Intravenous sotalol decreases transthoracic cardioversion energy requirement for chronic atrial fibrillation in humans: assessment of the electrophysiological effects by biatrial basket electrodes

OBJECTIVES: This study was undertaken to assess the effects of sotalol on the transthoracic cardioversion energy requirement for chronic atrial fibrillation (AF) and on the atrial electrograms during AF recorded by two basket electrodes. BACKGROUND: The effects of sotalol infusion on transthoracic electrical cardioversion for chronic atrial fibrillation in humans have not been well investigated. METHODS: We included 18 patients with persistent AF for more than three months. Atrial electrograms were recorded by two basket electrodes positioned in each atrium respectively. Transthoracic cardioversion was performed before and after sotalol 1.5 mg/kg i.v. infusion. RESULTS: In the 14 patients whose AF could be terminated by cardioversion before sotalol infusion, the atrial defibrillation energy was significantly reduced after sotalol infusion (236 +/- 74 jules [J] vs. 186 +/- 77 J; p < 0.01). Atrial fibrillation was refractory to cardioversion in four patients at baseline and was converted to sinus rhythm by cardioversion after sotalol infusion in two of them. We further divided the patients into two groups. Group A consisted of 10 patients in whom the energy requirement was decreased by sotalol while group B consisted of eight patients in whom the energy requirement was not decreased. The mean A-A (atrial local electrogram) intervals during AF were significantly increased after sotalol infusion in both groups, but the increment of A-A interval was significantly larger in group A than it was in group B patients (36 +/- 13 ms vs. 22 +/- 8 ms for the right atrium; 19 +/- 7 ms vs. 9 +/- 7 ms for the left atrium; both p < 0.05). The spatial and temporal dispersions of A-A intervals were not significantly changed after sotalol infusion in both atria in both groups. CONCLUSIONS: Sotalol decreases the atrial defibrillation energy requirement by increasing atrial refractoriness but not by decreasing the dispersion of refractoriness.     

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

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

Defibrillation-guided radiofrequency ablation of atrial fibrillation secondary to an atrial focus

OBJECTIVES: Our aim was to evaluate a potential focal source of atrial fibrillation (AF) by unmasking spontaneous early reinitiation of AF after transvenous atrial defibrillation (TADF), and to describe a method of using repeated TADF to map and ablate the focus. BACKGROUND: Atrial fibrillation may develop secondary to a rapidly discharging atrial focus that the atria cannot follow synchronously, with suppression of the focus once AF establishes. Focus mapping and radiofrequency (RF) ablation may be curative but is limited if the patient is in AF or if the focus is quiescent. Early reinitiation of AF has been observed following defibrillation, which might have a focal mechanism. METHODS: We performed TADF in patients with drug-refractory lone AF using electrodes in the right atrium (RA) and the coronary sinus. When reproducible early reinitiation of AF within 2 min after TADF was observed that exhibited a potential focal mechanism, both mapping and RF ablation were performed to suppress AF reinitiation. Clinical and ambulatory ECG monitoring was used to assess AF recurrence. RESULTS: A total of 44 lone AF patients (40 men, 4 women; 32 persistent, 12 paroxysmal AF) with a mean age of 58+/-13 years underwent TADF. Sixteen patients had early reinitiation of AF after TADF, nine (20%; 5 paroxysmal) exhibited a pattern of focal reinitiation. Earliest atrial activation was mapped to the right superior (n = 4) and the left superior (n = 3) pulmonary vein, just inside the orifice, in the seven patients who underwent further study. At the onset of AF reinitiation, the site of earliest activation was 86+/-38 ms ahead of the RA reference electrogram. The atrial activities from this site were fragmented and exhibited progressive cycle-length shortening with decremental conduction to the rest of the atrium until AF reinitiated. Radiofrequency ablation at the earliest activation site resulted in suppression of AF reinitiation despite pace-inducibility. Improved clinical outcome was observed over 8+/-4 months' follow-up. CONCLUSIONS: Transvenous atrial defibrillation can help to unmask, map, and ablate a potential atrial focus in patients with paroxysmal and persistent AF. A consistent atrial focus is the cause of early reinitiation of AF in 20% of patients with lone AF, and these patients may benefit from this technique.     

