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Journal of Cancer Research and Therapeutics, Vol. 7, No. 3, July-September, 2011, pp. 346-348 Letter to the Editor - Documenting a Case Rituximab induced myocardial infarction: A fatal drug reaction Palamalai Arunprasath1, Pakkirisamy Gobu1, Biswajit Dubashi2, Santhosh Satheesh1, Jayaraman Balachander1 1 Department of Cardiology, JIPMER, Puducherry, India Sir, Rituximab is chimeric anti-CD20 antibody used commonly in the treatment of various neoplasms, such as lymphomas and also in the treatment of rheumatoid arthritis. Infusion reactions are common following rituximab administration. Cardiotoxicity in the form of arrthymias is described usually as an adverse reaction. We report here a rare fatal infusion reaction, acute myocardial infarction following rituximab therapy for the treatment of testicular lymphoma. A 60-year-man having diabetes, presented with swelling in the right scrotum for 3 months. The patient was evaluated and diagnosed to have testicular lymphoma and subsequently underwent high orchidectomy. There were no stage B symptoms. Histopathology and immunohistochemistry revealed diffuse large B cell lymphoma with CD20, CD10 positive, and Tdt negative CD3-stained structure lymphocytes with increased ki67. Postoperative chemotherapy was planned. Prechemotherapy evaluation was done as per the protocol. The patient had no cardiac symptoms prior to chemotherapy. Baseline electrocardiogram and echocardiogram were normal. After informed consent, the patient was started on rituximab. He developed febrile reaction with rigors immediately following infusion. This reaction was managed with antihistamines and hydrocortisone injection. The patient complained of severe chest pain and sweating 15 min later. Urgent electrocardiogram revealed ST elevation in lateral leads, which did not subside even after stopping rituximab infusion and administration with sublingual nitrates. Pain persisted for more than 30 min and repeat electrocardiogram showed extensive anterior wall myocardial infarction [Figure - 1]. The patient was shifted to coronary care unit and thrombolyzed with streptokinase 1.5 million units over 45 min. There was more than 50% ST segment resolution at 90 min, suggestive of successful thrombolysis. Echocardiography showed regional wall motion abnormality of left anterior descending artery (LAD) territory with moderate left ventricular dysfunction (40%). Coronary angiography done at the time of discharge revealed spontaneous dissection of proximal left anterior descending artery with residual thrombus but with TIMI III flow [Figure - 2] and [Figure - 3]. No other significant coronary lesion was detected. Rituximab is a chimeric anti-CD20 antibody with high affinity for CD20 surface antigen on B lymphocytes of both normal and malignant origin. [ 1 ] It is used commonly against various hematologic malignancies, CD20 positive diffuse large B cell lymphoma, and stage III-IV follicular lymphoma. B lymphocytes play a pivotal role in the pathogenesis of rheumatoid arthritis and so rituximab is an approved agent in the management of patients with rheumatoid arthritis. Rituximab is generally well tolerated if given with adequate premedication except for minor infusion reactions. Fatal infusion reactions are rare, although well documented in the literature and occurred 80% of time with first infusion. [ 1 ] Risk of fatal infusion reactions is higher with high baseline CD20 positive B lymphocyte load. [2] Fatal infusion reactions include hypoxia, pulmonary infiltrates, acute respiratory distress syndrome, myocardial infarction, ventricular fibrillation, and cardiogenic shock. In severe cases, life-threatening cytokine release syndrome in the form of bronchospasm, hypotension, urticaria, and angioedema occurs. Cardiovascular toxicity in the form of cardiac dysrhythmias has been reported in 8% of patients treated with rituximab for lymphoma. Arrhythmias that occur may be due to release of cytokines, such as interleukin-6 and tumor necrosis factor-alpha. [3] Myocardial infarction is one of the fatal infusion reactions reported. The proposed mechanism for acute coronary syndrome following rituximab infusion is the release of cytokines, which cause vasoconstriction, platelet activation, and/or rupture of atherosclerotic plaque. [4] In our case it is likely that the patient had a pre-existing vulnerable plaque. Following the cytokine release with rituximab infusion the vulnerable plaque would have spontaneously ruptured or dissected creating an acute total occlusion and myocardial infarction. The angiographic evidence of spontaneous dissection and residual thrombus indicates this as a likely mechanism [Figure - 2] and [Figure - 3]. Vulnerable plaque rupture can happen in high-risk patients who have risk factors for coronary artery disease or pre-existing coronary artery disease. Anecdotal case reports on acute coronary syndrome following rituximab therapy have been reported in pre-existing coronary artery disease patients. In our case, the patient had diabetes and advanced age as risk factors but never had any symptoms of ischemic heart disease. Meticulous screening for ischemic heart disease may be necessary in high-risk subsets before starting on rituximab therapy. References
Copyright 2011 - Journal of Cancer Research and Therapeutics The following images related to this document are available:Photo images[cr11085f1.jpg] [cr11085f3.jpg] [cr11085f2.jpg] |
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