Department of Cardiology, Division of Medicine, MD Anderson Cancer Center, 1400 Pressler, Box 1451, Houston, TX, 77030, USA.
Curr Atheroscler Rep. 2018 Feb 8;20(2):10. doi: 10.1007/s11883-018-0702-5.
Numerous chemotherapeutic agents have been associated with the development of ischemia and arterial thrombosis. As newer therapies have been developed to treat cancer, some of these chemotherapy drugs have been implicated in the development of vascular disease. In this review, we will summarize the most common chemotherapeutic drug classes that may play a role in the development of ischemic heart disease.
Angiogenesis inhibitors, alkylating agents, antimetabolites, antimicrotubules, and proteasome inhibitors have a number of cardiovascular toxicities. The possible mechanisms of action of these drugs leading to ischemic complications are varied but include endothelial dysfunction, platelet aggregation, reduced levels of nitrous oxide (NO), and elevated levels of reactive oxygen species (ROS), and vasospasm. While some drugs act through multiple pathways that result in the development of ischemic heart disease, others such as the antimetabolites and antimicrotubules appear to primarily cause vasospasm. Furthermore, while aromatase inhibitors increase the risk of heart disease in comparison to tamoxifen in large studies, this finding likely occurs because of a protective role of tamoxifen on cardiovascular risk factors rather than a direct effect of aromatase inhibitors. Angiogenesis inhibitors, alkylating agents, antimetabolites, antimicrotubules, and proteasome inhibitors can lead to ischemic complications in patients with cancer. Many of these drugs have proven to be effective in improving cancer prognosis, but their possible cardiovascular effects have to be carefully monitored and treated. Treatment of ischemic complications in the setting of cancer therapy should focus on the optimal medical management of known cardiovascular risk factors and follow an evidence-based approach.
许多化疗药物与缺血和动脉血栓形成有关。随着治疗癌症的新疗法的发展，其中一些化疗药物与血管疾病的发生有关。在这篇综述中，我们将总结可能在缺血性心脏病发展中起作用的最常见的化疗药物类别。
血管生成抑制剂、烷化剂、抗代谢物、抗微管蛋白和蛋白酶体抑制剂都有许多心血管毒性。这些药物导致缺血性并发症的可能作用机制多种多样，包括内皮功能障碍、血小板聚集、一氧化氮（NO）水平降低和活性氧（ROS）水平升高，以及血管痉挛。虽然一些药物通过多种途径导致缺血性心脏病的发生，而其他药物如抗代谢物和抗微管蛋白似乎主要引起血管痉挛。此外，尽管芳香酶抑制剂在大型研究中与他莫昔芬相比增加了心脏病的风险，但这一发现可能是由于他莫昔芬对心血管危险因素的保护作用，而不是芳香酶抑制剂的直接作用。血管生成抑制剂、烷化剂、抗代谢物、抗微管蛋白和蛋白酶体抑制剂可导致癌症患者发生缺血性并发症。其中许多药物已被证明能有效改善癌症预后，但必须仔细监测和治疗其可能的心血管影响。癌症治疗中缺血性并发症的治疗应侧重于已知心血管危险因素的最佳药物治疗，并遵循循证方法。
