肿瘤细胞治疗研究
英文原题：Heart failure medication to prevent cancer therapy-related cardiac dysfunction: A narrative review.
肿瘤治疗的进展提高了癌症生存率，但也增加了癌症治疗相关心功能障碍（CTRCD）的临床发生率，这是一系列从亚临床生物标志物或应变异常到进行性心力衰竭和心源性休克的病症。
肿瘤治疗的进展提高了癌症生存率，但也增加了癌症治疗相关心功能障碍（CTRCD）的临床发生率，这是一系列从亚临床生物标志物或应变异常到进行性心力衰竭和心源性休克的病症。尽管以蒽环类药物为基础的治疗和人表皮生长因子受体2（HER2）靶向治疗仍是研究最广泛的原因，但更新的靶向药物和免疫治疗引入了额外的、机制不同的心脏毒性表型，包括内皮功能障碍和由后负荷驱动的心力衰竭（血管内皮生长因子[VEGF]通路抑制剂、蛋白酶体抑制剂）、与心律失常相关的心功能障碍（布鲁顿酪氨酸激酶抑制剂）以及细胞因子释放综合征背景下的炎症介导的心肌抑制（CAR-T[CAR-T]细胞和双特异性抗体）。本叙述性综述总结了在这一不断演变的背景下，预防性使用常规心力衰竭治疗的理由和现有证据。它进一步强调了当前的知识空白，特别是关于现代心力衰竭治疗和现代免疫介导的肿瘤治疗。
Advances in oncological therapies have improved cancer survival but also have increased the clinical incidence of cancer therapy-related cardiac dysfunction (CTRCD), a spectrum of conditions ranging from subclinical biomarker or strain abnormalities to progressive heart failure and cardiogenic shock. Whereas anthracycline-based and human epidermal growth receptor 2 (HER2)-targeted therapies remain the most extensively studied causes, newer targeted agents and immune-based therapies introduce additional, mechanistically distinct cardiotoxic phenotypes, including endothelial dysfunction and afterload-driven heart failure (vascular endothelial growth factor [VEGF]-pathway inhibitors, proteasome inhibitors), arrhythmia-associated cardiac dysfunction (Bruton tyrosine kinase inhibitors) and inflammation-mediated myocardial depression in the context of cytokine release syndromes (chimeric antigen receptor T [CAR-T] cells and bispecific antibodies). This narrative review summarises the rationale and available evidence for the preventive use of conventional heart failure therapies across this evolving landscape. It further highlights current gaps in knowledge, especially regarding modern heart failure therapies and modern immune-mediated oncological therapies.
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