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. Author manuscript; available in PMC: 2008 Apr 1.
Published in final edited form as: Heart Rhythm. 2007 Jan 7;4(5):638–647. doi: 10.1016/j.hrthm.2006.12.046

Figure 1. BayK8644–induced QT prolongation in a left ventricular canine wedge preparation and the effect of ranolazine.

Figure 1

A–C: Action potentials recorded from M and epicardial (Epi) cells together with a transmural ECG. BayK8644 (1 μM, 60 minutes of exposure) produces preferential prolongation of the M cell action potential [M cell: 250 to 325 ms (29.6%); Epi: 200 to 237 ms (18.5%)], leading to prolongation of the QT interval and increase in transmural dispersion of repolarization (TDR). Ranolazine (10 μM, 30 minutes of exposure) in the continued presence of BayK8644 (1 μM) causes little changes in the Epi action potential but abbreviates the duration of the M cell action potential, especially at the plateau level, resulting in a decrease in the amplitude of the T wave and the magnitude of TDR (from 74 to 54 ms). Basic cycle length = 2,000 ms. D, E: Rate dependence of the QT interval and TDR in the absence of presence of BayK8644 (1 μM), with and without ranolazine (10 μM).