Characterization of low right atrial isthmus as the slow conduction zone and pharmacological target in typical atrial flutter

BACKGROUND: Previous electrophysiological studies in patients with typical atrial flutter suggested that the slow conduction zone might be located in the low right atrial isthmus, which is a path formed by orifice of inferior vena cava, eustachian valve/ridge, coronary sinus ostium, and tricuspid annulus. The conduction characteristics during atrial pacing and responses to antiarrhythmic drugs of this anatomic isthmus were unknown. METHODS AND RESULTS: Forty-four patients, 20 patients with paroxysmal supraventricular tachycardia (group 1) and 24 patients with clinically documented paroxysmal typical atrial flutter (group 2), were studied. A 20-pole halo catheter was situated around the tricuspid annulus. Incremental pacing from the low right atrium and coronary sinus ostium was performed to measure the conduction time and velocity along the isthmus and lateral wall in the baseline state and after intravenous infusion of procainamide or sotalol. In both groups, conduction velocity in the isthmus during incremental pacing was significantly lower than that in the lateral wall before and after infusion of antiarrhythmic drugs. Furthermore, gradual conduction delay with unidirectional block in the isthmus was relevant to initiation of typical atrial flutter. Compared with group 1, group 2 had a lower conduction velocity in the isthmus and shorter right atrial refractory period. Procainamide significantly decreased the conduction velocity, but sotalol did not change it. In contrast, sotalol significantly prolonged the atrial refractory period with a higher extent than procainamide. After infusion of procainamide, the increase of conduction time in the isthmus accounted for 52+/-19% of the increase in flutter cycle length, and 5 of 12 patients (42%) had spontaneous termination of typical flutter. After infusion of sotalol, typical flutter was induced in only 6 of 12 patients (50%) without significant prolongation of flutter cycle length. CONCLUSIONS: The low right atrial isthmus with rate-dependent slow conduction properties is critical to initiation of typical human atrial flutter. It may be the potentially pharmacological target of antiarrhythmic drugs in the future.     

Effects of azimilide dihydrochloride on circus movement atrial flutter in the canine sterile pericarditis model

INTRODUCTION: The effects of a Class III agent, azimilide dihydrochloride, on atrial flutter circuits were studies in a functional model of single loop reentrant atrial flutter using dogs, 3 to 5 days after production of sterile pericarditis. METHODS AND RESULTS: A computerized mapping system was used to construct activation maps from 138 to 222 epicardial sites in the right atrium. Doses of 3, 10, and 30 mg/kg i.v. azimilide dihydrochloride were analyzed in 8 dogs in which sustained atrial flutter lasting more than 30 minutes was induced by burst pacing. Atrial flutter was always due to single loop circus movement reentry in the lower right atrium. At 3 mg/kg, azimilide dihydrochloride terminated atrial flutter in 2 dogs; however, atrial flutter was reinduced. At 10 mg/kg, atrial flutter was terminated in all 8 dogs but was reinduced in 4 dogs with slower rate. At 30 mg/kg, atrial flutter was terminated in the remaining 4 dogs and could not be reinduced. Atrial flutter cycle length always increased prior to termination. Isochronal activation maps showed that the increase in cycle length was due to additional conduction delays in the slow zone of the reentrant circuit. The site of termination was always located within the slow conduction zone situated in the lower right atrium between the line of functional conduction block and the AV ring. Effective refractory periods (ERPs) were measured at selected sites in the slow zone and normal zone at twice diastolic threshold for the 10 mg/kg dose. Azimilide preferentially prolonged ERP in the slow zone (42.4 +/- 20.1 msec, mean +/- SD) compared with the normal zone (23.3 +/- 15.4 msec, P < 0.0001). The increase in cycle length corresponded with the increase in ERP in the slow zone. CONCLUSIONS: In a functional model of circus movement atrial flutter, azimilide dihydrochloride terminates and prevents reinduction of atrial flutter by a preferential increase in refractoriness leading to further conduction delay and conduction block in the slow zone of the functional reentrant circuit.     

