Division of Thoracic Surgery, Department of Surgery, Northwestern University Feinberg School of Medicine, Chicago, Illinois.
Division of Thoracic Surgery, Department of Surgery, Northwestern University Feinberg School of Medicine, Chicago, Illinois.
Ann Thorac Surg. 2024 Jan;117(1):206-212. doi: 10.1016/j.athoracsur.2022.12.013. Epub 2022 Dec 12.
Primary graft dysfunction is a risk factor of early mortality after lung transplant. Models identifying patients at high risk for primary graft dysfunction are limited. We hypothesize high postreperfusion systolic pulmonary artery pressure is a clinical marker for primary graft dysfunction.
This is a retrospective review of 158 consecutive lung transplants performed at a single academic center from January 2020 through July 2022. Only bilateral lung transplants were included and patients with pretransplant extracorporeal life support were excluded.
Primary graft dysfunction occurred in 42.3% (n = 30). Patients with primary graft dysfunction had higher postreperfusion systolic pulmonary artery pressure (41 ± 9.1 mm Hg) than those without (31.5 ± 8.8 mm Hg) (P < .001). Logistic regression showed postreperfusion systolic pulmonary artery pressure is a predictor for primary graft dysfunction (odds ratio 1.14, 95% CI 1.06-1.24, P < .001). Postreperfusion systolic pulmonary artery pressure of 37 mm Hg was optimal for predicting primary graft dysfunction by Youden index. The receiver operating characteristic curve of postreperfusion systolic pulmonary artery pressure at 37 mm Hg (sensitivity 0.77, specificity 0.78, area under the curve 0.81), was superior to the prereperfusion pressure curve at 36 mm Hg (sensitivity 0.77, specificity 0.39, area under the curve 0.57) (P < .01).
Elevated postreperfusion systolic pulmonary artery pressure after lung transplant is predictive of primary graft dysfunction. Postreperfusion systolic pulmonary artery pressure is more indicative of primary graft dysfunction than prereperfusion systolic pulmonary artery pressure. Using postreperfusion systolic pulmonary artery pressure as a positive signal of primary graft dysfunction allows earlier intervention, which could improve outcomes.
原发性移植物功能障碍是肺移植后早期死亡的危险因素。目前用于识别原发性移植物功能障碍高危患者的模型十分有限。我们假设肺再灌注后收缩期肺动脉压升高是原发性移植物功能障碍的临床标志物。
这是一项回顾性研究,纳入了 2020 年 1 月至 2022 年 7 月期间在一家学术中心进行的 158 例连续肺移植患者。仅纳入了双侧肺移植患者,排除了移植前体外生命支持的患者。
原发性移植物功能障碍的发生率为 42.3%(n=30)。发生原发性移植物功能障碍的患者肺再灌注后收缩期肺动脉压(41±9.1mmHg)高于未发生原发性移植物功能障碍的患者(31.5±8.8mmHg)(P<0.001)。Logistic 回归分析显示,肺再灌注后收缩期肺动脉压是原发性移植物功能障碍的预测因子(比值比 1.14,95%置信区间 1.06-1.24,P<0.001)。通过约登指数,肺再灌注后收缩期肺动脉压 37mmHg 预测原发性移植物功能障碍的效果最佳。肺再灌注后收缩期肺动脉压 37mmHg 的受试者工作特征曲线(敏感性 0.77,特异性 0.78,曲线下面积 0.81)优于肺再灌注前收缩期肺动脉压 36mmHg 的曲线(敏感性 0.77,特异性 0.39,曲线下面积 0.57)(P<0.01)。
肺移植后肺再灌注后收缩期肺动脉压升高与原发性移植物功能障碍相关。肺再灌注后收缩期肺动脉压比肺再灌注前收缩期肺动脉压更能提示原发性移植物功能障碍。将肺再灌注后收缩期肺动脉压作为原发性移植物功能障碍的阳性信号,可以更早地进行干预,从而改善预后。