Cancer-induced cardiac dysfunction has become a major clinical challenge as advances in cancer therapies continue to extend patient survival. Once regarded as a secondary concern, cardiotoxicity is now recognized as a leading contributor to morbidity and mortality among cancer patients and survivors. Its pathophysiology is multifactorial, involving systemic inflammation (e.g., TNF-α, IL-6), oxidative stress driven by reactive oxygen species (ROS), neurohormonal imbalances (e.g., angiotensin II, endothelin-1), and metabolic disturbances. These mechanisms collectively promote cardiomyocyte apoptosis, atrophy, mitochondrial dysfunction, and impaired cardiac output. Cardiac complications may arise directly from cancer itself or as adverse effects of oncologic therapies such as anthracyclines, trastuzumab, and immune checkpoint inhibitors. These agents have been linked to heart failure (HF), systolic dysfunction, and cardiac atrophy, often progressing insidiously and underscoring the importance of early detection and careful monitoring. Current preventive and therapeutic strategies include pharmacological interventions such as ACE inhibitors, beta-blockers, statins, dexrazoxane, and endothelin receptor antagonists like atrasentan. Emerging compounds, particularly Withaferin A (WFA), have shown potential through their anti-inflammatory and cardiac protective properties. In addition, antioxidants and lifestyle modifications may provide supplementary cardioprotective benefits, while interventional cardiology procedures are increasingly considered in selected patients. Despite encouraging progress, standardized treatment protocols and robust long-term outcome data remain limited. Given the heterogeneity of cancer types and cardiovascular responses, a personalized and multidisciplinary approach is essential. Continued research and close collaboration between oncologists, cardiologists, and basic scientists will be the key to advancing care, reducing treatment-related morbidity, and ensuring that improvements in cancer survival are matched by preservation of cardiovascular health.
随着癌症治疗手段的进步不断延长患者生存期，癌症诱发的心功能不全已成为临床主要挑战。曾被视为次要问题的癌症治疗相关心脏毒性，现已被确认为癌症患者及幸存者发病和死亡的主要因素。其病理生理机制具有多因素性，涉及全身性炎症（如TNF-α、IL-6）、活性氧驱动的氧化应激、神经激素失衡（如血管紧张素II、内皮素-1）以及代谢紊乱。这些机制共同促进心肌细胞凋亡、萎缩、线粒体功能障碍及心输出量受损。心脏并发症可能直接由癌症本身引起，也可能源于蒽环类药物、曲妥珠单抗和免疫检查点抑制剂等肿瘤治疗的不良反应。这些药物与心力衰竭、收缩功能障碍及心脏萎缩相关，常呈隐匿性进展，凸显了早期发现和密切监测的重要性。当前预防和治疗策略包括药物干预，如血管紧张素转换酶抑制剂、β受体阻滞剂、他汀类药物、右雷佐生以及阿曲生坦等内皮素受体拮抗剂。新兴化合物特别是醉茄素A，通过其抗炎和心脏保护特性显示出潜力。此外，抗氧化剂和生活方式调整可提供辅助性心脏保护效益，而介入心脏病学手段在特定患者中也日益受到重视。尽管取得令人鼓舞的进展，标准化治疗方案和可靠的长期结局数据仍然有限。鉴于癌症类型和心血管反应的异质性，个体化多学科诊疗模式至关重要。肿瘤学家、心脏病学家和基础科研人员持续开展研究并保持紧密合作，将是推动诊疗进步、降低治疗相关发病率、确保癌症生存率提升与心血管健康维护同步实现的关键。
肿瘤(癌症)患者之家