B49-46 Life-threatening Cardiac Tamponade During Azacitidine Induction Therapy in a Patient With Acute Myeloid Leukemia

Abstract Introduction Cardiac tamponade is a life-threatening condition1. While it is most commonly associated with malignancy, infection, trauma, or autoimmune disease, drug-induced tamponade is a rare but important etiology to consider1. Case Presentation This is the case of a 78-year-old female with history of hyperparathyroidism, autoimmune hypothyroidism, and acute myeloid leukemia (AML) diagnosed one month prior. One week after her first treatment cycle with azacitidine, she was hospitalized for pericarditis and had clinical improvement when treated with colchicine. Given the close temporal relationship with azacitidine initiation and a negative infectious and rheumatologic workup, pericarditis was attributed to azacitidine-induced cardiotoxicity. She now presents with new-onset diaphoresis, lightheadedness, and pleuritic chest pain. On admission, she was tachycardic, normotensive, afebrile, and stable on room air. She appeared ill and pale. Cardiac auscultation revealed tachycardia with muffled heart sounds and jugular venous distension. Laboratory workup showed pancytopenia. Point-of-care cardiac ultrasound demonstrated large pericardial effusion with diastolic collapse of the right atrium and right ventricle, consistent with cardiac tamponade. She underwent emergent pericardiocentesis. Pericardial fluid culture, flow cytometry, and cytology were negative. She was diagnosed with recurrent pericarditis with progression to cardiac tamponade, consistent with azacitidine-induced cardiotoxicity. Discussion Azacitidine is a hypomethylating agent used in AML, with well-documented adverse effects involving the hematologic and gastrointestinal systems. While prior research has established an association between azacitidine, coronary vasospasm, pericarditis, and pericardial effusion2, reports of it causing cardiac tamponade are rare3. The mechanism is not understood, but hypothesized to result from an immune-mediated reaction, leading to pericardial irritation and effusion accumulation4. This case highlights the importance of point-of-care cardiac ultrasound as a simple, rapid, and effective tool for diagnosing pericardial effusion and tamponade. Early recognition and intervention are crucial, as drug-induced tamponade can be life-threatening if not promptly managed. Patients on azacitidine who present with chest pain should undergo thorough evaluation for potential cardiac complications. References: 1.Hwang SH. Pictorial Review of Tuberculosis involving the Pleura. European Congress of Radiology-ECR 2011; 2011: 2.Chu B, Venkatakrishnan A, Aggarwal P. Safety signal between azacitidine and pericarditis. Chemotherapy. 2023;68(2):115-118. 3.Krecak I, Supe M, Markov B, Skelin M, Lucijanic M. Fatal heart tamponade during induction treatment with azacitidine and venetoclax. Annals of hematology. 2024;103(11):4827-4829. 4.Goo K, Uy R, Roswarski J. Azacitidine-associated pleuropericardial effusion in myelodysplastic syndrome: A case report. Journal of Oncology Pharmacy Practice. 2019;25(5):1248-1252. This abstract is funded by: None