Introduction: Thalidomide was used first as a sedative and antiemetic agent. Soon Thalidomide`s teratogenic effects became apparent, and it was subsequently withdrawn from the market. However there is now a growing clinical interest in Thalidomide, and it is introduced as an antiangiogenic and immunomodulatory drug used primarily to treat multiple myeloma. Unforturately, an increase in the risk of venous thrombosis and pulmonary embolism was reported by several articles. However, arterial thrombosis associated with Thalidamide was very rare, especially coronary arteries. We report coronary arterial thrombosis induced by Thalidamide in a multiple myeloma patient. Case: A 58-year-old male patient who had been diagnosed with multiple myeloma was admitted to our cardiovascular center with chest pain. The patient``s history was unremarkable for any cardiopulmonary disease and for any cardiovascular risk factors. He has been treated with Thalidamide(200 mg/day) for 8 weeks. He had ST segments elevation in V1~V6, and poor R wave in V1~V4 and the Troponin-I and CK-MB were markedly elevated. After administration of Enoxaparin and loading dose Aspirin and Clopidogrel, he was emergently performed cardiac catherization, which revealed that total occlusion with large thrombus of distal left anterior descending artery, distal left circumflex artery and 1st diagonal artery. We performed percutaneous catheter thrombectomy and balloon angioplasty successfully and improved coronary artery flow. We also have treated with Tirofiban(Agrastat(R)) intravenously and Enoxaparin subcutaneously. We also let him stop taking Thalidomide. Meanwhile, 3 days later, the patient felt chest pain again, ST segments were elevated in all precordial leads, so we promptly performed coronary angiography that showed total occlusion at the same site of the previous study. We treated him as the same way of the past with aspiration thrombectomy and Tirofiban intravenously, Enoxaparin subcutaneuouly. The patient`s condition was stabilized after adequate treatment. 7 days later, we performed coronary angiography again that showed no evidence of occlusion. He was discharged with antiplatelets medication in stable condition without recurrence.