Conduction properties of the inferior vena cava-tricuspid annular isthmus in patients with typical atrial flutter

INTRODUCTION: A functional region of slow conduction located in the inferior right atrium has been postulated to be critical to the induction and maintenance of typical human atrial flutter. We reexamined the potential role of functional conduction delay in the annular isthmus between the tricuspid valve and the inferior vena cava; it is within this region that such delays have been postulated to occur, and where interruption of conduction by radiofrequency energy application has been shown to eliminate typical flutter. METHODS AND RESULTS: Thirty patients with type I atrial flutter (30 counterclockwise, 14 clockwise) were studied. Counterclockwise and clockwise isthmus activation times adjacent and parallel to the tricuspid valve were measured during three conditions: (1) atrial pacing in sinus rhythm, (2) atrial flutter, and (3) entrainment of atrial flutter. During pacing in sinus rhythm at progressively shorter cycle lengths, both counterclockwise and clockwise isthmus activation times remained unchanged; decremental conduction prior to flutter induction or loss of capture was not observed. Counterclockwise isthmus activation time did not significantly differ during flutter (68 +/- 23 msec), inferolateral tricuspid annulus pacing (71 +/- 23 msec), or entrainment of flutter (72 +/- 23 msec). Similarly, clockwise isthmus activation times did not significantly differ between flutter (65 +/- 22 msec), proximal coronary sinus pacing (73 +/- 21 msec), or entrainment of flutter (64 +/- 15 msec). CONCLUSION: Decremental conduction is not characteristic of activation through the isthmus when activation is assessed parallel and adjacent to the tricuspid annulus. Functional slowing or conduction delay does not develop in this region during typical atrial flutter.     

Conduction properties of the crista terminalis in patients with typical atrial flutter: basis for a line of block in the reentrant circuit

INTRODUCTION: Previous mapping studies in patients with typical atrial flutter have demonstrated the crista terminalis to be a posterior barrier of the reentrant circuit forming a line of block. However, the functional role of the crista terminalis in patients with or without a history of atrial flutter is not well known. The aim of this study was to determine whether the conduction properties of the crista terminalis are different between patients with and those without a history of atrial flutter. METHODS AND RESULTS: The study population consisted of 12 patients with clinically documented atrial flutter (group 1) and 12 patients with paroxysmal supraventricular tachycardia as well as induced atrial flutter (group 2). A 7-French, 20-pole, deflectable Halo catheter was positioned around the tricuspid annulus. A 7-French, 20-pole Crista catheter was placed along the crista terminalis identified by the recording of double potentials with opposite activation sequences during typical atrial flutter. After sinus rhythm was restored, pacing from the low posterior right atrium near the crista terminalis was performed at multiple cycle length to 2:1 atrial capture. No double potentials were recorded along the crista terminalis during sinus rhythm in both groups. In group 1, the longest pacing cycle length that resulted in a line of block with double potentials along the crista terminalis was 638 +/- 119 msec. After infusion of propranolol, it was prolonged to 832 +/- 93 msec without change of the interdeflection intervals of double potentials. In group 2, the longest pacing cycle length that resulted in a line of block with double potentials along the crista terminalis was 214 +/- 23 msec. After infusion of procainamide, it was prolonged to 306 +/- 36 msec with increase of interdeflection interval of double potentials. CONCLUSION: The crista terminalis forms a line of transverse conduction block during typical atrial flutter. Poor transverse conduction property in the crista terminalis may be the requisite substrate for clinical occurrence of typical atrial flutter.     

Characterization of the excitable gap in human type I atrial flutter

OBJECTIVES: We sought to characterize the excitable gap of the reentrant circuit in atrial flutter. BACKGROUND: The electrophysiologic substrate of typical atrial flutter has not been well characterized. Specifically, it is not known whether the properties of the tricuspid valve isthmus differ from those of the remainder of the circuit. METHODS: Resetting was performed from two sites within the circuit: proximal (site A) and distal (site B) to the isthmus in 14 patients with type I atrial flutter. Resetting response patterns and the location where interval-dependent conduction slowing occurred were assessed. RESULTS: Some duration of a flat resetting response (mean +/- SD 40.1 +/- 20.9 ms, 16 +/- 8% of the cycle length) was observed in 13 of 14 patients; 1 patient had a purely increasing response. During the increasing portion of the resetting curve, interval-dependent conduction delay most commonly occurred in the isthmus. In most cases, the resetting response was similar at both sites. In three patients, the resetting response differed significantly between the two sites; this finding suggests that paced beats may transiently change conduction within the circuit or the circuit path, or both. CONCLUSIONS: Some duration of a flat resetting response was observed in most cases of type I atrial flutter, signifying a fully excitable gap in all portions of the circuit. The isthmus represents the portion of the circuit most vulnerable to interval-dependent conduction delay at short coupling intervals.     

