title: Spatial and nonspatial influences on the TG-ST segment deflection of ischemia. Theoretical and experimental analysis in the pig.
abstract: Spatial and nonspatial aspects of TQ-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 (DeltaTQ-ST) was measured at 22 ischemic (IS) and nonischemic (NIS) epicardial sites overlying right (RV) and left (LV) ventricles. In IS regions, DeltaTQ-ST decreased according to LV > septum > RV and LV base > LV apex. In NIS regions, LV sites had negative (Neg) DeltaTQ-ST which increased as LV IS border was approached. However, RV NIS had positive (Pos) DeltaTQ-ST which again increased as RV IS border was approached. With large artery occlusion IS area increased 123+/-18%, DeltaTQ-ST at IS sites decreased (-38.1+/-3.6%), and sum of DeltaTQ-ST at IS sites increased by only 67.3+/-10.3%. In RV NIS Pos DeltaTQ-ST became Neg. With increased K(+), DeltaTQ-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.
mesh_terms: D000818:Animals; D003327:Coronary Disease / Q000503:physiopathology*; D003331:Coronary Vessels / Q000502:physiology; D004195:Disease Models, Animal; D004562:Electrocardiography; D004566:Electrodes; D008297:Male; D008433:Mathematics; D013552:Swine / Q000502:physiology*