Abstract: The patient was a 53-year-old male, cadre, who was admitted to the hospital for more than 20 days with paroxysmal precordial dullness. The episodes occurred mostly in the morning after waking up in the resting state and lasted from a few minutes to more than 10 minutes each time, and could resolve on their own. He had a history of hypertension for more than 10 years without treatment, and his blood pressure was about 160/100 mmHg. Smoking average 20 cigarettes/day × 20 years, drinking average 250ml/day × 20 years. Biochemical test report: CHOL 5,97mmol/L, TG 1,65mmol/L, HDL-C 1,20mmol/L, LDL-C 3,74mmol/L, VLDL 1,03mmol/L, GLU 5,0mmol/L. Cardiac ultrasound: normal internal diameter of each atrial cavity, normal left ventricular ejection fraction, septal thickening (14mm). Chest radiograph: no characteristic changes in cardiac shadow. Coronary angiography was performed and the results showed no abnormalities in the coronary arteries. He was discharged from the hospital with medication. On the third day after discharge, the patient again had a dull pain in the precordial region, which lasted for half an hour and could not be relieved on its own, and came to the hospital urgently. The symptoms lasted for about 1 hour in total. After 24 hours, myocardial enzymes: CK 374IU/L HBDH 253IU/L CKMB 33IU/L AST 55IU/L, ECG showed that V1-V3 was QS type, T wave was inverted. 48 hours ECG showed that V2 and V3 were rS type, and the patient had no symptoms such as chest tightness and shortness of breath. The patient did not have symptoms such as chest tightness and shortness of breath. Afterwards, the ECG was rechecked and V2 and V3 r waves were gradually higher and T wave inversions were gradually shallow. 2, Discussion: The patient did not see stenosis in the coronary artery, but had typical variant angina and acute myocardial infarction clinical manifestations, considering acute myocardial infarction due to coronary artery spasm. The basic lesion of coronary heart disease is atherosclerotic stenosis of coronary arteries, which leads to myocardial ischemia and loss of balance between myocardial hypoxia and oxygen supply causing angina pectoris and myocardial infarction, a concept that still serves as the theoretical basis of traditional treatment. However, in recent years, coronary artery spasm (CAS) has attracted a lot of attention from cardiologists. CAS can cause not only angina pectoris but also acute myocardial infarction, severe rhythm disturbances and sudden death. The specific mechanism is not very clear, but is mostly thought to be related to neural mechanisms, mechanical stimulation, and humoral stimulation. Heavy smoking is an important risk factor. Since acute thrombosis is accompanied by thrombus autolysis, and complete revascularization has myocardial cell necrosis, but the myocardial function is quickly restored, so the impact on cardiac function is smaller and the prognosis is better. Prevention of coronary artery spasm is the main strategy for this disease.