A mechanism for the electrocardiogram response to left ventricular hypertrophy and acute ischemia.
A proposed mechanism for explaining the electrocardiographic response in left ventricular hypertrophy and in subendocardial and epicardial acute ischemia was incorporated in a mathematical model of electrical heart activity. The model of hypertrophy was simply an increase in cell size, and the principal effect on the computer-generated 12-lead electrocardiograms (ECGs) was an increase in R-wave amplitude and ventricular activation time and a flattening or polarity reversal of the T wave. The model of acute ischemia was a reduction between plateau and resting potential of the transmembrane action potential. The principal effect on the computer-generated 12-lead ECGs was an S-T segment displacement up or down depending on the location of the lesion. This shift was linearly proportional to the severity of the ischemia, i.e., the reduction in electrical activity of the ischemic cell, and for a lesion of given severity the S-T segment shift was a measure of the area, not the volume, of ischemic tissue. Therefore, this model suggests that 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.
D003201:Computers; D003327:Coronary Disease / Q000503:physiopathology*; D004562:Electrocardiography; D006352:Heart Ventricles / Q000503:physiopathology*; D006801:Humans; D006984:Hypertrophy / Q000503:physiopathology; D008564:Membrane Potentials; D008954:Models, Biological