 227 +/- 29 to 296 +/- 62 ms (P < 0.01) but did not terminate AF1. ERP during AF1 prolonged from 169 +/- 24 to 219 +/- 41 ms (P < 0.01). Control EG was 57 +/- 16 ms or 25% +/- 6% of AF1 CL and on PA EG was 77 +/- 30 ms (P = 0.01), which was still 26% +/- 7% of the CL. Without drug, RRC was mixed in eight cases demonstrating an EG composed of fully excitable tissue (10 +/- 4 ms or 19% +/- 10% of the EG) and partially refractory tissue (48 +/- 18 ms). PA did not change the duration of the fully excitable region (13 +/- 10 ms or 19% +/- 15% of EG). Peak PA plasma concentration was 47 +/- 20 mumol/L. PA prolonged AF1 CL, ERP, and EG duration but did not change the proportion of AF1 CL occupied by the EG. The persistance of fully excitable tissue at the head of the wavefront in the presence of PA may largely explain its inefficacy in the acute termination of common AF1.