Treatment of type II endoleaks with a novel polyurethane thrombogenic foam: induction of endoleak thrombosis and elimination of intra-aneurysmal pressure in the canine model

OBJECTIVE: The clinical significance and treatment of retrograde collateral arterial perfusion of abdominal aortic aneurysms after endovascular repair (type II endoleak) have not been completely characterized. A canine abdominal aortic aneurysm model of type II endoleak with an implanted pressure transducer was used to evaluate the use of polyurethane foam to induce thrombosis of type II endoleaks. The effect on endoleak patency, intra-aneurysmal pressure, and thrombus histology was studied. METHODS: Prosthetic aneurysms with an intraluminal, solid-state, strain-gauge pressure transducer were created in the infrarenal aorta of 14 mongrel dogs. Aneurysm side-branch vessels were reimplanted into the prosthetic aneurysm of 10 animals by using a Carrel patch. Type II (retrograde) endoleaks were created by excluding the aneurysm from antegrade perfusion with an impermeable stent graft. Thrombosis of the type II endoleak was induced by implantation of polyurethane foam into the prosthetic aneurysm sac of four animals. Six animals with type II endoleaks were not treated. In four control animals, no collateral side branches were reimplanted, and therefore no endoleak was created. Intra-aneurysmal and systemic pressures were measured daily for 60 to 90 days after the implantation of the stent graft. Endoleak patency and flow were assessed during surgery and at the time of death by using angiographic imaging and duplex ultrasonography. Histologic analysis of the intra-aneurysmal thrombus was also performed. RESULTS: Intra-aneurysmal pressure values are indexed to systemic pressure and are represented as a percentage of the simultaneously obtained systemic pressure, which has a value of 1.0. All six animals with untreated type II endoleaks maintained patency of the endoleak and side-branch arteries throughout the study period. Compared with control aneurysms that had no endoleak, animals with patent type II endoleaks exhibited significantly higher intra-aneurysmal pressurization (systolic pressure: patent type II endoleak, 0.702 +/- 0.283; control, 0.172 +/- 0.091; P < .001; mean pressure: endoleak, 0.784 +/- 0.229; control, 0.137 +/- 0.102; P < .001; pulse pressure: endoleak, 0.406 +/- 0.248; control, 0.098 +/- 0.077; P < .001; P < .001 for comparison for all groups by analysis of variance). Treatment of the type II endoleak with polyurethane foam induced thrombosis of the endoleak and feeding side-branch arteries in all four animals with type II endoleaks. This resulted in intra-aneurysmal pressures statistically indistinguishable from the controls (systolic pressure, 0.183 +/- 0.08; mean pressure, 0.142 +/- 0.09; pulse pressure, 0.054 +/- 0.04; not significant). Angiography and histology documented persistent patency up to the time of death (mean, 64 days) for untreated type II endoleaks and confirmed thrombosis of polyurethane foam-treated endoleaks in all cases. CONCLUSIONS: Untreated type II endoleaks were associated with intra-aneurysmal pressures that were 70% to 80% of systemic pressure. Treatment with polyurethane foam resulted in a reduction of intra-aneurysmal pressure to a level that was indistinguishable from control aneurysms that had no endoleak. CLINICAL RELEVANCE: Endovascular repair of abdominal aortic aneurysms is dependent on the successful exclusion of the aneurysm from arterial circulation. Type II endoleaks originate from retrograde flow into the aneurysm sac. This study demonstrates the use of polyurethane foam to induce thrombosis in a canine model of a type II endoleak, thereby reducing intra-aneurysmal pressure to levels similar to levels in animals without endoleaks. This approach may be a strategy for future treatment of type II endoleaks.     

Characterization of retrograde collateral (type II) endoleak using a new canine model

