Marshall vein as arrhythmogenic source in patients with atrial fibrillation

Correlation between its anatomy and electrophysiological findings

Toshiya Kurotobi, Hiroshi Itoh, Koichi Inoue, Katsuomi Iwakura, Shigeo Kawano, Atsunori Okamura, Motoo Date, Kenshi Fujii

Research output: Contribution to journalArticle

53 Citations (Scopus)

Abstract

Background: Atrial fibrillation (AF) may originate from catecholamine-sensitive vein of Marshall (VOM) or its ligament in addition to pulmonary veins (PVs). The anatomy of VOM and its relation to arrhythmogenic foci in the left atrium are unknown. We studied the anatomy of VOM and its relation to foci in patients with AF. Methods: The study population consisted of 100 patients with AF (mean age, 62 years; chronic AF, n = 15). AF sources were determined at baseline and after isoproterenol administration without sedation. VOM was identified by balloon-occluded coronary sinus (CS) angiography. We determined its anatomy in relation to left PVs. Results: VOM was visualized in 73 patients (73%). Ninety-seven patients had 269 arrhythmogenic foci (PV, n = 77; non-PV, n = 48). Non-PV foci included left atrial posterior wall (24, 9%), left lateral area (12, 4.5%), roof (6, 2.2%), superior vena cava (28, 10.4%), crista terminalis (8, 3.0%), CS (10, 3.7%), and others (10, 3.7%). The incidence of PV foci in the left superior PV (LSPV) was significantly higher in patients with well-developed VOM than in those without (66% vs 42%, P <0.05). Twenty-eight patients had 30 non-PV foci around the LSPV ostium. We successfully ablated the non-PV foci at the distal end of VOM in 11 patients. The ends of the VOM branches were good markers to search for non-PV foci. Seven of 11 (64%) patients with successful ablation of non-PV foci were free from arrhythmia, whereas only 6 of 17 (35%) were free from arrhythmia in those with residual non-PV foci. Conclusions: To determine VOM anatomy is important to identify non-PV foci around the ends of VOM.

Original languageEnglish
Pages (from-to)1062-1067
Number of pages6
JournalJournal of Cardiovascular Electrophysiology
Volume17
Issue number10
DOIs
Publication statusPublished - Oct 2006
Externally publishedYes

Fingerprint

Atrial Fibrillation
Veins
Anatomy
Pulmonary Veins
carbosulfan
Coronary Sinus
Cardiac Arrhythmias
Superior Vena Cava
Heart Atria
Coronary Angiography
Isoproterenol
Ligaments
Catecholamines

Keywords

  • Atrial fibrillation
  • Atrial premature beats
  • Catheter ablation
  • Trigger
  • Vein of Marshall

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology

Cite this

Marshall vein as arrhythmogenic source in patients with atrial fibrillation : Correlation between its anatomy and electrophysiological findings. / Kurotobi, Toshiya; Itoh, Hiroshi; Inoue, Koichi; Iwakura, Katsuomi; Kawano, Shigeo; Okamura, Atsunori; Date, Motoo; Fujii, Kenshi.

In: Journal of Cardiovascular Electrophysiology, Vol. 17, No. 10, 10.2006, p. 1062-1067.

Research output: Contribution to journalArticle

Kurotobi, Toshiya ; Itoh, Hiroshi ; Inoue, Koichi ; Iwakura, Katsuomi ; Kawano, Shigeo ; Okamura, Atsunori ; Date, Motoo ; Fujii, Kenshi. / Marshall vein as arrhythmogenic source in patients with atrial fibrillation : Correlation between its anatomy and electrophysiological findings. In: Journal of Cardiovascular Electrophysiology. 2006 ; Vol. 17, No. 10. pp. 1062-1067.
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abstract = "Background: Atrial fibrillation (AF) may originate from catecholamine-sensitive vein of Marshall (VOM) or its ligament in addition to pulmonary veins (PVs). The anatomy of VOM and its relation to arrhythmogenic foci in the left atrium are unknown. We studied the anatomy of VOM and its relation to foci in patients with AF. Methods: The study population consisted of 100 patients with AF (mean age, 62 years; chronic AF, n = 15). AF sources were determined at baseline and after isoproterenol administration without sedation. VOM was identified by balloon-occluded coronary sinus (CS) angiography. We determined its anatomy in relation to left PVs. Results: VOM was visualized in 73 patients (73{\%}). Ninety-seven patients had 269 arrhythmogenic foci (PV, n = 77; non-PV, n = 48). Non-PV foci included left atrial posterior wall (24, 9{\%}), left lateral area (12, 4.5{\%}), roof (6, 2.2{\%}), superior vena cava (28, 10.4{\%}), crista terminalis (8, 3.0{\%}), CS (10, 3.7{\%}), and others (10, 3.7{\%}). The incidence of PV foci in the left superior PV (LSPV) was significantly higher in patients with well-developed VOM than in those without (66{\%} vs 42{\%}, P <0.05). Twenty-eight patients had 30 non-PV foci around the LSPV ostium. We successfully ablated the non-PV foci at the distal end of VOM in 11 patients. The ends of the VOM branches were good markers to search for non-PV foci. Seven of 11 (64{\%}) patients with successful ablation of non-PV foci were free from arrhythmia, whereas only 6 of 17 (35{\%}) were free from arrhythmia in those with residual non-PV foci. Conclusions: To determine VOM anatomy is important to identify non-PV foci around the ends of VOM.",
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T1 - Marshall vein as arrhythmogenic source in patients with atrial fibrillation