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.     

Role of the tricuspid annulus and the eustachian valve/ridge on atrial flutter. Relevance to catheter ablation of the septal isthmus and a new technique for rapid identification of ablation success

BACKGROUND: Typical atrial flutter (AFL) results from right atrial reentry by propagation through an isthmus between the inferior vena cava (IVC) and tricuspid annulus (TA). We postulated that the eustachian valve and ridge (EVR) forms a line of conduction block between the IVC and coronary sinus (CS) ostium and forms a second isthmus (septal isthmus) between the TA and CS ostium. METHODS AND RESULTS: Endocardial mapping in 30 patients with AFL demonstrated atrial activation around the TA in the counter-clockwise direction (left anterior oblique projection). Double atrial potentials were recorded along the EVR in all patients during AFL. Pacing either side of the EVR during sinus rhythm also produced double potentials, which indicated fixed anatomic block across EVR. Entrainment pacing at the septal isthmus and multiple sites around the TA produced a delta return interval < or = 8 ms in 14 of 15 patients tested. Catheter ablation eliminated AFL in all patients by ablation of the septal isthmus in 26 patients and the posterior isthmus in 4. AFL recurred in 2 of 12 patients (mean follow-up, 33.9 +/- 16.3 months) in whom ablation success was defined by the inability to reinduce AFL, compared with none of 18 patients (mean follow-up, 10.3 +/- 8.3 months) in whom success required formation of a complete line of conduction block between the TA and the EVR, identified by CS pacing that produced atrial activation around the TA only in the counterclockwise direction and by pacing the posterior TA with only clockwise atrial activation. CONCLUSIONS: (1) The EVR forms a line of fixed conduction block between the IVC and the CS; (2) the EVR and the TA provide boundaries for the AFL reentrant circuit; and (3) verification of a complete line of block between the TA and the EVR is a more reliable criterion for long-term ablation success.     

Detection of BK polyomavirus genotypes in healthy and HIV-positive children

BACKGROUND: Atrial flutter is a common arrhythmia which frequently recurs after cardioversion and is relatively difficult to control with antiarrhythmic agents. AIMS: To evaluate the success rate, recurrence rate and safety of radiofrequency, (RF) ablation for atrial flutter in a consecutive series of patients with drug refractory chronic or paroxysmal forms of the arrhythmia. METHODS: Electrophysiologic evaluation of atrial flutter included activation mapping with a 20 electrode halo catheter placed around the tricuspid annulus and entrainment mapping from within the low right atrial isthmus. After confirmation of the arrhythmia mechanism with these techniques, an anatomic approach was used to create a linear lesion between the inferior tricuspid annulus and the eustachian ridge at the anterior margin of the inferior vena cava. In order to demonstrate successful ablation, mapping techniques were employed to show that bi-directional conduction block was present in the low right atrial isthmus. RESULTS: Successful ablation was achieved in 26/27 patients (96%). In one patient with a grossly enlarged right atrium, isthmus block could not be achieved. Of the 26 patients with successful ablation, there has been one recurrence of typical flutter (4%) during a mean follow-up period of 5.5 +/- 2.7 months. This patient underwent a successful repeat ablation procedure. Of eight patients with documented clinical atrial fibrillation (in addition to atrial flutter) prior to the procedure, five continued to have atrial fibrillation following the ablation. There were no procedural complications and all patients had normal AV conduction at the completion of the ablation. CONCLUSIONS: RF ablation is a highly effective and safe procedure for cure of atrial flutter. In patients with chronic or recurrent forms of atrial flutter RF ablation should be considered as a first line therapeutic option.     

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.     

