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(Circulation. 2000;101:1503.)
© 2000 American Heart Association, Inc.
Brief Rapid Communications |
From Utah Valley Regional Medical Center, Provo, Utah (C.H.); the Division of Cardiology, Department of Medicine, Taichung Veterans General Hospital, Taichung, Taiwan (T.-J.W.); and the Division of Cardiology, Department of Medicine, Cedars-Sinai Medical Center and UCLA School of Medicine, Los Angeles, Calif (R.N.D., C.T.P., P.-S.C.).
Correspondence to Chun Hwang, MD, Central Utah Medical Clinic, 1055 North 500 West, Provo, Utah 84604.
| Abstract |
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Methods and ResultsA total of 28 consecutive patients with paroxysmal AF underwent balloon-occlusion coronary sinus angiograms to identify the vein of Marshall (VOM). Attempts were then made to advance a 1.5-French electrophysiological catheter into the VOM via the coronary sinus orifice. In 17 of the 28 patients (10 of 17 were men aged 38±15 years), cannulation was successful. Double potentials were registered in 8 of these 17 patients. The first potential corresponded with local left atrial activation. The second potential was shorter and narrower than the first. The sequence of activation in the second potential in the VOM was proximal to distal. In 6 patients with direct VOM recordings, we documented that the origin of AF was in the muscle bundle within the LOM. Radiofrequency catheter ablation aimed at the insertion site of the VOM successfully terminated AF in 4 of these 6 patients.
Conclusions(1) It is possible to cannulate and to record electrical potentials from the VOM. (2) The characteristics of the double potentials within the VOM suggest that the second potential is from the muscle bundle (Marshall bundle) within the LOM. (3) The Marshall bundle may be the origin of focal AF in some patients.
Key Words: arrhythmias electrophysiology catecholamines catheter ablation potentials
| Introduction |
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| Methods |
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3 antiarrhythmic
drugs, had recurrent symptomatic AF, and had no structural
heart disease. The electrophysiological
study and the radiofrequency ablation were performed in the same
session using standard procedures.6 Written, informed
consent was obtained before the study. All antiarrhythmic drugs were
discontinued for
5 half-lives. No patients were treated with
amiodarone. Fentanyl and Versed (midazolam) were used for
sedation. Three quadripolar catheters were inserted via the femoral
veins and positioned in the high right atrium,
atrioventricular junction, and right ventricle. A
luminal decapolar catheter was inserted via the right internal jugular
vein into the coronary sinus and advanced to the most distal
position. Via a transeptal approach, a standard ablation catheter was
inserted into the left atrium. The patients were anticoagulated with
heparin as soon as the catheters were placed. The activation times were
determined with the usual criteria.7 If atrial tachyarrhythmias did not occur spontaneously, we attempted to induce them with an isoproterenol (1 to 5 µg/min) infusion and, if necessary, by withdrawing sedatives. The left atrium was mapped to determine the earliest activation site at the onset of the atrial tachyarrhythmia. Radiofrequency ablation was done with a target temperature of 55°C delivered to the site of earliest activation. Multiple applications were performed until all atrial arrhythmias were eliminated.
VOM Recordings
In 28 consecutive patients, we performed balloon-occlusion
angiograms to identify the VOM. We then attempted to cannulate the VOM
using a 1.5-French quadripolar catheter (Cardima). Four
recording electrodes spaced 2 mm apart were built on the
catheter to register 2 bipolar electrograms. Electrograms were acquired
during sinus rhythm and during spontaneous or induced atrial
tachyarrhythmias. Filter and gain settings for VOM
recordings were the same as those for recordings from
the coronary sinus and pulmonary veins.
Data Analyses
The data were presented as mean±SD. Students
t tests were used to compare the means. P
0.05
was considered significant.
| Results |
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VOM Recordings
In 19 of the 28 patients, the VOM was visualized by
balloon-occlusion coronary sinus angiography. The VOM is the
first atrial branch of the coronary sinus, and it runs
obliquely toward the left superior pulmonary vein. The VOM was
successfully cannulated with the recording catheter in 17 of
the 19 patients. On average, 21±9 minutes were needed for successful
cannulation. These 17 patients were 38±15 years of age and included 10
men and 7 women. In comparison, the other 11 patients included 7 men
and 4 women who had an average age of 40±2 years
(P=NS).