OBJECTIVE: The clinical significance of retrograde collateral arterial perfusion of abdominal aortic aneurysms after endovascular repair (type II endoleak) has not been completely characterized. In this study a canine model was used to analyze intra-aneurysmal pressure, thrombus histologic characteristics, endoleak patency, and radiographic appearance of type II endoleaks originating from single and multiple aneurysm side branches. METHODS: Prosthetic aneurysms with an intraluminal solid-state strain-gauge pressure transducer were created in the infrarenal aorta of 14 mongrel dogs. A single collateral side branch was reimplanted in 4 animals, multiple side branches were reimplanted in 6 animals, and no side branches were reimplanted in 4 control animals. Intra-aneurysmal and systemic pressure was measured for 60 to 90 days after creation of the type II endoleak. Endoleak patency and flow were assessed with duplex ultrasound scanning and cine-magnetic resonance angiography. Histologic analysis of the intra-aneurysmal thrombus was also performed. RESULTS: Stent-graft exclusion reduced intra-aneurysmal pressure significantly in all animals, as compared with systemic pressure (P < .001). All intra-aneurysmal pressure values are indexed to the systemic pressure, and are represented as a percentage of the simultaneously obtained systemic pressure, which has a value of 1.0. Type II endoleaks originating from multiple side branches exhibited significantly increased intra-aneurysmal systolic pressure, mean pressure, and pulse pressure, as compared with endoleaks derived from either a single side branch (systolic pressure: multiple, 0.70 +/- 0.28 vs single, 0.50 +/- 0.19; P < .001; mean pressure: multiple, 0.78 +/- 0.23 vs single, 0.59 +/- 0.22, P < .001; pulse pressure: multiple, 0.41 +/- 0.25 vs single, 0.17 +/- 0.15, P < .001) or excluded control aneurysms that had no side branches and no endoleak (systolic pressure, 0.17 +/- 0.09; mean pressure, 0.14 +/- 0.10; pulse pressure, 0.098 +/- 0.08; P < .001). Cine-magnetic resonance angiograms and duplex ultrasound scans documented persistent patency of multiple branch endoleaks up to the time of euthanasia. In contrast, single side branch endoleaks thrombosed within 3 days (P < .001). Thrombus in the aneurysm sac in close proximity to the endoleak contained intact red blood cells and limited fibrin. Thrombus distant from the endoleak demonstrated extensive fibrin deposition and degraded red blood cells. CONCLUSION: The canine model may be used to reliably measure intra-aneurysmal pressure in the presence of patent and thrombosed type II endoleaks. In this model 2 or more side branches are necessary to maintain persistent patency of type II endoleaks. These endoleaks are associated with significantly elevated intra-aneurysmal pressure, that is, 70% to 80% of systemic pressure. These results suggest that persistent type II endoleaks have clinical significance. CLINICAL RELEVANCE: Endoleaks originating from retrograde flow in the side branch vessels of the aneurysm generate significant levels of intra-aneurysmal pressure, that is, 70% to 80% of systemic pressure. At least 2 patent side branch vessels appear to be necessary to cause persistent patency of type II endoleak in the canine model. Further studies will be necessary to enable more complete characterization of retrograde endoleaks and to extend these findings to allow clinical application. However, these results suggest that persistently patent type II endoleaks are clinical significance and may require more intensive follow-up intervention.     

Aneurysm sac pressure after EVAR: the role of endoleak.

OBJECTIVE: The relation between endoleak and aneurysm sac pressure is not completely clear. This review evaluates the effect of endoleaks on aneurysm sac pressure and summarizes the present knowledge regarding aneurysm sac pressure after EVAR. METHODS: A systematic search of literature was carried out using MEDLINE, EMBASE and Web of Science. Studies were included if aneurysm sac pressure measurements as well as systemic pressure measurements were performed during or after EVAR. Mean pressure indices (MPI), ratio mean aneurysm sac pressure to mean systemic pressure), in the absence of endoleaks and in the presence of different type of endoleaks were compared. RESULTS: Stent-graft deployment does not seem to result in immediate reduction of aneurysm sac in the absence of an endoleak. Aneurysm sac pressure is elevated in the presence of an endoleak. However, the MPIs differ widely between studies both in the absence and presence of an endoleak. CONCLUSION: MPI is not specific to the type of endoleak. This implies that the same type of endoleak does not necessarily pose the same MPI and by this the same hazard of aneurysm rupture, because the aneurysm sac pressure is directly related to the aneurysm wall stress.     

All sealed endoleaks are not the same: a treatment strategy based on an ex-vivo analysis.

PURPOSE: factors contributing to pressure transmission through thrombosed or sealed endoleaks have not been elucidated. The purpose of this investigation was to create an ex-vivo model that mimics patent and sealed endoleaks and that can quantitatively analyse the effects of length, diameter and thrombus on pressure transmission to the interior of the aneurysm sac. METHODS: In the ex-vivo model, endoleak channels (ELCs) of various lengths (2 cm, 6 cm, 10 cm) and diameters (0.6 cm, 1.0 cm, 1.4 cm) were constructed using polytetrafluoroethylene (PTFE) grafts and attached to an artificial aneurysm sac. These ELCs were incorporated within a mock circulation made of rubber tubing connected to a pulsatile pump. Peak systolic pressure (PSP) was recorded in the aneurysm sac, distal to each ELC. Subsequently the ELCs were filled with human thrombus, and the pressure measurements repeated (n =5). Data was evaluated by regression analysis. RESULTS: Peak systolic pressure in the artificial circulation was maintained at 150 mmHg. In the absence of thrombus pressure did not change across the ELC, regardless of its length or diameter. In the presence of organised thrombus, the pressure curves distal to the ELC were dampened, and the pressure reduction was directly proportional to the length and inversely proportional to the diameter of the ELC. Regression analysis indicated statistical significance. CONCLUSION: In the absence of thrombosis, pressure transmitted via an ELC to the aneurysm sac is unchanged regardless of its length or diameter. All sealed endoleaks also transmit pressure. However, when an endoleak has thrombosed, pressure reduction is directly proportional to the length and inversely proportional to the diameter of its channel. This ex-vivo model suggests that Type 2 endoleaks with longer channels and smaller diameters would derive a greater benefit from adjunctive manoeuvres (coil embolisation) that hasten thrombosis. On the other hand, thrombosis of endoleaks with short and wide channels (e.g. Type 1) may not result in substantial pressure reduction within the aneurysm sac and a successful outcome.     