Differential effect of adenosine on anterograde and retrograde fast pathway conduction in patients with atrioventricular nodal reentrant tachycardia

INTRODUCTION: Several studies have shown that the fast pathway is more responsive to adenosine than the slow pathway in patients with AV nodal reentrant tachycardia. Little information is available regarding the effect of adenosine on anterograde and retrograde fast pathway conduction. METHODS AND RESULTS: The effects of adenosine on anterograde and retrograde fast pathway conduction were evaluated in 116 patients (mean age 47 +/- 16 years) with typical AV nodal reentrant tachycardia. Each patient received 12 mg of adenosine during ventricular pacing at a cycle length 20 msec longer than the fast pathway VA block cycle length and during sinus rhythm or atrial pacing at 20 msec longer than the fast pathway AV block cycle length. Anterograde block occurred in 98% of patients compared with retrograde fast pathway block in 62% of patients (P < 0.001). Unresponsiveness of the retrograde fast pathway to adenosine was associated with a shorter AV block cycle length (374 +/- 78 vs 333 +/- 74 msec, P < 0.01), a shorter VA block cycle length (383 +/- 121 vs 307 +/- 49 msec, P < 0.001), and a shorter VA interval during tachycardia (53 +/- 23 vs 41 +/- 17 msec, P < 0.01). CONCLUSION: Although anterograde fast pathway conduction is almost always blocked by 12 mg of adenosine, retrograde fast pathway conduction is not blocked by adenosine in 38% of patients with typical AV nodal reentrant tachycardia. This indicates that the anterograde and retrograde fast pathways may be anatomically and/or functionally distinct. Unresponsiveness of VA conduction to adenosine is not a reliable indicator of an accessory pathway.     

New classification of moricizine and propafenone based on electrophysiologic and electrocardiographic data from isolated rabbit heart

Because the classification of propafenone and moricizine is not clear, we measured in 20 specifically equipped isolated rabbit hearts QRS duration, QT interval, action potential duration at 90% of repolarization (APD90), effective refractory period (ERP), conduction time (CT), and rise velocity (Rv) of the monophasic action potentials (AP) during exposure to moricizine and propafenone in comparison with procainamide. Propafenone and procainamide prolonged APD90 and JT. All drugs increased ERP. Propafenone demonstrated marked tonic sodium channel block. Onset of use-dependent kinetics (tau on), defined as change in Rv as fraction per beat at 300 ms cycle length (CL), were 0.047 +/- 0.004/beat for procainamide, 0.050 +/- 0.004/beat for propafenone, and 0.022 +/- 0.003/beat for miricizine. Recovery kinetics, defined as recovery of Rv after cessation of pacing, had a time constant of 5.3 +/- 0.7 s for procainamide, 6.3 +/- 0.8 s for propafenone, and 25.0 +/- 1.3 s for moricizine. Based on these data, moricizine must be classified as a Ic agent, whereas propafenone demonstrates pronounced tonic sodium channel block, in addition to its phasic block, which is similar to class Ia kinetics.     

Clinical study on 6 cases of urosepsis associated with septic shock

A linear lesion created at the right atrial isthmus by radiofrequency current application can successfully eliminate common atrial flutter (AF). The mechanism of unsuccessful cases has not yet been well delineated. This study sought to investigate the cause of unsuccessful cases of radiofrequency catheter ablation of AF. Sixty-six patients with refractory common AF were referred for radiofrequency catheter ablation. Radiofrequency current was applied to the right atrial isthmus between the inferior vena cava and tricuspid annulus or between the coronary sinus orifice and tricuspid annulus. In 5 (8%) of the 66 patients, a morphological change of the flutter wave was observed in the 12-lead ECG concomitant with the change of the atrial excitation sequence during the delivery of radiofrequency energy without the termination of atrial flutter. In 8 (12%) patients, the morphology of the new AF wave, which was provoked electrically after the termination of the original AF, was different, and the average flutter cycle length also differed in 3 cases (2%). The results of radiofrequency application could be misinterpreted as unsuccessful when the occurrence of another, different type of AF has been overlooked following the elimination of the original AF during the radiofrequency catheter ablation procedure. It is possible that the flutter circuit can take an alternative pathway despite the complete conduction block at the right atrial isthmus.     

Atrial flutter with 1:1 atrioventricular conduction caused by propafenone

We describe a case of 1:1 atrial flutter in a patient with coronary disease taking propafenone. In atrial flutter, the atrial rate is usually about 300 beats/min with 2:1 AV conduction and a ventricular rate of 150 beats/min. Class IA antiarrhythmic drugs, especially quinidine and disopyramide, may cause 1:1 AV response because they reduce atrial rate and are vagolytic. However, propafenone is a Class IC agent and has no anticholinergic properties, and the occurrence of 1:1 AV conduction at a rate of about 250 beats/min is an important side effect that, although uncommon, should be recognized.     

