Cardiologists and emergency physicians deal with patients with acute chest pain every day. The causes of chest pain are many and wide-ranging, and it is sometimes challenging to make the correct diagnosis and disposition in a timely manner. Coronary artery disease acute coronary syndrome is a common cause of chest pain and is a frequent differential diagnosis to consider. ECG and myocardial enzymatic changes are critical in the diagnosis of acute coronary syndrome, but sometimes the diagnosis is often overlooked when the particular subtype of acute coronary syndrome has negative myocardial enzymatic findings and the ECG presentation lacks specificity. The consequences are serious and can lead to disease progression or death of the patient. This particular type of unstable angina, Wellens syndrome, is described below in the context of a typical case. Case presentation: The patient, male, 71 years old, was admitted to the hospital with episodes of retrosternal sternal pain for 20 days, aggravated for 5 days. He denied hypertension, history of diabetes mellitus and had a history of heavy smoking for 40 years, smoking 40 paper cigarettes per day. On examination: BP 120/80 mmHg, both lungs without an ancient mu 50 beats/min, heart rhythm, no murmur, A2>P2, ECG: sinus bradycardia, some ST-T changes (see Figure 1). Cardiac enzymes: CK-Mb 20u/L, TnI 0.1ng/L, MYO 37U/L, UCG: left ventricular EF 60%, mitral regurgitation mild, left ventricular diastolic dysfunction, normal size of each chamber. Admission diagnosis: acute coronary syndrome of coronary artery disease, unstable angina pectoris. After admission, the patient had frequent angina attacks, up to 10 times a day, and often had resting attacks at night. The patient’s ECG showed inverted or bidirectional T waves in the precordial leads without chest pain (see Figure 1 and Figure 2), and the T waves could be pseudo-improved during chest pain attacks. Ventricular tachycardia and ventricular fibrillation occurred during the attack, cardioversion was given successfully, and myocardial TnI and CK-Mb were negative during hospitalization. Later, coronary angiography and PCI were performed (see Figure 3). The angina disappeared after the procedure and the patient was discharged 1 week later. The final diagnosis of coronary artery disease, Wellens syndrome, was made. Discussion: In 1982, Wellens et al, a Dutch physician, reported a group of unstable angina subtypes with crisis anterior descending proximal segment lesions, mainly characterized by symmetrical deep inversion of T waves or bidirectional T waves in leads V2 and V3 in the precordial region without significant ST-segment shift, pathological Q- or R-wave reduction, and normal cardiac enzymes. The main diagnostic points of Wellens syndrome include: ① Symmetric deep inversion or bidirectional T waves in the precordial region, usually in leads V2 and V3, but often extending to V1, V4, V5, or V6, with T wave changes occurring in the absence of chest pain, and pseudo-normalization during angina attacks. The patient may have ventricular arrhythmia or even ventricular tachycardia or ventricular fibrillation; ② ST may be pseudo-normalized or ST-segment elevation during the onset of symptoms; ③ there is no corresponding R-wave reduction and pathological Q-wave in the precordial region; ④ there is no or only mild ST-segment elevation.