Effects of different atrial pacing modes on atrial electrophysiology: implicating the mechanism of biatrial pacing in prevention of atrial fibrillation

BACKGROUND: Multiple-site atrial pacing has been shown to prevent recurrence of atrial fibrillation. However, information about the mechanisms of different atrial pacing modes in prevention of atrial fibrillation was not clear. METHODS AND RESULTS: Forty-two patients without structural heart disease were classified into group 1 and group 2 according to absence or presence of clinical atrial fibrillation, respectively. Atrial conduction time and electrogram width of the right posterior interatrial septum (RPS) were measured during drive-train stimulation (S1) and early extrastimulation (S2). The locations of S1 were the high right atrium (HRA), distal coronary sinus (DCS), or both sites simultaneously. Effective refractory periods (ERPs) of the HRA and DCS were also determined during S1 stimulation at each site and during biatrial pacing. The ERPs were not different between single-site atrial pacing and biatrial pacing. In contrast, early S2 stimulation at the HRA caused greater atrial conduction delay and greater increment of electrogram width of the RPS in patients with a history of atrial fibrillation. Biatrial pacing significantly reduced the conduction delay and electrogram width of the RPS caused by HRA extrastimulation. In addition, in 17 group 2 patients, atrial fibrillation was induced by an early HRA S2 coupled to HRA pacing. However, with the same coupling interval of S2 at HRA, only 6 of them had the arrhythmia induced during biatrial pacing. Furthermore, conduction delay and increase of electrogram width caused by early S2 at the HRA were reduced by biatrial pacing only in patients whose arrhythmia induction was successfully prevented by biatrial pacing. CONCLUSIONS: Biatrial pacing reduced both the atrial conduction delay and increase of electrogram width at the RPS caused by early S2 at HRA, and these effects could prevent induction of atrial fibrillation.     

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.     

An Italian experience of radiofrequency transcatheter ablation in type-I atrial flutter: the results and follow-up

BACKGROUND: Type I atrial flutter (AF) is a supraventricular tachycardia that is notoriously disabling and resistant to antiarrhythmic drugs. The introduction of an effective non-pharmacologic technique, such as radiofrequency catheter ablation (RF), opened new therapeutic prospects for the management of this arrhythmia. The aim of our study was to evaluate the long-term efficacy of atrial flutter RF using a successful procedure marker of bi-directional conduction block in the isthmus. METHODS: In the last consecutive 50 patients (pts) who underwent RF procedure for AF at our Center (46 pts during spontaneous or induced AF and 4 in sinus rhythm) after the successful interruption of AF we performed the usual reinduction attempts and well atrial pacing from 2 sites in the right atrium (in 18 pts before and after RF and in 32 only after RF). The sites of pacing were site 1: low lateral right atrium (LRA); site 2: proximal coronary sinus (PCS). The 50 pts consisted of 13 females, 37 males with a mean age of 62.5 +/- 9.7 years (35-83). The end-point for the procedure was: 1) abrupt interruption of AF; 2) inability to reinduce AF; 3) recognition of atrial activation sequence during pacing in LRA and in PCS compatible with conduction block in the isthmus. RESULTS: The RF was successful in terminating AF in all pts after 11 +/- 7 applications of energy. After ablation, sustained AF was no longer inducible by atrial pacing. After RF, during pacing in sinus rhythm from LRA, the lower septum and PCS presented a delayed activation after the His region. Similarly, during pacing from PCS after ablation, the atrial activation sequence was modified: the low lateral right atrium was now activated by a single front after the high lateral atrium. No acute complications were noted in any pts during or after procedure. AF recurred in 9 pts. Four pts now present chronic atrial fibrillation. The mean follow-up period is 14.8 +/- 8 months. All the patients were discharged without antiarrhythmic therapy. CONCLUSIONS: The mechanism of successful ablation is the bi-directional conduction block in the isthmus with the evidence of the changes in the right atrial activation sequence during atrial pacing in sinus rhythm in LRA and in PCS before and after RF.     