Early Reinitiation of Atrial Fibrillation Following External Electrical Cardioversion in Amiodarone-Treated Patients

Early reinitiation of atrial fibrillation (ERAF) following external or internal electrical cardioversion is one of the factors determining unsuccessful electrical cardioversion. Prevention of ERAF has not been studied systematically in patients on amiodarone therapy. Methods and Results: 22 patients had ERAF within 1[emsp4 ]min after external electrical cardioversion of atrial fibrillation. 11 patients were on amiodarone therapy and 11 patients had no antiarrhythmic medication. The effect of atropine, post-shock atrial pacing and intravenous ajmaline on ERAF was consecutively tested in these patients. Administration of atropine before repeated defibrillation or post-shock atrial pacing prevented ERAF in 9 of the 11 patients (82%) on amiodarone therapy but in only 3 of 11 patients (27%) without amiodarone (p<0.05). In the remaining patients, intravenous ajmaline was effective in the suppression of ERAF in 5 patients without amiodarone and in 1 patient with amiodarone. The PP interval preceding the atrial premature beat reinitiating atrial fibrillation was nonsignificantly longer in amiodarone-treated patients (1127±419[emsp4 ]ms) in comparison to patients without amiodarone (896±271[emsp4 ]ms). 27% of patients without amiodarone at the time of electrical cardioversion and 55% of patients with amiodarone remained in sinus rhythm during the follow-up of 29±14 and 30±14 months, respectively. Conclusions: ERAF in patients on amiodarone can be treated by atropine or atrial pacing to prevent bradycardia-dependent ERAF. ERAF in amiodarone-treated patients does not apparently predict late recurrence of atrial fibrillation on continued amiodarone therapy.     

Incidence and modes of onset of early reinitiation of atrial fibrillation after successful internal cardioversion, and its prevention by intravenous sotalol

OBJECTIVES—To study the incidence and mode of onset of early reinitiation of atrial fibrillation (ERAF) following successful internal cardioversion of chronic atrial fibrillation, and to determine the effects of sotalol in the prevention of ERAF.
DESIGN—The incidence and modes of onset of ERAF and the acute effects of intravenous sotalol in the prevention of ERAF were studied retrospectively.
SETTING—Electrophysiology laboratory at a university teaching hospital.
PATIENTS—64 patients, mean (SD) age 62 (10) years, who underwent internal cardioversion of chronic atrial fibrillation (mean duration of atrial fibrillation 31 (39) months).
MAIN OUTCOME MEASURES—ECGs and intracardiac electrograms recorded during the internal cardioversion of atrial fibrillation using 3/3 ms biphasic, R wave synchronised shocks.
RESULTS—52 patients (81%) had successful electrical cardioversion, and 20 (31%) of these had ERAF during the procedure. There was no clinical predictor for the occurrence of ERAF. Fifty eight episodes of ERAF were observed. Five ERAF episodes (9%) had preceding bradycardia and 53 (91%) of these were triggered by atrial premature beats with normal preceding heart rate. Atrial premature beats that reinitiated atrial fibrillation had a shorter coupling interval (333 (43) ms v 396 (100), p < 0.001) and a lower prematurity index (0.44 (0.11) v 0.55 (0.14), p < 0.001) than those that did not reinitiate atrial fibrillation. Repeated shock delivery and increasing the defibrillation energy did not prevent ERAF. Intravenous sotalol infusion decreased the numbers of atrial premature beats and prolonged their coupling interval, and prevented ERAF after repeated defibrillation in 83% of patients with ERAF.
CONCLUSIONS—ERAF is a significant clinical problem after successful internal cardioversion of chronic atrial fibrillation, and was observed in up to 31% of patients. In most episodes, ERAF was triggered by short coupling atrial premature beats with preceding normal heart rate. Intravenous sotalol was effective in preventing ERAF in most cases.


