| | The effect of endograft relining on sac expansion after endovascular aneurysm repair with the original-permeability Gore Excluder abdominal aortic aneurysm endoprosthesisPresented at the New England Society for Vascular Surgery Annual Meeting, Sept 22-24, Boston, Mass. Received 24 September 2006; accepted 11 December 2006. published online 20 February 2007. ObjectiveEndovascular abdominal aortic aneurysm repair (EVAR) with the original-permeability Excluder (W.L. Gore & Associates, Flagstaff, Ariz) has been associated with postoperative sac expansion in the absence of endoleak. In these cases, we have performed an endovascular revision, relining the original endograft with another Excluder, in an effort to arrest sac expansion by reducing permeability. We have studied these cases to determine the effect of relining on aneurysm expansion. MethodsPatients who demonstrated sac expansion (≥5 mm diameter, ≥5% three-dimensional volume) after EVAR with the original Excluder were evaluated. Between 1999 and 2004, the original-permeability endoprosthesis was used in 97 patients who underwent EVAR for asymptomatic abdominal aortic aneurysm (AAA). Sac expansion occurred in 24 patients, of which multiple imaging modalities showed 12 had expansion without demonstrable endoleak. Nine of the 12 have had endovascular relining, and five of these nine have >6 months follow-up to form the primary basis for this report. ResultsAAA size was stable or smaller in the first 6 months after the original EVAR for all patients. Once expansion began (typically in the time frame of 6 to 12 months), multimodality imaging showed no aneurysm spontaneously decreased in size without intervention, despite the absence of endoleak (n = 12). Expansion exceeded clinically significant thresholds at 30 months (mean) by diameter criteria and 22 months (mean) by three-dimensional volume criteria for the five patients with >6 months follow-up after relining. Endovascular relining was performed at a mean of 36 months, with a mean hospital stay of 1 day, and no morbidity or mortality. Over the entire duration of expansion (mean, 26 months), aneurysms expanded by 6.0 ± 1 mm/year diameter and by 12% ± 2%/year by three-dimensional volume. At a mean of 16 months follow-up after relining with another Excluder, the mean diameter decrease was 2.0 mm/year (P < .03) and the mean volume decrease was 2.6%/year (P < .01). After relining, all AAAs were smaller by diameter or volume, or both, exceeding thresholds defining shrinkage in two of the five with >6 months follow-up after relining. There was no rupture, migration, endoleak, conversion to open repair, or aneurysm-related death in any patient. ConclusionsIt appears from the initial follow-up that AAA expansion owing to permeability issues after EVAR with the original Excluder can be arrested by endovascular relining with a low-permeability Excluder endoprosthesis. The Excluder endoprosthesis (W. L. Gore & Associates, Flagstaff, Ariz) has a good safety profile for endovascular repair (EVAR) of abdominal aortic aneurysms (AAA).1, 2, 3 Despite this fact, several reports indicate a significant percentage of enlarging AAAs after repair with what is now known as the “original” Excluder.4, 5, 6, 7, 8 Of interest is that when AAAs enlarging after EVAR with the original Excluder are evaluated, most have no endoleak.7, 9 Most conversions to open repair have also involved expansion without detected endoleak, often referred to as endotension.9 Complications related to sac enlargement in the absence of endoleak appear to be uncommon, but rupture, loss of proximal seal zone, and conversion to open repair or other secondary interventions have been reported.1, 3, 7, 9, 10, 11, 12, 13 Partly because of the low number of reported complications, the true nature of endotension and its natural history are not entirely clear. Examination of fluid withdrawn from the sac by direct puncture, reports on the sac at the time of conversion, and explanted devices have all indicated that in many cases enlargement in the absence of endoleak with the original Excluder is due to material permeability.1, 9, 10, 14 The problem appears to have been corrected by changing the graft material in the newer low-permeability Excluder LP,8 but that does not address the problem of endotension in patients with the original Excluder. The problem may be solved by conversion to open repair, but this carries a significant risk to the patient. Less invasive options such as laparoscopic sac fenestration and aspiration of the sac have been performed but have not been successful.15 Our hypothesis for some time has been that sac expansion secondary to graft permeability can be arrested by relining the original-permeability endoprosthesis with another endoprosthesis. We performed the initial such procedure in 2002, and have performed relining more frequently recently, encouraged by information on explanted endografts (Fig 1) and the availability of the low-permeability Excluder endoprosthesis in 2004. Over time, it has become clear that the incidence of AAA enlargement without endoleak is significant. Thus, we