Gastrointestinal haemorrhage in extracorporeal membrane oxygenation: insights from the national inpatient sample

INTRODUCTION: Extracorporeal membrane oxygenation (ECMO) is associated with gastrointestinal haemorrhage (GIH), which may result from coagulopathy, systemic inflammation, reduced gastric perfusion, and arteriovenous malformation from non-pulsatile blood flow. Data are limited regarding the burden of this complication in the United States. MATERIAL AND METHODS: We analysed the National Inpatient Sample (NIS) database for the years 2007 to 2011 to identify hospitalisations in which an ECMO procedure was performed. Hospitalizations complicated by GIH in this cohort were then identified by relevant codes. RESULTS: Between 2007 and 2011, ECMO hospitalisations increased from 1869 to 3799 (p \u3c 0.01). The proportion of hospitalisations complicated by GIH increased from 2.12% in 2007 to 7.46% in 2011 (p \u3c 0.01). Gastrointestinal haemorrhage was more common in men (56.7%) and in Caucasians (57.4%). Common comorbidities in this population were renal failure (71%), anaemia (55%), and hypertension (26%). All-cause inpatient mortality showed a numerical but nonsignificant increase from 56.7% to 61.9% (p = 0.49). The average cost of care per hospitalisation with GIH associated with ECMO use increased from $132,420 in 2007 to$215,673 in 2011 (p \u3c 0.01). CONCLUSIONS: Gastrointestinal haemorrhage during ECMO hospitalisations occurred in small but significantly increasing proportions. The inpatient mortality rate and costs associated with GIH were substantial and increased significantly during the study period

Upfront dexrazoxane for the reduction of anthracycline-induced cardiotoxicity in adults with preexisting cardiomyopathy and cancer: a consecutive case series

Abstract Background Cardiotoxicity associated with anthracycline-based chemotherapies has limited their use in patients with preexisting cardiomyopathy or heart failure. Dexrazoxane protects against the cardiotoxic effects of anthracyclines, but in the USA and some European countries, its use had been restricted to adults with advanced breast cancer receiving a cumulative doxorubicin (an anthracycline) dose > 300 mg/m2. We evaluated the off-label use of dexrazoxane as a cardioprotectant in adult patients with preexisting cardiomyopathy, undergoing anthracycline chemotherapy. Methods Between July 2015 and June 2017, five consecutive patients, with preexisting, asymptomatic, systolic left ventricular (LV) dysfunction who required anthracycline-based chemotherapy, were concomitantly treated with off-label dexrazoxane, administered 30 min before each anthracycline dose, regardless of cancer type or stage. Demographic, cardiovascular, and cancer-related outcomes were compared to those of three consecutive patients with asymptomatic cardiomyopathy treated earlier at the same hospital without dexrazoxane. Results Mean age of the five dexrazoxane-treated patients and three patients treated without dexrazoxane was 70.6 and 72.6 years, respectively. All five dexrazoxane-treated patients successfully completed their planned chemotherapy (doxorubicin, 280 to 300 mg/m2). With dexrazoxane therapy, changes in LV systolic function were minimal with mean left ventricular ejection fraction (LVEF) decreasing from 39% at baseline to 34% after chemotherapy. None of the dexrazoxane-treated patients experienced symptomatic heart failure or elevated biomarkers (cardiac troponin I or brain natriuretic peptide). Of the three patients treated without dexrazoxane, two received doxorubicin (mean dose, 210 mg/m2), and one received daunorubicin (540 mg/m2). Anthracycline therapy resulted in a marked reduction in LVEF from 42.5% at baseline to 18%. All three developed symptomatic heart failure requiring hospitalization and intravenous diuretic therapy. Two of them died from cardiogenic shock and multi-organ failure. Conclusion The concomitant administration of dexrazoxane in patients with preexisting cardiomyopathy permitted successful delivery of anthracycline-based chemotherapy without cardiac decompensation. Larger prospective trials are warranted to examine the use of dexrazoxane as a cardioprotectant in patients with preexisting cardiomyopathy who require anthracyclines.https://deepblue.lib.umich.edu/bitstream/2027.42/147463/1/40959_2019_Article_36.pd

Electrocardiographic features of immune checkpoint inhibitor associated myocarditis.