Keywords: atrial fibrillation; low energy cardioversion; sotalol     

Limited benefit of septal pre-excitation in pace prevention of atrial fibrillation

BACKGROUND: Pre-excitation of the intra-atrial septum (IAS) by pacing at the ostium of the coronary sinus (CSO) can prevent atrial fibrillation (AF) in case of single atrial premature beats (APBs). We investigated whether pre-excitation of IAS, either by pacing at CSO or at the right ventricle in the presence of retrograde conduction (RV), can prevent atrial tachyarrhythmia triggered by single and multiple APBs. AF vulnerability was compared to pacing at the right atrium (RA) and sinus rhythm (SR). METHODS: Seventeen patients, age 52 +/- 21 years, who exhibited retrograde VA conduction and reproducible induction of atrial tachyarrhythmia during an electrophysiological procedure, were studied. Both during SR and pacing (S1-S1:600 ms) at RA, CSO, and right ventricle (RV), single (A1-S2:200 ms) and multiple premature stimuli (A1-S2-S3-S4:200-180-180 ms) were delivered at RA (4 x diastolic threshold). RESULTS: During pacing at RA, single and multiple APBs invariably induced runs of atrial tachyarrhythmia (mean duration 34 +/- 67 sec and 37 +/- 69 sec, range 1 sec to 20 min). During preventive pacing at CSO and RV, single APBs (A1-S2:200 ms) did not induce atrial arrhythmia (0 +/- 0 sec, 0 +/- 0 sec, P < 0.05 vs pacing at RA). In contrast, when multiple APBs were applied, pacing at CSO or RV failed to prevent initiation of AF (mean duration 36 +/- 63 sec, 38 +/- 65 sec, NS). Also during SR, single APBs did not induce AF (0 +/- 0 sec, P < 0.05 vs pacing at RA) whereas multiple APBs invariably induced AF (39 +/- 74 sec, NS). CONCLUSIONS: Compared to pacing at RA, pre-excitation of IAS either by pacing at CSO or at RV with retrograde conduction can prevent initiation of paroxysms of atrial tachyarrhythmia triggered by single but not by multiple right APBs. These findings imply that the potential benefit of choosing an optimal pacing site in patients requiring atrial-based pacing is limited. Moreover, in the absence of bradycardia, no specific pacing site offers incremental benefit over the natural "protective" effect of sinus rhythm.     

Efficacy and tolerability of continuous overdrive atrial pacing in atrial fibrillation.

Overdrive right atrial pacing has been used to prevent atrial fibrillation, but its efficacy in atrial fibrillation prevention and the patient tolerability and quality of life during high rate pacing remain uncertain. The objective of this study was to test the effects of a consistent atrial pacing algorithm that automatically paced the atrium at 30 ms shorter than the sinus P-P interval for atrial fibrillation prevention. Fifteen patients with sick sinus syndrome implanted with a Thera DR (model 7940 or 7960, Medtronic Inc.) were randomly programmed to rate adaptive dual chamber pacing (DDDR) or DDDR + consistent atrial pacing mode, each for an 8-week study period. The efficacy of consistent atrial pacing was assessed by the number of automatic mode switching and the number of premature atrial complexes. Symptoms and quality of life were assessed by the SF-36 quality of life questionnaire and an atrial fibrillation symptom checklist. The percentage of atrial pacing increased from 57 +/- 32% to 86 +/- 28%. Overall, there was no significant difference in the number of automatic mode switching episodes between DDDR and DDDR + consistent atrial pacing (47 +/- 90 vs 42 +/- 87, P > 0.05), but a significant reduction in premature atrial complexes by 74.7% (P < 0.001). There was no undue increase in atrial rate by the DDDR + consistent atrial pacing mode versus DDDR (63 +/- 13 vs 70 +/- 7 bpm). There was no significant difference in quality of life scores and symptom severity on frequency between the two modes of pacing, but a trend towards a lower frequency of symptoms in the DDDR + consistent atrial pacing mode compared with baseline (29.5 +/- 10.2 vs 25.1 +/- 9.7, P = 0.07). An algorithm that provides consistent atrial overdrive pacing can suppress atrial fibrillation triggering premature atrial complexes without the need to increase the overall atrial rate compared with conventional pacing. The algorithm appears to be well-tolerated, but further studies are needed to address the clinical impact of this atrial fibrillation prevention algorithm.     