Intra-aneurysm sac pressure--the holy grail of endoluminal grafting of AAA.

OBJECTIVES: To relate intra-aneurysm sac pressure during endoluminal AAA repair to early and late endoleak, as well as to the aneurysm size upon follow-up. DESIGN: Prospective clinical investigation. METHODS AND PATIENTS: In 46 patients who had their AAAs treated by a stent graft (group I), intra-operative pressure measurement was performed (aorta uni-iliac stent grafts: 25 cases, bifurcated stent grafts: 21 cases). In 18 patients with open repair (group II) flow in the inferior mesenteric artery, and the pressure in the aneurysm sac was measured, before and after aortic and iliac cross clamping. Values are given in median with range. RESULTS: In group I, complete exclusion of AAA (no endoleak on intra-operative control angiogram) resulted in a statistically significant decrease in mean sac pressure from 74 (55-101) to 47 (4-104) mmHg. Pulse pressure reduced from 67 (34-103) to 8 (0-74) mmHg. In 11 patients a proximal type I endoleak was sealed by balloon modeling, after which the mean sac pressure reduced from 63 (14-91) to 52 (4-74) mmHg (n.s. versus patients with primary seal). Intra-operative pressure did not correlate with change in AAA diameter during twelve months follow-up. In group II, cross clamping of the proximal aorta significantly reduced mean sac pressure to 32 (21-55) mmHg, and the pulse pressure to 0 (0-13) mmHg (p < 0.05). Subsequent cross clamping of the iliac arteries did not significantly change the pressures. CONCLUSIONS: Measurement of intra-aneurysm sac pressure can help to detect and treat endoleaks during endoluminal grafting. However, the intra-operative sac pressure did not predict the fate of aneurysm during follow up. Compared to open repair of AAA, the sac pressure after endoluminal grafting remains significantly higher, in relation to pulse pressure.     

A canine model to study the significance and hemodynamics of type II endoleaks

OBJECTIVE: The clinical significance of Type 2 endoleak after endovascular repair of abdominal aortic aneurysms (AAA) remains incompletely delineated. This study describes the development of a novel canine model that allows for continuous monitoring of intraaneurysmal pressure in the setting of Type 2 endoleak. METHODS: Infrarenal AAA were created in 10 mongrel dogs by implanting a prosthetic aneurysm containing an intraluminal, solid-state, strain gauge pressure transducer which is able to measure pressures in both solid and liquid media. A segment of native aorta with two or more patent side branch vessels was reimplanted into the prosthetic aneurysm using a Carrel patch. Four animals had two lumbar vessels implanted; two had two lumbar vessels and the caudal mesenteric artery implanted, and four control animals had no vessels reimplanted. Retrograde flow in the aneurysmal side branches caused a Type 2 endoleak after the aneurysm was excluded from antegrade flow by deploying a stent graft. Both systemic and intra-sac pressures were measured daily for up to 90 days after endovascular exclusion and indexed to systemic pressure. Endoleak patency and flow were assessed with digital subtraction angiography, duplex ultrasound, and cine-magnetic resonance angiography (MRA). Histological characterization of the intraaneurysmal contents was performed. RESULTS: Before endovascular exclusion, the systolic, mean arterial, and pulse pressure within the aneurysmal sac closely matched that of the systemic circulation (systolic, 0.96 +/- 0.22; mean, 0.94 +/- 0.21; pulse pressure, 0.97 +/- 0.22) (R value, 0.97). Endovascular exclusion in animals with no collateral side branch vessels resulted in no endoleak and significantly reduced intraaneurysmal pressure when compared to systemic pressure, with systolic, mean arterial, and pulse pressure 0.172 +/- 0.05, 0.137 +/- 0.05, and 0.098 +/- 0.02, respectively (P < 0.001). In animals with Type 2 endoleaks, the pressures were lower than systemic pressure, but statistically significant in their difference from the control group. The systolic pressure of those with Type 2 endoleaks was 0.702 +/- 0.048; mean arterial pressure was 0.784 +/- 0.028, and pulse pressure was 0.406 +/- 0.031 when indexed to systemic pressure (P < 0.001). Cine-MRA and Duplex ultrasound documented persistent patency of the Type 2 endoleaks throughout the study period in animals with multiple side branches. CONCLUSION: Intraaneurysmal pressure in the setting of Type 2 endoleaks may be accurately determined using this canine model. Intraaneurysmal pressure is maintained at a significant level in the context of this retrograde collateral perfusion, suggesting that persistent Type 2 endoleaks are of clinical significance. This model may serve to allow further evaluation and characterization of Type 2 endoleaks.     

