Department of Haematology and Transfusion Medicine, Carlo Poma Hospital, Mantova, Italy.
Department of Clinical Medicine and Surgery, Federico II University Hospital, Naples, Italy.
Semin Thromb Hemost. 2021 Nov;47(8):942-949. doi: 10.1055/s-0041-1733927. Epub 2021 Aug 31.
Cancer is associated with an increased incidence of both venous thromboembolism (VTE) and arterial thrombosis (cardiovascular events and ischemic stroke). Cancer-associated arterial thrombotic events are less well studied than VTE, but increasingly recognized, particularly in specific malignancies and in association with specific anticancer therapies. The pathogenesis of arterial thrombotic events in cancer is complex and involves generation of tumor-associated procoagulant factors and a variety of alterations in platelet function as well as in the coagulation and fibrinolytic systems, and endothelial injury and dysfunction, that combine to produce hypercoagulability. The multifactorial interaction between this prothrombotic state, the individual cardiovascular risk, advanced age and presence of comorbidities, and the specific neoplasm characteristics and therapy, may induce the vascular events. Recent studies based on population databases and prospective or retrospective analyses with prolonged follow-up highlight that cancer patients experience an increased (approximately 1.5-2-fold) risk of both cerebrovascular and cardiovascular events compared with noncancer individuals, which peaks in the time period of the diagnosis of cancer but may persist for years. Beyond the type of cancer, the risk reflects the tumor burden, being higher in advanced stages and metastatic cancers. The occurrence of arterial thromboembolic events is also associated with increased overall mortality. We here present an update of the pathophysiology, risk factors, clinical evidence, and treatment considerations on cancer-associated arterial thrombosis, in the light of the need for specific multidisciplinary prevention and surveillance strategies in this setting, in the frame of cardio-oncology approaches.
癌症与静脉血栓栓塞症（VTE）和动脉血栓形成（心血管事件和缺血性中风）的发生率增加有关。与 VTE 相比，癌症相关的动脉血栓栓塞事件研究得较少，但越来越受到重视，尤其是在某些特定的恶性肿瘤和与特定的抗癌治疗相关的情况下。癌症相关的动脉血栓形成事件的发病机制较为复杂，涉及肿瘤相关促凝因子的产生，以及血小板功能、凝血和纤维蛋白溶解系统以及内皮损伤和功能障碍的多种改变，这些因素共同导致高凝状态。这种促凝状态、个体心血管风险、高龄和合并症的多因素相互作用，以及特定的肿瘤特征和治疗方法，可能会引发血管事件。最近基于人群数据库的研究以及前瞻性或回顾性分析（随访时间较长）强调，与非癌症个体相比，癌症患者发生脑血管和心血管事件的风险增加（约 1.5-2 倍），这一风险在癌症诊断期间达到峰值，但可能持续多年。除了癌症类型外，风险还反映了肿瘤负担，在晚期和转移性癌症中更高。动脉血栓栓塞事件的发生也与总体死亡率的增加有关。我们根据心血管肿瘤学方法的需要，在此背景下提出了癌症相关动脉血栓形成的病理生理学、危险因素、临床证据和治疗注意事项的最新更新。
