Notes: Conduction Properties of the Crista Terminalis. Introduction: Previous mapping studies in patients with typical atrial flutter have demonstrated the crista terminalis to he a posterior harrier 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.

Notes: We present a case of primary hyperparathyroidism with hypercalcemia in a patient who had spontaneous attacks of ventricular tachycardia. Right ventricular burst pacing reproducibly induced ventricular tachycardia in the electrophysiological laboratory after intravenous administration of calcium-gluconate, and verapamil could terminate the tachycardia. After resection of the parathyroid adenoma, the calcium level was restored to normal, and ventricular tachycardia did not occur again during the follow-up period,

Notes: HSIEH, M.-H., et al.: Mechanism of Spontaneous Transition from Typical Atrial Flutter to Atrial Fibrillation: Role of Ectopic Atrial Fibrillation Foci. Paroxysmal AF has been known to be initiated by ectopic beats, especially in the pulmonary veins (PVs), and radiofrequency catheter ablation could cure it. We considered that the spontaneous transition from typical atrial flutter to AF also could be initiated by ectopic beats. Twenty patients (18 men, mean age 66 ± 14 years) with episodes of spontaneous transition from typical atrial flutter to AF were included in this study. They underwent detailed mapping of both atria. All the patients had spontaneous AF initiated by ectopic beats, and all of them had typical atrial flutter and spontaneous transition from typical atrial flutter (12 patients with counterclockwise atrial flutter and 8 patients with clockwise atrial flutter) to AF. The transition was initiated by ectopic beats from the PVs (17 foci, 85%), crista terminalis (2 foci, 10%), and superior vena cava (1 focus, 5%). After successful ablation of AF foci, typical atrial flutter was induced again, but no spontaneous transition was found after at least 10 minutes of observation. We concluded that paroxysmal AF and spontaneous transition from typical atrial flutter to AF were initiated by ectopic beats, and successful catheter ablation of the ectopic foci can eliminate paroxysmal AF and spontaneous transition from typical atrial flutter to AF.

Notes: Background: Junctional rhythm (JR) is commonly observed during radiofrequency (RF) ablation of the slow pathway for atrioventricular (AV) nodal reentrant tachycardia. However, the atrial activation pattern and conduction time from the His-bundle region to the atria recorded during JR in different types of AV nodal reentrant tachycardia have not been fully defined. Methods: Forty-five patients who underwent RF ablation of the slow pathway for AV nodal reentrant tachycardia were included; 27 patients with slow-fast, 11 patients with slow-intermediate, and 7 patients with fast-slow AV nodal reentrant tachycardia. The atrial activation pattern and HA interval (from the His-bundle potential to the atrial recording of the high right atrial catheter) during AV nodal reentrant tachycardia (HASVT) and JR (HAJR) were analyzed. Results: In all patients with slow-fast AV nodal reentrant tachycardia, the atrial activation sequence recorded during JR was similar to that of the retrograde fast pathway, and transient retrograde conduction block during JR was found in 1 (4%) patient. The HAJR was significantly shorter than the HASVT (57 ± 24 vs 68 ± 21 ms, P 〈 0.01). In patients with slow-intermediate AV nodal reentrant tachycardia, the atrial activation sequence of the JR was similar to that of the retrograde fast pathway in 5 (45%), and to that of the retrograde intermediate pathway in 6 (55%) patients. Transient retrograde conduction block during JR was noted in 1 (9%) patient. The HAJR was also significantly shorter than the HASVT (145 ± 27 vs 168 ± 29 ms, P = 0.014). In patients with fast-slow AV nodal reentrant tachycardia, retrograde conduction with block during JR was noted in 7 (100%) patients. The incidence of retrograde conduction block during JR was higher in fast-slow AV nodal reentrant tachycardia than slow-fast (7/7 vs 1/11, P 〈 0.01) and slow-intermediate AV nodal reentrant tachycardia (7/7 vs 1/27, P 〈 0.01). Conclusions: In patients with slow-fast and slow-intermediate AV nodal reentrant tachycardia, the JR during ablation of the slow pathway conducted to the atria through the fast or intermediate pathway. In patients with fast-slow AV nodal reentrant tachycardia, there was no retrograde conduction during JR. These findings suggested there were different characteristics of the JR during slow-pathway ablation of different types of AV nodal reentrant tachycardia.