All Sealed Endoleaks are not the Same: A Treatment Strategy Based on an ex-vivo Analysis

Purpose factors contributing to pressure transmission through thrombosed or sealed endoleaks have not been elucidated. The purpose of this investigation was to create an ex-vivo model that mimics patent and sealed endoleaks and that can quantitatively analyse the effects of length, diameter and thrombus on pressure transmission to the interior of the aneurysm sac. Methods in the ex-vivo model, endoleak channels (ELCs) of various lengths (2 cm, 6 cm, 10 cm) and diameters (0.6 cm, 1.0 cm, 1.4 cm) were constructed using polytetrafluoroethylene (PTFE) grafts and attached to an artificial aneurysm sac. These ELCs were incorporated within a mock circulation made of rubber tubing connected to a pulsatile pump. Peak systolic pressure (PSP) was recorded in the aneurysm sac, distal to each ELC. Subsequently the ELCs were filled with human thrombus, and the pressure measurements repeated (n =5). Data was evaluated by regression analysis. Resultspeak systolic pressure in the artificial circulation was maintained at 150 mmHg. In the absence of thrombus pressure did not change across the ELC, regardless of its length or diameter. In the presence of organised thrombus, the pressure curves distal to the ELC were dampened, and the pressure reduction was directly proportional to the length and inversely proportional to the diameter of the ELC. Regression analysis indicated statistical significance. Conclusions in the absence of thrombosis, pressure transmitted via an ELC to the aneurysm sac is unchanged regardless of its length or diameter. All sealed endoleaks also transmit pressure. However, when an endoleak has thrombosed, pressure reduction is directly proportional to the length and inversely proportional to the diameter of its channel. This ex-vivo model suggests that Type 2 endoleaks with longer channels and smaller diameters would derive a greater benefit from adjunctive manoeuvres (coil embolisation) that hasten thrombosis. On the other hand, thrombosis of endoleaks with short and wide channels (e.g. Type 1) may not result in substantial pressure reduction within the aneurysm sac and a successful outcome.     

Intra-aneurysmal pressure after incomplete endovascular exclusion.

PURPOSE: An endoleak results from the incomplete endovascular exclusion of an aneurysm. We developed an experimental model to analyze hemodynamic changes within the aneurysm sac in the presence of an endoleak, with and without a simulated open collateral branch. METHODS: With a latex aneurysm model connected to a pulsatile pump, pressures were measured simultaneously within the system (systemic pressure) and the aneurysm sac (intrasac pressure). The experiments were performed without endoleak (control group) and after creating a 3.5-mm (group 1), 4.5-mm (group 2), and 6-mm (group 3) diameter orifice in the endograft, simulating an endoleak. Pressures were also registered with and without a patent aneurysm side branch. RESULTS: In each endoleak group, the intrasac diastolic pressure (DP) and mean pressure (MP) were significantly higher than the systemic DP and MP (P =.01, P =.006, and P =.001, respectively), although the pressure curve was damped. The presence of an open side branch significantly reduced the intrasac DP and MP. CONCLUSION: In this model, intrasac pressures were significantly higher than systemic pressures in the presence of all endoleaks, even the smallest ones. Intrasac pressures higher than systemic pressure may pose a high risk for aneurysm rupture. Although patent side branches significantly reduce these pressures, the aggressive management of an endoleak should be pursued.     

Significance of endotension,endoleak, and aneurysm pulsatility after endovascular repair

OBJECTIVE: The lack of aneurysm pulsatility after endovascular aneurysm repair (EVAR) is deemed by some an important guide to the effectiveness of exclusion. However, factors that contribute to aneurysm pulsatility after EVAR have not been elucidated. This study quantitatively analyzed the effects of systemic pressure, aneurysm sac pressure, endoleak, branch outflow from aneurysm sac, and intra-sac thrombus on aneurysm pulsatility after EVAR. METHODS: In an ex vivo model, an artificial aneurysm sac was incorporated within a mock circulation comprised of rubber tubing and a pulsatile pump. The aneurysm sac was then completely excluded from the circulatory circuit with two types of stent-grafts, ie, supported and unsupported, and heparinized canine blood was circulated. Systemic circulation and aneurysm sac pressure was recorded in the absence and presence of endoleaks, and simulated open and closed lumbar branch outflow from the aneurysm sac. The aneurysm sac was then filled with organized human thrombus, and all pressure measurements were repeated. Two observers blinded to the above-mentioned variables independently evaluated aneurysm sac pulsatility with palpation in five separate experiments. Analysis of variance was performed, with significance accepted at P =.05. RESULTS: Systemic pressure was simulated in the artificial circulation to range from 100/60 to 180/60 mm Hg. Regardless of the simulated lumbar branch outflow from the aneurysm, sac pressure was directly related to the presence of endoleak (P <.001). Aneurysm sac pulsatility was present only when the lumbar branch outflow was patent and not dependent on sac pressures. Aneurysm sac thrombosis or type of stent-graft did not influence sac pressure and pulsatility. CONCLUSIONS: In this model, after EVAR pulsatility depends on aneurysm sac outflow, regardless of endoleak, sac thrombosis, sac pressure, or stent-graft. Furthermore, persistent pulsatility does not predict systemic intra-sac pressure, nor does lack of pulsatility reflect freedom of the aneurysm sac from systemic pressurization. This ex vivo model suggests that aneurysm pulsatility is an unreliable guide for predicting aneurysm sac pressurization after EVAR. Other diagnostic methods must be used to assess successful aneurysm exclusion.     

