Stimulation of pathologic electrocardiograms: the role of Durrer layers in the normal, the hypertrophied and the ischemic heart.
A mechanism is described which explains the electrocardiographic manifestations of cellular hypertrophy and acute ischemia. This mechanism arises from neighboring cells having different transmembrane action potentials, and it has been called the "contiguity effect". The contiguity effect of adjacent "Durrer layers" (defined in the paper) gives rise to the T-wave distortions in hypertrophy and is also responsible for the polarity of the normal T-wave. This mechanism has been incorporated in a computer model of electrical heart activity which generates high fidelity 12-lead electrocardiograms. It is shown that the increase in R-wave amplitude and in ventricular activation time, and the flattening and/or polarity reversal of the T-wave in hypertrophy is due to an increase in the size of myocardial cells, and the S-T segment shift in acute ischemia is produced by the contiguity effect between normal and ischemic cells. For a lesion of given size, the S-T segment shift is linearly proportional to the "severity"; i.e., the reduction in electrical activity, of ischemic cells, and fora lesion of given severity, the S-T segment shift is a measure of the area, not the volume, of ischemic tissue. Therefore, a direct correlation does not necessarily exist between volume measuring tests (such as serum enzyme values in the case of necrosis) and S-T segment shifts in acute ischemia.
D006332:Cardiomegaly / Q000175:diagnosis*; D003327:Coronary Disease / Q000175:diagnosis*; D004562:Electrocardiography / Q000379:methods*; D006321:Heart / Q000502:physiology*; D006801:Humans; D008961:Models, Structural; D016276:Ventricular Function