We present a case of 51-year-old female patient who was admitted at the Clinic of Nephrology and Clinical Immunology. The patient was hospitalized 5 months prior in a regional institution due to type 2 acute respiratory insufficiency, as well as elevated values of D-dimer (9730ng/ml). Thoracic computed tomography (CT) scan was performed natively and with contrast, pleural effusions were observed on both sides (up to 12 mm on the right, and up to 5 mm on the left) as well as three ulcers on the aortic arch up to 5 mm in diameter. During hospitalization, a sudden onset of intense chest pain occurred, followed by a development of heart failure to the level of cardiogenic shock. Electrocardiography showed signs of ST-elevated myocardial infarction (STEMI) of the anterior wall, and an increase in cardiospecific enzymes (high-sensitivity cardiac troponin I (hs-cTnI) 20 000 ng/ml, creatin kinase MB (CK-MB) 259 IU/L), after which the patient transferred to a reference health facility. Arterial hypertension, hypercholesterolemia and smoking are among the risk factors for developing acute coronary syndrome. Coronary angiography was performed, which verified the narrowing of the ostial segment of the left anterior descending artery (LAD). Bearing in mind the previously mentioned ulcer and coronary angiography findings, percutaneous coronary intervention (PCI) was performed with drug-eluting stent (DES) implantation in left anterior descending artery (LAD). Echocardiography verified ischemic cardiomyopathy with ejection fraction (EF) 38%. Due to the appearance of back pain and quantitative disturbance of consciousness, as well as hemodynamic instability and differences in arterial blood pressure on upper extremities, urgent CT angiography was performed, which indicated an occlusion of the left common carotid artery (ACC), subclavian and axillary arteries as well as a penetrating aortic ulcer localized infrarenal (Photo 1). In the further course of treatment, left-sided weakness of the body was registered in the objective finding. Head CT scan was performed, which showed an acute ischemic lesion with a diameter of 13 mm, high parietal on the right, as well as a chronic ischemic lesion with a diameter of 9 mm on the front right. A neurologist was consulted, who indicated the continuation of dual antiplatelet therapy, and proposed additional imaging diagnostics and immunological testing. Upon admission to the Clinic of Nephrology and Clinical Immunology, further examinations were performed, including Doppler ultrasonography of carotid and vertebral arteries, which registered left occlusion, right ACC/external carotid artery (ACE) stenosis with suspected “macaroni sign”, as well as suspected left vertebral artery (AV) occlusion; the finding was described to correspond to Takayasu arteritis. MRI with MRA were performed and showed chronic (micro) ischemic frontoparietal lesions on the right, and to a lesser extent on the left; on the absence of flow in the extracranial segment of the left AV as well as multiple stenoses on the longer segment of the left internal carotid artery (ACI) as well as a stenosis by about 60-70% of the right ACI on the retreat (Photo 2). CT angiography of the head and neck was also performed, the following was observed: occlusion of the left ACC along its entire length, stenosis of the right and left ACI, occlusion of the left a. subclaviae, as well as moderate narrowing of the truncus brachiocephalicus and right a. subclaviae. Laboratory tests verified negative anti-nuclear antibodies on primate liver and Hep-2 cells, negative anti cytoplasmic antibodies (ANCA), anti Beta2 glycoprotein IgG and anti Beta2 glycoprotein IgM antibodies (Ab), anti-cardiolipin Ab and lupus anticoagulant, elevated erythrocyte sedimentation rate (ESR) 56mm/h and a C-reactive protein (CRP) of 54 mg/L. After all the tests that were performed, a final diagnosis of Takayasu arteritis was established and corticosteroids were included in the therapy (primarily in pulse doses) with the first pulse of cyclophosphamide (CYP) of 1000mg. The patient was in a further hospital course in good general condition, with regression of all the previously mentioned problems, and was discharged for outpatient treatment at a dose of prednisolone and CYP monthly pulses. The values of inflammatory biomarkers, after treatment, were in a significant decline in regard to initial values (ESR 26 mm/h, CRP 2.5 mg/L). On the first check up the patient was feeling well, with no neurological and cardiac problems.