Hypogastric artery aneurysm rupture after endovascular graft exclusion with shrinkage of the aneurysm: significance of endotension from a "virtual," or thrombosed type II endoleak

Type II endoleaks, resulting from retrograde branch flow, after endovascular graft aneurysm exclusion are considered benign because they usually thrombose and are commonly associated with stable or shrinking aneurysm sacs. We report a hypogastric artery aneurysm rupture from endotension from an undetected, thrombosed Type II endoleak, associated with sac shrinkage. The patient had undergone an endovascular graft repair of a 4-cm right common iliac artery and 9-cm hypogastric artery aneurysm with distal hypogastric artery coil embolization. Serial computed tomography scans revealed no endoleak and a hypogastric aneurysm thrombosis with shrinkage. Eighteen months later, the aneurysm ruptured as a result of pressurization from backbleeding, patent branches.     

Evaluation of the accuracy of a wireless pressure sensor in a canine model of retrograde-collateral (type II) endoleak and correlation with histologic analysis

BACKGROUND: The utility of intra-aneurysmal pressure determination is dependent on the ability to measure pressure in the presence of endoleak and thrombosis. In this study, the accuracy of a CardioMEMS wireless pressure sensor (CardioMEMS, Atlanta, Ga) transducer in the presence of thrombus associated with type II endoleak was measured. METHODS: Type II endoleaks were created in four mongrel dogs by implanting four collateral arterial side branches (lumbar and caudal mesenteric arteries) as a Carrel patch onto a 3-cm prosthetic polytetrafluoroethylene abdominal aortic aneurysm (AAA). The aneurysm was excluded 2 weeks later from antegrade perfusion by a stent graft. The wireless pressure sensor was positioned in the AAA external to the stent graft. A Konigsberg intraluminal solid-state strain-gauge pressure transducer (Konigsberg Instruments, Pasadena, Calif) that is accurate in the presence of thrombus served as the control to determine AAA pressure. Both of the transducers were implanted on the luminal surface of the aneurysm, 180 degrees opposite from the Carrel patch and endoleak channel. Intra-aneurysmal pressure resulting from the type II endoleak was measured twice daily for 4 weeks using both transducers. A total of 56 pre-exclusion and 224 post-exclusion distinct pressure determinations were made. Intra-aneurysmal pressure was indexed to the systemic pressure that was simultaneously measured by a strain-gauge pressure transducer implanted in the native aorta. Histologic analysis of the aneurysm contents was performed with hematoxylin and eosin. RESULTS: The intra-aneurysmal systolic, mean, and pulse pressures produced by the type II endoleak were significantly lower than systemic pressure in all animals and were < 60% of systemic pressure (P < .001). Close correlation between the wireless transducer and the control strain-gauge transducer was observed (R = 0.83, P < .001). Arteriography and Doppler ultrasound documented retrograde flow through the aneurysm side branches and persistent endoleak patency up to the time of euthanasia. Pathologic analysis demonstrated the endoleak channel to be patent and separated from the transducers by thrombus, which surrounded both transducers. CONCLUSIONS: Intra-aneurysmal pressure generated by type II endoleaks may be accurately measured through thrombus using a wireless pressure sensor in the canine model. The wireless sensor has the potential for clinical applicability in diagnosing and characterizing type II endoleaks.     

Hypogastric artery aneurysm rupture after endovascular graft exclusion with shrinkage of the aneurysm: Significance of endotension from a “virtual,” or thrombosed type II endoleak

Type II endoleaks, resulting from retrograde branch flow, after endovascular graft aneurysm exclusion are considered benign because they usually thrombose and are commonly associated with stable or shrinking aneurysm sacs. We report a hypogastric artery aneurysm rupture from endotension from an undetected, thrombosed Type II endoleak, associated with sac shrinkage. The patient had undergone an endovascular graft repair of a 4-cm right common iliac artery and 9-cm hypogastric artery aneurysm with distal hypogastric artery coil embolization. Serial computed tomography scans revealed no endoleak and a hypogastric aneurysm thrombosis with shrinkage. Eighteen months later, the aneurysm ruptured as a result of pressurization from backbleeding, patent branches. (J Vasc Surg 2001;33:1271-4.)     