Immediate Reinitiation of Atrial Fibrillation Following Internal Atrial Defibrillation

Immediate Reinitiation of AF. Introduction: Although the recurrence rate of atrial fibrillation has been reported to be similar to that after external and internal cardioversion, little is known about immediate reinitiation of atrial fibrillation (IRAF) following internal cardioversion. Methods and Results: Thirty-eight patients (24 men; mean age 63 ± 13 years) underwent internal atrial defibrillation. Catheter-based defibrillation electrodes were positioned in the anterolateral right atrium and the coronary sinus. All patients were cardioverted at a mean threshold of 4.6 ± 3.4 J. Five of 38 patients (13%) had 1 to 4 episodes of IRAF. No difference in clinical and echocardiographic characteristics were observed when patients with and without IRAF were compared. Atrial fibrillation was always reinitiated by an atrial premature beat. When the earliest atrial endocardial activation time on the defibrillation catheters was analyzed, these atrial premature heats did not seem to originate from the defibrillation catheters. Twenty-one patients had atrial premature heats without IRAF. When the coupling intervals of the first atrial premature heat in patients without and with IRAF after conversion were compared, a significant difference was found (661 ± 229 vs 418 ± 79 msec, P < 0.05). IRAF was successfully treated with repeated shock delivery after the administration of atropine in 1 patient and intravenous flecainide in 2. Only repeated shock delivery was sufficient to treat IRAF in another 2 patients. Late recurrences of atrial fibrillation occurred in 3 of 5 with IRAK and in 19 of 33 patients without IRAF (P = NS). Conclusion: IRAF after internal atrial defibrillation occurred in 13% of patients, was always initiated by an atrial premature heat having a short coupling interval not originating from the defibrillation catheters, and was prevented by repeated shock delivery with or without preceding administration of pharmacologic agents. IRAF did not predict early recurrences of the arrhythmia after discharge from the hospital, emphasizing the necessity to treat immediate reinitiation promptly to achieve a successful cardioversion.     

Beneficial effects of biatrial pacing on cardiac function in patients with bradycardia -- tachycardia syndrome.

BACKGROUND: Biatrial (BiA) pacing prevents atrial fibrillation. By an unknown mechanism. The purpose of this study was to use Doppler echocardiography to evaluate the hemodynamic effects during BiA pacing. METHODS AND RESULTS: The subjects were 7 patients with bradycardia - tachycardia syndrome with an implanted pacemaker. Atrial pacing sites were the right atrial appendage (RAA) and coronary sinus. P wave duration during BiA pacing (123 +/-16 ms) was significantly shorter than during either RAA pacing (167+/-19 ms, p<0.05) or sinus rhythm (148+/-12 ms, p<0.05). Doppler echocardiography revealed a greater cardiac output during BiA pacing than during RAA pacing (4.1+/-1.1 vs 3.5+/-0.7 L/min, p=0.042). The Doppler waveform of transmitral flow indicated that the left ventricular contraction interrupted the atrial filling wave during RAA pacing. The interval between the end of the atrial filling wave of transmitral flow and the mitral valvular closing sound was significantly increased by BiA pacing compared with RAA pacing (56+/-65 vs 40+/-57 ms, p=0.047). CONCLUSION: Cardiac hemodynamics were improved by BiA pacing and reduction of left atrial load may be one of the mechanisms.     

Permanent, direct His-bundle pacing: a novel approach to cardiac pacing in patients with normal His-Purkinje activation

BACKGROUND: Direct His-bundle pacing (DHBP) produces synchronous ventricular depolarization and improved cardiac function relative to apical pacing. Although it has been performed transiently in the electrophysiology laboratory and persistently in open-chested canines, permanent DHBP in humans has not been achieved. METHODS AND RESULTS: A total of 18 patients aged 69+/-10 years who had a history of chronic atrial fibrillation, dilated cardiomyopathy, and normal activation (ie, QRS< or =120 ms) were screened for permanent DHBP using an electrophysiology catheter. In 14 patients, the His bundle could be reliably stimulated. Of these 14, permanent DHBP using a fixed screw-in lead was successful in 12 patients. Radiofrequency atrioventricular node ablation was performed in patients exhibiting a fast ventricular response. All patients received single-chamber rate-responsive pacemakers. Acute pacing thresholds were 2.4+/-1.0 V at a pulse duration of 0.5 ms. Lead complications included exit block requiring reoperative adjustment and gross lead dislodgment. Echocardiographic improvement in heart function was shown by reductions in the left ventricular end-diastolic dimension from 59+/-8 to 52+/-6 mm (P相似文献   