Coronary sinus pacing initiates counterclockwise atrial flutter while pacing from the low lateral right atrium initiates clockwise atrial flutter. Analysis of episodes of direct initiation of atrial flutter

INTRODUCTION: Rapid atrial pacing in sinus rhythm may directly induce atrial flutter without provoking intervening atrial fibrillation, or initiate atrial flutter indirectly, by a conversion from an episode of transient atrial fibrillation provoked by rapid atrial pacing. The present study was performed to examine whether or not the direct induction of clockwise or counterclockwise atrial flutter was pacing-site (right or left atrium) dependent. METHODS AND RESULTS: We analyzed the mode of direct induction of atrial flutter by rapid atrial pacing. In 46 patients with a history of atrial flutter, rapid atrial pacing with 3 to 20 stimuli (cycle length = 500 - 170 ms) was performed in sinus rhythm to induce atrial flutter from 3 atrial sites, including the high right atrium, the low lateral right atrium, and the proximal coronary sinus, while recording multiple intracardiac electrograms of the atria. Direct induction of atrial flutter by rapid atrial pacing was a rare phenomenon and was documented only 22 times in 15 patients: 3, 11, and 8 times during stimulation, respectively, from the high right atrium, low lateral right atrium, and the proximal coronary sinus. Counterclockwise atrial flutter (12 times) was more frequently induced with stimulation from the proximal coronary sinus than from the low lateral right atrium (8 vs 1, P = .0001); clockwise atrial flutter (10 times) was induced exclusively from the low lateral right atrium (P = .0001 for low lateral right atrium vs proximal coronary sinus, P = .011 for low lateral right atrium vs high right atrium). CONCLUSIONS: Direct induction of either counterclockwise or clockwise atrial flutter was definitively pacing-site dependent; low lateral right atrial pacing induced clockwise, while proximal coronary sinus pacing induced counterclockwise atrial flutter. Anatomic correlation between the flutter circuit and the atrial pacing site may play an important role in the inducibility of counterclockwise or clockwise atrial flutter.     

Prevention of recurrent atrial fibrillation with chronic dual-site right atrial pacing

OBJECTIVES: We investigated 1) the feasibility, safety and efficacy of multisite right atrial pacing for prevention of atrial fibrillation (AF); and 2) the ability of atrial pacing in single- and dual-site modes to increase arrhythmia-free intervals in patients with drug-refractory AF. BACKGROUND: We recently developed and applied a novel technique of dual-site right atrial pacing in an unselected group of consecutive patients with AF requiring demand pacing. A prospective crossover study design was used to evaluate single- and dual-site right atrial pacing modes. METHODS: The frequency of AF during the 3 months before pacemaker implantation was analyzed. Consecutive consenting patients underwent insertion of two atrial leads and one ventricular lead with a DDDR pulse generator. Patients were placed in a dual-site pacing mode for the first 3 months and subsequently mode switched to single site pacing for 3 months. Mode switching was repeated at 6-month intervals thereafter. RESULTS: Atrial pacing resulted in a marked decline in AF recurrences (p < 0.001). During dual-site pacing with an optimal drug regimen, there was no AF recurrence in any patient compared with five recurrences in 12 patients during single-site pacing (p = 0.03). The mean (+/-SD) arrhythmia-free interval before pacing (14 +/- 14 days) was prolonged with dual- (89 +/- 7 days, p < 0.0001) and single-site pacing (76 +/- 27 days, p < 0.0001). Symptomatic AF episodes showed a declining trend during dual- and single-site pacing compared with those during the preimplantation period (p = 0.10). Mean antiarrhythmic drug use for all classes declined from 4 +/- 1.9 drugs before implantation to 1.5 +/- 0.5 (p < 0.01) drugs after implantation. Twelve (80%) of 15 patients remained in atrial paced rhythm at 13 +/- 3 months. CONCLUSIONS: We conclude that multisite right atrial pacing is feasible, effective and safe for long-term application. Atrial pacing significantly prolongs arrhythmia-free intervals in patients with drug-refractory paroxysmal AF. Dual-site right atrial pacing may offer additional benefits and should be considered either as the primary mode or in patients unresponsive to single-site pacing.     