BACKGROUND: Myocarditis is a highly morbid complication of immune checkpoint inhibitor (ICI) use that remains inadequately characterized. The QRS duration and the QTc interval are standardized electrocardiographic measures that are prolonged in other cardiac conditions; however, there are no data on their utility in ICI myocarditis. METHODS: From an international registry, ECG parameters were compared between 140 myocarditis cases and 179 controls across multiple time points (pre-ICI, on ICI prior to myocarditis, and at the time of myocarditis). The association between ECG values and major adverse cardiac events (MACE) was also tested. RESULTS: Both the QRS duration and QTc interval were similar between cases and controls prior to myocarditis. When compared with controls on an ICI (93±19 ms) or to baseline prior to myocarditis (97±19 ms), the QRS duration prolonged with myocarditis (110±22 ms, p CONCLUSIONS: The QRS duration is increased in ICI myocarditis and is associated with increased MACE risk. Use of this widely available ECG parameter may aid in ICI myocarditis diagnosis and risk-stratification

Management of cardiac disease in cancer patients throughout oncological treatment: ESMO consensus recommendations.

peer reviewedCancer and cardiovascular (CV) disease are the most prevalent diseases in the developed world. Evidence increasingly shows that these conditions are interlinked through common risk factors, coincident in an ageing population, and are connected biologically through some deleterious effects of anticancer treatment on CV health. Anticancer therapies can cause a wide spectrum of short- and long-term cardiotoxic effects. An explosion of novel cancer therapies has revolutionised this field and dramatically altered cancer prognosis. Nevertheless, these new therapies have introduced unexpected CV complications beyond heart failure. Common CV toxicities related to cancer therapy are defined, along with suggested strategies for prevention, detection and treatment. This ESMO consensus article proposes to define CV toxicities related to cancer or its therapies and provide guidance regarding prevention, screening, monitoring and treatment of CV toxicity. The majority of anticancer therapies are associated with some CV toxicity, ranging from asymptomatic and transient to more clinically significant and long-lasting cardiac events. It is critical however, that concerns about potential CV damage resulting from anticancer therapies should be weighed against the potential benefits of cancer therapy, including benefits in overall survival. CV disease in patients with cancer is complex and treatment needs to be individualised. The scope of cardio-oncology is wide and includes prevention, detection, monitoring and treatment of CV toxicity related to cancer therapy, and also ensuring the safe development of future novel cancer treatments that minimise the impact on CV health. It is anticipated that the management strategies discussed herein will be suitable for the majority of patients. Nonetheless, the clinical judgment of physicians remains extremely important; hence, when using these best clinical practices to inform treatment options and decisions, practitioners should also consider the individual circumstances of their patients on a case-by-case basis

T-cell Immunotherapy and Cardiovascular Disease: Chimeric Antigen Receptor T-cell and Bispecific T-cell Engager Therapies.

Chimeric antigen receptor (CAR) T-cell and bispecific T-cell engager (BiTE) therapies have revolutionized the treatment of refractory or relapsed leukemia and lymphoma. Increased use of these therapies has revealed signals of significant cardiotoxicity, including cardiomyopathy/heart failure, arrhythmia, myocardial injury, hemodynamic instability, and cardiovascular death mainly in the context of a profound inflammatory response to CAR T-cell antitumor effects known as cytokine release syndrome (CRS). Preexisting cardiovascular risk factors and disease may increase the risk of such cardiotoxicity. High index of suspicion and close monitoring is required for prompt recognition. Supportive hemodynamic care and targeted anti-IL-6 therapy, as well as possibly broader immunosuppression with corticosteroids, are the cornerstones of the management

Cardiotoxicity of T-Cell Antineoplastic Therapies: JACC: CardioOncology Primer.

T-cell therapies, such as chimeric antigen receptor (CAR) T-cell, bispecific T-cell engager (BiTE) and tumor-infiltrating lymphocyte (TIL) therapies, fight cancer cells harboring specific tumor antigens. However, activation of the immune response by these therapies can lead to a systemic inflammatory response, termed cytokine release syndrome (CRS), that can result in adverse events, including cardiotoxicity. Retrospective studies have shown that cardiovascular complications occur in 10% to 20% of patients who develop high-grade CRS after CAR T-cell therapy and can include cardiomyopathy, heart failure, arrhythmias, and myocardial infarction. While cardiotoxicities have been less commonly reported with BiTE and TIL therapies, systematic surveillance for cardiotoxicity has not been performed. Patients undergoing T-cell therapies should be screened for cardiovascular conditions that may not be able to withstand the hemodynamic perturbations imposed by CRS. Generalized management of CRS, including the use of the interleukin-6 antagonist, tocilizumab, for high-grade CRS, is used to mitigate the risk of cardiotoxicity