T2 - Correlation between its anatomy and electrophysiological findings

AU - Kurotobi, Toshiya

AU - Itoh, Hiroshi

AU - Inoue, Koichi

AU - Iwakura, Katsuomi

AU - Kawano, Shigeo

AU - Okamura, Atsunori

AU - Date, Motoo

AU - Fujii, Kenshi

PY - 2006/10

Y1 - 2006/10

N2 - Background: Atrial fibrillation (AF) may originate from catecholamine-sensitive vein of Marshall (VOM) or its ligament in addition to pulmonary veins (PVs). The anatomy of VOM and its relation to arrhythmogenic foci in the left atrium are unknown. We studied the anatomy of VOM and its relation to foci in patients with AF. Methods: The study population consisted of 100 patients with AF (mean age, 62 years; chronic AF, n = 15). AF sources were determined at baseline and after isoproterenol administration without sedation. VOM was identified by balloon-occluded coronary sinus (CS) angiography. We determined its anatomy in relation to left PVs. Results: VOM was visualized in 73 patients (73%). Ninety-seven patients had 269 arrhythmogenic foci (PV, n = 77; non-PV, n = 48). Non-PV foci included left atrial posterior wall (24, 9%), left lateral area (12, 4.5%), roof (6, 2.2%), superior vena cava (28, 10.4%), crista terminalis (8, 3.0%), CS (10, 3.7%), and others (10, 3.7%). The incidence of PV foci in the left superior PV (LSPV) was significantly higher in patients with well-developed VOM than in those without (66% vs 42%, P <0.05). Twenty-eight patients had 30 non-PV foci around the LSPV ostium. We successfully ablated the non-PV foci at the distal end of VOM in 11 patients. The ends of the VOM branches were good markers to search for non-PV foci. Seven of 11 (64%) patients with successful ablation of non-PV foci were free from arrhythmia, whereas only 6 of 17 (35%) were free from arrhythmia in those with residual non-PV foci. Conclusions: To determine VOM anatomy is important to identify non-PV foci around the ends of VOM.

AB - Background: Atrial fibrillation (AF) may originate from catecholamine-sensitive vein of Marshall (VOM) or its ligament in addition to pulmonary veins (PVs). The anatomy of VOM and its relation to arrhythmogenic foci in the left atrium are unknown. We studied the anatomy of VOM and its relation to foci in patients with AF. Methods: The study population consisted of 100 patients with AF (mean age, 62 years; chronic AF, n = 15). AF sources were determined at baseline and after isoproterenol administration without sedation. VOM was identified by balloon-occluded coronary sinus (CS) angiography. We determined its anatomy in relation to left PVs. Results: VOM was visualized in 73 patients (73%). Ninety-seven patients had 269 arrhythmogenic foci (PV, n = 77; non-PV, n = 48). Non-PV foci included left atrial posterior wall (24, 9%), left lateral area (12, 4.5%), roof (6, 2.2%), superior vena cava (28, 10.4%), crista terminalis (8, 3.0%), CS (10, 3.7%), and others (10, 3.7%). The incidence of PV foci in the left superior PV (LSPV) was significantly higher in patients with well-developed VOM than in those without (66% vs 42%, P <0.05). Twenty-eight patients had 30 non-PV foci around the LSPV ostium. We successfully ablated the non-PV foci at the distal end of VOM in 11 patients. The ends of the VOM branches were good markers to search for non-PV foci. Seven of 11 (64%) patients with successful ablation of non-PV foci were free from arrhythmia, whereas only 6 of 17 (35%) were free from arrhythmia in those with residual non-PV foci. Conclusions: To determine VOM anatomy is important to identify non-PV foci around the ends of VOM.

KW - Atrial fibrillation

KW - Atrial premature beats

KW - Catheter ablation

KW - Trigger

KW - Vein of Marshall

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