Exercise-induced ST elevation in patients without myocardial infarction.

Abstract

SUMMARY A review of 6040 consecutive exercise tests yielded 106 patients without previous myocardial infarction (MI) who had exercise-induced ST elevation (. 0.5 mm in a 15-lead ECG system). In 46, ST elevation was correlated with left ventriculography and coronary angiography. Coronary artery disease (CAD) (> 70% narrowing) was detected in 40 of 46 patients: 12 patients had one-vessel disease, 13 had two-vessel disease, and 15 had three-vessel disease. Resting ventriculograms were normal in 36 of 40 patients. Of 21 patients with anterior (V,-V3) ST glutamic oxaloacetic transaminase). All patients who did not fulfill the above criteria (i.e., those in whom an infarction was uncertain) were rejected from the study; patients who either fulfilled or had none of these criteria were included in the study.Of the 6040 patients tested, 399 (6.6%) had exerciseinduced ST elevation and a myocardial infarction. The majority (95%) of the 399 patients had ST elevation over the area of infarction. One hundred six patients (1.7% of the total population) developed ST elevation and had no evidence of a myocardial infarction, LVH or bundle branch block and were not taking digitalis. Forty-six patients in this latter group had undergone diagnostic cardiac catheterization. Another 21 patients with LVH and 12 patients taking digitalis also had exercise-related ST elevation. Six patients with LVH, one of whom was also taking digitalis, were catheterized. The stress tests were carried out according to either the multistaged Bruce or Balke protocols.'2 13 Each patient's blood pressure was monitored by indirect sphygmomanometry. Also, all patients were questioned during and after the exercise test about the development of symptoms. Angina pectoris was recorded if a patient developed exertional or postexer-

Significance of exercise‐induced ST changes in leads AVR, V5, and V1. Discrimination of patients with single‐ or multivessel coronary artery disease

“…1 On the other hand, the appearance of exercise-induced ST-segment elevation, although significantly less frequent than ST depression, seems to indicate a particular myocardial region, with ischemia either by coronary spasm or by severe narrowing of the coronary vessels in patients without prior myocardial infarction. [2][3][4][5][6][7] Consequently, the estimation of ST elevation in particular leads might be useful for identifying ischemic my-ocardial regions during exercise testing. Progress in this field appears to be promising, as reported recently by two studies, in which the value of ST elevation in the "pseudo-intracavitary" lead aVR and in lead V 1 was appreciated.…”

Nonischemic ST-Segment Elevation Induced by Negative Inotropic Agents

“…However, persistent STsegment elevation is sometimes observed in patients with ventricular aneurysm, 3 and exercise or dobutamine stressinduced ST-segment elevation has been observed after MI, possibly due to ventricular asynergy. 4,5 Thus, it is important to determine whether myocardial ischemia is present in these patients. The present results showed that nonischemic ST-segment elevation was induced by regional ventricular dyskinesia, indicating that regional wall motion abnormalities can cause ST-segment elevation in the absence of coronary stenotic lesions and that ST-segment elevation is not always a good marker of myocardial ischemia.…”

“…3 In addition, an exercise or dobutamine stress-test sometimes induces ST-segment elevation in patients with an old anteroseptal MI, probably due to asynergy. 4,5 These findings suggest that regional ventricular dyskinesia is a possible mechanism for ST-segment elevation unrelated to myocardial ischemia.We investigated the role of regional ventricular dyskinesia in ST-segment elevation not associated with ischemia in a canine model of regional ventricular dyskinesia produced with negative inotropic agents. …”

Stretch-Activated Ion Channel Blocker Gadolinium Attenuates Ischemic ST-Segment Elevation in Canine Myocardium

“…After the recording of baseline measurements (control), the coronary bypass was occluded again for 5 min followed by 15 Regional transmural ischemia causes both ST-segment elevation and systolic elongation (bulging) of the myocardium. Mechanical stretch might alter the transmembrane potentioal via stretch-activated ion channels (SAC); however, the role of SAC on ischemic ST-segment elevation has not yet fully studied.…”