Department of Vascular and Endovascular Surgery, University of Texas-Southwestern, Dallas, Texas 75390-9157, USA.
J Endovasc Ther. 2011 Aug;18(4):601-6. doi: 10.1583/11-3469.1.
To evaluate the effects of type II endoleaks and sac pressurization on stent-graft displacement following endovascular aneurysm repair (EVAR).
Experimental silicone infrarenal aneurysm (6-cm) models were "treated" with a Talent stent-graft deployed with 20-mm proximal and distal landing zones. Inflow and outflow vessels were created as part of the silicone model to control flow into the aneurysm sac. All aneurysm models were uniform, with a diameter neck of 31 mm, a neck length of 20 mm, and iliac artery diameters of 16 mm. The aortic model was secured in a water bath to a pulsatile pump under physiological conditions; the output phase ratio (%systole/%diastole) was set at 65/35 with a pump rate of 80 beats per minute. Commercially available bifurcated stent-grafts were then displaced in vitro utilizing a linear motion apparatus attached to a force gauge. The mean arterial pressure (MAP) and pulse pressure (PP) at the aortic inflow were 60.1 ± 3.1 and 38.3 ± 7.8 mmHg, respectively. Peak force to cause initial stent-graft migration with and without a type II endoleak was recorded and compared.
In aneurysm sacs with no endoleak, the MAP and sac PP were 32 ± 6.4 and 6 ± 1.3 mmHg, respectively (p<0.01). In aneurysm sacs with a type II endoleak, the MAP and sac PP were 54.1 ± 9.7 and 16.1 ± 4.1 mmHg, respectively (p<0.02). Peak force to initiate migration was 16.0 ± 1.41 N (range 15-18) with no endoleak vs. 23.2 ± 2.2 N (range 20-25) in those with a type IIa endoleak and 23.5 ± 2.5 N (range 20-26) in those with a type IIb endoleak (p<0.001).
Type II endoleaks are associated with a significantly increased sac pressure. Increased sac pressurization from type II endoleaks results in a significantly greater force to displace a stent-graft longitudinally. Type II endoleaks may therefore inhibit migration and offer a benefit following EVAR; however, clinical correlation of these results is required.
评估 II 型内漏和瘤囊内压对血管内动脉瘤修复（EVAR）后支架移植物移位的影响。
实验性硅胶腹主动脉瘤（6cm）模型采用 Talent 支架移植物进行“治疗”，近端和远端着陆区各有 20mm。流入和流出血管作为硅胶模型的一部分进行创建，以控制流入瘤囊的血流。所有的动脉瘤模型都是统一的，颈直径为 31mm，颈长 20mm，髂动脉直径为 16mm。主动脉模型被固定在水浴中，通过生理条件下的脉动泵；输出相位比（%收缩/%舒张）设定为 65/35，泵速为每分钟 80 次。然后，使用附接到力计的线性运动装置将商用分叉支架移植物在体外移位。主动脉流入处的平均动脉压（MAP）和脉搏压（PP）分别为 60.1±3.1mmHg 和 38.3±7.8mmHg。记录并比较有和没有 II 型内漏时导致支架初始迁移的峰值力。
在没有内漏的瘤囊中，MAP 和瘤囊 PP 分别为 32±6.4mmHg 和 6±1.3mmHg（p<0.01）。在有 II 型内漏的瘤囊中，MAP 和瘤囊 PP 分别为 54.1±9.7mmHg 和 16.1±4.1mmHg（p<0.02）。无内漏时引发迁移的峰值力为 16.0±1.41N（范围 15-18），而 IIa 型内漏时为 23.2±2.2N（范围 20-25），IIb 型内漏时为 23.5±2.5N（范围 20-26）（p<0.001）。
II 型内漏与瘤囊内压显著升高有关。来自 II 型内漏的瘤囊内压升高会导致支架移植物纵向移位的力显著增加。因此，II 型内漏可能会抑制 EVAR 后的迁移并提供益处；然而，需要对这些结果进行临床相关性研究。
