Reciprocal ST Segment Changes in Acute Myocardial Infarction; Informative or Incidental?

Abstract

The majority of patients show elevation of the ST segment of the surface electrocardiogram during the acute phase of transmural myocardial infarction. In a significant proportion of such patients, depression of the ST segment is observed in an area of myocardium away from the infarcted territory. In spite of the recognition of this reciprocal ST segment depression for some decades, its aetiology and diagnostic and prognostic significance have been elusive and the subject of controversy. There is general, but not uniform, agreement that patients showing reciprocal ST segment depression usually have more extensive myocardial damage than those without reciprocal changes. Assessments have included echocardiography [1], radionuclide ventriculography for ejection fraction and wall motion abnormalities [2, 3], thallium perfusion scintigraphy [4], enzyme release [2, 5] and in-hospital complications including heart failure and dysrhythmias [6]. It is logical to assume that the longer-term prognosis of such patients is somewhat less good, although evidence is limited and based on series too small to provide reliable prognostic information [7, 8]. Two general views have been advanced to explain reciprocal ST segment changes in acute myocardial infarction. The first contends that ST segment depression in areas presumably remote from the infarct territory is an electrical phenomenon related to the extent of ST segment elevation over the infarct territory. The second contends that ischaemia 'at a distance' underlies the ST segment depression, related to compromise of myocardial perfusion either from the same or a different artery to that supplying the infarct territory. It is likely that neither view is exclusively correct because of time-related changes in currents of injury after myocardial infarction. Thus, it was shown over 25 years ago in a canine model that ST segment elevation from the anterior epicardial electrogram after left anterior descending coronary artery ligation was associated immediately with ST segment depression on the epicardial surface of the posterior wall, directly opposite the evolving infarct [9]. Within 20 min, however electrodes on the periphery of the infarct that had recorded ST segment elevation initially showed ST segment depression as a marker of local myocardial injury. Clearly, the 12 lead body surface electrocardiogram is insufficient to differentiate reliably between such non-infarct and peri-infarct phenomena. Transient reciprocal ST segment changes, for example during coronary angioplasty [10,11], do not necessarily reflect currents of injury during evolving myocardial infarction. Protagonists of these two viewpoints have examined the predictive value of reciprocal ST