Monophasic action potentials of the right atrium in patients with paroxysmal atrial fibrillation

To investigate the mechanism of atrial fibrillation (AF), monophasic action potentials (MAPs) from the atrial myocardium were studied in 7 patients with paroxysmal AF (PAF) and in 7 control individuals. The MAPs were recorded using a contact catheter during sinus rhythm and continuous pacing at the high right atrium (HRA) with pacing cycle lengths of 600, 500 and 400 ms. MAPs were obtained from 6 sites in each participant. The MAPD90 was measured from onset to 90% of MAP repolarization. Average, maximal and minimal MAPD90 (avMAPD90, maxMAPD90 and minMAPD90) were obtained from all participants. The dispersion of MAPD90 (dispMAPD90) was defined as the difference between maxMAPD90 and minMAPD90. The width of each atrial potential (WAP) and the wavelength index (WLI=MAPD90/WAP) were determined. Average, maximal and minimal WLI (avWLI, maxWLI and minWLI) were obtained from all participants. The avMAPD90 and maxMAPD90 did not significantly differ between the 2 groups. The minMAPD90 in the PAF group was significantly smaller than that in the control group at HRA pacing with cycle lengths of 500 and 400 ms (210+/-18ms vs 245+/-14 ms, p<0.05; 207+/-23 ms vs 238+/-20 ms, p<0.05; respectively). The dispMAPD90 was significantly longer in the PAF group than in the control group during sinus and HRA pacing. The WAP value did not differ between the 2 groups. The minWLI in the PAF group was significantly smaller than that in the control group at HRA pacing with cycle lengths of 500 and 400 ms (3.3+/-0.5 vs 3.8+/-0.3, p<0.05; 3.2+/-0.4 vs 3.7+/-0.3, p<0.02). A shortened and widened dispersion of atrial refractoriness may play an important role in the genesis of AF. Furthermore, smaller wavelengths may form in the atrium of patients with PAF.     

Effect of Bachmann's bundle pacing on atrial fibrillation: electrophysiologic assessment

BACKGROUND: It has recently been reported that simultaneous multisite atrial pacing, Bachmann's bundle (BB) pacing, and coronary sinus (CS) pacing are useful for preventing the induction of atrial fibrillation (AF). HYPOTHESIS: We investigated whether a simple pacing approach via BB could reduce the induction of AF by extrastimuli (S2) from the right atrial appendage (RAA). METHODS: Programmed electrical stimulation was performed from the RAA and the area of BB at the superior aspect of the atrial septum, and bipolar recordings were obtained from the RAA, BB, and CS in 14 patients. RESULTS: In five patients, AF was induced with critically timed RAA-S2 delivered during RAA pacing. However, AF was not induced in any patient when RAA-S2 was delivered during BB pacing. The duration of the P wave during BB pacing was significantly shorter than that during RAA pacing and sinus rhythm (BB 80 +/- 16 ms vs. RAA 106 +/- 36 ms vs. sinus rhythm 100 +/- 24 ms, p < 0.05). The intra-atrial conduction time to the distal coronary sinus (CSd) caused by early S2 at the RAA was significantly reduced by BB pacing (BB 114 +/- 22 ms vs. RAA 157 +/- 35 ms, p < 0.001). CONCLUSION: Bachmann's bundle pacing reduces atrial conduction time caused by RAA-S2 and may be useful for preventing the induction of AF.     

The effects of class IA antiarrhythmic drug on the common type of atrial flutter in combination with pacing therapy

In 11 patients with common type of atrial flutter (common AF), rapid atrial pacing from the high right atrium was performed before and/or after class Ia antiarrhythmic drug administration, confirming transient entrainment by decreasing the pacing cycle length by 10 ms. In 10 patients before the drug administration, common AF was not interrupted although the pacing cycle length was decreased to 200 ms in 5 patients, accelerated atrial flutter or atrial fibrillation was induced in 4 patients, and common AF was converted into sinus rhythm in only 1 patient. After the drug administration common AF was converted into sinus rhythm in 5 out of 6 patients. The class Ia antiarrhythmic drug prolonged the common AF cycle length (255 +/- 12 ms vs. 298 +/- 37 ms, p less than 0.005) and widened the entrainment zone (64 +/- 7 ms vs. 90 +/- 20 ms, p less than 0.05). The widening of the entrainment zone and the prolongation of the common AF cycle length facilitate the successful conversion of common AF at a longer pacing cycle length, which would not precipitate atrial fibrillation or accelerated atrial flutter. The combination therapy of rapid atrial pacing and the class Ia antiarrhythmic drug is thought to be useful in the therapy of common AF.     

