Rest Of Atrium Research Articles

Apparent short PR interval during atrial tachycardia: what is the mechanism?

A 69-year-old woman with an incessant narrow QRS tachycardia underwent catheter ablation 5 days after failed ablation attempt at another center. Figure 1a shows 12-lead ECG of the tachycardia with a PR interval = 80 ms and cycle length of 450 ms. Ventricular overdrive pacing showed ventriculoatrial dissociation. Figure 1b shows atrial overdrive pacing with the cycle length of 420 ms, with PR interval of 160 ms, which excludes very long PR interval manifesting as apparent short PR interval. In addition incremental atrial pacing showed a Wenckebach point of 350 ms and no preexcitation. Pacing during sinus rhythm with the same cycle length (420 ms) generated a PR interval of 160 ms. Figure 2 shows activation mapping of atrial tachycardia in right atrium with the earliest activation recorded in fast pathway region near His (Fig. 2b). Activation mapping also showed slow conduction from this point (Fig. 2a, b) to the rest of atria (Fig. 2c), which was responsible for the apparent short PR interval. Radiofrequency ablation (Navistar 4 mm, Biosense Webster Inc, Diamond Bar, California, USA) at the earliest activation point (30 W, 50 C) slowed down and then terminated the atrial tachycardia with transient first degree atrioventricular (AV) block. The P wave morphology was not compatible with a septal atrial tachycardia; however, we postulated that delayed and changed atrial activation pattern due to earlier linear ablation lesions as shown in activation mapping may have resulted the observed apparent short PR interval and unusual changed P wave morphology (Fig. 2) [1, 2]. In conclusion, the slow conduction from the earliest activation point to the rest of the right and left atria despite normal conduction to and through the AV node resulted in the delayed atrial depolarization which in turn caused the apparent short PR interval during atrial tachycardia in the absence of an accessory pathway. During catheter ablation the patient transiently developed first degree AV Block. We used a low power setting to avoid high-degree AV block; however, using cryoablation with EnSite NavX Navigation system (St. Jude Medical, Inc. St. Paul, MN) could have been a safe alternative for catheter ablation in this area. Junctional tachycardia should be considered in the differential diagnosis. However, in this case the earliest activation would be at the AV node region. As shown in Fig. 2, the earliest activation during tachycardia was superior and posterior to the fast pathway/AV node region. In addition, the polarity of the P wave and its relation to QRS complex (short PR) argues against junctional tachycardia. Finally, the total atrial activation time was 160 ms which excludes macro-reentry as the underlying mechanism of the tachycardia. True focal atrial tachycardia due to abnormal automaticity or microreentry remains the possible mechanism of this tachycardia.

Local conduction block of the atria by premature stimulus in a patient with Brugada syndrome

A 46-year-old man with type II Brugada electrocardiogram pattern changed to a type I Brugada type electrocardiogram pattern by class I antiarrhythmic drug (pilsicainide) underwent electrophysiologic study. Ventricular fibrillation was induced by double extrastimuli from the right ventricular (RV) apex. Monophasic action potentials (MAPs) were then recorded from the high right atrium. Duration of MAP at a coupling interval of 220 milliseconds was 122 milliseconds, and local activation of S2 spread to the left atrium. However, MAP at a coupling interval of 210 milliseconds was 112 milliseconds, and local activation of S2 failed to spread to the rest of atrium.