The effect of conductivity on ST-segment epicardial potentials arising from subendocardial ischemia.

Abstract

We quantify and provide biophysical explanations for some aspects of the relationship between the bidomain conductivities and ST-segment epicardial potentials that result from subendocardial ischemia. We performed computer simulations of ischemia with a realistic whole heart model. The model included a patch of subendocardial ischemic tissue of variable transmural thickness with reduced action potential amplitude. We also varied both intracellular and extracellular conductivities of the heart and the conductivity of ventricular blood in the simulations. At medium or high thicknesses of transmural ischemia (i.e., at least 40% thickness through the heart wall), a consistent pattern of two minima of the epicardial potential over opposite sides of the boundary between healthy and ischemic tissue appeared on the epicardium over a wide range of conductivity values. The magnitude of the net epicardial potential difference, the epicardial maximum minus the epicardial minimum, was strongly correlated to the intracellular to extracellular conductivity ratios both along and across fibers. Anisotropy of the ischemic source region was critical in predicting epicardial potentials, whereas anisotropy of the heart away from the ischemic region had a less significant impact on epicardial potentials. Subendocardial ischemia that extends through at least 40% of the heart wall is manifest on the epicardium by at least one area of ST-segment depression located over a boundary between ischemic and healthy tissue. The magnitude of the depression is a function of the bidomain conductivity values.