Revisiting low-voltage interpretation: Chamber-specific relationships between myocardial wall thickness and omnipolar voltage

Electrogram voltage reflects multiple factors, including viable myocardial mass, structural integrity, electrode configuration, catheter orientation, and activation sequence. How local myocardial wall thickness (WT) contributes to voltage amplitude in structurally intact myocardium remains incompletely defined. This study examined the chamber-specific relationships between directly measured WT and unipolar voltage (Uni-V), omnipolar voltage (Omni-V), and peak frequency (PF) in structurally intact swine myocardium. High-resolution electroanatomic maps were created in 25 swine. Radiofrequency (RF) lesions were used as anatomical tags to ensure precise spatial correlation between electrophysiological data and post-mortem WT measurements. A total of 340 atrial and 304 ventricular sites were analyzed. In the atria, WT correlated significantly with Omni-V (R²=0.54, P < 0.0001). This correlation improved after excluding trabeculated regions (R²=0.60, P < 0.0001) and was strongest in non-trabeculated regions with WT < 4 mm (R²=0.65, P < 0.0001). Uni-V also correlated with atrial WT, but less strongly (R²=0.29, P < 0.0001). In contrast, ventricular WT showed only weak associations with Omni-V (R²=0.02, P = 0.07) and Uni-V (R²=0.016, P = 0.06). PF did not correlate with WT in either chamber. In structurally intact swine myocardium, WT was associated with voltage amplitude primarily in the atrium, with a stronger relationship for Omni-V than Uni-V, particularly in thin, non-trabeculated regions. Ventricular WT showed only weak associations with voltage, and PF was independent of WT. These findings indicate that WT is one anatomical contributor to voltage amplitude under healthy conditions, particularly in the atrium, but should not support using voltage as a direct surrogate for physical tissue thickness or for interpreting voltage behavior in diseased substrate. In structurally intact swine myocardium, atrial wall thickness correlated with omnipolar voltage, whereas ventricular wall thickness showed only weak voltage associations, highlighting chamber-specific anatomical contributors to electrogram amplitude. In a 25-swine structurally intact heart model, high-resolution electroanatomic maps were generated and compared with direct anatomical measurements of myocardial WT at sites marked by RF fiducial tags. In the atria, Omni-V showed a strong positive association with WT, particularly in thin, non-trabeculated myocardium with WT <4 mm. This relationship was weaker for Uni-V and was reduced in trabeculated atrial regions. In contrast, WT–voltage coupling was weak in the ventricles, and PF did not correlate with WT in either chamber. These findings suggest that local WT may be one anatomical contributor to voltage amplitude in structurally intact atrial myocardium, particularly when assessed using Omni-V, whereas voltage amplitude should not be interpreted as a direct surrogate for tissue thickness or extrapolated to diseased ventricular substrate.