Conduction slowing and a focal scar are jointly required for sustained ventricular reentry in diabetic cardiomyopathy.

Diabetic cardiomyopathy increases the risk of ventricular tachycardia and fibrillation through ionic and structural remodeling, but whether the reentrant substrate arises from a diffuse slow-conduction (fibrotic) substrate, a focal scar, or from repolarization remodeling remains unclear. Using a three-dimensional monodomain model (truncated-ellipsoid left ventricle; ToR-ORd ionic model with six diabetic current-scaling factors), I performed a controlled ablation study (in-silico knockout, not catheter ablation) in which diffuse fibrosis and connexin-43 remodeling were reduced tissue conductivity, patchy fibrosis discrete inexcitable elements, and a focal scar an inexcitable transmural wedge, with reentry tested by an S1-S2 protocol. Diabetic remodeling slowed conduction (≍60 to 13 cm/s) and prolonged the QT interval (255 to 301 ms). Sustained reentry required slow conduction and a focal scar: a scar at normal conduction did not reenter, and a slow-conduction substrate without a scar did not - at any patchy-fibrosis density, nor with spatially correlated or strandlike fibrosis textures (0/14); only their combination produced scar-anchored reentry. Disabling ionic remodeling did not abolish reentry, and a conductivity sweep confined reentry to a conduction-velocity window, identifying conduction slowing, not repolarization, as the driver of reentry maintenance; findings reproduced at a finer, independent discretization, though conduction-velocity and block thresholds are effective, resolution-dependent values (coarse grid; robustness check, not mesh convergence). Because the focal scar reflects concomitant ischemic injury and the diffuse slow-conduction substrate is invisible to late-gadolinium-enhancement (LGE), detecting this two-hit substrate would require pairing LGE with diffuse-fibrosis (T1/extracellular-volume) mapping for risk stratification in diabetic patients with a scar.