Spatial and Nonspatial Influences on the TQ-ST Segment Deflection of Ischemia

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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 (ΔTQ-ST) was measured at 22 ischemic (IS) and nonischemic (NIS) epicardial sites overlying right (RV) and left (LV) ventricles. In IS regions, ΔTQ-ST decreased according to LV > septum > RV and LV base > LV apex. In NIS regions, LV sites had negative (Neg) ΔTQ-ST which increased as LV IS border was approached. However, RV NIS had positive (Pos) ΔTQ-ST which again increased as RV IS border was approached. With large artery occlusion IS area increased 123±18%, ΔTQ-ST at IS sites decreased (−38.1±3.6%), and sum of ΔTQ-ST at IS sites increased by only 67.3±10.3%. In RV NIS Pos ΔTQ-ST became Neg. With increased K+, ΔTQ-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.