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Michael Brunner, Xuwen Peng, Gong Xin Liu, Xiao-Qin Ren, Ohad Ziv, Bum-Rak Choi, Rajesh Mathur, Mohammed Hajjiri, Katja E. Odening, Eric Steinberg, Eduardo J. Folco, Ekatherini Pringa, Jason Centracchio, Roland R. Macharzina, Tammy Donahay, Lorraine Schofield, Naveed Rana, Malcolm Kirk, Gary F. Mitchell, Athena Poppas, Manfred Zehender, Gideon Koren
Published in Volume 118, Issue 6
J Clin Invest. 2008; 118(6):2246–2259 doi:10.1172/JCI33578
Abstract | Full text | PDF
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Figure 8
Activation maps of VF initiation in an LQT2 heart.

(A) APD map. The red dotted line marks the interventricular septum. The APD map in LQT2 shows increased dispersion, mostly in the mid LV region. (B) Trace of action potentials during initial period of VF. (C) Series of activation maps marked in panel B. Isochronal lines are drawn every 2-ms interval, and lighter color represents earlier activation. Panel no. 1 shows activation pattern of the paced beat. The following beats (nos. 2 and 3) encounter conduction block where the APD is longer (see panel A). Therefore, the LV activated via the apical free wall where APD is shorter and tissue is recovered from the previous beat. The next activation (no. 4) appears from the RV and propagates toward the mid LV. A similar wave front (no. 5) encounters conduction block (red straight line) in the region where APD is longer and forms a rotation (no. 6), initiating VF (no. 7 and no. 8). This initiation highlights APD dispersion as an important mechanism in arrhythmia formation in this LQT2 model. (D and E) Traces and activation maps from LMC and LQT1 hearts. Traces and maps were taken at the shortest cycle length that did not cause 2:1 block. Both LMC and LQT1 showed uninterrupted conduction from the stimulation sites to the rest of the heart without rotation or conduction blocks.