A 72-year-old man was admitted to the hospital for elective carotid endarterectomy surgery due to an asymptomatic 95% internal carotid artery stenosis. His medical history was significant for multiple vascular operations; he had a carotid endarterectomy on the opposite side 2 years earlier and repeated lower-extremity arterial bypass procedures for intermittent claudication. He had insulin-dependent diabetes mellitus and ischemic heart disease status post, and a coronary artery bypass graft surgery 7 years earlier for left-main and triple-vessel coronary artery disease. He had grade IIa stable angina pectoris, essential hypertension, and mild renal failure, but no history of congestive heart failure.
An electrocardiogram (ECG) revealed left ventricular hypertrophy, left anterior hemiblock, and right bundle branch block. The patient underwent carotid endarterectomy under general anesthesia. Just before the induction of anesthesia the patient was connected to the 12-lead ST-trend monitor, and a baseline, resting ECG was acquired. The operation itself was uneventful. At the end of the surgery, the patient was extubated, neurologically intact, and hemodynamically stable. In the recovery room, he reported pain in his neck, presumably from the sur-gery, and received repeated intravenous doses of morphine. Despite the absence of chest pain, myocardial ischemia was suspected and, although the patient was participating in a study and the monitoring was supposed to be blinded, the ST-trends were made available for the treating physician.
The figure demonstrates the ST and heart rate trends of the patient before the induction of anesthesia and for the next 24 hours. The patient developed prolonged (190 minutes) ST-segment depression-type ischemia, which started at the end of surgery on emergence from anesthesia, in accordance with a moderate increase in heart rate. Although the ischemic ECG changes reverted to baseline at the end of the ischemic episode, 10 hours later, his serum troponin I increased to 10.2 ng/mL, and then to 32.1 ng/mL the next morning. The figure shows marked ST-segment depression in the anterior leads (367 microvolts) during peak ischemia compared with the patient’s baseline.
This patient had prolonged silent ST-segment depression-type ischemia and subsequent myocardial infarction (MI). The MI could have gone completely unnoticed if we had not performed the continuous ECG monitoring and routine troponin I measurements used for the study protocol. The ECG changes that occurred during ischemia completely returned to baseline, despite the elevation of troponin I to 20 times the upper limit of normal. This case demonstrates how, unless one uses continuous ST-trend monitoring, diagnosing MI by single snapshots of 12-lead ECGs in patients with baseline ECG abnormalities can be difficult.