The difficult electrocardiographic diagnosis of myocardial infarction

A review of data on patients suffering from acute pancreatitis provides few instances wherein electrocardiographic evidence of acute myocardial injury or necrosis developed under circumstances in which concomitant coronary insufficiency was not a more likely cause of the myocardial damage. Experimentally induced acute pancreatitis and the intravenous injection of pancreatic enzymes were not attended by electrocardiographic changes of the kind associated with myocardial infarction. Therefore, if a patient suffering from acute pancreatitis develops electrocardiographic changes indicative of acute myocardial infarction, it is likely that a disparity between coronary flow and myocardial need has resulted in myocardial infarction. Intracranial hemorrhage or trauma commonly induces cardiac arrhythmias and changes in T waves, probably by increased vagal stimulation. However, the eletrocardiographic changes described in all except one of the reports reviewed supply only inferential evidence of myocardial injury. Unless other clinical evidence supports existence of myocardial infarction, that diagnosis rests insecurely. Electrocardiographic evidence of confluent myocardial scar rarely is encountered in patients having primary myocardial disease. This conclusion is consonant with the disseminated focal myocardial changes that characterize this type of myocardial disease morphologically. Segmental and T wave changes in acute pericarditis may mimic those of myocardial infarction; the presence of pathologic Q waves, however, is distinctive of infarction. Cor pulmonale, acute or chronic, may simulate posterior myocardial infarction, but only rarely in a degree sufficient to induce sustained justified confusion. A major acute myoccardial infarction may prove difficult of diagnosis when the infarct is transmural but of small circumference, when it is confined to subendocardium, or to the lateral or posterolateral wall of the left ventricle. The nature of electrocardiographic changes induced by such lesions and the basis for their peculiar features are reviewed. Healed myocardial infarcts frequently produce no electrocardiographic changes permitting recognition of the scar. Such scarring almost certainly is responsible for some instances of major shifts in mean electrical axis to the left (left-axis deviation of −30 to −90, S 2S 3 pattern). However, review of two pathologic studies supports the judgment that uncomplicated left-axis deviation is a perilous sole criterion on