Conversion efficacy and safety of intravenous ibutilide compared with intravenous procainamide in patients with atrial flutter or fibrillation

OBJECTIVES: This multicenter study compared the efficacy and safety of ibutilide versus procainamide for conversion of recent-onset atrial flutter or fibrillation. BACKGROUND: Ibutilide fumarate is an intravenous (IV) class III antiarrhythmic agent that has been shown to be significantly more effective than placebo in the pharmacologic conversion of atrial flutter and fibrillation to sinus rhythm. Procainamide is commonly used for conversion of recent-onset atrial fibrillation to normal sinus rhythm. METHODS: One hundred twenty-seven patients (age range 22 to 92 years) with atrial flutter or fibrillation of 3 h to 90 days' (mean 21 days) duration were randomized to receive either two 10-min IV infusions of 1 mg of ibutilide fumarate, separated by a 10-min infusion of 5% dextrose in sterile water, or three successive 10-min IV infusions of 400 mg of procainamide hydrochloride. RESULTS: Of the 127 patients, 120 were evaluated for efficacy: 35 (58.3%) of 60 in the ibutilide group compared with 11 (18.3%) of 60 in the procainamide group had successful termination within 1.5 h of treatment (p < 0.0001). Seven patients were found to have violated the protocol and were not included in the final evaluation. In the patients with atrial flutter, ibutilide had a significantly higher success rate than procainamide (76% [13 of 17] vs. 14% [3 of 22], p=0.001). Similarly, in the atrial fibrillation group, ibutilide had a significantly higher success rate than procainamide (51% [22 of 43] vs. 21% [8 of 38], p=0.005). One patient who received ibutilide, which was found to be a protocol violation, had sustained polymorphic ventricular tachycardia requiring direct current cardioversion. Seven patients who received procainamide became hypotensive. CONCLUSIONS: This study establishes the superior efficacy of ibutilide over procainamide when administered to patients to convert either atrial fibrillation or atrial flutter to sinus rhythm. Hypotension was the major adverse effect seen with procainamide. A low incidence of serious proarrhythmia was seen with the administration of ibutilide occurring at the end of infusion.     

Isolated paralysis of the ramus marginalis mandibulae nervi facialis: clinical aspects, etiology, diagnosis and therapy. An overview]

INTRODUCTION: Little is known about the predictors of recurrent atrial flutter or fibrillation after successful radiofrequency ablation of typical atrial flutter. In addition, there is only limited evidence suggesting that elimination of atrial flutter would modify the natural history of atrial fibrillation in patients who experienced both of these arrhythmias. The aims of the present study were to investigate the long-term results of radiofrequency catheter ablation and to examine the predictors for late occurrence of atrial fibrillation in a large population with typical atrial flutter. METHODS AND RESULTS: The study population consisted of 144 patients (mean age 56 +/- 18 years) with successful ablation of clinically documented typical atrial flutter. In the first 50 patients, successful ablation was defined as termination and noninducibility of atrial flutter; for the subsequent 94 patients, successful ablation was defined as achievement of bidirectional isthmus conduction block and no induction of atrial flutter. The clinical and echocardiographic variables were analyzed in relation to the late occurrence of atrial flutter or fibrillation. Over the follow-up period of 17 +/- 13 months, 14 (9.7%) patients had recurrence of typical atrial flutter. In the first 50 patients, 8 (16%) had recurrence of atrial flutter, compared with only 6 (6%) of the following 94 patients. Patients with incomplete isthmus block had a significantly higher incidence of recurrent atrial flutter than those with complete isthmus block (6/16 vs 0/78, P < 0.0001) in the following 94 patients. There was no predictor for recurrence of atrial flutter after successful ablation as determined by univariate and multivariate analysis. Although successful ablation of atrial flutter eliminated atrial fibrillation in 45% of patients with a prior history of atrial fibrillation, 31 (21.5%) of 144 patients undergoing this procedure developed atrial fibrillation during the follow-up period. Univariate analysis revealed that three clinical variables were related to the occurrence of atrial fibrillation: (1) the presence of structural heart disease; (2) a history of atrial fibrillation before ablation; and (3) inducible sustained atrial fibrillation after ablation. By multivariate analysis, only a history of atrial fibrillation and inducible sustained atrial fibrillation could predict the late development of atrial fibrillation after atrial flutter ablation. CONCLUSION: Radiofrequency catheter ablation of typical atrial flutter is highly effective and associated with a low recurrence rate of atrial flutter, but atrial fibrillation continues to be a long-term risk for patients undergoing this procedure. The presence of structural heart disease and prior spontaneous or inducible sustained atrial fibrillation increases the risk of developing atrial fibrillation.     

