The cardiac toxicity of radiotherapy – a review of characteristics, mechanisms, diagnosis, and prevention

Abstract

Purpose: Radiation-induced heart disease (RIHD) is one of the most serious complications of radiotherapy. The purpose of this paper is to review recent researches about cardiac toxicity of radiotherapy in clinical characteristics, mechanisms, diagnosis, and prevention. Conclusions: Powered by the rapid development of medicine, the overall survival (OS) of cancer has been improved significantly. Surgery, chemotherapy, and radiotherapy (RT) are three critical ways in the comprehensive treatments of cancer. There is a consensus that early diagnosis and interventions for the prevention of RIHD are crucial. This review concludes recent clinical and experimental studies on RIHD. RIHD, a heterogeneous and serious disease, is a spectrum of heart disease including myocardial disease, pericarditis, coronary artery disease, valvular heart disease, and conduction system dysfunction. Mean heart dose, biomarkers, and detecting techniques are important components in detecting heart injury. Improvements in radiotherapy regimens remain the primary goal of prevention. Further investigation is needed beyond the observation period of most of these studies.

Myocardial Ischemia Related to Common Cancer Therapy—Prevention Insights

“…Endovascular thrombosis and capillary luminal stenosis determine a reduction in capillary density [ 135 ]. The endothelial dysfunction is responsible not only for impaired vascular reactivity, e.g., coronary spasm or persistent vasoconstriction, but also acts synergistically with sustained inflammation to maintain the prothrombotic environment [ 136 ].…”

Quantitative assessment of radiotherapy-induced myocardial damage using MRI: A systematic review

“…In brief, on the subcellular level, oxidative stress and the in ammatory response within endothelial cells are responsible for the production of numerous cytokines (e.g. interleukin [IL]-1, IL-6, IL-8, IL-18, tumor necrosis factor [TNF]-α)) associated with RT-induced cardiotoxicity (e.g., brosis) [10], [11]. High concentrations of free radicals (primarily reactive oxygen species (ROS)) produced by RT dysregulate enzymatic activity, increase lipid peroxidation, and induce cellular damage and/or death.…”

“…High concentrations of free radicals (primarily reactive oxygen species (ROS)) produced by RT dysregulate enzymatic activity, increase lipid peroxidation, and induce cellular damage and/or death. Indeed, ROS can increase hypertrophy and brosis and trigger the release of calcium leading to cellular apoptosis and necrosis [11]. ROS also impair mitochondrial function.…”

Modulators of radiation-induced cardiopulmonary toxicities for non-small cell lung cancer: Integrated cytokines, single nucleotide variants, and HBP systems imaging

“…Cytokine release syndrome has been linked with life-threatening cardiovascular complications including hypotension, shock, tachycardia, arrhythmias (ranging from asymptomatic prolonged corrected QT interval to supraventricular tachycardia, atrial fibrillation, flutter, and ventricular arrhythmias (e.g., Torsade de Pointes), left ventricular dysfunction, heart failure, and cardiovascular death. Another proposed mechanism for radiation-induced cardiopulmonary toxicity is the formation of microvascular and macrovascular thrombi that result from the radiation-induced activation of platelets, neutrophils, and other proteins, which can contribute to vascular occlusion by microvascular thrombosis and myocardial infarction ( 43 , 44 ). Further understanding of how cytokines that affect inflammatory processes affect RT-induced cardiopulmonary toxicity (and vice versa) may improve the effectiveness of RT for cancer.…”