High resolution mapping of the pulmonary vein and the vein of marshall during induced atrial fibrillation and atrial tachycardia in a canine model of pacing-induced congestive heart failure
Yuji Okuyama, MD, PhD*,
Yasushi Miyauchi, MD*,
Angela M. Park, MD*,
Akira Hamabe, MD*,
Shengmei Zhou, MD*,
Hideki Hayashi, MD*,
Mizuho Miyauchi, MD*,
Chikaya Omichi, MD*,
Hui-Nam Pak, MD*,
Lauren A. Brodsky, BA*,
William J. Mandel, MD*,
Michael C. Fishbein, MD ,
Hrayr S. Karagueuzian, PhD* and
Peng-Sheng Chen, MD*,*
* Division of Cardiology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA
Department of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California, Los Angeles, California, USA
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Figure 1 Spontaneous atrial tachycardia (AT) to atrial fibrillation (AF) transition preceded by fractionated activity in the right inferior pulmonary vein (RIPV). Asterisks separate AT from AF. CL = cycle length; I = surface ECG lead I; LAA = left atrial appendage; LIPV = left inferior pulmonary vein; LSPV = left superior pulmonary vein; RSPV = right superior pulmonary vein.
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Figure 2 Atrial fibrillation (AF) termination. Burst pacing from the left atrium appendage induced a brief episode of AF. After the termination of the fractionated activity in RMPV and LSPV (asterisks), AF converted to AT. Large positive P waves (arrows) are compatible with organized atrial activations. The AT then spontaneously terminated. II = surface ECG lead II. Abbreviations as in Figure 1.
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Figure 3 Computerized mapping of focal activations in a pulmonary vein (PV). (A) Bipolar electrograms. The electrode locations a–e are marked in panel B. The patterns of activation of beats B, C, and D in panel A are shown by isochronal maps in panels B, C, and D, respectively. The dotted line in panel B shows the junction between PV and left atrium (LA). Black arrows indicate the site of earliest activation in the PV. LIPV = left inferior pulmonary vein.
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Figure 4 Complex activation in the right superior pulmonary vein (RSPV) during atrial fibrillation. (A) Electrograms from the RSPV (a–e locations are indicated in the lower panels), left atrium (LA), and right atrium (RA) are shown. The patterns of activation during the time period bracketed by the two vertical red lines are shown in panel B. The activation rate in the LA was faster than that in the RA. Conduction delay or block (double line segments) in the PV was frequently observed in electrodes c, d, and e. In the left side of the mapped area, activation from proximal to distal PV and activations from distal to proximal PV are seen. Numbers at the bottom show the times of data acquisition in ms, with the beginning of data acquisition as time zero. The wavefront is labeled red.
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Figure 5 Computerized mapping of atrial fibrillation (AF) termination. (A) Electrograms from the right superior pulmonary vein (a–h locations are indicated in the lower panels) and left atrium (LA) are shown. Complex activity was seen during AF from the beginning until activation #1. At that time, the activation patterns abruptly changed to regular activity (beats 1, 2, and 3) before a long pause, which was followed by a final activation in pulmonary vein (PV) (beat 4) and then by sinus rhythm. In (B), the first six panels show complex activations in the PV during AF. Activation patterns indicated by numbers 1 to 4 in the upper panel of A are shown in the bottom row. An isochronal map of beat 1 shows an activation that invaded the PV from the LA. Beats 2 to 4 show that the early activation sites (blue arrows in bottom panel) were in the PV, with wavefronts propagating in the direction of the LA and the distal PV.
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Figure 6 The vein of Marshall (VOM) activations during sinus rhythm and during atrial fibrillation (AF) are shown. Panel A depicts an actual electrogram from site e in panel C during AF. A and M indicate atrial and VOM activations, respectively. Panel B shows actual activations during one beat of sinus rhythm, and the actual VOM activations recorded in activations 1, 3, 4, and 5 of panel C (local atrial electrograms were omitted). The isochronal maps of sinus rhythm and seven consecutive VOM activations during AF are shown in panel C.
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Figure 7 Atrial tachycardia originating from the left superior pulmonary vein (LSPV). (A) Surface echocardiogram and bipolar electrograms are depicted from sites shown in panel B. All bipolar electrodes registered the same activation cycle length (147 ms). The vein of Marshall (VOM) activations (red asterisks) occurred at longer cycle lengths than in the atria, suggesting intermittent conduction blocks from the left atrium (LA) to the VOM. Earliest activation (a) was found in the proximal LSPV, near the LA–LSPV junction.
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Figure 8 Pattern of fibrosis in experimental animals. Interstitial fibrosis (blue staining) is present in pulmonary vein (A), left atrium (B), and right atrium (C). In left ventricle (D), fibrosis is limited to the pacing site (*). (All trichrome stain: A,B,C x 40; D x 12.5.)
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