Atypical form of the fourth criterion for transient entrainment

The typical fourth criterion for transient entrainment is defined when both a sudden shortening in conduction interval to and a distinct change in electrogram morphology at a bipolar recording site are demonstrated while performing overdrive pacing of a reentrant tachycardia from a single pacing site at two different constant rates. The purpose of this article was to test the hypothesis that if an intracardiac recording site showing both orthodromic and antidromic capture with entrainment pacing is located suitably distant from the circuit, sudden shortening in conduction interval to that site may occur without any significant change in the bipolar electrogram morphology (i.e., atypical form of the fourth criterion). Atrial overdrive pacing of orthodromic tachycardia was performed in 20 patients with either left anterior (12 patients) or left posterior (8 patients) accessory pathways. We investigated the effects of overdrive pacing from the proximal or distal coronary sinus, specifically effects on the electrogram interval and the electrogram morphology at the right atrial appendage. Overdrive pacing of orthodromic tachycardia from the proximal coronary sinus was performed in 10 of the 12 patients with left anterior accessory pathways; those 10 patients demonstrated the first entrainment criterion at the right atrial appendage site. Overdrive pacing of orthodromic tachycardia at still shorter cycle lengths demonstrated a sudden shortening in conduction interval to the right atrial appendage site. Despite shortening in conduction interval the morphology of the right atrial appendage electrogram was completely or almost identical to that during orthodromic tachycardia, indicating an atypical form of the fourth criterion. This criterion was not demonstrated in patients with left posterior accessory pathways. Thus, atypical fourth entrainment criterion was demonstrated during overdrive pacing of orthodromic tachycardia from the proximal coronary sinus only in patients with left anterior accessory pathways. Demonstration of atypical fourth criterion seems largely dependent on the location of the accessory pathway, the pacing, and the recording sites.     

Atrial electrograms and activation sequences in the transition between atrial fibrillation and atrial flutter

INTRODUCTION: The electrophysiologic mechanism of atrial fibrillation (AF) has a wide spectrum, and it seems that some atrial regions are essential for the occurrence of a particular type of AF. We focused on one type of AF: AF associated with typical atrial flutter (AFL), which was right atrial (RA) arrhythmia, and sought to investigate intra-atrial electrograms and activation sequences in the transition between AF and AFL. METHODS AND RESULTS: Intra-atrial electrograms and activation sequences in the RA free wall and the septum were evaluated in the transition between AF and AFL in seven patients without organic heart disease (all men; mean age 57+/-11 years). In five episodes of the conversion of AFL into AF, the AFL cycle length was shortened (from 211+/-6 msec in stable AFL to 190+/-15 msec before the conversion, P, 0.001). Interruption of the AFL wavefront and an abrupt activation sequential change induced by a premature atrial impulse resulted in fractionation and disorganization of the septal electrograms. During sustained AF, septal electrograms were persistently fractionated with disorganized activation sequences. However, the RA free-wall electrograms were organized, and the activation sequence was predominantly craniocaudal rather than caudocranial throughout AF. In 12 episodes of the conversion of AF into AFL, the AF cycle length measured in the RA free wall increased (from 165+/-26 msec at the onset of AF to 180+/-24 msec before the conversion, P, 0.001). AFL resumed when fractionated septal electrograms were separated and organized to the caudocranial direction, despite the RA free-wall electrograms remaining discrete and sharp with an isoelectric line. CONCLUSION: Changes of the electrogram and activation sequence in the atrial septum played an important role in the transition between AF and AFL.     

Chronic rapid atrial pacing. Structural, functional, and electrophysiological characteristics of a new model of sustained atrial fibrillation