Sotalol reverses remodeled action potential in patients with chronic atrial fibrillation but does not prevent arrhythmia recurrence

INTRODUCTION: Recurrence of atrial fibrillation (AF) may be related to AF-induced electrical remodeling characterized by shortening of the atrial action potential duration (APD) and loss of its rate adaptation. We investigated the effects of pretreatment with oral d,l-sotalol on rate-dependent changes in atrial monophasic action potential (MAP) duration after cardioversion of chronic AF with reference to the efficacy in preventing the arrhythmia recurrence. METHODS AND RESULTS: MAPs were recorded from the right atrium at six pacing cycle lengths (CLs) from 300 to 750 ms in 19 chronic AF patients after electrical cardioversion; 9 had been pretreated with oral d,l-sotalol (196 +/- 42 mg/day) for 7 days and 10 were untreated. MAP duration at 90% repolarization (MAPD90) in 11 control patients increased progressively with increases in CLs from 209 +/- 19 ms at CL = 300 ms to 264 +/- 28 ms at CL = 750 ms. In AF patients without sotalol, the CL-MAPD relation was shifted downward and flattened at longer CLs; MAPD90 values were 206 +/- 11 ms and 227 +/- 16 ms at CLs of 300 and 750 ms, respectively. MAPD90 values at CLs > or =500 ms in AF were significantly shorter than controls. In AF patients with sotalol, the normal CL-MAPD relation was preserved; MAPD90 increased from 226 +/- 19 ms to 282 +/- 46 ms in the CL range. AF recurred within 2 weeks after cardioversion in 14 of 24 patients pretreated with d,l-sotalol (216 +/- 51 mg/day) despite of continuation of sotalol treatment. CONCLUSION: Sotalol reverses AF-induced decrease in MAPD adaptation to rate in the atria of chronic AF patients, but this effect does not lead to prevention of AF recurrence.     

Role of KATP channels in repetitive induction of ventricular fibrillation.

AIM: Patients with sustained ventricular tachyarrhythmias are at high risk for sudden cardiac death. The mechanisms leading to multiple temporally related episodes of ventricular fibrillation (VF) are not yet fully elucidated, and treatment options are limited. We investigated whether K(ATP)-channels could be involved in triggering VF. METHODS: We determined postarrhythmic changes of monophasic action potentials (MAP) after repetitive induction of VF in 32 Langendorff-perfused rabbit hearts. RESULTS: Postarrhythmic action potential duration (APD) was significantly shorter compared with baseline (100 +/- 12 ms vs. 140 +/- 8 ms, P < 0.05). With increasing numbers of VF and shortening of recovery intervals between VF episodes (2 min) inducibility of VF increased, and abbreviation of APD became more prominent (90 +/- 5 ms vs. 130 +/- 4 ms, P < 0.05). Pre-treatment with the selective K(ATP) blocking agent HMR 1883 led to a significant increase of postarrhythmic APDs compared with control hearts (100 +/- 12 ms vs. 118 +/- 3 ms, P = 0.0013). Moreover, HMR 1883 significantly reduced inducibility of VF and increased the rate of successful defibrillation. CONCLUSIONS: Repetitive episodes of VF result in postarrhythmic abbreviation of APDs, a phenomenon thought to be of potential relevance for incessant tachyarrhythmias in patients. Prevention of postarrhythmic MAP-shortening by HMR 1883 might be useful in suppressing VF.     

