Cardiac Toxicity During Rituximab Administration

Garypidou, Vassilia; Perifanis, Vassilios; Τζιόμαλος, Κωνσταντίνος; Theodoridou, Stamatia

doi:10.1080/10428190310001607160

Cited by 19 publications

(11 citation statements)

References 2 publications

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“…However, rituximab infusion is known to be associated with the release of cytokines, such as interleukin-6 and tumor necrosis factor-a. 2 Such cytokine storms are postulated to lead to vasoconstriction, platelet activation, and rupture of atherosclerotic plaque, 3 thus leading to acute ischemic syndromes. Armitage and colleagues 4 described the cases of 3 patients with lymphoproliferative disorders who experienced ACS associated with an initial infusion of rituximab.…”

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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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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“…However, clinical manifestations such as myocardial infarction, ventricular fibrillation, and cardiogenic shock, which occur due to cytokine release occurring within a few hours of initiation the first infusion, have been reported [28][29][30]. Garypidou and coworkers reported a case that presented with substernal pain radiating in neck and left arm, along with palpitations 4 h after the initiation of the first infusion of rituximab and that showed sinus tachycardia without ST segment changes at the electrocardiogram [10]. No changes in serum cardiac markers or ECG were observed within the few days following the cessation of rituximab.…”

Section: Discussionmentioning

confidence: 94%

“…The prevalence of the significant cardiotoxicity increases linearly with cumulative doxorubicin dose, reaches approximately 7.5% at the cumulative dose of 550 mg/m 2 , but then onwards starts to increase steeply [9]. In spite of the fact that cardiac toxicity after the initial infusion of rituximab has been reported [10], it is not known whether the addition of rituximab to CHOP results in increased cardiac toxicity.…”

Section: Introductionmentioning

confidence: 99%

Addition of rituximab to chop does not increase the risk of cardiotoxicity in patients with non-Hodgkin’s lymphoma

et al. 2008

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“…Hypotension, angioedema, hypoxia, and bronchospasm can also be seen in up to 10% of cases (10,11). With previously reported cases of angina, ACS, and arrhythmias with rituximab infusion (14-25), FDA has cautiously provided recommendations to discontinue infusions for serious or life-threatening cardiac arrhythmias and perform cardiac monitoring during and after all infusions of rituximab for patients who develop clinically significant arrhythmias, or who have a history of arrhythmia or angina (12). However, these current recommendations do not sufficiently address the cardiovascular concerns related to rituximab treatment, since cases with adverse cardiovascular effects following rituximab infusion have been additionally reported as shown in Table 1.…”

Section: Discussionmentioning

confidence: 99%

Non-ischemic cardiomyopathy after rituximab treatment for membranous nephropathy

et al. 2016

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Rituximab is an anti-CD20 monoclonal antibody frequently used for the treatment of non-Hodgkin’s lymphoma, chronic lymphocytic leukemia (CLL), rheumatoid arthritis (RA), and anti-neutrophilic cytoplasmic antibody (ANCA)-associated vasculitis. In addition, rituximab has recently been increasingly used as an off-label treatment in a number of inflammatory and systemic autoimmune diseases. It is advised that rituximab infusion may cause infusion reactions and adverse cardiac effects including arrhythmia and angina, especially in patients with prior history of cardiovascular diseases. However, its detailed cardiotoxicity profile and effects on cardiac function were not well described. We report a 51-year-old man who developed non-ischemic cardiomyopathy after rituximab treatment for membranous nephropathy. The patient experienced reduced cardiac functions within 48 hours after the initial infusion, which remained markedly reduced at 9-month follow-up. As the utility of rituximab expands, physicians must be aware of this serious cardiovascular adverse effect.

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Cardiac Toxicity During Rituximab Administration

Cited by 19 publications

References 2 publications

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

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

Addition of rituximab to chop does not increase the risk of cardiotoxicity in patients with non-Hodgkin’s lymphoma

Non-ischemic cardiomyopathy after rituximab treatment for membranous nephropathy

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