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首页> 外文期刊>American Journal of Neuroradiology >Can Induction of Systemic Hypotension Help Prevent Nidus Rupture Complicating Arteriovenous Malformation Embolization?: Analysis of Underlying Mechanisms Achieved Using a Theoretical Model
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Can Induction of Systemic Hypotension Help Prevent Nidus Rupture Complicating Arteriovenous Malformation Embolization?: Analysis of Underlying Mechanisms Achieved Using a Theoretical Model

机译：全身性低血压的诱导能否帮助防止Nidus破裂使动静脉畸形栓塞复杂化？：使用理论模型分析潜在的机制

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BACKGROUND AND PURPOSE: Nidus rupture is a serious complication of intracranial arteriovenous malformation (AVM) embolotherapy, but its pathogenetic mechanisms are not well described. An AVM model based on electrical network analysis was used to investigate theoretically the potential role of hemodynamic perturbations for elevating the risk of nidus vessel rupture (Rrupt) after simulated AVM embolotherapy, and to assess the potential benefit of systemic hypotension for preventing rupture. METHODS: Five separate hypothetical mechanisms for nidus hemorrhage were studied: 1) intranidal rerouting of blood pressure; 2) extranidal rerouting of blood pressure; 3) occlusion of draining veins with glue; 4) delayed thrombosis of draining veins; and 5) excessively high injection pressures proximal to the nidus. Simulated occlusion of vessels or elevated injection pressures were implemented into the AVM model, and electrical circuit analysis revealed the consequent changes in intranidal flow, pressure, and Rrupt for the nidus vessels. An expression for Rrupt was derived based on the functional distribution of the critical radii of component vessels. If AVM rupture was observed (Rrupt =" BORDER="0">100%) at systemic normotension (mean pressure [P] = 74 mm Hg), the theoretical embolization was repeated under systemic hypotension (minor P = 70 mm Hg, moderate P = 50 mm Hg, or profound P = 25 mm Hg) to assess the potential benefit of this maneuver in reducing hemorrhage rates. RESULTS: All five pathogenetic mechanisms under investigation were able to produce rupture of AVMs during or after embolotherapy. These different mechanisms had in common the capability of generating surges in intranidal hemodynamic parameters resulting in nidus vessel rupture. The theoretical induction of systemic hypotension during and after treatment was shown to be of significant benefit in attenuating these surges and reducing Rrupt to safer levels below 100%. CONCLUSION: The induction of systemic hypotension during and after AVM embolization would appear theoretically to be of potential use in preventing iatrogenic nidus hemorrhage. The described AVM model should serve as a useful research tool for further theoretical investigations of AVM embolotherapy and its hemodynamic sequelae.
机译：背景与目的：Nidus破裂是颅内动静脉畸形（AVM）栓塞治疗的严重并发症，但其致病机理尚未得到很好的描述。理论上，基于网络分析的AVM 模型用于研究 血流动力学扰动 可能对增加股动脉血管破裂风险的潜在作用（R 模拟AVM栓塞治疗后的 rupt ），并评估系统性低血压预防破裂的潜在益处。 方法：研究了5种假想性尼杜斯出血的假想机制：1）血压向神经内改变方向； 2） 血压的颅外改道； 3）用胶水堵住 静脉； 4）引流静脉血栓延迟；和 5）靠近nidus的注射压力过高。 模拟血管闭塞或注射压力升高 应用于AVM模型，电路 分析显示，nidus血管的随之而来的潮气变化， 压力和R rupt 。根据组成容器的 临界半径的功能分布，得出 R rupt 的表达式。如果在系统性正常血压（平均压力[P] = 74 ）下观察到AVM破裂 （R rupt = BORDER =“ 0”> 100％） > mm Hg），在全身性低血压（低P = 70 mm Hg，中P = 50 mm Hg或深层 P = 25 mm Hg）下重复理论栓塞评估此操作 降低出血率的潜在益处。 结果：正在研究的所有五种致病机制 均能够在AVM破裂期间引起AVM破裂。 这些不同的机制具有共同的能力，可以在肾内血流动力学参数中产生 激增，从而导致nidus 血管破裂。治疗期间和治疗后的全身性低血压 被证明在减轻这些潮涌和将R rupt 降低到安全水平 方面具有显着的益处。 sup>低于100％。 结论：归纳法从理论上讲，AVM栓塞期间和之后的系统性低血压有可能潜在地用于预防医源性病灶出血。所描述的 AVM模型应作为进一步研究AVM栓塞治疗及其血液动力学 后遗症的理论研究有用的工具。

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  • 来源
    《American Journal of Neuroradiology》 |2000年第7期|1255-1267|共13页
  • 作者

    Tarik F. Massoud; George J. Hademenos; William L. Young; Erzhen Gao; John Pile-Spellman;

  • 作者单位

    From the Division of Interventional Neuroradiology and Department of Radiological Sciences (T.F.M., G.J.H.), University of California at Los Angeles School of Medicine, Los Angeles Departments of Radiology (T.F.M., W.L.Y., J.P.-S.), Anesthesiology (W.L.Y.), and Neurological Surgery (W.L.Y., J.P.-S.), College of Physicians and Surgeons, and the Department of Electrical Engineering (E.G.), Columbia University, New York, New York.;

    From the Division of Interventional Neuroradiology and Department of Radiological Sciences (T.F.M., G.J.H.), University of California at Los Angeles School of Medicine, Los Angeles Departments of Radiology (T.F.M., W.L.Y., J.P.-S.), Anesthesiology (W.L.Y.), and Neurological Surgery (W.L.Y., J.P.-S.), College of Physicians and Surgeons, and the Department of Electrical Engineering (E.G.), Columbia University, New York, New York.;

    From the Division of Interventional Neuroradiology and Department of Radiological Sciences (T.F.M., G.J.H.), University of California at Los Angeles School of Medicine, Los Angeles Departments of Radiology (T.F.M., W.L.Y., J.P.-S.), Anesthesiology (W.L.Y.), and Neurological Surgery (W.L.Y., J.P.-S.), College of Physicians and Surgeons, and the Department of Electrical Engineering (E.G.), Columbia University, New York, New York.;

    From the Division of Interventional Neuroradiology and Department of Radiological Sciences (T.F.M., G.J.H.), University of California at Los Angeles School of Medicine, Los Angeles Departments of Radiology (T.F.M., W.L.Y., J.P.-S.), Anesthesiology (W.L.Y.), and Neurological Surgery (W.L.Y., J.P.-S.), College of Physicians and Surgeons, and the Department of Electrical Engineering (E.G.), Columbia University, New York, New York.;

    From the Division of Interventional Neuroradiology and Department of Radiological Sciences (T.F.M., G.J.H.), University of California at Los Angeles School of Medicine, Los Angeles Departments of Radiology (T.F.M., W.L.Y., J.P.-S.), Anesthesiology (W.L.Y.), and Neurological Surgery (W.L.Y., J.P.-S.), College of Physicians and Surgeons, and the Department of Electrical Engineering (E.G.), Columbia University, New York, New York.;

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