Progressive action potential duration shortening and the conversion from atrial flutter to atrial fibrillation in the isolated canine right atrium
Tsu-Juey Wu, MD*,*  ,
Young-Hoon Kim, MD, FACC,
Masaaki Yashima, MD,
Charles A. Athill, MD,
Chih-Tai Ting, MD, PhD*,
Hrayr S. Karagueuzian, PhD, FACC and
Peng-Sheng Chen, MD, FACC
* Division of Cardiology, Department of Medicine, Taichung Veterans General Hospital and Institute of Clinical Medicine, Cardiovascular Research Center, National Yang-Ming University School of Medicine, Taipei, Taiwan
Division of Cardiology, Department of Medicine, Cedars-Sinai Medical Center and University of California at Los Angeles School of Medicine, Los Angeles, California, USA
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Figure 1 (A) Activation pattern during S1 pacing in isolated canine right atrial endocardial tissue (tissue no. 10). The S1 pacing was applied at the left edge of the representative tissue (B). (A) Color-coded isochronal activation map during S1 pacing, demonstrating the nonuniformity of the conduction velocity, which, along the central line during S1 pacing, is 122 cm/s. The site for S2 stimulation is marked by a black square. (B) Gross endocardial structures, including part of the crista terminalis (CT) and pectinate muscle bundles in the atrial tissue. These pectinate muscle bundles were either tightly attached to the atrial free wall ("ridge-like" structure, white arrows) or discontinuous with the atrial free wall ("bridge-like" structure, red probe). An asterisk marked the site for S1 pacing. To better correlate the endocardial activation patterns with the underlying anatomic structures, the endocardial tissue was displayed by a mirror image. The white outline in part B indicates the location of the recording plaque.
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Figure 2 The insertion site of a large pectinate muscle to the underlying atrial tissue, serving as an anchoring site for re-entrant wave fronts (data from tissue no. 10). During ACh infusion (1 µmol/l), a single and stationary re-entry was induced. The pathway of the tip of the re-entrant wave front circled in a clockwise direction (A to E) around the insertion site of a large pectinate muscle to the underlying atrial tissue (see Fig. 1B). (F) The location of channels (Chn) around the insertion site. (G) The actual electrograms registered by these channels during stationary re-entry. During re-entry, the pseudo-ECG recording reveals regular tachycardia (H).
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Figure 3 Conversion from "flutter-like" to "fibrillation-like" activity by increasing the concentration of ACh (2.5 µmol/l) (data from tissue no. 10). (A to G) The re-entrant wave front became nonstationary. (G) The daughter wave front (asterisk) arising from the wave break spontaneously detached from the anchoring site and propagated outside the mapped area. (H) The path and direction of the tip of the re-entrant wave front (white lines). (I) The simultaneous pseudo-ECG shows fibrillation-like activity. The double bars in parts G and H indicate the site of spontaneous wave break.
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Figure 4 Another example of nonstationary re-entry with continuous wave breaks during fibrillation (2.5 µmol/l of ACh, data from tissue no. 9). (A to H) A re-entrant wave front with counterclockwise rotation and a moving core. (I) The trajectory of the tip of the re-entrant wave front. During re-entry with a moving core, continuous wave breaks were also observed. The double bars in B, E and H indicate the sites of spontaneous wave break. (J) The simultaneous pseudo-electrocardiogram recording reveals "fibrillation-like" activity. (K) A typical example of spontaneous wave breaks. Seven daughter wave fronts arose from a wave front of breakthrough. The wave fronts of breakthrough in parts A, G and K are marked by white squares.
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Figure 5 A different form of in vitro fibrillation during ACh infusion of a high concentration (5 µmol/l) (data from tissue no. 10). (A) A snapshot of dynamic display shows that there were multiple wave fronts (up to five) during fibrillation. All of these wave fronts activated rapidly and repetitively, as shown in the isochronal activation maps (B to D). These maps demonstrate the activation patterns of three consecutive beats in the white outlined area in part A. Each letter (a to c) in part A shows the recording site for a corresponding channel (Chn) in part E. Note that the activation patterns were similar among the maps in parts B to D. In addition, the activations in each channel of part E were relatively regular in rhythm and uniform in morphology. These findings indicate that these wave fronts were stationary in character. However, as shown in part E, the activation cycle lengths were different among these wave fronts. The simultaneous pseudo-electrocardiogram recording reveals "fibrillation-like" activity (F). The numbers in part B indicate the channel numbers. The numbers in parts C and D indicate the activation times. ACL = activation cycle length.
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Figure 6 Effects of acetylcholine (ACh) on conduction velocity (CV) and transmembrane potential (TMP) characteristics. (A and B) Data from tissue no. 8 show that ACh had no effect on the CV during S1 pacing. The CV along a central line during baseline and ACh (5 µmol/l) infusion was 94 cm/s. (C to F) A series of TMP recordings during different concentrations of ACh (data from tissue no. 10). (C) At baseline (no ACh), the action potential duration (APD90) during S1 pacing was 123 ms. There were only short runs of repetitive beats (<5 beats) induced. (D) During the infusion of 1 µmol/l of ACh, the APD90 was shortened to 70 ms. The S2 pacing induced a stable re-entry, anchoring to a large pectinate muscle (see Figs. 1B and 2). (E) Once ACh was raised to 2.5 µmol/l, the APD90 was shortened to 50 ms. The S2 pacing consistently induced nonstationary re-entry with a moving core (see Fig. 3). Note that during fibrillation, TMP recordings with variable APD90 values and low amplitudes were frequently observed (vertical arrows). (F) However, by further shortening the APD90 to 22 ms during 5 µmol/l of ACh infusion, multiple, but stationary wave fronts were induced by S2 pacing (see Fig. 5). The APD90 values and amplitudes of TMP recordings became relatively constant. PCL = pacing cycle length.
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