have continually updated and reviewed all patients at our institution that underwent placement of the original-permeability Excluder endoprosthesis, experienced sac expansion in the absence of endoleak, and underwent endovascular relining with Excluder components. At this point we believe the series has sufficient procedures and length of follow-up to form this preliminary report. Methods  Patients All patients undergoing endovascular abdominal aortic aneurysm repair at Dartmouth-Hitchcock Medical Center are prospectively entered into a database, including serial three-dimensional (3D) imaging and standard anatomic measurements. All patients who underwent elective EVAR of an AAA using an original-permeability Excluder endoprosthesis were included in our initial review. The review was used to determine the number of AAAs with expansion as defined by Society of Vascular Surgery (SVS) standards (≥5 mm maximum AAA diameter or ≥5% sac expansion by 3D volume),16, 17 the proportion expanding without endoleak, and the number that underwent endovascular relining procedures. Operative technique for primary endovascular abdominal aortic aneurysm repair All patients underwent primary repair of their AAA with the original-permeability Excluder endoprosthesis according the manufacturer’s instructions for use.18 All EVARs were performed in the operating room with a 12-inch digital C-arm fluoroscopy unit (GE/OEC 9800, GE Medical Systems, Milwaukee, Wis; or previously, Philips BV 312, Philips Medical Systems, Santa Ana, Calif) and carbon-fiber table. Completion arteriography was always performed, with antegrade contrast injection at the proximal attachment site and separate retrograde injection in both iliac arteries. Other injection sites (junction injection, separate views) were used as necessary if endoleak was present to rule out type I or type III endoleak. Imaging Preoperative and postoperative imaging was primarily spiral computed tomography (CT) with 3D reconstruction and Computer Aided Measurement, Planning and Simulation (3D CAMPS) software (Preview M2S, formerly Medical Metrix Solutions, West Lebanon, NH). Scans covered a volume from the celiac to the common femoral arteries using a scan protocol with the 3D CAMPS technique, which has been previously published in detail.19, 20, 21 Electronic data from CT angiography (CTA) or magnetic resonance angiography (MRA) was sent in Digital Imaging and Communication in Medicine (DICOM) format for postprocessing by M2S, including multiplanar reformats encompassing the entire volume of the scan in sagittal, coronal, and axial planes at 0.75-mm to 2-mm intervals and orthogonal reformats (perpendicular to the vessel) at 1-mm intervals. Measurements were performed using validated techniques, including electronic calipers and standard measurement definitions including SVS Reporting Standards.16, 17 Key anatomic parameters included maximum AAA diameter change and 3D volume change measured from the lowest renal artery to the aortic bifurcation and from the lowest renal artery to the common iliac artery bifurcation to capture changes in patients with iliac aneurysms. Diameters were measured orthogonal to the vessel (ie, in a plane at a right angle to the centerline of the lumen). Methods for 3D volume measurements used standard 3D reconstruction techniques described previously,19, 20, 21, 22 which were validated on phantoms of known size and clinically on aortic aneurysms, with interobserver variability <5%. As determined from both interobserver variability and SVS Reporting Standards, the thresholds used to define expansion or shrinkage were ≥5 mm for diameter and ≥5% for 3D volume.16, 21 Spiral CT, 3D reconstruction images, and morphometric data for all patients were prospectively collected and entered into a database for comparison of aneurysm morphology over time. These data were used for patient evaluation and management purposes as standard of care. Patient follow-up All patients were scheduled for interval follow-up at 1, 6, and 12 months, with annual visits thereafter. Interim visits were scheduled as clinically indicated. Each visit included a patient interview, review of systems, physical examination, determination of ankle-brachial index if indicated, and CT scan with 3D reconstruction including volume measurements. Abdominal radiographs (four views) were performed to evaluate for fracture or according to clinical trial protocol. Additional studies, including duplex ultrasonography and angiography, were performed as clinically indicated. If relining was performed, patients were scheduled for interval follow-up at 1, 6, and 12 months, with annual visits thereafter. Evaluation before secondary intervention Any patient who had experienced significant sac expansion by volume or diameter criteria was carefully examined for endoleak. Multimodality imaging methods, including CT, delayed-contrast CT, delayed-contrast MRA, duplex, and arteriography, were used for further evaluation of potential endoleak as deemed appropriate by the surgeon. All patients had delayed-contrast CTA as the minimum extent of further