In 8 of the 17 patients in whom the VOM was successfully
cannulated, double potentials were registered both inside the left
superior pulmonary vein and inside the VOM (Figure 1
). The first potential corresponded to
local left atrial activation, and the second was shorter and narrower
than the first. During sinus rhythm, the activation sequence of the
second potential within the VOM was proximal to distal. The timing of
the second potential in the left superior pulmonary vein was
similar to that registered in the distal VOM (Figure 1A
). The
interval between the first and the second potential was 64.3±9.2 ms in
the pulmonary vein and 73.0±8.5 ms in the distal VOM
(P=NS). The temporal separation between the local atrial
electrograms and the VOM electrograms gradually shortened as the
catheter pulled back from the most distal to the most proximal position
in the VOM (Figures 1A
to 1C).
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Fusion of the 2 electrograms (Figure 1C
) indicated that the
catheter was at the site where the Marshall bundle inserts into the
muscle tract surrounding the coronary sinus or the left atrium.
A total of 8 episodes of spontaneous AF occurred in 6 of these 8
patients. Rapid activation of the Marshall bundle preceded the onset of
AF (Figure 2
). Radiofrequency catheter
ablation (Figure 2
), guided by the VOM catheter (Figure 1E
), successfully terminated atrial
tachyarrhythmias and prevented its reinduction in 4 of
these 6 patients. No radiofrequency applications were needed in the
pulmonary veins. During a follow-up of 3.9±2.6 months, none of
these 4 patients had recurrent AF.
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In 2 of the 17 patients, the VOM recording showed double potentials during sinus rhythm. However, AF originated from the right superior pulmonary vein. The VOM catheter failed to register double potentials in the remaining 7 patients, and AF did not originate in this area.
Among the 28 patients who underwent VOM angiographic studies, 2 had a dissection of the VOM and 1 had a dissection of coronary sinus. These complications did not result in pericardial effusion, tamponade, or hemodynamic compromises. No long-term complications occurred in patients in the study.
| Discussion |
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LOM as a Source of Focal AF
In humans, the sinus node is not the only pacemaker. Boineau et
al8 demonstrated widely distributed atrial pacemaker
complexes in the human heart. In the isolated, perfused canine right
atrium, ectopic pacemaker activity was most often found near the sinus
node or the crista terminalis.9 These pacemakers may
exhibit different responses to norepinephrine and
acetylcholine. Scherlag et al3 reported that sympathetic
stimulation could also induce left atrial ectopic activity. To study
the source of these ectopic activities, we performed a computerized
mapping study in the isolated-perfused canine left
atrium.1 We found that isoproterenol can cause automatic
rhythm with this preparation. On the basis of these findings, we
hypothesized that the Marshall bundle may serve as a source of focal AF
in humans.
In the present study, we successfully cannulated the VOM and recorded sharp potentials directly from the catheter within the VOM. Because the VOM is an epicardial structure and the recording site was not close to the pulmonary veins, it is unlikely that these sharp second potentials originated from the extension of the atrial musculature into the pulmonary veins.10 Rapid activation of the Marshall bundle might serve as a trigger of atrial arrhythmias, including AF. Finally, we were able to use the VOM catheter as a guide for radiofrequency ablation. A radiofrequency lesion placed in the posterolateral left atrium between the Marshall bundle insertion and the ostium of the left inferior pulmonary vein resulted in successful treatment of the focal AF. This finding suggests that the trigger of the focal AF episodes resides not within the pulmonary veins, but in the Marshall bundle.
Limitations of the Study
One limitation of the present study is that successful
cannulation of the VOM was not achieved in all patients. The potential
complications related to the dissection of the veins are other
limitations. Furthermore, in some patients, double potentials were not
registered within the VOM. This procedure (VOM cannulation and
recording) may not be applicable to all patients. However,
these limitations do not invalidate our conclusion that in some
patients, the Marshall bundle is a source of focal AF.
| Acknowledgments |
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Received November 30, 1999; revision received February 1, 2000; accepted February 8, 2000.
| References |
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