A 65-year-old male, who was a current smoker with hypertension, was admitted to our hospital with chest pain radiating to the jaw for 6 months and aggravation for 1 month. Chest pain induced by activity persisted for approximately 10–20 minutes each time, and was gradually alleviated after rest. Physical examination revealed an anxious appearance. His pulse rate was 54 beats/min, his blood pressure was 121/73 mmHg, and his respiratory rate was 16 breaths/min. The initial ECG showed slight ST-segment elevation in Ι, aVL with T-wave inversion in the inferior leads (Fig. 1A). The cardiac troponin I level was 0.07(normal value 0-0.09 ng/ml) and all other basic laboratory tests were within normal limits. An echocardiogram showed that ventricular diastolic function had decreased. He was treated with aspirin, ticagrelor, enoxaparin sodium, amlodipine, atorvastatin and isosorbide mononitrate. One day after admission, the patient presented with sudden chest pain radiating to the jaws with diaphoresis while he was defecating. An ECG was performed, showing upsloping ST-segment depression up to 6 mm at the J point from V1 to V6, I, aVL; tall symmetrical T waves in leads V2-V5 together with a 1 mm J point elevation in the lead aVR; and elevation at the J point in the inferior leads with a heart rate of 34 times/min (Fig. 1B). At the same time, after performing a long II lead ECG, cardiac arrhythmia was revealed, including sinus bradycardia, atrioventricular (AV) junctional escape beats and AV junctional rhythm (Fig. 2). After the administration of nitroglycerin (5 mg) three minutes later, the patient became symptom-free, and repeated ECG showed that the pattern had returned to its former shape. We recognized the de Winter ECG pattern, which should be treated as the ST-elevation equivalent. However, given the stable hemodynamic status, and relief of chest pain after treatment, the cardiac catheterization laboratory was not activated immediately.
Twenty hours later, a coronary arteriogram was performed, confirming total occlusion of the proximal right coronary artery (RCA) with collateral circulation (Fig. 3) from the left coronary artery and no significant lesions at the LAD or the left main artery; the LCX was almost completely occluded at its middle portion, followed by insertion of a drug-eluting stent (Fig. 3). A few days later, the patient was discharged without any sign of complications.