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Mechanisms and clinical course of cardiovascular toxicity of cancer treatment I. Oncology.
Seminars in Oncology ( IF 4 ) Pub Date : 2019-11-11 , DOI: 10.1053/j.seminoncol.2019.10.006
Edward T H Yeh 1 , Michael S Ewer 2 , Javid Moslehi 3 , Monika Dlugosz-Danecka 4 , Jose Banchs 2 , Hui-Ming Chang 1 , Giorgio Minotti 5
Affiliation  

The opening session of Second International Colloquium on Cardio-Oncology addressed two areas of vital interest. The first reviewed new thoughts related to established agents. While anthracycline cardiotoxicity has been studied and reviewed extensively, ongoing research attempting to understand why it appears the mechanism(s) of toxicity differs from that of oncologic efficacy continue to evoke comment and intriguing speculation. Better understanding of the role of β-topoisomerase II in toxicity has advanced our understanding of the cascade of events that lead to heart failure. Additionally, the cardioprotective role of dexrazoxane fits well with our new understanding of how β-topoisomerase II works. Beyond the anthracyclines, new insight is providing us insight to better understand the impact on cardiac function seen with other agents including those targeting HER2 and several tyrosine-kinase inhibitors. Unlike the anthracyclines, these agents affect cardiac function in ways that are less direct, and therefore have different characteristics and should be thought of in alternate ways. This new knowledge regarding established agents furthers our understanding of the spectrum of cardiotoxicity and cardiac dysfunction in the cancer patient. The session also addressed cardiovascular toxicities of newer and established agents beyond myocardial dysfunction including effects on the vasculature. These agents cause changes that may be temporary or permanent, and that range from subclinical to life-threatening. The session ended with a discussion of the cardiac effects of immune checkpoint inhibitors. These agents can cause rare and sometimes fatal cardiac inflammation, for which long-term follow up may be required.

中文翻译:

癌症治疗心血管毒性的机制和临床过程I.肿瘤学。

第二届国际肿瘤学国际学术讨论会的开幕会议讨论了两个极为重要的领域。首先回顾了与已建立的特工有关的新思想。尽管已经对蒽环类药物的心脏毒性进行了广泛的研究和审查,但正在进行的试图理解其毒性机制与肿瘤功效不同的正在进行的研究继续引起评论和有趣的猜测。更好地了解β-拓扑异构酶II在毒性中的作用,使我们对导致心力衰竭的一系列事件有了更深入的了解。此外,右雷佐生的心脏保护作用与我们对β-拓扑异构酶II如何起作用的新认识非常吻合。除了蒽环以外,新的见识为我们提供了见解,以便更好地了解其他药物(包括靶向HER2的药物和几种酪氨酸激酶抑制剂)对心脏功能的影响。与蒽环类药物不同,这些药物以不太直接的方式影响心脏功能,因此具有不同的特征,应以其他方式考虑。关于已建立的药物的新知识进一步加深了我们对癌症患者心脏毒性和心脏功能障碍的认识。会议还讨论了除心肌功能障碍以外的新药和已确立药物的心血管毒性,包括对脉管系统的影响。这些因素导致的变化可能是暂时的或永久的,范围从亚临床到危及生命。会议结束时讨论了免疫检查点抑制剂对心脏的影响。这些药物可引起罕见的,有时甚至是致命的心脏炎症,可能需要长期随访。
更新日期:2019-11-11
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