Imaging the dynamics and microstructure of fibrin clot polymerization in cardiac surgical patients using spectrally encoded confocal microscopy.

Imaging the dynamics and microstructure of fibrin clot polymerization in cardiac surgical patients using spectrally encoded confocal microscopy.
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使用光谱编码共聚焦显微镜对心脏手术患者的纤维蛋白凝块聚合的动力学和微观结构进行成像。

DOI:
10.1002/ajh.26217
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发表时间:
2021
影响因子:
12.8
通讯作者:
Nadkarni,SeemantiniK
Nadkarni,SeemantiniK
中科院分区:
医学1区
文献类型:
--
作者:
Tshikudi,DianeM;Simandoux,Olivier;Kang,Dongkyun;VanCott,ElizabethM;Andrawes,MichaelN;Yelin,Dvir;Nadkarni,SeemantiniK

文献摘要

相似文献

在体外循环(CPB)心脏手术中,止血平衡的改变可能会破坏纤维蛋白的组装,使患者易发生围手术期出血。我们研究了一种称为光谱编码共聚焦显微镜(SECM)的新型设备的效用,用于评估CPB患者在肝素和鱼精蛋白治疗后的纤维蛋白凝块聚合。SECM是一种新颖的、高速的光学方法,用于在三维立体视野(165 × 4000 × 36 μm)上以高空间分辨率(1.0 μm)可视化和量化纤维蛋白凝块形成。SECM的测量灵敏度首先通过在正常受试者的血浆样品中加入肝素和鱼精蛋白来确定。接下来,对CPB患者的血浆样本进行SECM,以量化CPB暴露对纤维蛋白凝块动力学和微观结构的改变程度。在加标样品中,随着肝素浓度的增加,纤维蛋白时间延长(4.4±1.8 ~ 49.3±16.8 min,p< 0.001),纤维蛋白网络密度降低(0.079±0.010 ~ 0.001±0.002 A.U,p< 0.001)。此外,在鱼精蛋白处理的样品中,纤维蛋白网络密度没有恢复到基线水平。在CPB患者中,SECM报告蛋白蛋白化样本中的纤维蛋白网络密度(0.055±0.01 au[任意单位])低于基线值(0.066±0.009 au)。(p = 0.03),尽管类似纤维蛋白时间(基线= 6.0±1.3,鱼精蛋白= 6.4±1.6分钟,p = 0.5)。在这些患者中,包括纤维蛋白异质性、长度和直线度在内的附加指标被量化。值得注意的是,SECM显示,鱼精蛋白与CPB暴露后,纤维蛋白凝块更加不均匀(基线= 0.11±0.02 A)。U,鱼精蛋白= 0.08±0.01 A。U,p= 0.008),较直的纤维(基线= 0.918±0.003A)。U,鱼精蛋白= 0.928±0.0006 a.u p< 0.001)。通过提供快速可视化和量化纤维蛋白凝块微观结构的能力,SECM可以为评估心脏手术患者的凝块稳定性和止血提供一种新的方法。
During cardiac surgery with cardiopulmonary bypass (CPB), altered hemostatic balance may disrupt fibrin assembly, predisposing patients to perioperative hemorrhage. We investigated the utility of a novel device termed spectrally‐encoded confocal microscopy (SECM) for assessing fibrin clot polymerization following heparin and protamine administration in CPB patients. SECM is a novel, high‐speed optical approach to visualize and quantify fibrin clot formation in three dimensions with high spatial resolution (1.0 μm) over a volumetric field‐of‐view (165 × 4000 × 36 μm). The measurement sensitivity of SECM was first determined using plasma samples from normal subjects spiked with heparin and protamine. Next, SECM was performed in plasma samples from patients on CPB to quantify the extent to which fibrin clot dynamics and microstructure were altered by CPB exposure. In spiked samples, prolonged fibrin time (4.4 ± 1.8 to 49.3 ± 16.8 min,p< 0.001) and diminished fibrin network density (0.079 ± 0.010 to 0.001 ± 0.002 A.U,p< 0.001) with increasing heparin concentration were reported by SECM. Furthermore, fibrin network density was not restored to baseline levels in protamine‐treated samples. In CPB patients, SECM reported lower fibrin network density in protaminized samples (0.055 ± 0.01 A.U. [Arbitrary units]) vs baseline values (0.066 ± 0.009 A.U.) (p= 0.03) despite comparable fibrin time (baseline = 6.0 ± 1.3, protamine = 6.4 ± 1.6 min,p= 0.5). In these patients, additional metrics including fibrin heterogeneity, length and straightness were quantified. Note, SECM revealed that following protamine administration with CPB exposure, fibrin clots were more heterogeneous (baseline = 0.11 ± 0.02 A.U, protamine = 0.08 ± 0.01 A.U,p= 0.008) with straighter fibers (baseline = 0.918 ± 0.003A.U, protamine = 0.928 ± 0.0006A.U.p< 0.001). By providing the capability to rapidly visualize and quantify fibrin clot microstructure, SECM could furnish a new approach for assessing clot stability and hemostasis in cardiac surgical patients.