Notes: Several atrial pacing modes have been reported to be effective in the prevention of atrial fibrillation (AF); they included biatrial pacing, dual site right atrial pacing, Bachmann's bundle (BB) pacing, and coronary sinus pacing. However, the relative efficacy and electrophysiological mechanisms of these pacing modes in the prevention of AF are not clear. In 15 patients (age 54 ± 14 years) with paroxysmal AF, P wave duration, effective refractory period, and atrial conduction time were determined with six different atrial drive pacings, that were right atrial appendage (RAA), BB, right posterior interatrial septum (RPS), distal coronary sinus (DCS), RAA plus RPS simultaneously (DSA), and RAA plus DCS simultaneously (BiA). All these patients consistently had AF induced with early RAA extrastimulation coupling to RAA drive pacing. No patient had AF induced with RAA extrastimulation coupled to BB, RPS, or DCS drive pacing, but seven and eight patients had AF induced with RAA extrastimulation coupled to DSA and BiA drive pacing, respectively. The P wave duration was longest during RAA pacing, and became shorter during other atrial pacing modes. Analysis of electrophysiological change showed that early RAA extrastimulation coupled to RAA drive pacing caused the longest atrial conduction delay among these atrial pacing modes; BB, RPS, and DCS drive pacing caused a greater reduction of this conduction delay than DSA and BiA drive pacing. In addition, the effective refractory periods of RAA determined with BB, RPS, and DCS drive pacing were similar and longer than that determined with DSA and BiA drive pacing. In patients with paroxysmal AF, this arrhythmia was readily induced with RAA extrastimuli coupled to RAA drive pacing. BB, RPS, and DCS pacing were similar and more effective than DSA and BiA pacing in preventing AF.

Notes: TAI, C.-T., et al.: Differentiating the Ligament of Marshall from the Pulmonary Vein Musculature Potentials in Patients with Paroxysmal Atrial Fibrillation: Electrophysiological Characteristics and Results of Radiofrequency Ablation. It was reported that paroxysmal atrial fibrillation (PAF) can be initiated by ectopic atrial beats originating from the pulmonary vein (PV) or left atrial tract (LAT) within the ligament of Marshall (LOM). The aim of this study was to differentiate the LAT from the PV potentials, and to investigate the results of radiofrequency ablation guided by these potentials. Ten patients (age 60 ± 12 years) with PAF who had a recording of double potentials (DPs) in or around the left PV were included. Group I had five patients with the second deflection of DPs (D2) due to activation of the LAT, and Group II had five patients with D2 due to activation of the PV musculature. There were no significant difference in the isoelectric interval between DPs, the activation time, and amplitude of D2 between Groups I and II. During distal coronary sinus (CS) pacing, the CS ostium (CSO) to D2 interval was shorter compared with that during sinus rhythm in Group I (39 ± 19 vs 71 ± 25 ms, P = 0.04), but was longer in Group II (96 ± 16 vs 44 ± 19 ms, P = 0.04). During ectopic activation, three patients in Group I, but no Group II patients, had transformation of recorded DPs into triple potentials. Radiofrequency ablation guided by the earliest activation of the LAT potential was performed with transient suppression of PAF, but ablation guided by the earliest activation of the PV potentials had a high success rate in eliminating PAF. In conclusion, differentiating the LAT from the PV potentials for initiation of PAF is feasible by an electrophysiological approach, and may be important for radiofrequency ablation of PAF.

Notes: The authors developed a canine model of pacing induced cardio my apathy to study the possible mechanisms of ibutilide induced torsades de pointes (TP) in heart failure. Thirteen dogs received intravenous ibutilide after acute AV block for 60 minutes, and after implantation of a VVI pacemaker, with a rate of 270 beats/min for 2–3 weeks. Twelve-lead ECG and right and left ventricle monophasic action potentials were recorded at different right ventricle pacing cycle lengths from 600 ms to 1200 ms during the study. The results showed ibutilide could significantly prolong ventricular repolarization and increase the dispersion in a dose dependent and reverse use dependent manner. Furthermore, after ihutilide administration, cardiomyopathic dogs had a greater dispersion of ventricular repolarization, and also had higher incidences of early afterdepolarizations and spontaneous or pacing induced TP than acute AV block dogs.

