Rituximab induced myocardial infarction: A fatal drug reaction

Arunprasath, Palamalai; Packirisamy, Gobu; Dubashi, Biswajit; Satheesh, Santhosh; Balachander, Jayaraman

doi:10.4103/0973-1482.87003

Cited by 35 publications

(18 citation statements)

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“…Interleukin-6, tumor necrosis factor-alpha, and other cytokines released after rituximab use may lead to cardiac arrhythmias, vasoconstriction, platelet activation, and/or rupture of atherosclerotic plaque [7,8]. In treatment of diffuse large B-cell lymphoma, addition of rituximab to cyclophosphamide-doxorubicin-vincristine-prednisolone (CHOP) chemotherapy regimen did not change the cardiotoxicity risk [9].…”

Section: Discussionmentioning

confidence: 99%

Cardiotoxicity following cyclophosphamide therapy: a case report

2014

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IntroductionCardiac toxicity is one of the life-threatening complications of cancer therapy. Systemic anticancer treatments may exert their own toxic effects or can aggravate adverse effects of other drugs. We report a case of cyclophosphamide-induced cardiotoxicity in a patient with normal cardiac functions before chemotherapy.Case presentationA 66-year-old Caucasian woman with a mediastinal mass diagnosed with Burkitt lymphoma underwent chemotherapy with rituximab-hyperfractionated-cyclophosphamide-vincristine-doxorubicin-dexamethasone. On the seventh day of chemotherapy, she developed dyspnea. An electrocardiogram demonstrated low voltage in the limb and precordial leads. It also showed diffusely increased myocardial echogenicity, mild pericardial and pleural effusion, generally impaired biventricular systolic functions with a left ventricular ejection fraction of 31%, and right ventricular mid-apical akinesia, even though she had normal biventricular functions before chemotherapy. Cyclophosphamide-induced cardiotoxicity was suspected and she was given treatment for congestive heart failure. Her dyspnea decreased and she was discharged on the tenth day with a left ventricular ejection fraction of 37% and normal right ventricular function. After 1 month, echocardiography showed normal biventricular functions with a left ventricular ejection fraction of 60%.ConclusionsDrug-induced cardiotoxicity, therefore, should be taken into consideration when using cyclophosphamide therapy, especially when anthracyclines are co-administered. Close communication between hematologists and cardiologists is required.

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Section: Discussionmentioning

confidence: 99%

Cardiotoxicity following cyclophosphamide therapy: a case report

2014

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“…Armitage and colleagues 4 described the cases of 3 patients with lymphoproliferative disorders who experienced ACS associated with an initial infusion of rituximab. Arunprasath and associates 5 have reported on one such patient who was managed conservatively after an infusion with rituximab-precipitated AMI.…”

Section: Discussionmentioning

confidence: 99%

Rituximab-Vincristine Chemotherapy-Induced Acute Anterior Wall Myocardial Infarction with Cardiogenic Shock

Roy

Khanna²,

Senguttuvan³

2014

Texas Heart Institute Journal

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1 Chemotherapy-induced left ventricular (LV) dysfunction is often encountered in clinical practice, but chemotherapy-mediated ischemic syndromes are rarely seen. The incidence of acute myocardial infarction (AMI) after chemotherapy varies from 1% to 5%.1 We describe the case of an elderly man with non-Hodgkin lymphoma (NHL) who developed AMI after the administration of chemotherapeutic agents. Case ReportA 68-year-old man with coronary artery disease (CAD) and severe single-vessel disease of the left anterior descending coronary artery (LAD) had undergone coronary angioplasty with a 3 × 18-mm bare-metal stent. Four years later, while under evaluation for neck and abdominal pain, he was diagnosed with NHL (diffuse large β-cell lymphoma). His LV function, as evaluated with 2-dimensional transthoracic echocardiography (TTE) before chemotherapy, was normal, and he was free of angina. He received chemotherapy that included rituximab, cyclophosphamide, vincristine, and prednisolone (R-CVP).Forty-eight hours later, he had sudden-onset heaviness of the chest and difficulty in breathing. On examination, his heart rate was 150 beats/min, his blood pressure was 80/60 mmHg, and crepitations could be heard bilaterally over his entire chest. He was immediately intubated and started on intravenous diuretic agents and inotropic support. An electrocardiogram was indicative of ST-elevation anterior-wall myocardial infarction, and TTE showed severely hypokinetic myocardium (involving the LAD territory), with an estimated LV ejection fraction of 0.30. He was transferred for diagnostic angiography and primary percutaneous coronary intervention. Before the procedure, the patient received a loading dose of aspirin and clopidogrel; then an intra-aortic balloon pump was inserted. A left coronary angiogram revealed a patent stent in the mid-LAD with a discrete, thrombotic, tight stenosis proximal to the stent; there was slow flow in the LAD and substantial ostio-proximal disease of the left circumflex coronary artery (LCx) and first obtuse marginal branch (Fig. 1). A right coronary angiogram showed diffuse but insignificant disease. After cannulating the left coronary system with a Judkin left 3.5 catheter, we crossed the LAD lesion with a floppy wire and stented it with a 3 × 13-mm bare-metal stent, without predilation. In view of his hemodynamic instability, we also performed stenting (without predila-

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“…34 Therefore, they are considered to provide more benefit with fewer incidences of undesirable complications. Most known side effects are related to the blockage of target growth factors.…”

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confidence: 99%