Morelli Marco Bruno, Bongiovanni Chiara, Da Pra Silvia, Miano Carmen, Sacchi Francesca, Lauriola Mattia, D'Uva Gabriele
Scientific and Technological Pole, IRCCS MultiMedica, Milan, Italy.
National Laboratory of Molecular Biology and Stem Cell Engineering, National Institute of Biostructures and Biosystems (INBB), Bologna, Italy.
Front Cardiovasc Med. 2022 Apr 15;9:847012. doi: 10.3389/fcvm.2022.847012. eCollection 2022.
Chemotherapy and targeted therapies have significantly improved the prognosis of oncology patients. However, these antineoplastic treatments may also induce adverse cardiovascular effects, which may lead to acute or delayed onset of cardiac dysfunction. These common cardiovascular complications, commonly referred to as cardiotoxicity, not only may require the modification, suspension, or withdrawal of life-saving antineoplastic therapies, with the risk of reducing their efficacy, but can also strongly impact the quality of life and overall survival, regardless of the oncological prognosis. The onset of cardiotoxicity may depend on the class, dose, route, and duration of administration of anticancer drugs, as well as on individual risk factors. Importantly, the cardiotoxic side effects may be reversible, if cardiac function is restored upon discontinuation of the therapy, or irreversible, characterized by injury and loss of cardiac muscle cells. Subclinical myocardial dysfunction induced by anticancer therapies may also subsequently evolve in symptomatic congestive heart failure. Hence, there is an urgent need for cardioprotective therapies to reduce the clinical and subclinical cardiotoxicity onset and progression and to limit the acute or chronic manifestation of cardiac damages. In this review, we summarize the knowledge regarding the cellular and molecular mechanisms contributing to the onset of cardiotoxicity associated with common classes of chemotherapy and targeted therapy drugs. Furthermore, we describe and discuss current and potential strategies to cope with the cardiotoxic side effects as well as cardioprotective preventive approaches that may be useful to flank anticancer therapies.
化疗和靶向治疗显著改善了肿瘤患者的预后。然而，这些抗肿瘤治疗也可能诱发不良心血管效应，进而导致心脏功能障碍的急性发作或延迟发作。这些常见的心血管并发症，通常被称为心脏毒性，不仅可能需要调整、暂停或停止挽救生命的抗肿瘤治疗，存在降低其疗效的风险，而且还会严重影响生活质量和总生存期，无论肿瘤预后如何。心脏毒性的发作可能取决于抗癌药物的类别、剂量、给药途径和持续时间，以及个体风险因素。重要的是，心脏毒性副作用可能是可逆的，即停药后心脏功能得以恢复，也可能是不可逆的，其特征为心肌细胞损伤和丧失。抗癌治疗诱导的亚临床心肌功能障碍随后也可能演变为有症状的充血性心力衰竭。因此，迫切需要心脏保护疗法，以减少临床和亚临床心脏毒性的发作和进展，并限制心脏损害的急性或慢性表现。在本综述中，我们总结了关于常见化疗药物和靶向治疗药物相关心脏毒性发作的细胞和分子机制的知识。此外，我们描述并讨论了应对心脏毒性副作用的当前和潜在策略，以及可能有助于辅助抗癌治疗的心脏保护预防方法。