Notes: Complete or incomplete bidirectional isthmus conduction block after linear ablation of atrial flutter is difficult to interpret without detailed multiple electrodes mapping along the tricuspid an-nulus and the low right atrial isthmus area. The influence of isthmus block on the intraatrial septal and coronary sinus activation has not been assessed by endocardial mapping. This study was designed to analyze the intraartial and interatrial activation times in a retrospective fashion to investigate (1) whether isthmus conduction block can change the coronary sinus activation sequence during low lateral right atrial pacing, and (2) the correlation between change of coronary sinus activation time and isthmus conduction block. Sixty-five consecutive patients (mean age, 57 ± 18 years) with clinically documented typical atrial flutter were studied. A 20-pole “Halo” catheter was placed around the tricuspid annulus including the entire low right atrial isthmus to verify complete bidirectional isthmus block. Activation time from ostium to distal coronary sinus (OCS→DCS), and interatrial septum and isthmus activation times during right atrial pacing were analyzed and compared before and after incomplete or complete isthmus block. Complete bidirectional isthmus block was achieved in 50 (77%) patients. During low lateral right atrial pacing, linear ablation at low right atrial isthmus results in a significant delay of activation in all coronary sinus recording sites with greater extent at the ostium area without influence on interatrial septum activation in complete and incomplete isthmus conduction block. The difference of the OCS→DCS interval before and after ablation, Δ (OCS→DCS), was well correlated with results of isthmus conduction block and significantly longer in patients with complete than those with incomplete isthmus block (34 ± 11 vs 11 ± 8 ms, P 〈 0.001), thereby allowing a value of 20 ms as a discriminative parameter to differentiate incomplete (〈20 ms) from complete (〈 20 ms) isthmus counterclockwise conduction block with a sensitivity of 96% and a specificity of 88%. In conclusion, creation of a line of block at the inferior vena cava-tricuspid annulus isthmus could change coronary sinus activation sequence during low lateral right atrial pacing in sinus rhythm. The change of coronary sinus activation time after linear ablation, Δ (OCS→DCS), was well correlated with isthmus conduction block by using a value ≥ 20 ms to discern complete counterclockwise isthmus block.

Notes: Early recurrence of atrial fibrillation (AF) has been reported to occur in a significant number of patients after internal cardioversion. However, information about early recurrence of AF after external cardioversion has never been reported. The present study was conducted to investigate the clinical and electrophysiological characteristics of early recurrence of AF and its role in failure of cardioversion in patients with chronic AF. Methods and Results: The study included 50 consecutive patients, age 69 ± 9, with a history of chronic AF for more than 3 months duration and electrical cardioversion. They were divided into two groups according to the presence (group 1) or absence (group 2) of early recurrence of AF. There were 13 (26%) patients in group 1 and 37 (74%) patients in group 2. The age, gender, duration of AF, left ventricular function, left atrial dimension, and underlying heart disease were similar between group 1 and 2. Forty-five patients were successfully converted to sinus rhythm with a mean energy of 158 ± 57 J. Among those who failed to be converted to sinus rhythm, 4 (80%) belonged to group 1 and 1 (20%) belonged to group 2. The early recurrences of AF were initiated with consecutive APDs; but the numbers of APD in the first 30 seconds after cardioversion were similar between group 1 and 2. However, the coupling interval of the second APD was shorter in group 1 than group 2 (188 ± 22 vs 324 ± 59 ms, P = 0.003). Nine of the 13 early recurrences were prevented by an increase of shock energy (n = 3) or intravenous amiodarone infusion (n = 6). There were no differences in duration of follow-up, recurrence rate, and time interval to recurrence between group 1 and group 2. Early recurrence of AF occurred in 26% of chronic AF patients who underwent external electrical cardioversion and was a major cause of failure in cardioversion. Early recurrence of AF was initiated by APDs with decreasing coupling intervals and could be prevented with an increase of shock energy or amiodarone.