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Updated: Oct 19, 2026

Estimating Bilateral Atrial Function by Cardiovascular Magnetic Resonance Feature Tracking in Patients with Paroxysmal Atrial Fibrillation
Published on: July 20, 2022
Localized bigeminal activity in the left atrial posterior wall preceding atrial fibrillation initiation
Ko Abe1, Kazuhiro Nagaoka1, Yasushi Mukai2
1Department of Cardiovascular Medicine, St. Mary's Hospital, Kurume, Japan.
Abstract:
Bigeminal activity of the pulmonary veins is considered an indicator of arrhythmogenic triggers of atrial fibrillation (AF). However, few reports have described localized bigeminal activity originating from non-pulmonary vein regions. We observed the phenomenon of local bigeminal activities, which did not develop into premature atrial contraction, in a restricted area of left atrial posterior wall (LAPW), preceding the initiation of the AF. Radiofrequency ablation targeting the site of these bigeminal activities transiently suppressed AF, and subsequent linear ablation connecting the site to the adjacent low-voltage region resulted in durable elimination of AF. The spatial relationship between the localized activity and the low-voltage substrate suggests that conduction abnormalities within diseased atrial myocardium may have contributed to the observed phenomenon. This case highlights the potential role of localized electrical activity arising near a low-voltage substrate of the LAPW in AF initiation and may provide insights into the electrophysiological mechanisms of non-pulmonary vein triggers.
Learning Objective:
Left atrial posterior wall (LAPW) is known to be one of the non-pulmonary vein (PV) origins triggering atrial fibrillation (AF). While bigeminal activity originating from PVs or superior vena cava has been associated with arrhythmogenic triggers, similar activity originating from non-PV origin, such as LAPW, has rarely been described. This case indicates that localized bigeminal activity occurring near a low-voltage substrate of the LAPW may precede AF initiation and provides new insights into non-PV arrhythmogenic substrates as the target of ablation.
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