Table 6 Comparison of the conventional and the proposed ECG interpretation of the ischemic ECG changes

Normal ECG before the onset of plaque rupture

Hyperacute T wave changes - increased T wave amplitude and width; QT prolongs; some ST segment elevation

altered repolarization of the involved left ventricle wall is not optimally buffered by the still normal repolarization of septal muscle and right ventricle

If walls of both ventricles are synchronous in repolarization, right ventricle and septal muscle reduce the left ventricle dominance. If the left ventricle wall is delayed, the resulting T wave increases

Marked ST elevation with hyperacute T wave changes

altered distribution of ventricular charges in diastole and systole displaces the systolic attractor from the diastolic attractor

any asymmetry in the systolic or in the diastolic ventricular electric field changes the position of the thoracic field center in that heart cycle phase.

Pathologic Q waves appear (necrosis), ST elevation decreases, T waves begin to invert

reduced quantity of repolarised tissue near the “UP” electrode allows the right ventricle structure to prevail during depolarization, when the septal muscle is already depolarized, resulting in Q waves

reduced quantity of tissue able to repolarise near the “UP” electrode allows the septal and right ventricle muscles to prevail and thus Pathologic Q waves and T wave inversion inverse T waves.

Pathologic Q waves and T wave inversion (necrosis with fibrosis)

Pathologic Q waves, upright T waves (fibrosis)

Q waves may get smaller or disappear with time

cicatrisation physically reduces the electrically “dead” area, so the surrounding muscle can oppose the prevailing right ventricle and septal muscles

The remaining left ventricle muscle tissue becomes able to repolarise and the new electric balance between two walls and septal muscle is achieved.