ST-segment mapping. Realistic and unrealistic expectations.

DURING THE LAST FEW YEARS considerable interest has developed in the possibility that some of the myocardial damage consequent to coronary occlusion may be averted.' To explore this possibility there is a critical need for techniques capable of testing the hypothesis that a given intervention is capable of protecting ischemic myocardium. Since it has long been appreciated that myocardial ischemia produces changes in the ST segment, it was natural to attempt to utilize this portion of the electrocardiogram as an index of ischemic injury.2 The purpose of this editorial is to review the electrophysiologic basis for deviation of the ST segment and to place into perspective its potential value and limitations in assessing the efficacy of interventions designed to limit infarct size. In 1920, Pardee directed attention to this portion of the electrocardiogram when he described elevation of the ST segment as a clinical sign of myocardial ischemia following coronary occlusion.3 Wilson,4 Bailey,' Rakita5 and their respective collaborators noted that following experimental ligation of a coronary artery, epicardial leads showed ST-segment elevation. Sometimes ST-segment depressions occurred at the junction of the cyanotic and normal zones. The electrophysiologic basis of changes in the ST segment in myocardial ischemia has not been completely clarified,7 and there is a great need to obtain an electrical model of the sequential changes that take place from the onset of ischemia to the stage of chronic infarction. It has been postulated that following repolarization of normal tissue the resting membrane potential of ischemic cells is lower than that of normal cells and for this reason a "current of injury" flows across the boundary between the normally polarized region and the ischemic zone. According to this concept this current disappears when the entire heart is depolarized during excitation and the elevated ST segment results from a depressed T-Q segment.8 It has also been suggested that ST-segment elevation may occur as a result of failure of the injured area to depolarize during excitation,9 which results in current flow during depolarization across the boundary between the partially polarized, injured region and the depolarized normal zone.