Abstract
Chemotherapy-associated myocardial toxicity is increasingly recognized with the expanding armamentarium of novel chemotherapeutic agents. The onset of cardiotoxicity during cancer therapy represents a major concern and often involves clinical uncertainties and complex therapeutic decisions, reflecting a compromise between potential benefits and harm. Furthermore, the improved cancer survival has led to cardiovascular complications becoming clinically relevant, potentially contributing to premature morbidity and mortality among cancer survivors. Specific higher-risk populations of cancer patients can benefit from prevention and screening measures during the course of cancer therapies. The pathobiology of chemotherapy-induced myocardial dysfunction is complex, and the individual patient risk for heart failure entails a multifactorial interaction between the selected chemotherapeutic regimen, traditional cardiovascular risk factors, and individual susceptibility. Treatment with several specific chemotherapeutic agents, including anthracyclines, proteasome inhibitors, epidermal growth factor receptor inhibitors, vascular endothelial growth factor inhibitors, and immune checkpoint inhibitors imparts increased risk for cardiotoxicity that results from specific therapy-related mechanisms. We review the pathophysiology, risk factors, and imaging considerations as well as patient surveillance, prevention, and treatment approaches to mitigate cardiotoxicity prior, during, and after chemotherapy. The complexity of decision-making in these patients requires viable discussion and partnership between cardiologists and oncologists aiming together to eradicate cancer while preventing cardiotoxic sequelae.
Highlights
Chemotherapy-associated myocardial toxicity is increasingly recognized with the expanding armamentarium of novel chemotherapeutic agents
The improved cancer survival has led to cardiovascular complications becoming clinically relevant many years after cancer diagnosis, and cardiovascular diseases are currently considered the main cause of death in cancer survivors
In the US, the Food and Drug Administration (FDA) has approved DRZ only in patients who have received more than 300 mg/m2 of doxorubicin for metastatic breast cancer and who may benefit from continued doxorubicin treatment.[69]
Summary
Chemotherapy-associated myocardial toxicity is increasingly recognized with the expanding armamentarium of novel chemotherapeutic agents. The improved cancer survival has led to cardiovascular complications becoming clinically relevant many years after cancer diagnosis, and cardiovascular diseases are currently considered the main cause of death in cancer survivors This is especially relevant for pediatric and young cancer survivors who have demonstrated increased rates of cardiovascular disease several decades after therapy.[1,2] an increasing number of patients are receiving longterm or lifelong cancer therapies with potential cardiovascular adverse effects. Cardiac toxicity may lead to premature morbidity and death among cancer survivors.[3] Beyond long-term cardiovascular complications, the onset of cardiotoxicity during cancer therapy represents a major concern and often involves clinical uncertainties and complex therapeutic decisions, reflecting a compromise between potential benefits and harm. Doxorubicin exerts its tumoricidal activity via binding to topoisomerase-IIα (Top2α),[21] an enzyme found predominantly in dividing cells and required for DNA replication. Mice with a cardiac-specific deletion of Top2β are protected from doxorubicin-induced cardiotoxicity.[22]
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