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In the case of adenosine-sensitive atrial tachycardia originating near the atrioventricular (AV) node, overdrive pacing from the anterior right atrium showed constant and progressive fusion, indicating that the pacing site is proximal to slow conduction. Shortening the pacing cycle length prolonged conduction times to the orthodromic capture sites; they remained unchanged at the antidromic capture sites. Limited decremental conduction property in the slow conduction zone supports the hypothesis that AV node-like tissue remnants along the AV annulus are involved.

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Cardiac pacemaking remains an unsolved matter from many perspectives. Extensive experimental and computational studies have been performed to describe the sinoatrial physiology across different scales, from the molecular to clinical levels. Nevertheless, the mechanism by which a heartbeat is generated inside the sinoatrial node and propagated to the working myocardium is not fully understood at present.

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A 70-year-old man with hypertensive heart disease underwent catheter ablation of persistent atrial fibrillation. After completing the pulmonary vein isolation, atrial burst pacing induced an annular atrial tachycardia (AT). Overdrive pacing exhibited constant fusion, indicating a macroreentrant mechanism of the AT.

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