Drug-Related Cardiotoxicity for the Treatment of Haematological Malignancies in Elderly

Abstract

Several publications have focused on the cardiotoxicity of specific classes of hematological therapeutic agents such as antracyclines and cyclofosfamide. Cardiotoxicity of cancer chemotherapeutics is a problem for patients of all ages, but it increases with age. Toxicity can also develop months after the last chemotherapy dose, and late reactions can be seen years later when they present as new-onset cardiomyopathy. No data are available about the cardiotoxicity of non-chemotherapy agents currently used as preferred therapy for hematological malignancy in elderly. In this review we have provided a summary of the cardiovascular toxic effects produced by different drugs and therapeutic agents. Early identification of patients who are at risk for cardiotoxicity should be a primary goal for hematologists in the development of personalized antineoplastic therapeutic strategies or interventions. Thus, the discovery of new biomarkers to identify patients at a high risk for the development of these complications is a high priority. Although targeted therapies such as imatinib and anti-CD20 antibody such rituximab are considered less toxic and better tolerated by patients compared with classic chemotherapy drugs, certain cardiological complications can be very serious and as these agents have been in use for a limited period of time.

Perspective Chapter: Magnetoliposomes - A Recent Development as Recent Advances in the Field of Controlled Release Drug Delivery

“…Doxorubicin (DOX) is one example of an effective anticancer drug with adverse effects on many organs. The greatest clinical problem with the use of conventional anthracyclines is cardiovascular complications, which mainly concern patients with significant risk factors for the development of heart failure [7][8][9]. Pegylated liposomal doxorubicin under the name Doxil® is a commercially used form of an enclosed drug and was the first liposomal formulation approved by the US Food and Drug Administration (FDA) [10].…”

Putative Mechanisms Underlying Cardiovascular Disease Associated with Clonal Hematopoiesis of Indeterminate Potential

“…For example, patients with acute leukemia exhibit increased left ventricle masses and volumes and decreased global longitudinal strain before chemotherapy, demonstrating an inherent CV deficit in patients with hematological malignancies ( Assuncao et al., 2017 ). In addition, patients with hematological malignancies can exhibit CVD and CV toxicities to chemotherapy, and these toxicities appear to increase with age, suggesting that these patients may also be more susceptible to CV injury ( Dickerson et al., 2019 ; Malato et al., 2010 ). It is currently unclear if CHIP contributes to these pathologies; however, a more thorough understanding of the role of CHIP in CVD may help identify patients who will be more susceptible to the development of CVD and CV toxicities.…”

Reversal of cardiomyopathy with tocilizumab in a case of HIV‐negative Castleman's disease

“…Although a definite causal relationship is difficult to establish, we believe the former is the more likely scenario for the following reasons: (i) Initially, the patient improved significantly on rituximab. The fact that lymphadenopathy was unchanged when she presented with heart failure (three weeks after discontinuation of rituximab) suggests that persistence of lymphadenopathy and her newonset heart failure were both caused by CD; (ii) Although cardiotoxicity is a well-described, albeit rare, side effect of rituximab (14), it most commonly occurs shortly after initiating the first infusion (15,16) and is an acute event in the form of arrhythmias or ischemia (17). This is thought to be caused by a typically self-limited 'cytokine release syndrome,' which, if not rapidly fatal, usually lasts only up to a day.…”