Pulsatile wall motion and blood pressure in aneurysms with open and thrombosed endoleaks--comparison of a wall track system and M-mode ultrasound scanning: an in vitro and animal study

OBJECTIVE: Pulsatile wall motion has been suggested as a means by which to evaluate abdominal aortic aneurysms after exclusion from the circulation to determine whether the treatment has been effective. The objective of this study was to investigate the relations between pulsatile wall motion and both the mean and pulse pressures within the aneurysmal sac for both patent and thrombosed endoleaks. Furthermore, we compared the measurements of pulsatile wall motion by means of M-mode ultrasound scanning and a wall track system to determine the most reliable technique. METHODS: First, interobserver and intraobserver variability of M-mode ultrasound scan measurements was determined at different pressure levels in a cow iliac artery placed in an in vitro circulation. M-mode ultrasound scanning and a wall track system were compared in the same model. Second, in an animal experiment, an aneurysm and endoleak model with both patent and thrombosed endoleaks was created. Systemic and aneurysmal mean and pulse pressures were recorded synchronically with pulsatile wall motion by means of M-mode ultrasound scanning and a wall track system. RESULTS: The intraobserver and interobserver variability values for M-mode ultrasound scan measurement in vitro were 0.11 mm (SD = 0.10 mm) and 0.15 mm (SD = 0.13 mm), respectively. In the animal study, a significant difference existed with respect to the level of pulse pressure within the aneurysmal sac between the group with pulsatile wall motion and the group without such motion (P <.0001). The presence of pulsatile wall motion was not correlated with the level of aneurysmal mean pressure. The level of pulsatile wall motion determined by means of M-mode ultrasound scanning correlated well with the level determined by means of the wall track system (r = 0. 74; P =.01). For the level of pulsatile wall motion determined by means of M-mode ultrasound scanning, a significant difference between patent and thrombosed endoleaks existed (P =.04). For detecting endoleaks, the sensitivity and specificity of pulsatile wall motion as determined by means of the wall track system were 52% and 100%, respectively, and the sensitivity and specificity of pulsatile wall motion as determined by means of M-mode ultrasound scanning were 64% and 67%, respectively. For the detection of pulse pressure in the aneurysmal sac, the sensitivity and specificity of pulsatile wall motion as determined by means of the wall track system were 76% and 100%, respectively, and the sensitivity and specificity of pulsatile wall motion as determined by means of M-mode ultrasound scanning were 90% and 71%, respectively. CONCLUSIONS: We found that pulsatile wall motion is correlated with aneurysmal pulse pressure but not with the mean level of pressure inside the aneurysm. Although measurements of pulsatile wall motion are of great theoretic value when groups of patients who have undergone endovascular aneurysm repair are being compared, this method appears to be unreliable in a clinical setting with respect to determining whether the aneurysmal sac is still pressurized in individual patients.     

Relationship between preoperative patency of the inferior mesenteric artery and subsequent occurrence of type II endoleak in patients undergoing endovascular repair of abdominal aortic aneurysms

OBJECTIVES: The purpose of this study was (1) to find out whether preoperative inferior mesenteric artery (IMA) patency (on radiographic imaging) predicts IMA-related endoleaks after endovascular repair of infrarenal abdominal aortic aneurysms, (2) to determine feasibility of measuring aneurysm sac pressures in patients with endoleaks, and (3) to report early evidence of effective endovascular obliteration of IMA endoleaks. METHODS: We studied 76 consecutive cases of infrarenal aortic aneurysms that were repaired with an endovascular approach (March 1998-April 1999). RESULTS: There were 13 (17%) endoleaks persistent 30 days after the procedure. Eleven (85%) of these 13 were IMA-related endoleaks, which were documented with selective superior mesenteric artery angiography. The preoperative finding (on computed tomographic scan) of a patent IMA does not always predict an IMA-related endoleak, but results in a statistically and clinically significant higher ratio of patients with IMA-related endoleaks in the immediate postoperative period (24% versus 3%, P <.035). In eight of the 11 patients with persistent IMA-related endoleaks, measurement of intra-aneurysm sac pressures was possible, and six of these patients had systemic pressures within the excluded aneurysm sac. Nine (82%) of 11 IMA-related endoleaks were successfully obliterated by means of selective IMA embolization. CONCLUSIONS: Many endoleaks are caused by a patent IMA, and this can result in persistence of systemic pressure within the aneurysm sac. The preoperative finding (on computed tomographic scan) of a patent IMA is a predictor of increased rates of IMA endoleaks, and IMA endoleaks can be successfully obliterated through endovascular procedures, after endovascular abdominal aortic aneurysm repair.     

