From the Department of Radiology (M.M.H., E.C.B., S.M.), Department of Biomedical Statistics and Informatics (W.S.H.), and Department of Pulmonary and Critical Care Medicine (V.N.I.), Mayo Clinic, 200 First St SW, Rochester, MN 55905.
Radiology. 2019 Sep;292(3):762-770. doi: 10.1148/radiol.2019180978. Epub 2019 Jul 30.
Background Embolization is the standard of care for treatment of pulmonary arteriovenous malformations (PAVMs). Persistence of PAVMs after embolization occurs for undefined reasons but may include inflammation related to smoking in dysregulated angiogenesis. Purpose To determine whether patients with hereditary hemorrhagic telangiectasia (HHT) who smoke tobacco are more prone to PAVM persistence after embolization. Materials and Methods Patients with HHT treated for PAVMs between January 2000 and August 2017 were retrospectively identified. Only PAVMs with no previous treatment and patients with both clinical and imaging follow-up were included. Age, sex, PAVM characteristics (size, complexity, and location), embolization material used, microcatheter type, smoking history, active tobacco use, and other risk factors for arterial disease were analyzed by using a multivariate Cox proportional hazards model to determine risk factors for persistence. Results Five-year persistence-free survival rates in nonsmokers, smokers of 1-20 pack-years, and smokers of more than 20 pack-years were 12.2%, 21.9%, and 37.4% respectively. Smokers with more than 20 pack-years relative to nonsmokers had greater risk of persistence after adjusting for arterial feeder size (hazard ratio, 3.8; 95% confidence interval [CI]: 1.5, 10.0; = .007). Patients who reported active tobacco use at the time of PAVM embolization had a 5-year cumulative incidence of persistence of 26.3% compared with 13.5% in inactive smokers. After adjusting for arterial feeder size, the risk of persistence was greater in tobacco users versus inactive smokers at the time of treatment (hazard ratio, 2.4; 95% CI: 1.2, 4.7; = .01). Conclusion Smoking is associated with pulmonary arteriovenous malformation persistence after embolization in patients with hereditary hemorrhagic telangiectasia. See also the editorial by Trerotola and Pyeritz in this issue.
栓塞是治疗肺动静脉畸形(PAVM)的标准治疗方法。栓塞后 PAVM 持续存在的原因尚不清楚,但可能包括与吸烟相关的炎症,以及血管生成失调。目的:确定患有遗传性出血性毛细血管扩张症(HHT)且吸烟的患者在栓塞后更易发生 PAVM 持续存在。材料和方法:回顾性确定了 2000 年 1 月至 2017 年 8 月期间接受 PAVM 治疗的 HHT 患者。仅纳入无既往治疗且具有临床和影像学随访的患者。通过多变量 Cox 比例风险模型分析患者的年龄、性别、PAVM 特征(大小、复杂性和位置)、使用的栓塞材料、微导管类型、吸烟史、主动吸烟和其他动脉疾病的危险因素,以确定持续性的危险因素。结果:在不吸烟者、吸烟 1-20 包年者和吸烟超过 20 包年者中,5 年无持续性生存率分别为 12.2%、21.9%和 37.4%。在校正动脉供体大小后,与不吸烟者相比,吸烟超过 20 包年者的持续性风险更高(风险比,3.8;95%置信区间[CI]:1.5,10.0; =.007)。在 PAVM 栓塞时报告主动吸烟的患者,5 年内持续性累积发生率为 26.3%,而不吸烟者为 13.5%。在校正动脉供体大小后,在治疗时吸烟与不吸烟者相比,持续性风险更高(风险比,2.4;95%CI:1.2,4.7; =.01)。结论:吸烟与遗传性出血性毛细血管扩张症患者栓塞后肺动静脉畸形持续存在有关。本期杂志还刊登了 Trerotola 和 Pyeritz 的社论。