Department of Medicine, University of Toronto, Toronto, Ontario, Canada; Institute for Clinical Evaluative Sciences, Toronto, Ontario, Canada; Institute of Health Policy, Management and Evaluation, University of Toronto, Toronto, Ontario, Canada; Women's College Hospital, Toronto, Ontario, Canada.
Department of Medicine, University of Toronto, Toronto, Ontario, Canada; Princess Margaret Cancer Centre, Toronto, Ontario, Canada.
Cancer Treat Rev. 2017 Feb;53:120-127. doi: 10.1016/j.ctrv.2016.12.002. Epub 2016 Dec 30.
The cardiovascular risk of angiogenesis inhibitors is not well-quantified. We hypothesized that, compared to direct vascular endothelial growth factor (VEGF) inhibitors (anti-VEGF antibodies or decoy receptors), small molecule agents have higher risk due to their less specific mechanism.
We searched the MEDLINE, EMBASE, and Cochrane Central Register of Controlled Trials for phase III randomised controlled trials comparing angiogenesis inhibitor-based therapy to other systemic therapy. Outcomes evaluated were hypertension, severe hypertension, cardiac dysfunction, congestive heart failure, cardiac ischemia, arterial thromboembolism, venous thromboembolism, and fatal cardiovascular events. Data were pooled using Mantel-Haenszel random effects method to generate odds ratios (OR).
We identified 77 studies meeting inclusion criteria. Compared to routine care, angiogenesis inhibitors were associated with a higher risk of hypertension (OR 5.28 [4.53-6.15], number needed to harm [NNH] 6), severe hypertension (OR 5.59 [4.67-6.69], NNH 17), cardiac ischemia (OR 2.83 [1.72-4.65], NNH 85) and cardiac dysfunction (OR 1.35 [1.06-1.70], NNH 139). VEGF inhibitors were associated with an increased risk of arterial thromboembolism (OR 1.52 [1.17-1.98], NNH 141). No significant interaction was observed between the two drug subgroups for any outcomes. We identified no significant increase in the risk of the other outcomes evaluated.
Angiogenesis inhibitors increase the risk of hypertension, arterial thromboembolism, cardiac ischemia and cardiac dysfunction. There was no significant difference in cardiovascular risk between direct VEGF inhibitors and small molecule agents.
血管生成抑制剂的心血管风险尚未得到充分评估。我们假设,与直接血管内皮生长因子(VEGF)抑制剂(抗 VEGF 抗体或诱饵受体)相比,小分子药物由于其机制不够特异,风险更高。
我们检索了 MEDLINE、EMBASE 和 Cochrane 对照试验中心注册库,以查找比较血管生成抑制剂治疗与其他全身治疗的 III 期随机对照试验。评估的结局为高血压、重度高血压、心功能障碍、充血性心力衰竭、心肌缺血、动脉血栓栓塞、静脉血栓栓塞和致命性心血管事件。使用 Mantel-Haenszel 随机效应法对数据进行汇总,生成比值比(OR)。
我们确定了符合纳入标准的 77 项研究。与常规治疗相比,血管生成抑制剂与高血压(OR 5.28 [4.53-6.15],危害比[NNH] 6)、重度高血压(OR 5.59 [4.67-6.69],NNH 17)、心肌缺血(OR 2.83 [1.72-4.65],NNH 85)和心功能障碍(OR 1.35 [1.06-1.70],NNH 139)的风险增加相关。VEGF 抑制剂与动脉血栓栓塞的风险增加相关(OR 1.52 [1.17-1.98],NNH 141)。对于任何结局,我们都没有观察到两个药物亚组之间存在显著的交互作用。我们没有发现其他评估结局的风险增加。
血管生成抑制剂增加高血压、动脉血栓栓塞、心肌缺血和心功能障碍的风险。直接 VEGF 抑制剂和小分子药物之间的心血管风险没有显著差异。