Distribution of Sac Pressure in an Experimental Aneurysm Model after Endovascular Repair: The Effect of Endoleak Types I and II
Distribution of Sac Pressure in an Experimental Aneurysm Model after Endovascular Repair: The Effect of Endoleak Types I and II
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血管内修复后实验性动脉瘤模型中囊压的分布：I 型和 II 型内漏的影响
DOI：
10.1177/152660280301000317
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发表时间：
2003
期刊：
影响因子：
--
通讯作者：
M. Goldman
中科院分区：
文献类型：
--
作者：
E. Xenos;S. Stevens;M. Freeman;J. Pacanowski;D. Cassada;M. Goldman
目的：在实验性动脉瘤模型中研究覆膜支架隔绝前后以及存在单独I型和II型内漏时动脉瘤壁上的应变/压力（S/P）差异分布。研究方法：将两个锥形椭圆形Gore-Tex补片缝合到8 mm Gore-Tex管移植物的前后纵向动脉切开处，从而形成梭形动脉瘤。将2个S/P探头放置在近端瘤颈附近的近端瘤囊处，2个放置在瘤囊直径最宽的部位，2个放置在远端瘤颈附近的瘤囊处。使用10 mm覆膜支架排除了与脉动泵系统连接的动脉瘤。分别创建和测试I型和II型内漏。在体循环收缩压（BP）为80、110和150 mmHg时获得S/P测量值。通过在囊内注射凝血酶和钙诱导囊内容物血栓形成。血管造影用于验证囊内是否存在血流。结果：与排除前相比，动脉瘤排除导致所有3个BP水平的S/P显著降低（p，0.05）。囊内血栓未改变被排除囊内的S/P（所有3个BP水平的p <0.05）。在存在近端I型内漏的情况下，S/P分布不均匀，近端瘤颈的S/P接近排除前的S/P（所有3个BP水平的无移植物与I型内漏的p 0.05）。在存在血栓的情况下也是如此。有II型内漏时，S/P分布更均匀，与无内漏时的压力相比没有显著升高（p.0.05，所有3个BP水平的移植物与II型内漏）。血栓对具有II型内漏的腔内S/P没有影响。当BP 5150 mmHg时，与II型内漏相比，I型内漏的Intrasac S/P显著更高（p50.008）。结论：动脉瘤的腔内隔绝术可使动脉瘤囊内的S/P均匀降低。I型内漏（而非II型内漏）导致近端瘤颈附近的瘤囊区域的S/P显著更高。血栓不会导致动脉瘤囊内S/P分布的显著差异。血管内治疗杂志2003;10：516-523
Purpose: To study in an experimental aneurysm model the differential distribution of strain/ pressure (S/P) on the aneurysm wall before and after endograft exclusion and in the presence of individual type I and type II endoleaks. Methods: Two tapered elliptical Gore-Tex patches were sutured to an anterior and posterior longitudinal arteriotomy of an 8-mm Gore-Tex tube graft, thus creating a fusiform aneurysm. Two S/P transducers were placed at the proximal sac adjacent to the proximal neck, 2 at the site of the widest sac diameter, and 2 at the sac adjacent to the distal neck. The aneurysm, which was connected to a pulsatile pump system, was excluded using a 10mm endograft. Type I and type II endoleaks were created and tested individually. S/P measurements were obtained at systemic systolic pressures (BP) of 80, 110, and 150 mmHg. Thrombosis of the sac contents was induced by injection of thrombin and calcium in the sac. Angiography was used to verify presence or absence of flow in the sac. Results: Aneurysm exclusion resulted in significant S/P reductions at all 3 BP levels versus prior to exclusion (p,0.05). Thrombus in the sac did not alter S/P in the excluded sac (p.0.05 for all 3 BP levels). In the presence of a proximal type I endoleak, S/P distribution was not uniform, and S/P at the proximal neck was close to S/P prior to exclusion (p.0.05 no graft versus type I endoleak for all 3 BP levels). This was also true in the presence of thrombus. With a type II endoleak, S/P was more evenly distributed and was not significantly elevated compared to the pressure without an endoleak (p.0.05, graft versus type II endoleak for all 3 BP levels). Thrombus had no effect on intrasac S/P with a type II endoleak. Intrasac S/P was significantly higher in the presence of a type I endoleak compared to a type II endoleak when BP5150 mmHg (p50.008). Conclusions: Endovascular exclusion of an aneurysm results in uniform S/P reduction in the aneurysm sac. Type I endoleak, but not type II endoleak, results in significantly higher S/P in an area of the sac adjacent to the proximal neck. Thrombus does not result in significantly different S/P distribution in the aneurysm sac. J Endovasc Ther 2003;10:516–523