Complex electrophysiological characteristics in atrioventricular nodal reentrant tachycardia with continuous atrioventricular node function curves

BACKGROUND: Although typical atrioventricular nodal reentrant tachycardia (AVNRT) with discontinuous AV node function curves has been well studied, there has been a lack of any significant information about AVNRT without evidence of dual AV nodal pathway physiology during atrial extrastimulus testing or atrial pacing. METHODS AND RESULTS: Group 1 included 9 patients with continuous curves during atrial extrastimulus testing but without a jump (> or = 50 ms) of the atrial-His bundle (AH) interval during incremental atrial pacing. The maximal AH interval during atrial pacing (266 +/- 61 versus 168 +/- 27 ms, P = .007) or extrastimulus testing (290 +/- 60 versus 176 +/- 18 ms, P = .005) shortened significantly after ablation. Antegrade and retrograde AV node properties were similar before and after ablation. Group 2 included 14 patients with continuous curves and a jump of the AH interval during incremental atrial pacing. The atrial pacing cycle length with 1:1 AV conduction and effective refractory period (ERP) of the antegrade AV node increased significantly, whereas the maximal AH interval during atrial pacing (358 +/- 70 versus 203 +/- 28 ms, P = .001) or extrastimulus testing (338 +/- 75 versus 196 +/- 34 ms, P = .002) shortened significantly after ablation. Group 3 included 24 patients with discontinuous curves. The maximal AH interval during atrial pacing or extrastimulus testing and the ERP of the antegrade fast AV node shortened, whereas the ERP of the antegrade AV node increased significantly after ablation. The maximal AH interval before ablation, extent of decrease in maximal AH interval after ablation, ERP of the retrograde AV node before ablation, and tachycardia cycle length were significantly shorter in group 1 than groups 2 and 3. CONCLUSIONS: In AVNRT with continuous AV node function curves, dual AV nodal pathway physiology may or may not be demonstrated during atrial pacing. Significant shortening of the maximal AH interval during atrial pacing after radiofrequency ablation suggests successful elimination of AVNRT.     

Frequency-dependent effects of propafenone decrease with duration of ventricular tachycardia in isolated guinea pig hearts

Na+ channel blockers terminate tachyarrhythmias primarily by rate-dependent effects. The purpose of this study was to investigate the use-dependent effects of propafenone in isolated guinea pig and rabbit hearts perfused by the method of Langendorff. In the presence of propafenone (0.3 microM) during ventricular pacing, an abrupt decrease of the pacing cycle length (220 ms to 120 ms) slowed the intraventricular conduction with a transient peak QRS prolongation of 33.8 +/- 2.0% after 5.7 +/- 0.5 s (P < 0.01) which subsequently decreased to a steady state of 14.0 +/- 2.5% after 38.0 +/- 5.5 s (mean +/- S.E.M.; n = 10; P < 0.01). The ventricular effective refractory period was significantly prolonged if evaluated by a train of 10 basic stimuli (S1) (interstimulus interval: 120 ms) followed by a premature stimulus (S2). However, when the train of basic stimuli was increased the effective refractory period diminished progressively. An initial increase in total activation time vanished with continued rapid ventricular stimulation. These effects may be explained by a shortening of the action potential during high rates resulting in a decreased binding of propafenone to Na+ channels.     

Induction of atrioventricular node reentrant tachycardia with adenosine: differential effect of adenosine on fast and slow atrioventricular node pathways

