Obstacle-induced transition from ventricular fibrillation to tachycardia in isolated swine right ventricles
Insights into the transition dynamics and implications for the critical mass
Miguel Valderrábano, MDa,
Young-Hoon Kim, MD, FACCa,
Masaaki Yashima, MDa,
Tsu-Juey Wu, MDa,
Hrayr S. Karagueuzian, PhD, FACCa and
Peng-Sheng Chen, MD, FACCa
a Division of Cardiology, Department of Medicine, Cedars-Sinai Medical Center, and UCLA School of Medicine, Los Angeles, California, USA
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Figure 1 Recording methods. (A) Schematic representation of the tissue preparation. (B) Electrode distribution. The shaded area shows the location of electrodes used for calculations in Table 1.
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Figure 2 Transition from VF to VT by attaching a RWF to the obstacle and PM insertion. The numbers above the snapshots indicate time after the beginning of data acquisition. Panels A–I show activation during VF (panels A and B) and the transition to VT (panels C–I). Panels J and K show a schematic representation: wavefronts marked as an asterisk and a diamond activate the obstacle’s boundaries. Later on, a wavefront marked with a circle attached to it. Conduction time was longest when turning around the PM. Panel L shows the mapped tissue, with PM next to the obstacle. Note that activation maps are mirror-images of the mapped endocardial side. Therefore, panel J was shown in its mirror-image to match with the activation maps. Panel M shows local electrograms of selected channels (marked with numbers in panels J and K). Panel N shows the pECG, with the transition from VF to VT.
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Figure 3 Transition from VF to VT by formation of a figure-eight. Panel A, activation during VF. Panels B–H, transition to VT by formation of a figure-eight. See text for details. Panel I, schematic representation, with conduction velocities in different portions of the reentrant circuit (the slowest in the isthmus). Panel J shows the tissue with the PM next to the obstacle and an isthmus in between the two. Panel K, shows local electrograms of channels marked in panel I. Wavefronts marked with asterisk and plus sign in panel B are the initiators of VT. Channel 5, located at the isthmus, is shared by both circuits and shows double potentials. Panel L, pECG of the transition from VF to VT.
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Figure 4 Core size calculation in figure-eight and single RWF VT. Panels A–G, example of a figure-eight pattern, where the core of the right-most reentrant circuit is formed by the obstacle (8-mm diameter). In the left, the RWF rotates counterclockwise. By consecutively joining the red dots, the core of this RWF can be delineated. In panel G, numbers show the location of the channels whose local electrograms are selected for demonstration in panel I. Also shown are the conduction velocities that are uniform around the obstacle but slowest in regions of increased curvature around the PM. Panels J–R, on a different tissue, the same method applied to a case of single RWF rotating clockwise. The core of this rotation is formed in part by the hole. However, when the activation proceeds inferior to the hole, it goes downward, where the PM was located (panels K, L and M). In panel M, the activation again contacts the hole’s boundaries. By joining the red dots, the area surrounded by the activation next to the hole can be identified (the PM insertion) and its area calculated. The summation of this area and the area of the hole is considered the core size. Panel P shows selected channels whose electrograms are shown in panel R, and conduction time longer around the PM. Panels H and Q are mirror-images of the respective tissues.
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