In the fibrosis group, VF was driven predominantly by disorganised activity in CF, RDs were detected 26±7% of time comparative to 51.2±4% in DF and 69.5±8% in PF group (p=0.001). PF stabilised RDs, average maximum rotations for a single RD in PF were 31.6±7.1 comparative to 12.5±1.7 in DF and 6.4±1.1 in CF, p<0.001. VF organisation measured by FDI was higher in PF (PF: 0.61±0.07, DF: 0.47±0.04, CF: 0.33±0.03, p=0.004) (figure 1 ). In the GJ modulation group, maximum rotations for a RD increased

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... with RTG (0nm: 5.4±0.45 vs 80nM: 48.20±12.32, p<0.001) and decreased with CBX (0mM: 8.0±1.3 vs 50mM: 0.3±0.3, p<0.001). Proportion of time RDs were detected in VF increased with RTG (0nM: 44±6 vs 80nM: 93±2, p<0.001) and decreased with CBX (0mM: 61±9% vs 50mM: 3±2%, p<0.001). FDI increased with RTG (0nM: 0.53±0.04 vs 80nM: 0.78±0.3, p<0.001) and decreased with CBX (0mM: 0.60±0.05 vs 50mM: 0.17 ±0.03, p<0.001) (figure 2 ). Conclusion VF mechanisms occur along a spectrum between organised activity with discrete drivers and disorganised myocardial activation. The degree of GJ coupling and ventricular fibrosis are key determinants of the underlying mechanism of VF. Enhanced GJ coupling and patchy fibrosis organised fibrillation and stabilised RDs, whilst GJ uncoupling and compact fibrosis disorganised VF. This study presents a unifying explanation for the numerous mechanisms reported for sustaining fibrillation. Characterising the degree and pattern of fibrosis in patient groups vulnerable to VF might be beneficial in identifying patients with targetable substrate, and GJ modulation might be a potential therapeutic target.