Department of Cardiovascular Disease, Mayo Clinic, Phoenix, Arizona, USA.
Curr Opin Cardiol. 2019 May;34(3):289-295. doi: 10.1097/HCO.0000000000000617.
Advances in cancer treatments have resulted in significant improvements in survival. Anthracycline chemotherapeutics play a major role in the treatment of hematologic malignancies and solid tumors; however, there is a risk of anthracycline cardiomyopathy in survivors. This focused review will provide a historical context on anthracycline cardiomyopathy and will also review pathophysiologic mechanisms of cardiotoxicity, dosage recommendations, prognosis, and outcomes.
Anthracycline inhibition of topoisomerase 2β in cardiomyocytes is believed to be the dominant mechanism of anthracycline-related cardiotoxicity. Emerging data suggest that downregulation of the RNA-binding protein quaking 5 may also be contributing. There is continued lack of agreement regarding what dosage of anthracycline is associated with the highest risk of cardiotoxicity.
Ongoing research into the mechanisms of anthracycline cardiotoxicity is warranted to allow for the development of targeted preventive therapies. A consensus definition of anthracycline cardiomyopathy will facilitate analyses of existing data and allow for the conduction of prospective clinical trials in this area.
癌症治疗的进展显著提高了患者的生存率。蒽环类化疗药物在血液系统恶性肿瘤和实体瘤的治疗中发挥着重要作用；然而，幸存者存在罹患蒽环类心肌病的风险。本次重点综述将提供蒽环类心肌病的历史背景，并回顾其心脏毒性的病理生理机制、剂量建议、预后和结果。
蒽环类药物抑制心肌细胞中的拓扑异构酶 2β，被认为是蒽环类相关心脏毒性的主要机制。新出现的数据表明，RNA 结合蛋白 quaking 5 的下调也可能起作用。关于哪种剂量的蒽环类药物与心脏毒性风险最高，仍缺乏共识。
有必要对蒽环类药物心脏毒性的机制进行持续研究，以开发有针对性的预防疗法。蒽环类心肌病的共识定义将有助于分析现有数据，并在该领域开展前瞻性临床试验。
