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(Circulation. 2002;105:2112.)
© 2002 American Heart Association, Inc.

Images in Cardiovascular Medicine

Radiofrequency Ablation of a Focal Atrial Tachycardia Originating From the Marshall Ligament as a Trigger for Atrial Fibrillation

Kostas P. Polymeropoulos, MD; Luz Maria Rodriguez, MD; Carl Timmermans, MD; H.J.J. Wellens, MD

From the Department of Cardiology, Academic Hospital Maastricht, Maastricht, the Netherlands.

Correspondence to Luz Maria Rodriguez, MD, Department of Cardiology, Academic Hospital Maastricht, Cardiovascular Research Institute Maastricht (CARIM), P. Debyelaan 25, 6202 AZ, Mastricht, The Netherlands. E-mail LM.Rodriguez@ cardio.azm.nl

A 66-year-old woman with a history of typical atrial flutter and atrial fibrillation was referred to our institution for radiofrequency ablation. In 1997, her atrial flutter was successfully ablated. During the next 4 years, she remained free of both arrhythmias. In 2001, the patient presented again with atrial fibrillation. During the subsequent electrophysiological study, the index arrhythmia was an incessant atrial tachycardia (AT), 170 bpm (Figure 1, left). A 3-dimensional electroanatomic map (CARTO; Biosense Webster, Inc) of the right atrium (RA) during tachycardia clearly demonstrated a tachycardia originating in the left atrium (LA) (Figure 2). Mapping of the LA through a transseptal puncture revealed an AT arising from a posterolateral LA focus, between the left superior pulmonary vein ostium and the atrioventricular groove (Figure 2). Endocardial recordings during AT from this region showed a discrete electrical potential (Marshall potential) preceding the atrial electrogram (Figure 1, right). Radiofrequency ablation targeting this area of early activation was successfully performed. The patient remains free of atrial arrhythmias at 3-month follow-up. This case indicates that in this particular patient, 2 triggers for atrial fibrillation were documented: an isthmus-dependent atrial flutter and an AT originating from the Marshall ligament.

View larger version (85K): [in this window] [in a new window]   Figure 1. Left, AT with a cycle length of 320 ms, with isoelectric P waves in leads I and aVL and positive P waves in the inferior and precordial leads, with 2:1 atrioventricular conduction. Right, Endocardial recordings during AT of the RA and the LA. Note the Marshall potential preceding the atrial electrogram recorded with the mapping/ablation catheter (RF), positioned between the left superior pulmonary vein and the coronary sinus. From top to bottom, ECG leads I and III; bipolar intracardiac recordings from distal (HBEd) and proximal (HBEp) His bundle; high septal (H1920), lateral (H1516), and low (H0102) RA; distal (CSd), medial (CSm), and proximal (CSp) coronary sinus.

View larger version (31K): [in this window] [in a new window]   Figure 2. Three-dimensional CARTO electroanatomic map of the RA and LA showing the endocardial activation sequence during AT in a posteroanterior projection (A) and a left anterior oblique projection (B). Earliest activation (red color) occurs in the posterolateral region close to the atrioventricular groove with activation spreading gradually from that region over the entire LA. Right atrial activation occurs through a superior connection (Bachmann’s bundle) activating the right septum and the rest of the RA from superior to inferior. This activation is blocked in a bidirectional manner in the cavotricuspid isthmus, as the result of the previous radiofrequency ablation. TV indicates tricuspid valve; MV, mitral valve; HIS, His bundle; CS, coronary sinus; LSPV, left superior pulmonary vein; LIPV, left inferior pulmonary vein; and LMPV, left intermediate pulmonary vein. Red dots indicate radiofrequency applications.

Footnotes

The editor of Images in Cardiovascular Medicine is Hugh A. McAllister, Jr, MD, Chief, Department of Pathology, St Luke’s Episcopal Hospital and Texas Heart Institute, and Clinical Professor of Pathology, University of Texas Medical School and Baylor College of Medicine.

Circulation encourages readers to submit cardiovascular images to the Circulation Editorial Office, St Luke’s Episcopal Hospital/Texas Heart Institute, 6720 Bertner Ave, MC1-267, Houston, TX 77030.

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