The vascular endothelial growth factor (VEGF) signaling pathway (VSP) fulfills a cardinal role in endothelial cells and its inhibition has profound cardiovascular impact. This is true not only for the normal vasculature but also for the tumor vasculature when VSP inhibitors are used as anti-angiogenic therapies. Generalized endothelial dysfunction predisposes to vasoconstriction, atherosclerosis, platelet activation, and thrombosis (arterial more than venous). All of these have been reported with VSP inhibitors and collectively give rise to vascular toxicities, the most concerning of which are arterial thromboembolic events (ATE). VSP inhibitors include antibodies, acting extracelluarly on VEGF, such as bevacizumab and tyrosine kinases inhibitors, acting intracellularly on the kinase domain of VEGF receptors, such as sunintib and sorafenib. The addition of bevacizumab and VSP tyrosine kinase inhibitor therapy to the cancer treatment regimen is associated with a 1.5–2.5-fold and 2.3–4.6-fold increase risk of ATEs, respectively. Risk factors for ATEs while on VSP inhibitor therapy include age older than 65 years, previous thromboembolic events, history of atherosclerotic disease, and duration of VSP inhibitor therapy. In clinical practice, hypertension remains the most commonly noted vascular manifestation of VSP inhibition. Optimal blood pressure goals and preferred therapeutic strategies toward reaching these goals are not defined at present. This review summarizes current data on this topic and proposes a more intensive management approach to patients undergoing VSP inhibitor therapy including Systolic Blood PRessure Intervention Trial (SPRINT) blood pressure goals, pleiotropic vasoprotective agents such as angiotensin converting enzyme inhibitors, amlodipine, and carvedilol, high-dose statin therapy, and aspirin.

血管内皮生长因子（VEGF）信号通路（VSP）在内皮细胞中起着重要作用，其抑制作用对心血管具有深远的影响。当使用VSP抑制剂作为抗血管生成疗法时，不仅对于正常脉管系统，而且对于肿瘤脉管系统都是如此。广泛性的内皮功能障碍易导致血管收缩，动脉粥样硬化，血小板活化和血栓形成（动脉多于静脉）。所有这些都已被VSP抑制剂报道，并共同引起血管毒性，其中最令人关注的是动脉血栓栓塞事件（ATE）。VSP抑制剂包括在细胞外作用于VEGF的抗体，例如贝伐单抗和酪氨酸激酶抑制剂，在细胞内作用于VEGF受体的激酶结构域，例如舒尼替尼和索拉非尼。在癌症治疗方案中加入贝伐单抗和VSP酪氨酸激酶抑制剂治疗分别使ATE的风险增加1.5-2.5倍和2.3-4.6倍。接受VSP抑制剂治疗时发生ATE的危险因素包括65岁以上的年龄，先前的血栓栓塞事件，动脉粥样硬化病史以及VSP抑制剂治疗的持续时间。在临床实践中，高血压仍然是最常见的VSP抑制血管表现。目前尚未确定最佳血压目标和实现这些目标的首选治疗策略。这篇评论总结了有关该主题的最新数据，并为接受VSP抑制剂治疗的患者提出了一种更深入的管理方法，包括收缩压介入试验（SPRINT）血压目标，