Notes: Introduction: The structural changes of the superior caval vein, pulmonary veins, and left atrium in atrial fibrillation initiated by superior caval vein ectopy have not been reported. Methods and Results: Nine patients with atrial fibrillation initiated by superior caval vein ectopic beats (male = 5, 54 ± 10 years) and 15 control (n = 15, male =  10, 52 ±  8 years) without any cardiac arrhythmias were included in this study. Using gadolinium-enhanced magnetic resonant angiography with three-dimensional reconstruction, the parameters of the superior caval vein morphology (length, various diameters, area, eccentricity, and volume) were measured. The morphological parameters of the four pulmonary veins (diameter, ostial area, and eccentricity) were also measured at the pulmonary vein–left atrial junction in an oblique sagittal section from the multiple-plane reconstruction images. The left atrial diameters and volume were measured. The different morphological parameters were compared between the two groups. The patients with atrial fibrillation initiated by superior caval vein ectopic beats exhibited a more eccentric structure of the second part of the superior caval vein as compared to the control group. All the ectopic beats initiating atrial fibrillation were located in the second part of the superior caval vein. Furthermore, the patients with atrial fibrillation initiated by superior caval vein ectopic beats had a larger superior caval vein volume, left atrial volume, and pulmonary vein size, and more eccentric pulmonary vein ostia than the controls. Conclusion: Structural changes of the superior caval vein were demonstrated in the patients with atrial fibrillation initiated by superior caval vein ectopic beats. These findings might explain the arrhythmogenic mechanism of atrial fibrillation initiated by superior caval vein ectopy.

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

Notes: We report a case with SVC ectopy initiating AF; the origin and breakout point of the sinus node was inside the SVC, and the SVC ectopy was conducted through the same path as the sinus node activation to depolarize the right atrium. Injury to the sinus node happened after successful isolation of SVC.

Notes: Introduction: Adenosine can terminate most focal atrial tachycardias (ATs). However, information about the termination mechanism is limited. This study investigated the effects and mechanism of adenosine on terminating focal AT using a three-dimensional noncontact mapping system. Methods and Results: The study consisted of 7 patients (4 men and 3 women; age 44 ± 29 years) with focal AT. Cycle length variation and atrial activation pattern at baseline and just before AT termination by adenosine (3–12mg) were analyzed. Noncontact mapping demonstrated focal AT propagated from the origin (O) with preferential conduction and spread away from the breakout sites to the whole atrium. Compared to baseline AT, termination episodes revealed higher mean beat-to-beat variation of AT cycle length (11.7 ± 11.7 msec vs 4.7 ± 4.5 msec, P 〈 0.001) and standard deviation of normalized AT cycle length (0.033 ± 0.014 vs 0.011 ± 0.005, P 〈 0.001). In termination episodes, adenosine significantly decreased the peak negative voltage of AT-O (–27.2 ± 15.3%, P 〈 0.01), preferential conduction (proximal: –32.1 ± 18.7, mid: –28.4 ± 22.8, distal portion: –29.6 ± 21.4%, P 〈 0.01), and breakout (–31.4 ± 12.5%, P 〈 0.01). However, adenosine did not affect voltage in nontermination episodes. Adenosine shifted the locations of AT-O in 5 of 10 AT episodes with termination. Mean number of shifting AT-O was 2.4 ± 1.5 (range 1–4), with maximum shifting distance of 15.0 ± 3.1 (range 10–19) mm. Focal activation at AT-O simply disappeared in all termination episodes and therefore was not due to conduction block within preferential conduction or breakout site. Catheter ablation lesions covered 50% of total shifting origins, without late recurrence. Conclusion: Adenosine-induced AT termination was associated with significantly decreased electrogram voltage, shifting AT-O locations, and disappearance of focal activation.

