Search for author "Zhilin Qu"

Figure 1. Spatially concordant (A) and discordant (B) APD alternans in simulated 2D cardiac tissue. A, Top traces show that simulated action potentials from sites a and b both alternate in a long-short pattern during pacing at 220-ms CL. Second panel shows that the spatial APD distribution is either long (blue) or short (red for each beat). Third panel shows that the APD dispersion (gray scale) for either long or short beats is minimal. Bottom panel shows simulated electrocardiogram (ECG), with T wave alternans. B, Top traces show that at a pacing CL of 180 ms, simulated action potentials from site a now alternate short-long, whereas at the same time, action potentials from site b alternate long–short. Second panel shows the spatial APD distribution, with a nodal line (white) with no APD alternation separating the out-of-phase top and bottom regions. Third panel shows that the APD dispersion is markedly enhanced, with the steepest gradient (black) located at the nodal line. Bottom panel shows simulated ECG, with both T wave and QRS alternans (attributable to engagement of CV restitution), as observed experimentally.10 Simulations used a modified Luo–Rudy action potential model described previously.11Show Less

Figure 3. Cobweb diagram of APD alternans arising from steep APD restitution slope, after Nolasco and Dahlen.15 Blue line shows the APD restitution curve, and red line shows the CL=APD+DI line. The top graph illustrates the effects of a perturbation, which shortens DI (asterisk), displacing the system from its unstable equilibrium point (solid black circle at the intersection of the two lines), resulting in persistent APD alternans, as shown in the bottom trace. See text for details.Show Less

Figure 5. Cobweb diagram of Cai alternans. A, Blue line shows the relationship between SR Ca release vs SR Ca load, with slope m in Equation 1. Red line indicates the conservation of Ca between beats as a function of SR Ca release slope (m) and sequestration efficiency (u) in Equation 2. The top graph illustrates the effects of a perturbation that induces a change in SR Ca load (asterisk), displacing the system from its equilibrium point (solid black circle at the intersection of the two lines). For m=3 and u=0.75 (normal heart), the beat-to-beat change in SR Ca release converges back to its equilibrium value over the ensuing beats. See text for details. B, In contrast, when m=8 (corresponding an increase in fractional SR Ca release slope), the equilibrium point becomes unstable, and alternans grows with each beat, although u is unchanged. C, Unstable alternans also occurs when m remains low3 but u decreases (0.45), indicating reduced SR Ca sequestration efficiency.Show Less

Figure 7. Formation of spatially discordant alternans by CV restitution (A) or an ectopic beat (B). Superimposed traces of membrane voltage vs time show action potential (AP) characteristics along the length of a simulated 1D cable of cardiac cells, stimulated at the top of the cable and propagating to the bottom with a wavefront velocity (CV) corresponding to the slope of the line formed by the AP upstrokes. A, CV restitution mechanism: spatially concordant APD alternans is already present when the pacing rate is increased further to engage CV restitution. The slowed CV causes the DI to increase slightly but progressively as the impulse propagates from the top to the bottom of the cable, creating dispersion of APD that is amplified during the subsequent beats until reaching a maintained steady state. Note that the pattern, once formed, is maintained indefinitely (right panels). See text for details. B, Ectopic beat mechanism: an ectopic beat arising from a different location (the bottom of the cable) creates the gradient in DI from top to bottom, which induces spatially nonuniform APD alternans. See text for details. The spatially discordance is transient, unlike the CV restitution mechanism. Adapted with permission from Watanabe et al.9Show Less