OBJECTIVES: This study sought to evaluate the sensitivity of fast and slow atrioventricular (AV) node pathways to incremental doses of adenosine in patients with typical AV node reentrant tachycardia. BACKGROUND: Although adenosine is known to depress conduction through the AV node, the relative sensitivity to adenosine of the anterograde fast and slow pathways in patients with dual AV node pathways and typical AV node reentrant tachycardia has not previously been studied. METHODS: Sixteen patients with dual AV node physiology and typical AV node reentrant tachycardia and 10 control patients were given incremental doses of adenosine during atrial pacing. RESULTS: In 14 of 16 patients with dual-AV node physiology, administration of small doses of adenosine during atrial pacing led consistently to transient block of impulse conduction in the fast pathway before block in the slow pathway, resulting in abrupt prolongation of the AH interval with continued 1:1 AV conduction. The mean (+/- SD) doses of adenosine required to cause conduction block in the fast and slow pathways were 2.7 +/- 3.0 and 7.2 +/- 4.7 mg, respectively (p = 0.004). In 9 of 16 patients, administration of low dose adenosine led to initiation of AV node reentrant tachycardia. The control patients showed no abrupt increases in AH interval with administration of adenosine during atrial pacing. CONCLUSIONS: In most patients with dual AV node pathways and typical AV node reentrant tachycardia, the fast pathway is more sensitive than the slow pathway to the effects of adenosine.     

Procainamide induced change of the width of the zone of entrainment and its relation to the inducibility of reentrant ventricular tachycardia

Procainamide depresses conduction velocity and prolongs refractoriness in myocardium responsible for reentrant VT, but the mechanism by which the induction of VT is suppressed after procainamide administration remains to be determined. In the present study, the relationship between electrophysiological parameters and the noninducibility of VT was assessed during procainamide therapy with a special reference to the change of an excitable gap. Clinically documented monomorphic sustained VT was induced in 30 patients and, utilizing the phenomenon of transient entrainment, the zone of entrainment was measured as the difference between the cycle length of VT and the longest paced cycle length interrupting VT (block cycle length) which was determined as the paced cycle length decreased in steps of 10 ms, and used as an index of the excitable gap. The effective refractory period was measured at the pacing site and the paced QRS duration was used as an index of the global conduction time in the ventricle. The cycle length of VT, the block cycle length, and the width of the zone of entrainment were determined and compared between the responders and nonresponders. In 15 patients, these parameters were determined at the intermediate dose and related to subsequent noninducibility at the final dose. At the final doses of procainamide, VT was suppressed in 8 (26.7%) of 30 patients. However, the cycle length of VT, the block cycle length, and the width of the zone of entrainment were unable to predict the drug efficacy, i.e., noninducibility. The change in the effective refractory period at the pacing site or the width of the paced QRS duration was not different between the responders and nonresponders. Among the variables, only the width of the zone of entrainment showed a significant narrowing in the responders at the intermediate dose of procainamide, and it was smaller than that of the nonresponders. The significant narrowing of the width of the zone of entrainment was associated with the subsequent noninducibility of VT at the final dose. The present study showed that the baseline cycle length of VT, the block cycle length, the drug induced change of the effective refractory period, or the paced QRS duration was not a predictor of the noninducibility after procainamide administration. However, a significant narrowing of the width of the zone of entrainment at the intermediate dose was associated with the noninducibility of VT at the final dose.     

Electrophysiological effects of catheter ablation of inferior vena cava-tricuspid annulus isthmus in common atrial flutter

BACKGROUND: The electrophysiological mechanisms for successful catheter ablation of atrial flutter (AFI) targeting the inferior vena cava-tricuspid annulus (IVC-TA) isthmus have not been determined. METHODS AND RESULTS: Twenty patients with common AFI were studied. All had inducible common AFI, and 8 of them had both common and reverse AFI. Right atrial (RA) activation sequences were investigated during pacing from sites proximal (low lateral RA) and distal (proximal coronary sinus) to the IVC-TA isthmus both during entrainment of common or reverse AFI and during pacing in sinus rhythm. This was repeated after ablation. During pacing in sinus rhythm from the low lateral RA, the septum was activated by caudocranial and craniocaudal wave fronts. Similarly, during pacing from the proximal coronary sinus, the lateral RA was activated by two wave fronts. Catheter ablation of the IVC-TA isthmus induced dramatic changes in mapping due to the loss of caudocranial wave front in all but 1 patient. The septum and the lateral RA were activated by a single craniocaudal front as during entrainment of reverse or common AFI, respectively. After a follow-up of 8 +/- 2 months, common or reverse AFI occurred in 4 patients. Two had no or only unidirectional changes in the isthmus conduction induced by ablation. The other 2 had a late recovery of conduction. CONCLUSIONS: The present study provides evidence that the mechanism of successful AFI ablation targeting the IVC-TA isthmus is local bidirectional conduction block. This change can be used as a new and complementary electrophysiological end point for the procedure. AFI recurrences are associated with failure to achieve a permanent block.