Characterization of right atrial substrate in patients with supraventricular tachyarrhythmias

Right atrial substrate of supraventricular tachyarrhythmias. BACKGROUND: Voltage mapping has been used to detect diseased myocardium. However, accurate determination of the local atrial voltage at the same site, and simultaneous recordings from multiple mapping sites were limited. The purpose of this study was to investigate the right atrial (RA) substrate properties in patients with supraventricular tachyarrhythmias (SVT). METHODS AND RESULTS: Forty patients (aged 55+/-20 years) undergoing noncontact mapping and ablation of SVT constituted the study population. There were eight patients with atrioventricular node reentrant tachycardia (AVNRT), eight patients with focal atrial tachycardia (AT), 14 patients with atrial flutter (AFL), and 10 patients with atrial fibrillation (AF). The mean peak negative voltage (PNV) was analyzed in virtual unipolar electrograms, which were obtained from 256 equally distributed RA endocardial sites during sinus rhythm (SR), atrial pacing, and tachycardia. The mean PNV of global RA during SR (-1.34+/-0.22 vs. -0.90+/-0.40 vs. -1.00+/-0.36 vs. -0.85+/-0.35 mV, P=0.04), atrial pacing at cycle lengths of 500 ms (-1.30+/-0.29 vs. -0.70+/-0.35 vs. -0.76+/-0.25 vs. -0.64+/-0.26 mV, P=0.02), and 300 ms (-1.54+/-0.47 vs. -0.94+/-0.21 vs. -0.75+/-0.27 vs. -0.57+/-0.22 mV, P<0.01) were significantly greater in patients with AVNRT compared to AT, AFL, and AF. Furthermore, the mean PNV decreased during atrial pacing with shorter pacing cycle length was demonstrated only in patients with AFL and AF. CONCLUSION: Negative unipolar voltage analysis of global RA showed different RA substrate characteristics during various SVT. The substrate property of activation and cycle length-dependent voltage reduction may be related to the development of AFL and AF.     

Autonomically induced conversion of pulmonary vein focal firing into atrial fibrillation

OBJECTIVES: This study was designed to determine the mechanism(s) whereby focal firing from pulmonary veins (PVs) is converted into atrial fibrillation (AF). BACKGROUND: The mechanism(s) whereby PV focal firing or even a single PV depolarization is converted into AF is unknown. METHODS: In 14 anesthetized dogs a right thoracotomy was performed to expose the right superior pulmonary vein (RSPV). An octapolar electrode catheter was sutured alongside the RSPV so that the distal electrode pair was adjacent to the fat pad containing autonomic ganglia (AG) at the veno-left atrial (LA) junction. An acrylic plaque electrode on the fat pad allowed AG stimulation at voltages ranging from 0.6 to 4.0 V. Multi-electrode catheters were sutured to the atria with their distal electrode pairs at the fat pad-atrial junctions. Right superior pulmonary vein focal firing consisted of S(1)-S(1) = 330 ms followed by as many as 11 atrial premature depolarizations (APDs) (A(2)-A(12)) whose coupling interval just exceeded RSPV refractoriness. RESULTS: Autonomic ganglia stimulation, without atrial excitation, caused a reduction in heart rate (HR): control 142 +/- 15/min, 4.0 V; 75 +/- 30/min, p /=9.3 V. CONCLUSIONS: The effects of AG stimulation at the base of the RSPV can provide a substrate for the conversion of PV firing into AF.     

Localization of arrhythmogenic triggers of atrial fibrillation

INTRODUCTION: Mapping procedures to identify triggers of atrial fibrillation from pulmonary veins (PVs) are not well established. We sought to determine the value of multipolar recordings from the coronary sinus (CS) and crista terminalis (CT) for identifying the origin of paced and atrial premature depolarizations (APDs) initiating atrial fibrillation from left versus right PVs. METHODS AND RESULTS: Fifteen patients with paroxysmal atrial fibrillation refractory to medications had decapolar catheters (5-mm electrode, 2-mm interelectrode spacing) placed in the CS and posterior medial to the CT. Bipolar electrograms were recorded at each site. Electroanatomic left atrial endocardial maps were created in sinus rhythm, and each PV was identified and paced. During spontaneous APDs initiating atrial fibrillation and PV pace maps, the atrial activation and the earliest electrogram at CS and CT were compared. PV sites were designated as sites of origin of APDs when (1) intracardiac electrograms in the CS and CT during arrhythmogenic APDs matched those of PV pace maps, (2) local activation preceded CS and CT recordings by at least 40 msec (all sites), and (3) atrial depolarizations were eliminated by application of radiofrequency energy (24/26 sites). Pacing from each of the 30 right PV sites resulted in proximal to distal CS activation and later recordings at the CS than the CT (earliest CS-CT activation range: -15 to -58 msec, mean -32 +/- 12). In contrast, pacing from the left PV sites typically (28/30 sites) activated the CS from the distal to proximal poles and demonstrated simultaneous or earlier (CS-CT range: -14 to +54 msec, mean 13 +/- 17) recordings of the CS than the CT (P < 0.0001). For 13 APDs mapped to the right PVs, CS minus CT activation was -17 to -49 msec (mean -31 +/- 8). For 13 APDs localized to the left PVs, the CS minus CT activation time ranged from -8 to +28 msec (mean 14 +/- 15). CONCLUSION: Activation sequence mapping from multipolar catheters placed in the CS and along the posterior medial CT rapidly differentiates right and left PV sites of origin of atrial depolarization.     

