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

Abstract

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-

Thrombosis in Autoimmune Diseases: A Role for Immunosuppressive Treatments?

“…93 In some case reports, cardiac adverse events were correlated with rituximab infusion for oncohematological disorders, in combination with other chemotherapeutic agents. 94,95 Similar data were found for autoimmune diseases, 96,97 even if, recently, a large cohort study found that rates of cardiac (and stroke) events in RA subjects treated with rituximab were consistent with rates found in general RA population in an 11-year follow-up. 98 Another monoclonal antibody used in RA is tocilizumab, an anti-IL-6 receptor antibody.…”

Phase II clinical trial testing the safety of a humanised monoclonal antibody anti-CD20 in patients with heart failure with reduced ejection fraction, ICFEr-RITU2: study protocol

“…We considered a convenience sample of 10 patients from our heart failure clinic since the previously reported incidence of acute coronary syndrome (ACS) and atrial and ventricular arrhythmias with the use of rituximab is <0.1% and 7.6%, respectively 8. Regarding the worsening of left ventricle ejection fraction (LVEF) attributed to rituximab, the incidence is limited to case reports only, wherefore it is impossible to precisely determine the incidence 9.…”

Management of Ischemic Coronary Disease in Patients Receiving Chemotherapy: an Uncharted Clinical Challenge

“…There have been multiple case reports of acute coronary events precipitated by infusion of various chemotherapeutic agents [4][5][6][7][8][9][10][11][12][13][14][15][16][17]. Several mechanisms have been proposed, including vasospastic phenomena, endothelial and mitochondrial cytotoxicity, cell-cycle arrest of cardiac endothelial cells, and even release of cytokines leading to plaque rupture and platelet activation [14,15,[18][19][20][21]. The variability in proposed mechanisms reflects the variability in site of action and downstream effects of cancer-specific treatment leading to ischemia.…”