Abstract

The genesis of the electrocardiogram in patients with myocardial infarction is a subject which has stimulated extensive discussion as well as several excellent investigations. It is now recognized that initial, mid-temporal, and terminal QRS ab­ normalities occur in patients with chronic myo­ cardial infarction. Wilson and co-investigators' initially postulated the window theory to explain the abnormal Q wave in the electrocardiogram in myocardial infarction. Their studies were based on the experimental production of myocardial lesions in dogs. It was their conclusion that Q waves resulted from an electric al window in the depolarization wavefront wh ich resulted in the transmission of the left ventricular ca vity poten­ tial to the torso through this opening. Presently there me two theories which have been postulated to explain the mechanism of terminal QRS ab­ normalities in infarction. The se changes, variously referred to as peri-infarction, post-infarction, and parietal block, were ascribed to delayed excitation of the epicardium overlying sub-endocardial in­ farction by Bayley, and to abnormal conduction in the Purkinje network of the left ventricle with delayed onset ofendocardial activation by Grant. The recent ventricular activation studies by Durrer and co-workers! demonstrated that Q waves were present on the epicardium of dogs overlying regions of sub-endocardial infarction. Larger and longer Q waves were found on the epi­ cardium over a larger sub-endocardial infarct and QS complexes were observed over region s of trans­ mural infarction. In addition, Durrer's group noted delay in excitation of the epicardium re

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call