BACKGROUND: Despite the clinical importance of atrial fibrillation (AF), the development of chronic nonvalvular AF models has been difficult. Animal models of sustained AF have been developed primarily in the short-term setting. Recently, models of chronic ventricular myopathy and fibrillation have been developed after several weeks of continuous rapid ventricular pacing. We hypothesized that chronic rapid atrial pacing would lead to atrial myopathy, yielding a reproducible model of sustained AF. METHODS AND RESULTS: Twenty-two halothane-anesthetized mongrel dogs underwent insertion of a transvenous lead at the right atrial appendage that was continuously paced at 400 beats per minute for 6 weeks. Two-dimensional echocardiography was performed in 11 dogs to assess the effects of rapid atrial pacing on atrial size. Atrial vulnerability was defined as the ability to induce sustained repetitive atrial responses during programmed electrical stimulation and was assessed by extrastimulus and burst-pacing techniques. Effective refractory period (ERP) was measured at two endocardial sites in the right atrium. Sustained AF was defined as AF > or = 15 minutes. In animals with sustained AF, 10 quadripolar epicardial electrodes were surgically attached to the right and left atria. The local atrial fibrillatory cycle length (AFCL) was measured in a 20-second window, and the mean AFCL was measured at each site. Marked biatrial enlargement was documented; after 6 weeks of continuous rapid atrial pacing, the left atrium was 7.8 +/- 1 cm2 at baseline versus 11.3 +/- 1 cm2 after pacing, and the right atrium was 4.3 +/- 0.7 cm2 at baseline versus 7.2 +/- 1.3 cm2 after pacing. An increase in atrial area of at least 40% was necessary to induce sustained AF and was strongly correlated with the inducibility of AF (r = .87). Electron microscopy of atrial tissue demonstrated structural changes that were characterized by an increase in mitochondrial size and number and by disruption of the sarcoplasmic reticulum. After 6 weeks of continuous rapid atrial pacing, sustained AF was induced in 18 dogs (82%) and nonsustained AF was induced in 2 dogs (9%). AF occurred spontaneously in 4 dogs (18%). Right atrial ERP, measured at cycle lengths of 400 and 300 milliseconds at baseline, was significantly shortened after pacing, from 150 +/- 8 to 127 +/- 10 milliseconds and from 147 +/- 11 to 123 +/- 12 milliseconds, respectively (P < .001). This finding was highly predictive of inducibility of AF (90%). Increased atrial area (40%) and ERP shortening were highly predictive for the induction of sustained AF (88%). Local epicardial ERP correlated well with local AFCL (R2 = .93). Mean AFCL was significantly shorter in the left atrium (81 +/- 8 milliseconds) compared with the right atrium 94 +/- 9 milliseconds (P < .05). An area in the posterior left atrium was consistently found to have a shorter AFCL (74 +/- 5 milliseconds). Cryoablation of this area was attempted in 11 dogs. In 9 dogs (82%; mean, 9.0 +/- 4.0; range, 5 to 14), AF was terminated and no longer induced after serial cryoablation. CONCLUSIONS: Sustained AF was readily inducible in most dogs (82%) after rapid atrial pacing. This model was consistently associated with biatrial myopathy and marked changes in atrial vulnerability. An area in the posterior left atrium was uniformly shown to have the shortest AFCL. The results of restoration of sinus rhythm and prevention of inducibility of AF after cryoablation of this area of the left atrium suggest that this area may be critical in the maintenance of AF in this model.     

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.     

Unusual resetting patterns in response to single atrial extrastimuli during AV junctional reentrant tachycardia

INTRODUCTION: Two unusual resetting patterns were observed in two patients with slow-fast AV junctional reentrant tachycardia (AVJRT) submitted to an electrophysiologic study. METHODS AND RESULTS: After AVJRT induction, resetting was evaluated by introducing single extrastimuli at progressively shorter coupling intervals from the high right atrium (HRA) and the proximal coronary sinus (CS). An alteration in the return cycle length duration allowed demonstration of resetting. In the first patient, during and AVJRT with a large excitable gap, properly timed extrastimuli delivered both from the HRA and CS simultaneously reset the tachycardia and advanced the H electrogram of the preceding tachycardia beat. In the second patient, both HRA and CS stimulation apparently failed to reset AVJRT (return cycle length unchanged), but, at critical coupling intervals, the cycle length duration of the tachycardia beat following the return cycle was consistently shortened. CONCLUSION: During slow-fast AVJRT, single atrial stimulation from sites remote to the reentrant circuit may result in unusual resetting patterns. Further studies are required to evidence the full spectrum of resetting in AVJRT.     

Modulation of atrial repolarization by site of pacing in the isolated rabbit heart

BACKGROUND: Single-site or multisite atrial pacing may reduce the incidence of atrial fibrillation in humans. The therapeutic mechanisms may include synchronization of atrial repolarization (repolarization "memory") and/or decreased dispersion of atrial repolarization. These responses have not been well documented in intact atria. METHODS AND RESULTS: Monophasic action potential recordings were made from six atrial epicardial sites in 39 isolated perfused rabbit heart preparations during 3 hours of continuous right atrial, left atrial, or biatrial pacing. Action potential recordings obtained at times 0, 45, 90, 135, and 180 minutes were computer analyzed for activation time (AT) and 90% action potential duration (APD) at each site. No consistent relationship could be demonstrated between APD and AT at any time during atrial pacing (all P > .05). On average, left atrial APDs were longer than right atrial APDs by up to 6.3 ms at all times, regardless of the site of pacing (P < or = .05). At all times, dispersion of atrial repolarization was minimized by left atrial pacing compared with right atrial pacing (21.6 +/- 9.1 versus 32.4 +/- 15.1 ms, respectively, at time 0; P < .05). Biatrial pacing provided no further reduction in dispersion of repolarization compared with left atrial pacing (all P > .05). CONCLUSIONS: No relationship can be demonstrated between atrial AT and APD in the isolated rabbit heart preparation. This differs from ventricular repolarization "memory," which is demonstrable under the same conditions. Left atrial APD is, on average, longer than right atrial APD, suggesting spatial heterogeneity in repolarization. Dispersion of atrial repolarization is minimized by left atrial pacing in this preparation with no further advantage to biatrial pacing.     

