The Electrophysiology of a Single MI
Click to Enlarge In A, note the rapid and synchronous programming of endocardial activation by the specialized ventricular conduction system results in the normal symmetrical activation of both inferior and anterosuperior walls and this balancing is associated with the absence of significant Q-waves. In B, to generate the Q-wave, an unbalancing of these forces is necessary. The normal anterosuperior LV forces, together with the loss of inferior forces due to the MI, are both essential to the development of the inferior Q-waves. In addition to Q-waves, the mid and late inferior R-waves are typically prolonged and notched. This is caused by the delayed activation of the subepicardial layers overlying the infarct, which blocks direct endo to epicardial activation in this region. Just as with unbalanced activation generates the Q-wave, repolarization is similarly unbalanced, resulting in negative inferior T-waves even though the IMI is old. The large IMI in C is associated with larger Q-waves, small terminal r-waves, and left axis deviation, all due to loss of a large mass of inferior myocardium and the predominance of opposing forces in the anterosuperior wall. The figure emphasizes the balance of inferior and superior wall forces that are necessary to produce the inferior Q-waves and axis shift. Finally, note in both the small and large IMIs the Purkinje system is not affected, i.e. no conduction system disease, fascicular block, etc.

The Electrophysiology of Two Opposing MIs
Click to Enlarge Two infarcts that are spatially opposed (180°) each affects the ECG manifestations of the other MI and no significant Q-waves may be present. Instead of Q-waves in either the inferior (lead III) or anterosuperior (lead aVL), complex, oscillating, notched, and low voltage waveforms referred to as M and W complexes are present, and these indicate two opposing MIs and are equivalent to opposing Q-waves which cannot exist in this condition.


Ischemic Cardiomyopathy (ICMP)
Click to Enlarge Patients surviving with multiple MIs and repeated ischemic insults may develop a unique and readily recognizable ECG morphology characterized by QRS widening, increased QRS voltage in the chest leads, low voltage in the limb leads with multiple notching and a jerky progression of R and S waves in the V leads, all atypical for classical left bundle branch block.