Abstract

supplied an appreciable amount of anterior and inferior left ventricular myocardium. Dunn et al.’ found that exercise-induced ST segment elevation in ECG leads V, or aVL was highly specific for the presence of LAD coronary artery stenosis and reversible anterior wall myocardial ischemia. Alternatively, we cannot exclude the possibility that coexistent coronary vasospasm superimposed on a critical coronary stenosis was responsible for the observed exercise-induced ST segment elevation, although there were no associated clinical features or abnormal ST segment shifts during ambulatory ECG monitoring to support this. Weiner et al6 have previously described exercise-induced ST segment elevation during the recovery phase of exercise testing in four patients with variant angina, two of whom had associated fixed coronary stenoses. Three of their patients exhibited ST segment depression during exercise, and ST segment elevation was not observed until 2 or 3 minutes after the cessation of exercise.6 We hypothesize that this patient developed subendocardial &hernia manifested by ST segment depression at a significant level of exercise (rate-pressure product 25,000), which rapidly progressed to “silent” transmural myocardial ischemia at maximal exercise and early into recovery. Undoubtedly, the exercise test was continued beyond the point of diagnostic ischemic ST segment changes because of the patient’s asymptomatic status. The subsequent appearance of marked anterior wall ST segment elevation delineated the presence of a strikingly positive exercise study, which ultimately led to catheterization and angioplasty. We conclude that asymptomatic exercise-induced ST segment elevation in the absence of prior ECG Q waves may be a manifestation of significant “silent myocardial ischemia,” presumably due to highgrade fixed coronary artery disease and/or superimposed coronary vasospasm. These findings should prompt consideration for urgent invasive evaluation.

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