New diagnostic finding to assess para-Hisian pacing observed in a patient with a permanent form of junctional reciprocating tachycardia

Para-Hisian pacing, a useful method to differentiate conduction over an accessory pathway from conduction over the AV node, is assessed essentially by comparing the timing of local atrial electrograms between His-bundle captured beats and His-bundle noncaptured beats. We describe the case of a patient with a permanent form of junctional reciprocating tachycardia, in whom an atrial double potential was recorded only during the tachycardia at the right posterior septum. During para-Hisian pacing, a morphologic change in the atrial electrogram at the posterior septum was also identified, as well as a change in the retrograde atrial sequence. Since the morphologic change of atrial electrograms during para-Hisian pacing cannot be demonstrated in a patient without an accessory pathway, this new finding could be considered a new additional diagnostic criterion suggesting the presence of an accessory pathway.     

Configuration of unipolar atrial electrograms during electrically induced atrial fibrillation in humans

BACKGROUND: During atrial fibrillation (AF), the atrium is activated by multiple wavelets that continuously change in size and direction. The aim of this study was to correlate the temporal variation in AF electrogram configuration with the varying spatial patterns of activation. METHODS AND RESULTS: In a group of 25 Wolff-Parkinson-White patients undergoing cardiac surgery, the free wall of the right atrium was mapped (244 points) during electrically induced AF. The unipolar electrograms recorded during 4 seconds of AF were classified into four categories: (1) single deflections, (2) short-double potentials, (3) long-double potentials, and (4) fragmented potentials. The proportion of these four types of electrograms during AF was as follows: singles, 77 +/- 12%; short-doubles, 7 +/- 3%; long-doubles, 10 +/- 7%; and fragmented, 6 +/- 4%. Electrogram morphology was an indicator for rapid uniform conduction (single potentials; positive predictive value [PPV] of 0.96), collision (short-double potentials; PPV of 0.33), conduction block (long-double potentials; PPV of 0.84), and pivoting points or slow conduction (fragmented potentials; PPV of 0.87). In type I, II, and III AF, the proportion of long-double potentials was 4 +/- 2%, 12 +/- 3%, and 18 +/- 7% (P < .05); the proportion of fragmented complexes was 2 +/- 2%, 6 +/- 3%, and 10 +/- 4% (P < .05), respectively. During electrically induced and self-terminating episodes of AF, no preferential anatomic sites for double or fragmented potentials were found in the right atrium. CONCLUSIONS: The morphology of single unipolar electrograms during AF reflects the occurrence of various specific patterns of conduction. This might be used to differentiate between different types of AF and to identify regions with structural conduction disturbances involved in perpetuation of chronic AF.     

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.     

Radiofrequency catheter ablation of concealed atrioventricular accessory pathways using a "simultaneous pacing method"

The retrograde atrial potential at a successful ablation site is usually obscured by the wide and large ventricular potential during atrioventricular reentrant tachycardia or ventricular pacing, which makes it difficult to determine the appropriate ablation site for a concealed accessory pathway. A pacing maneuver named the "simultaneous pacing method" is proposed herein to differentiate the retrograde atrial potential from the ventricular potential for a successful ablation of the concealed accessory pathway. Catheter ablation was performed in 12 patients with a single left free-wall concealed accessory pathway. The atrial insertion site was determined by the simultaneous pacing method in six patients (group I) and by ventricular pacing in six patients (group II). In the simultaneous pacing method, electrograms recorded during ventricular pacing in the earliest retrograde atrial activation site are a fusion of the ventricular potential and the following retrograde atrial potential. When atrial and ventricular pacings are performed simultaneously (simultaneous pacing), the end portion of the electrograms recorded at the same site is solely the ventricular component, because atrial is activated earlier. The atrial potential can be confirmed during ventricular pacing in comparison with the electrograms during the "simultaneous pacing." Radiofrequency catheter ablation was successful in eliminating conduction through the accessory pathway in all 12 patients. The radiofrequency applications in group I were significantly fewer than those in group II (1.7 +/- 1.0 in group I, 5.3 +/- 3.2 in group II, P < 0.05). The total procedure time in group I was significantly shorter than in group II (57.8 +/- 15.7 vs 106.7 +/- 41.6 mins in group II, respectively, P < 0.05). The fluoroscopy time in group I was significantly shorter than in group II (54.0 +/- 7.9 vs 81.3 +/- 26.3 mins, respectively, P < 0.05). We were able to determine the atrial insertion site of accessory pathways by the simultaneous pacing method. The simultaneous pacing method was useful in eliminating concealed left free-wall accessory pathways.     

