Trocciola Susan M, Dayal Rajeev, Chaer Rabih A, Lin Stephanie C, DeRubertis Brian, Ryer Evan J, Hynececk Robert L, Pierce Matthew J, Prince Martin, Badimon Juan, Marin Michael L, Fuster Valentin, Kent K Craig, Faries Peter L
Department of Surgery, New York Presbyterian Hospital, Cornell University, New York, NY 10021, USA.
J Vasc Surg. 2006 Jan;43(1):109-16. doi: 10.1016/j.jvs.2005.09.023.
This study used a canine model of abdominal aortic aneurysms (AAAs) to compare intra-aneurysmal pressure and thrombus formation after exclusion with Dacron and expanded polytetrafluoroethylene (ePTFE) stent-grafts.
Prosthetic AAAs with implanted strain-gauge pressure transducers were treated by stent-graft exclusion using Food and Drug Administration-approved devices in 10 mongrel dogs: five Dacron (AneuRx) and five ePTFE (original Excluder). Intra-aneurysmal pressure was measured over 4 weeks after AAA exclusion and indexed to the systemic pressure, represented as a percentage of a simultaneously obtained systemic pressure (value = 1.0). Magnetic resonance imaging (MRI) of the intra-aneurysmal thrombus was performed at 1, 2, and 4 weeks after exclusion and expressed as a signal-to-noise ratio (S:N) to control for background signal intensity. Comparisons of pressures and S:N between the two stent-grafts was analyzed with the Student's t test. Intra-aneurysmal thrombus was characterized histologically.
In animals excluded with both Dacron and ePTFE stent-grafts, the intra-aneurysmal pressure was nonpulsatile and reduced to <30% of systemic pressure. Significantly greater pressure transmission was observed after AAA exclusion using ePTFE compared with Dacron stent grafts (systolic pressure: ePTFE, 0.28 +/- 0.12 vs Dacron, 0.11 +/- 0.02, P < .001; mean pressure: ePTFE, 0.16 +/- 0.08 vs Dacron, 0.06 +/- 0.02, P < .001). MRI confirmed the absence of perfusion in all aneurysms. The T1-weighted signal intensity remained persistently elevated (S:N at 1 week, 2.7 +/- 0.4 vs 2 weeks, 4.0 +/- 0.2 vs 4 weeks, 5.4 +/- 1.3) in ePTFE-treated intra-aneurysmal thrombus, suggesting an absence of thrombus organization. In contrast, progressive evolution of T1 signal intensity in aneurysms excluded by Dacron stent-grafts was consistent with maturation from intact red blood cells (S:N at 1 week, 3.3 +/- 0.4) to methemoglobin (S:N at 2 weeks, 6.1 +/- 0.8), and then hemosiderin and ferritin (S:N at 4 weeks, 2.4 +/- 0.5). Histologically, ePTFE-excluded aneurysms contained poorly organized thrombus with red blood cell fragments and haphazardly arranged fibrin deposition indicative of active remodeling and continued influx of transudated serum. In aneurysms excluded by Dacron stent-grafts, dense, mature collagenous connective tissue and organized fibrin were present, indicative of greater thrombus organization.
Stent-graft treatment reduces intra-aneurysmal pressure to <30% of systemic pressure when no endoleak is present; however, significantly greater pressure is present in aneurysms treated with porous ePTFE stent-grafts than Dacron grafts. Histologic and MRI imaging analysis suggest that active transudation of serous blood components may be contributing to this increased intra-aneurysmal pressure.
本研究采用犬腹主动脉瘤(AAA)模型,比较用涤纶和膨体聚四氟乙烯(ePTFE)覆膜支架隔绝术后瘤内压力和血栓形成情况。
在10只杂种犬中,使用经美国食品药品监督管理局批准的器械,通过覆膜支架隔绝术治疗植入应变片压力传感器的人工AAA:5只用涤纶(AneuRx),5只用ePTFE(初代Excluder)。在AAA隔绝术后4周测量瘤内压力,并与体循环压力进行指数化,以同时获得的体循环压力的百分比表示(数值=1.0)。在隔绝术后1、2和4周对瘤内血栓进行磁共振成像(MRI),并以信噪比(S:N)表示,以控制背景信号强度。用Student t检验分析两种覆膜支架之间的压力和S:N比较。对瘤内血栓进行组织学特征分析。
在用涤纶和ePTFE覆膜支架隔绝的动物中,瘤内压力无搏动,降至体循环压力的<30%。与涤纶覆膜支架相比,使用ePTFE进行AAA隔绝术后观察到明显更大的压力传递(收缩压:ePTFE,0.28±0.12 vs涤纶,0.11±0.02,P<.001;平均压力:ePTFE,0.16±0.08 vs涤纶,0.06±0.02,P<.001)。MRI证实所有动脉瘤均无灌注。在ePTFE治疗的瘤内血栓中,T1加权信号强度持续升高(1周时S:N,2.7±0.4 vs 2周时,4.0±0.2 vs 4周时,5.4±1.3),提示血栓无机化。相比之下,涤纶覆膜支架隔绝的动脉瘤中T1信号强度的逐渐演变与从完整红细胞(1周时S:N,3.3±0.4)到高铁血红蛋白(2周时S:N,6.1±0.⑧),再到含铁血黄素和铁蛋白(4周时S:N,2.4±0.5)的成熟过程一致。组织学上.ePTFE隔绝的动脉瘤含有组织不良的血栓,有红细胞碎片和随意排列表示活跃重塑和渗出血清持续流入的纤维蛋白沉积。在涤纶覆膜支架隔绝的动脉瘤中,存在致密、成熟的胶原结缔组织和有组织的纤维蛋白,表示血栓有更大程度的机化。
当无内漏时,覆膜支架治疗可将瘤内压力降至体循环压力的<30%;然而,用多孔ePTFE覆膜支架治疗的动脉瘤中的压力明显高于涤纶覆膜支架。组织学和MRI成像分析表明,浆液性血液成分的活跃渗出可能是导致瘤内压力升高的原因。