Notes: Introduction: Previous literature has documented the association between narrow QRS supraventricular tachycardia (SVT) and pronounced ST-T segment change. The aim of this study was to evaluate repolarization changes during SVT initiation and demonstrate the possible mechanism. Methods and Results: Fifty-one consecutive patients (20 men and 31 women; mean age 46.1 ± 16.4 years) with narrow QRS SVT (32 patients with AV nodal reentrant tachycardia and 19 patients with AV reentrant tachycardia) were included. We retrospectively analyzed the intracardiac recordings and ST-T segment changes on 12-lead surface ECGs during SVT initiation. Twenty-six (51%) patients developed ST segment repolarization changes during SVT initiation. Patients with shorter baseline sinus cycle length, shorter tachycardia cycle length, elevated systolic blood pressure before tachycardia induction, and greater reduction of systolic blood pressure had a higher incidence of repolarization changes. However, multivariate analysis showed that reduction of systolic blood pressure after SVT induction was the only independent predictor of repolarization changes. Furthermore, the maximal degree of ST segment depression during SVT correlated with the reduction of systolic blood pressure (r = 0.75, P 〈 0.001). Conclusion: Repolarization changes during SVT initiation were caused mainly by concurrent hemodynamic change after SVT initiation with abrupt cycle length shortening.

Notes: Introduction: Understanding the structural remodeling and reverse remodeling of the left atrium (LA) and pulmonary vein (PV) after radiofrequency ablation of atrial fibrillation (AF) may provide important insights into the mechanism and management of AF. This study used magnetic resonance angiographic (MRA) images to investigate changes in PV and LA morphologies before and more than 1 year after ablation. Method and Results: Forty-five patients (36 men and 9 women, mean age 60 ± 13 years) who underwent MRA before and more than 12 months (mean 21 ± 11) after ablation of paroxysmal AF were included in the study. The patients were divided into two groups: group I included 35 patients without AF recurrence, and group II included 10 patients with late (〉1 month postablation) recurrence of AF. The sizes of the LA and nonablated PV were compared before and after ablation. In group I, significant reduction of ostial area of both superior PVs was noted (left superior PV: from 2.85 ± 0.67 to 2.59 ± 0.73 cm2; right superior PV: from 2.89 ± 0.85 to 2.60 ± 0.73 cm2, both P 〈 0.001). Geometric alteration toward a round shape was noted in the ostia of superior PVs during follow-up (eccentricity of right superior PV and left superior PV decreased from 0.31 ± 0.10 to 0.22 ± 0.13 and from 0.27 ± 0.11 to 0.19 ± 0.13, respectively, oth P 〈 0.01). However, LA volume showed only borderline reduction (from 61.52 ± 19.06 to 56.64 ± 17.13 mL, P = 0.05). In group II, significant dilation of the LA (from 61.14 ± 17.54 to 78.73 ± 25.27 mL, P = 0.004) and right superior PV (from 3.41 ± 1.12 to 4.08 ± 1.31 cm2, P = 0.016) was noted during follow-up. Ostial area and eccentricity of the left superior, left inferior, and right inferior PVs and LA were similar before and after ablation. Conclusion: Structural remodeling of the superior PVs and LA can be reversible after successful ablation without AF recurrence; however, late recurrence of AF is associated with progressive LA dilation.

Notes: Paroxysmal atrial fibrillation (PAF) can be initiated by ectopic activation from the crista terminalis. The crista terminalis conduction gap is also a critical isthmus in atrial reentrant arrhythmias like upper and lower loop reentry. The aim of this study was to investigate the mechanism and results of catheter ablation for complex atrial arrhythmias originating from the crista terminalis using the noncontact mapping system (NCM). The study population consisted of six patients (5 men, 1 woman; 70 ± 9 years) with drug refractory PAF and typical/atypical atrial flutter. NCM identified the earliest ectopic activation originating from the crista terminalis in these six patients. The reentry circuit of atypical atrial flutter propagated around the upper crista terminalis in five patients, and lower crista terminalis in one patient. The reentry circuit of atypical atrial flutter and the initial reentry circuit of AF conducted through the crista terminalis gap in all patients. Radiofrequency applications were delivered on the sites of ectopy, which initiated AF. Substrate modification was also performed over the crista terminalis gap (six patients) and cavotricuspid isthmus (three patients) responsible for the reentry. During a mean follow-up of 9 ± 5 months (range 5–18 months), five patients were free of AF without antiarrhythmic drugs, and one patient did not have AF or atrial flutter using propafenone. NCM demonstrated the mechanism of crista terminalis ectopy-initiating AF and associated typical/atypical atrial flutter. Catheter ablation of crista terminalis ectopy and substrate for the reentry guided by NCM successfully eliminated these atrial arrhythmias.

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.