Direct conversion of atrial flutter to sinus rhythm with low-output, short-duration transesophageal atrial pacing

BACKGROUND AND HYPOTHESIS: Transesophageal atrial pacing (TAP) is useful for terminating paroxysmal non-self terminating atrial flutter (PAF); however, high output pacing of long stimulus duration causes severe symptoms such as chest pain. The objective of this study was to investigate the effect of low-output, short-duration TAP on the conversion of PAF. METHODS: We applied low-output (within 15 mA with a pulse duration of 10 ms), short-duration (within 4 s) TAP in 31 patients (50 +/- 19 years) with PAF. Transesophageal pacing was delivered with 10 pulses of burst pacing at intervals that were 20 ms shorter than those of the flutter wave length. When the conversion was unsuccessful, we delivered 20 pulses of burst pacing. RESULTS: Sixteen patients (52%) were converted directly to sinus rhythm and 12 (38%) to atrial fibrillation. Transesophageal pacing was ineffective in 3 (10%) patients. The duration of atrial flutter, maximum flutter wave amplitude, effective pacing intervals, underlying heart diseases, and cardiac function were not different between patients who had direct conversion to sinus rhythm and those converted to atrial fibrillation. The patients who had direct conversion to sinus rhythm had longer flutter wave cycle lengths than those converted to atrial fibrillation (248 vs. 221 ms, p < 0.005). No patient had complications and complained of any symptoms. CONCLUSION: Low-output, short-duration TAP was useful to convert PAF directly to sinus rhythm without side effects.     

VDDR pacing after His-bundle ablation for paroxysmal atrial fibrillation: a pilot study

His-bundle ablation followed by pacemaker implantation is today a widely accepted therapeutic choice when drug refractoriness of symptomatic AF is evident. The selection of pacing mode in patients suffering from paroxysmal AF is still controversial. Preservation of AV synchrony is an attractive option in patients with paroxysmal AF who undergo His-bundle ablation. The purpose of this study was to examine prospectively the contribution of VDDR pacing for preservation of AV synchrony. After His-bundle ablation a VDDR pacing system was implanted in 17 patients with paroxysmal AF, and all antiarrhythmic drugs were withdrawn. The endpoint of the study was defined as the onset of chronic AF. To document the onset of chronic AF 48-hour Holter recordings were made every 6-8 weeks. After a mean followup of 18.2 (range 14-21) months, VDDR pacing is still operative in 13 patients (77%). Four patients developed chronic AF after a mean follow-up of 6 months. Of several baseline characteristics, only the intraatrial P wave at implantation was significantly smaller in patients developing chronic AF than in patients in whom the VDDR mode is still operative. This pilot study suggests that VDDR pacing is an attractive pacing method for patients with paroxysmal AF after His-bundle ablation. A low intraatrial P wave electrogram at implant was associated with a higher risk for the development of chronic AF.     

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.     

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.     

Permanent pervenous atrial pacing

A new J-lead has now been designed and manufactured for both animal and clinical studies. This lead has silastic tines proximal to the electrode, arranged so that they become entangled in the trabeculae of the appendage and hold the lead in place. Studies in ten dogs have shown excellent tissue fixation at the site of the tines, and only minimal scarring occurs at the site of the terminal electrode, with preservation of good P-wave amplitude and good stimulating thresholds for a period of four to five months (Figure 8, see next page). The lead designed for humans has been used successfully in 12 patients. Follow-up now extends to 19 months, with stable P-wave-triggered atrial pacing in eight patients, fixed rate atrial pacing in one, and A-V synchronized pacing in three. No lead dislodgement has occurred.