Importance of the "atrial kick" in determining the effective mitral valve orifice area in mitral stenosis

Atrial fibrillation with a rapid ventricular response in patients with mitral stenosis (MS) is often accompanied by pulmonary congestion and reduced cardiac output owing to a diminished diastolic filling period and the loss of the end-diastolic left ventricular (LV) pressure increment. To test the hypothesis that loss of atrial contraction (atrial kick) also results in a decrease in effective mitral valve orifice area, 6 patients with pure, isolated MS were studied in sinus rhythm during atrial pacing and simultaneous atrioventricular pacing. Atrial pacing at 140 beats/min caused no significant change from baseline in cardiac output or mitral valve area, but there was a decrease in LV end-diastolic volume and ejection fraction as well as an increase in left atrial pressure and mean diastolic gradient. Simultaneous atrioventricular pacing (to eliminate atrial kick) induced a decrease in cardiac output (4.4 +/- 0.9 vs 5.2 +/- 0.8 liters/min at 110 beats/min, 4.2 +/- 0.9 vs 5.1 +/- 0.9 liters/min at 140 beats/min; p less than 0.05) and LV end-diastolic volume (77 +/- 27 vs 93 +/- 29 ml at 110 beats/min, 54 +/- 17 vs 65 +/- 19 ml at 140 beats/min; p less than 0.05), an increase in left atrial pressure (28 +/- 3 vs 20 +/- 5 mm Hg at 110 beats/min, 30 +/- 4 vs 25 +/- 5 mm Hg at 140 beats/min; p less than 0.05), and a decrease in mitral valve area (1.2 +/- 0.4 vs 1.4 +/- 0.5 cm2 at 110 beats/min, 1.2 +/- 0.4 vs 1.4 +/- 0.4 cm2 at 140 beats/min; p less than 0.05). Thus, loss of atrial kick may cause pulmonary congestion and reduced cardiac output in patients with MS, partly because of a decrease in effective mitral valve area.     

Atrial defibrillation threshold in humans minutes after atrial fibrillation induction; "A stitch in time saves nine".

AIMS: To assess the effects of atrial fibrillation duration on the defibrillation threshold in atrial fibrillation patients seconds or minutes after initiation of the arrhythmia. METHODS AND RESULTS: Nineteen patients with recurrent symptomatic atrial fibrillation were evaluated. After programmed induction of atrial fibrillation, the defibrillation threshold was assessed after two sequential periods of arrhythmia in the same patient: an "ultrashort" period of 30 s duration and a "short" period, which lasted 10 min. After the specified period, internal cardioversion was attempted using a balloon-guided catheter that allows the delivery of biphasic shocks between one electrode array placed in the left pulmonary artery and a proximal electrode array on the lateral right atrial wall. The defibrillation threshold was assessed with energy steps of 0.5 J with a starting level of 0.5 J. Mean time from induction to successful defibrillation was 92+/-30 s after the "ultrashort" period of atrial fibrillation and 910+/-86 s after the short period. The defibrillation threshold was significantly greater after 10 min of atrial fibrillation than after 30 s of arrhythmia (2.32+/-0.61 J vs 1.31+/-0.66 J, P<0.001). Clinical data were not found to affect the defibrillation threshold. CONCLUSIONS: Prolongation of atrial fibrillation over minutes in patients with paroxysmal arrhythmia increases the energy requirements for successful defibrillation.