Pathophysiology of atrial fibrillation (AF) remains unclear. Interactions between scar and conduction velocity (CV) and their impact on wavefront propagation in sinus rhythm (SR) and rotational activity burden in AF were evaluated. Local activation times (LATs) and voltage data were obtained from patients undergoing ablation for persistent AF. Omnipolar voltage (OV) and bipolar voltage (BV) data were obtained during AF and sinus rhythm (SR) at pacing intervals (PIs) of 600ms and 250ms. LATs were used to determine CV dynamics and their relationship to the underlying voltage and pivot points in SR. Computational modelling studies were performed to evaluate the impact of CVs and fibrosis on rotational activity burden in AF. Data from 60 patients with a total of 2,085,600 LAT and voltage points analyzed (34,760±5689 points/patient). Voltage determined CV dynamics. Enhanced CV heterogeneity sites were predominantly mapped to low voltage zones (LVZs) [0.2-0.49mV] (129/168, 76.8%) rather than LVZs [<0.2mV] and frequently co-located to pivot points (151/168, 89.9%). AF OV maps correlated better with SR BV 250ms than 600ms maps thereby representing fixed and functional remodeling. SR maps at 250ms compared to 600ms harbored greater number of pivot points. Increased CV slowing and functional remodeling on computational models resulted in a greater rotational activity burden. CV dynamics are impacted by the degree of scar. CV heterogeneity and functional remodeling impacts wavefront propagation in SR and rotational activity burden in AF. This study provides insight to the pathophysiology of AF and identifies potential novel ablation targets.