A patient in their 60s with a history of hypertension presented to the emergency department with sudden chest pain radiating to the back and sweating for 2 hours without relief. Initial physical examination results revealed blood pressure of 140/78 mm Hg, a pulse rate of 74/min, and a respiratory rate of 20/min. An initial 12-lead electrocardiogram (ECG) was obtained (Figure, A).
Questions: What is the cause of these ST-T changes? Are these ST-segment elevations harmless artifact or critical fact? What is the most likely diagnosis and the management for the diagnosis?
The initial ECG showed ST-segment elevations (STEs) in leads I, II, III, aVF, V5, and V6; ST-segment depression (STD) in lead aVR; and broadening and biphasic T waves of bizarre configuration in leads I, II, aVR, aVL, and aVF. Two clues suggested the diagnosis of artifact in the first ECG: (1) presence of bizarre T waves in all limb leads, except lead III, and (2) significant difference in corrected QT (QTc) interval between leads II and III. However, there was an acute myocardial infarction (AMI) caused by acute occlusion of the left circumflex coronary artery (LCx) concealed beneath these harmless artifacts. A few clues in the first ECG suggest the diagnosis of AMI caused by acute occlusion of LCx: (1) STE in leads III, V5, and V6; (2) STD in leads V2 and V31; and (3) R-wave prominence (R-wave amplitude/S-wave amplitude [R/S] > 1) in lead V2.2 After repositioning electrodes, an 18-lead ECG was obtained 2 minutes later, showing a normal QTc interval and disappearance of the bizarre T waves in the limb leads, confirming that there was artifact before; it also showed STE in leads II, III, aVF, and V7 through V9 (Figure, B). Higher STE in lead II than III when ST was isoelectric in lead I, STE in extended leads V7 through V9, and STD in lead aVR during inferior STE also highly suggested an AMI caused by acute occlusion of LCx.3- 5