Clinical Significance of Type II Endoleak after Endovascular Repair of Abdominal Aortic Aneurysm

Type II endoleaks after endovascular repair of abdominal aortic aneurysm (EVAR) are a result of retrograde flow from arterial branches (e.g., lumbar and inferior mesenteric) refilling the aneurysm sac, which has been excluded by the stent graft. Controversy continues with regard to the clinical significance and treatment of type II endoleaks. To develop recommendations for management, we analyzed outcome data from 10 EVAR trials completed over the last 5 years involving a total of 2,617 cases. The incidence of type II endoleak at discharge or 30 days was 6-17%, at 6 months 4.5-8%, and at 1 year 1-5%. Successful resolution of endoleak following secondary interventions was observed in 11-100% of cases. There were 10 conversions to open repair and no ruptures related to type II endoleak. In patients observed for 12 months with computed tomography and/or ultrasound, approximately one-half of type II endoleaks disappeared spontaneously. In the absence of a type I endoleak, our analysis of the current literature suggests that intervention for type II endoleak should be undertaken for abdominal aortic aneurysm sac enlargement occurring after 6 months, persistence for >12 months without abdominal aortic aneurysm sac enlargement, or an aneurysm sac pressure >20% of systolic blood pressure; translumbar aneurysm sac thrombosis and intra-arterial feeding vessel occlusion appear to be prudent management options. Presented at the Twenty-second Annual Meeting of the Southern California Vascular Surgery Society, San Diego, CA, May 1, 2004.     

Infrarenal Abdominal Aortic Aneurysm Complicated by Persistent Endotension After Endovascular Repair: Report of a Case

Endoleak and endotension may prevent the successful exclusion of an aneurysm after endovascular aortic aneurysm repair (EVAR). The pressurization in the excluded aneurysm sac caused by endotension may lead to rupture of the aneurysm; however, the cause of endotension and its underlying mechanisms remain unclear. We report a case of infrarenal abdominal aortic aneurysm (AAA) complicated by persistent endotension after EVAR. Although no endoleaks were found on conventional double-phase computed tomographic scans, a thrombosed endoleak existed in the side branch and attachment site of the endograft. After treating the undetectable thrombosed endoleaks, physical examination revealed that the pressure of the excluded aneurysm had diminished, with shrinkage of the aneurysm. This case report suggests that a high-pressure undetectable type I or type II endoleak could be a major cause of endotension. Thus, postoperative evaluation of the attachment site of an endograft is important after EVAR.     

腹主动脉瘤腔内修复术中瘤腔内压力监测的意义

目的 探讨腹主动脉瘤腔内修复术(endovascular aneurysm repair,EVAR)中瘤腔内压力监测的意义.方法 选择2006年4月至2007年3月12例肾下腹主动脉瘤腔内修复术病例,瘤体最大直径(5.83±0.95)cm.术中应用测压导管监测治疗前、后瘤腔内压力的变化,观察内漏类型、部位及随访结果与压力的关系.结果 12例支架型血管(stent-graft,SG)释放前瘤腔内压力约等于体循环压.EVAR后11例瘤腔内收缩压下降＞40%,其中7例下降≥50%;1例无明显改变.12例脉压差下降＞30%,其中6例下降＞75%.术后随访无内漏发生,无动脉瘤相关死亡.5例收缩压下降＞50%的病例瘤径出现不同程度的缩小(1.6～3.1 mm),压力未下降的l例瘤径增长3.2 mm,余6例瘤径无明显变化.结论 腹主动脉瘤腔内修复术中瘤腔内压力监测可了解手术前后压力的变化,从而判断腔内治疗效果.     

Endoleakage after stent-graft treatment of abdominal aneurysm: Implications on pressure and imaging—an in vitro study

Background: Endoleakage is a fairly common problem after endovascular repair of abdominal aortic aneurysm and may prevent successful exclusion of the aneurysm. The consequences of endoleakage in terms of pressure in the aneurysmal sac are not exactly known. Moreover, the diagnosis of endoleakage is a problem because visualization of endoleaks can be difficult. Method: With an ex vivo model of circulation with an artificial aneurysm managed by means of a tube graft, studies were performed to evaluate precisely known diameters of endoleaks with both imaging techniques (computed tomography and digital subtraction angiography) and pressure measurements of the aneurysmal sac. The experiments were performed without endoleak (controls) and with 1.231-French (0.410 mm), 3-French (1 mm), and 7-French (2.33 mm) endoleaks. Pressure and imaging were evaluated in the absence and presence of a simulated open lumbar artery. The pressure in the prosthesis and in the aneurysmal sac were recorded simultaneously. Digital subtraction angiography with and without a Lucite acrylic plate, computed tomographic angiography, and delayed computed tomographic angiography were performed. For the first experiments, the aneurysmal sac was filled with starch solution. All tests were repeated with fresh thrombus in the aneurysmal sac. Results: Each endoleak was associated with a diastolic pressure in the aneurysmal sac that was identical to diastolic systemic pressure, although the pressure curve was damped. At digital subtraction angiography without a Lucite acrylic plate, the 1.231-French (0.410 mm) endoleak was visualized without an open lumbar artery. When a Lucite acrylic plate was added, the endoleak was not visible until a lumbar artery was opened. In the presence of thrombus within the aneurysmal sac, all endoleaks were not visualized at digital subtraction angiography. At computed tomographic angiography, all endoleaks were not visualized in the absence of a thrombus mass in the aneurysmal sac. In the presence of thrombus within the aneurysmal sac, the 1.231-French (0.410 mm) endoleak became visible after opening of a simulated lumbar artery. At delayed computed tomographic angiography, all endoleaks were visualized without and with thrombus. Conclusion: Every endoleak, even a very small one, caused pressure greater than systemic diastolic pressure within the aneurysmal sac. However, small endoleaks were not visualized with digital subtraction angiography and computed tomographic angiography, whereas all endoleaks were visualized with a delayed computed tomographic angiography protocol. We believe that follow-up examinations after stent graft placement for aortic aneurysms should focus on pressure measurements, but until this is clinically feasible, delayed computed tomographic angiography should be performed. (J Vasc Surg 1998;28:234-41.)     

