A B S T R A C T Spatial and nonspatial aspects ofTQ-ST segment mapping were studied with the solid angle theorem and randomly coded data from 15,000 electrograms of 160 anterior descending artery occlusions each of 100-s duration performed in 18 pigs. Factors analyzed included electrode location, ischemic area and shape, wall thickness, and increases in plasma potassium (K+). Change from control in the TQ-ST recorded at 60 s (ATQ-ST) was measured at 22 ischemic (IS) and nonischemic (NIS) epicardial sites overlying right (RV) and left (LV) ventricles. In IS regions, ATQ-ST decreased according to LV > septum > RV and LV base > LV apex. In NIS regions, LV sites had negative (Neg) ATQ-ST which increased as LV IS border was approached. However, RV NIS had positive (Pos) ATQ-ST which again increased as RV IS border was approached. With large artery occlusion IS area increased 123+18%, ATQ-ST at IS sites decreased (-38.1+3.6%), and sum of ATQ-ST at IS sites increased by only 67.3±10.3%. In RV NIS Pos ATQ-ST became Neg. With increased K+, ATQ-ST decreased proportionately to log K+ (r = 0.97±0.01) at IS and NIS sites on the epicardium and precordium. TQ-ST at 60 s was obliterated when K+ = 8.7+0.2 mM. All findings were significant (P < 0.005) and agreed with the solid angle theorem. Thus, a transmembrane potential difference and current flow at the IS boundary alone are responsible for the TQ-ST. Nonspatial factors affect the magnitude of transmembrane potential difference, while spatial factors alter the position of the boundary to the electrode site.