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. 2019 Dec 16;12(12):e007571. doi: 10.1161/CIRCEP.119.007571

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© 2019 The Authors.

Circulation: Arrhythmia and Electrophysiology is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDerivs License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made.

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Figure 6. — Cellular and tissue mechanisms of arrhythmogenesis in long QT syndrome (LQTS) type 1 (LQT1). A, Single-cell action potential duration (APD) vs P_Ca for LQT1 (left) and LQTS type 2 (LQT2; right). Arrow marks P_Ca where repolarization failure (RF) occurs. B, Single-cell voltage, I_Kr, and I_Ks vs time for LQT1 (top) and LQT2 (bottom) at 3 P_Ca values. C, Line scans of voltage in a 1-dimensional cable for P_Ca=3.1 µm/s at pacing cycle length (PCL)=500 ms (left, corresponding to the fourth ECG in Figure 5A) and P_Ca=4.1 µm/s at PCL=1000 ms (right, corresponding to the fifth ECG in Figure 5A) in LQT1, showing repolarization failure in the center of the cable generating new premature ventricular complexes.