Hsing Deyin D, Stock Arabela C, Greenwald Bruce M, Bacha Emile A, Flynn Patrick A, Carroll Sheila J, Dayton Jeffrey D, Prockop Susan E, Qiu Yuqing, Almeida Dena, Tamura Shoran, Hajjar Katherine A
Division of Pediatric Critical Care Medicine, Department of Pediatrics, Weill Cornell Medicine, New York City, NY.
Division of Cardiac Critical Care Medicine, Heart Institute, Johns Hopkins All Children's Hospital, St. Petersburg, FL.
Crit Care Explor. 2023 Feb 10;5(2):e0862. doi: 10.1097/CCE.0000000000000862. eCollection 2023 Feb.
The primary objective of this study was to determine whether expression of the multifunctional and adherens junction-regulating protein, annexin A2 (A2), is altered following cardiopulmonary bypass (CPB). A secondary objective was to determine whether depletion of A2 is associated with post-CPB organ dysfunction in children.
In a prospective, observational study conducted over a 1-year period in children undergoing cardiac surgery requiring CPB, we analyzed A2 expression in peripheral blood mononuclear cells at different time points. We then assessed the relationship of A2 expression with organ function at each time point in the early postoperative period.
Twenty-three-bed mixed PICU in a tertiary academic center.
Patients 1 month to 18 years old undergoing cardiac surgery requiring CPB.
We analyzed A2 expression in 22 enrolled subjects ( = 9, 1-23 mo old; = 13, 2-18 yr old) and found a proteolysis-mediated decline in intact A2 immediately after bypass ( = 0.0009), reaching a median of 4% of baseline at 6 hours after bypass ( < 0.0001), and recovery by postoperative day 1. The degree of A2 depletion immediately after bypass in 1-23-month-olds correlated strongly with the extent of organ dysfunction, as measured by PICU admission Vasoactive-Ventilation-Renal ( = 0.004) and PEdiatric Logistic Organ Dysfunction-2 ( = 0.039) scores on postoperative day 1. A2 depletion immediately after bypass also correlated with more protracted requirement for both respiratory support ( = 0.007) and invasive ventilation ( = 0.013) in the 1-23-month-olds.
The degree of depletion of A2 following CPB correlates with more severe organ dysfunction, especially acute respiratory compromise in children under 2 years. These findings suggest that loss of A2 may contribute to pulmonary microvascular leak in young children following CPB.
本研究的主要目的是确定多功能且调节黏附连接的蛋白膜联蛋白A2(A2)在体外循环(CPB)后表达是否发生改变。次要目的是确定A2的减少是否与儿童CPB术后器官功能障碍相关。
在一项对需要CPB的心脏手术患儿进行的为期1年的前瞻性观察研究中,我们分析了不同时间点外周血单核细胞中A2的表达。然后我们评估了术后早期各时间点A2表达与器官功能的关系。
一所三级学术中心拥有23张床位的混合儿科重症监护病房。
年龄在1个月至18岁之间、需要CPB进行心脏手术的患者。
我们分析了22名入组受试者(n = 9,1 - 23个月大;n = 13,2 - 18岁)中A2的表达,发现体外循环后立即出现由蛋白水解介导的完整A2下降(P = 0.0009),在体外循环后6小时降至基线的中位数4%(P < 0.0001),并在术后第1天恢复。1 - 23个月大的患儿体外循环后立即出现的A2减少程度与器官功能障碍程度密切相关,术后第1天通过儿科重症监护病房入院时血管活性 - 通气 - 肾脏(P = 0.004)和儿科逻辑器官功能障碍 - 2(P = 0.039)评分来衡量。1 - 23个月大的患儿体外循环后立即出现的A2减少也与对呼吸支持(P = 0.007)和有创通气(P = 0.013)的更持久需求相关。
CPB后A2的减少程度与更严重的器官功能障碍相关,尤其是2岁以下儿童的急性呼吸功能不全。这些发现表明A2的丧失可能导致幼儿CPB后肺微血管渗漏。