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. Author manuscript; available in PMC: 2010 Feb 1.
Published in final edited form as: Heart Rhythm. 2008 Nov 8;6(2):251–259. doi: 10.1016/j.hrthm.2008.11.008

Figure 5. Heart failure enhances susceptibility to spatially discordant APD-ALT.

Figure 5

Figure 5

Panel A. Volume averaged ECG and representative epicardial and endocardial optically recorded action potentials from a normal and HF heart at a pacing HR of 180 bpm. L signifies a long AP, S a short AP, and APD is shown below in ms. In HF, alternans which is out of phase between EPI and ENDO cells (DIS-ALT) is observed at this HR, but not in normals. Panel B. Transmural maps of APD-ALT magnitude (contour intensity) and phase (contour color, red is +phase, blue is -phase). At lower HR (top) concordant alternans (i.e. one color) is extensively distributed across the transmural surface in HF but not in normals. At faster HR (bottom), concordant alternans is transformed to DIS-ALT in HF only, as myocytes near the EPI and ENDO surfaces begin alternating with opposite phase, depicted by the presence of both red and blue contours. Panel C. Left. Summary data from all Vm experiments, demonstrating that HF lowers the HR threshold for the development of DIS-ALT (increases susceptibility to DIS-ALT) and that DISALT was observed more frequently in HF (Right).