Background-Epicardial mapping has demonstrated that atrial substrate may play a role in the characteristics of the resulting atrial fibrillation (AF). However, it is not known if these differences also occur in three dimensions.

Introduction The effect of the heart failure substrate on the initiation of ventricular fibrillation (VF), and its resulting mechanism is not known. The objective of this study was to determine the effects of substrate on VF initiation and its spatiotemporal organization in the heart failure model. Methods Optical action potentials were recorded from LV wedge preparations from either structurally normal hearts (control, n=11) or from congestive heart failure (CHF, n=7), at the epicardial surface, endocardial surface which included a papillary muscle, and a transmural cross section. Action potential duration (APD80) was determined, and VF was initiated. A fast Fourier-transform was calculated, and the dominant frequency (DF) was determined. Results The CHF group showed increased VF vulnerability (69% vs 26%, p<0.03), and every mapped surface showed an APD80 gradient which included islands of higher APDs on the transmural surface (M-cells) which was not observed in controls. VF in the CHF group was characterized by stable, discrete high DF areas that correlated to either foci or spiral waves located on the transmural surface at the site of the papillary muscle. Overall the top 10% of DFs correlated to an APD of 101 ms while the bottom 10% of DFs correlated to an APD of 126 ms (p<0.01). Conclusion In the CHF model, APD gradients correlated with an increased vulnerability to VF, and the highest stable DFs were located on the transmural surface which was not seen in Controls. This indicates that the CHF substrate creates unique APD and DF characteristics.

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