Aneurysm sac pressure measurements after endovascular repair of abdominal aortic aneurysms

OBJECTIVES: The goal of endovascular grafting of abdominal aortic aneurysms (AAAs) is to exclude the aneurysm sac from systemic pressure and thereby decrease the risk of rupture. Unlike conventional open surgery, branch vessels in the sac (eg, lumbar artery and inferior mesenteric artery [IMA]) are not ligated and can potentially transmit pressure. The purpose of our investigation was to evaluate the feasibility of various interventional techniques for measuring pressure within the aneurysm sac in patients who had undergone endovascular repair of AAAs. METHODS: Sac pressure measurements were performed in 21 patients who had undergone stent graft repair of AAAs. Seventeen of 21 patients had endoleaks demonstrated on 30-day computed tomographic (CT) scans. Access to the aneurysm sac in these patients was through direct translumbar sac puncture (5 patients), through a patent IMA accessed via the superior mesenteric artery (SMA) (9 patients), or by direct cannulation around attachment sites (3 patients). Four patients had perioperative pressure measurements obtained through catheters positioned along side of the endovascular graft at the time of its deployment. Two of these catheters were left in position for 30 hours during which time CT and conventional angiography were performed. Pressures were determined with standard arterial-line pressure transduction techniques and compared with systemic pressure in each patient. RESULTS: Elevated sac pressure was found in all patients. The sac pressure in patients with endoleaks was found to be systemic (15 patients) or near systemic (2 patients) and all had pulsatile waveforms. Elevated sac pressures were also found in patients without CT or angiographic evidence of endoleak (2 patients). Injection of the sacs in two of these patients revealed a patent lumbar artery and an IMA. CONCLUSIONS: It is possible to measure pressures from within the aneurysm sac in patients with stent grafts with a variety of techniques. Patients may continue to have pressurized AAA sacs despite endovascular AAA repair. Endoleaks transmit pulsatile pressure into the aneurysm sac regardless of the type. It is possible to have systemic sac pressures without evidence of endoleaks on CT or angiography.     

Noninvasive intrasac pressure measurement and the influence of type 2 and type 3 endoleaks in an animal model of abdominal aortic aneurysm

The objective of this study was to noninvasively detect pressure changes within an excluded aneurysm sac in an animal model of abdominal aortic aneurysm (AAA) and to study the influence of type 2 and 3 endoleaks. A porcine model of AAA that allows for the creation of type 2 and 3 endoleaks was used. A miniaturized pressure monitoring device (3 x 9 x 1.5 mm; Remon Medical Technologies, Caesarea, Israel) was implanted within the surgically created and excluded aneurysm sac. The pressure monitoring device is an ultrasound-based system that allows for pressure measurements in a noninvasive, transcutaneous fashion. In addition, catheter-based pressures were taken within the aorta and directly in the AAA sac. Noninvasive measurements were taken in a transcutaneous fashion between the initial operation and the time of sacrifice, when the type 3 endoleak was created (2 weeks). The median mean arterial pressure was 66 mm Hg (range 55-120 mm Hg; N = 8). The median noninvasive sac pressure with a type 2 endoleak was 48 mm Hg (range 39-90 mm Hg; N = 8) and was almost identical to the catheter-based measurements. Noninvasive pressures could be measured as early as postprocedure day 1. Two animals had follow-up that suggested closure of the type 2 endoleak during the observation period. With the creation of the type 3 endoleak, the catheter and noninvasive sac pressure and waveform changed from a flatline trace to a higher-pressure pulsatile trace (median 54 mm Hg; range 46-81 mm Hg; N = 8), reproducing the arterial pressure and waveform. This is the first study, to our knowledge, that demonstrates the efficacy of a noninvasive, miniaturized pressure monitoring device in identifying pressure changes in an excluded aneurysm sac with type 2 and type 3 endoleaks. This technology holds great promise for follow-up of patients and identification of sac pressure changes after EVAR and may allow a change in the current follow-up strategy.