IntroductionThrombotic thrombocytopenic purpura (TTP) is a rare thrombotic microangiopathy that manifests as microangiopathic hemolytic anemia, severe thrombocytopenia, and ischemia damage to important organs caused by platelet-rich thrombi produced in the microvasculature. TTP is caused by a congenital or acquired lack of the von Willebrand factor-cleaving protease, ADAMTS13 (A Disintegrin and Metalloproteinase with a Thrombospondin type 1 motif, member 13). Anti-ADAMTS13 autoantibodies are the primary cause of ADAMTS13 deficiency, which can be idiopathic or associated with various pathological processes such as neoplasias, infections, and autoimmune disorders like systemic lupus erythematous (SLE) 1. If left untreated, TTP is a dangerous illness with a high death rate. The prognosis has significantly improved with therapeutic plasma exchange (TPE), and mortality has dropped from 85%-100% to 10%-30% 2, 3. TPE is a technique that involves separating blood cells from plasma. When elements in the plasma are responsible for the pathophysiology of the disease, this approach is employed. This method is used as a treatment method for various diseases, but the reason for using TPE in a patient suffering from acquired TTP is to remove Anti-ADAMTS13 autoantibodies. Relapse happens in 40% of patients, and there are cases that are resistant to treatment. Various immunosuppressive medications, including rituximab (RTX), have been used in these cases 4. TTP is relatively uncommon in SLE patients. It is unknown how often TTP occurs overall in SLE patients; however, it has been estimated to be as low as 0.5% 5. Instances of simultaneous TTP and SLE are often discussed in the medical literature in patients who have substantial renal dysfunction and lupus activity 6. Here we present a clinical case of a woman who developed myocardial infarction (MI) in the context of TTP. After further investigation, undiagnosed SLE disease was suggested as the cause of TTP.