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Focal Atrial Tachycardia. 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.(J Cardiovasc Electrophysiol, Vol. 15, pp. 1-7, December 2004) [ABSTRACT FROM AUTHOR]

LIN, Y.-J.,et al.: Electrophysiological Mechanisms and Catheter Ablation of Complex Atrial Arrhythmias from Crista Terminalis: Insight from Three-Dimensional Noncontact Mapping. 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.(PACE 2004; 27:1231–1239) [ABSTRACT FROM AUTHOR]