Electrocardiographic ischemic patterns without coronary artery disease.

ST segment deviation is commonly accepted as a sign of myocardial ischemia. Whether indicative of actual myocardial ischemia or not, ST segment changes have been and continue to be generally interpreted as “ischemic ST deviation,” “subendocardial injury,” “coronary insufficiency,” or even “myocardial infarction.” The use of any of these terms intimates coronary artery disease and tends to leave one with an ominous feeling about the patient’s prognosis. Such ominous prognostic feelings on the part of the clinician may lead him to recommend drastic changes in the patient’s way of living. Such recommendations either directly or indirectly indicate to the patient that from that time forward his life is in jeopardy, and he must be extremely careful. Whether or not such drastic steps are necessary following all cases of actual proved coronary artery disease is not a point to be considered here, but it is obvious that such total-life modifying recommendations are contraindicated when there is no coronary artery disease. latrogenic heart disease is disabling to a patient, and is unnecessary if the clinician clearly understands when electrocardiographic changes are significant and when they are not. “Ischemic patterns” refers to those ST segment changes (elevation and depression) which have been commonly considered to be the result of myocardial ischemia. These same electrocardiographic changes are encountered in a wide variety of clinical conditions without other evidence of coronary artery disease. “Non-ischemic” electrocardiographic changes have received sporadic attention, but little effort has been made to establish a common denominator to explain these ST changes. This paper represents an attempt in this direction. Definitive understanding of the nature of ST deviation has been hampered, both clinically and experimentally by the relative lack of concern as to whether the direction of the shift was upward or downward. It has been generally assumed that epicardial ST segment depression is reciprocal to ST segment elevation on the subendocardial layers of the wall of the heart; elevation or depression in a given lead being dependent on the point of observation, i.e., on the position of the electrode with regard to the area of myocardial injury. Recently published experiments1 demonstrate that ST segment depression is a manifestation of primary epicardial change, as is ST segment elevation. Primary ST segment depression over the epicardial surface of the heart has been experimentally produced without ischemia by per-