Barachini Serena, Ghelardoni Sandra, Varga Zoltán V, Mehanna Radwa A, Montt-Guevara Maria Magdalena, Ferdinandy Péter, Madonna Rosalinda
Department of Clinical and Experimental Medicine, Laboratory for Cell Therapy, University of Pisa, Pisa, Italy.
Department of Pathology, Laboratory of Biochemistry, University of Pisa, Pisa, Italy.
Vascul Pharmacol. 2023 Dec;153:107223. doi: 10.1016/j.vph.2023.107223. Epub 2023 Sep 8.
With the improvement in cancer prognosis due to advances in antitumor therapeutic protocols and new targeted and immunotherapies, we are witnessing a growing increase in survival, however, at the same timeincrease in morbidity among cancer survivors as a consequences of the increased cardiovascular adverse effects of antineoplastic drugs. Common cardiovascular complications of antineoplastic therapies may include cardiac complications such as arrhythmias, myocardial ischemia, left ventricular dysfunction culminating in heart failure as well as vascular complications including arterial hypertension, thromboembolic events, and accelerated atherosclerosis. The toxicity results from the fact that these drugs not only target cancer cells but also affect normal cells within the cardiovascular system. In this article, we review the clinical features and main mechanisms implicated in antineoplastic drug-induced cardiovascular toxicity, including oxidative stress, inflammation, immunothrombosis and growth factors-induced signaling pathways.
随着抗肿瘤治疗方案以及新的靶向和免疫疗法的进展,癌症预后有所改善,我们看到生存率不断提高,然而,与此同时,由于抗肿瘤药物心血管不良反应增加,癌症幸存者的发病率也在上升。抗肿瘤治疗常见的心血管并发症可能包括心脏并发症,如心律失常、心肌缺血、最终导致心力衰竭的左心室功能障碍,以及血管并发症,包括动脉高血压、血栓栓塞事件和加速动脉粥样硬化。毒性产生的原因是这些药物不仅靶向癌细胞,还会影响心血管系统内的正常细胞。在本文中,我们综述了抗肿瘤药物诱导心血管毒性的临床特征和主要机制,包括氧化应激、炎症、免疫血栓形成和生长因子诱导的信号通路。