evaluation, with a delay of 3 to 5 minutes for venous phase contrast enhancement.20 Angiography was also performed at the time of relining to confirm the absence of endoleak in all cases. Patients with expansion and endoleak of any kind were excluded from analysis in this study. Those patients with sac expansion in the absence of endoleak had discussion of the options, including closer follow-up, conversion to open repair, or a relining procedure. Secondary interventions Secondary interventions described in this study consisted of relining the original-permeability Excluder endoprosthesis with another set of Excluder components. The goal of relining in each case was to cover any portion of the original endograft that was within the aneurysm sac not in apposition to vessel, as shown in Fig 2. Preoperative 3D CAMPS was used in a fashion similar to the original EVAR placement to review each patient’s images, and a plan was designed to cover the original-permeability endoprosthesis if no endoleak was detected at angiography. Relining was performed with Excluder components in all cases. An original Excluder was used for the initial case in 2002, and low-permeability Excluder components were always used after their release in August 2004. All patients were then followed up postoperatively in a manner similar to the first intervention. Statistical analysis The size change for each 6-month interval and for the duration of the expansion and relining time periods were analyzed with the Statview statistical software package (SAS Institute, Cary NC). Analysis of variance or t test were used where appropriate to delineate quantitative changes over time. Although sac size change in our overall series and in this cohort appeared consistent with a normal distribution, we also evaluated the changes for key differences with nonparametric methods (Wilcoxon signed rank test), and presented ranges of the data to avoid any concern about the normality of the data. All P values shown to be significant by parametric methods were also significant (P < .05) by nonparametric methods. Results  Patient population Between 1999 and 2004, EVAR was performed electively on 97 patients for asymptomatic AAA using the original-permeability Excluder endoprosthesis (a subset of nearly 500 endovascular repairs). Mean follow-up for these 97 patients was 33 months at the time of the analysis. Sac expansion has been detected by both diameter and volume criteria in 24 of 97 patients, and 12 of these were enlarging with no demonstrable endoleak on multiple imaging modalities (the other 12 had type II endoleak during expansion). Four other patients were enlarging by volume criteria only, none with endoleak. All patients had evaluation to rule out endoleak as described in the Methods section. All patients considered for relining had arterial-phase CTA, delayed-contrast venous-phase CTA, and angiography as a minimum, and some also had duplex or MRA, or both. Of the patients enlarging without apparent endoleak, nine have undergone relining procedures, and five of these nine have >6 months’ follow-up after relining to form the primary basis for this report. The mean follow-up after relining was 16 months (range, 7 to 24 months). Patient characteristics and demographics for the five patients with longer follow-up are summarized in Table I. | | |  | Patient characteristics | |  |
|---|
 | Age (mean years) | 74 |  |  | Male Sex | 80% |  |  | History of coronary disease | 60% |  |  | History of renal insufficiency | 20% |  |  | History of hypertension | 100% |  |  | History of hyperlipidemia | 40% |  |  | Anticoagulation | |  |  | Aspirin | 100% |  |  | Warfarin | 0% |  |  | Average time to 5 mm sac expansion by diameter, months | 30 |  |  | Average time to 5% growth by volume, months | 22 |  |  | Average duration of follow-up | |  |  | Before relining, months (range) | 36 (28-46) |  |  | After relining, months (range) | 14 (10-24) |  | | | |
Duration of follow-up and time to clinically significant expansion For the five patients with ≥6 months’ follow-up after relining, expansion began in the 6-month to 12-month time period in four, and in the 12-month to 24-month time period for the other. The mean time to exceed the threshold defining sac expansion was 22 months by 3D volume criteria and 30 months by diameter criteria. The mean duration of follow-up from primary EVAR to endovascular relining was 36 months (range, 28 to 46 months). Overall AAA enlargement at the time of relining was a 10.5-mm increase in maximal diameter and 26% increase in 3D volume relative to the smallest size of the aneurysm postoperatively. Mean AAA diameter at relining was 6.3 cm by CT orthogonal cross section (see Methods). Expansion rates were slower in the patients who were relined more recently or have not yet been relined (see “Pattern of sac behavior,” which follows). The endovascular relining procedure Various strategies were used for relining (Fig 2). Three of the five patients with longer follow-up underwent relining of the limbs of the graft only, with the limbs in standard position. One additional patient underwent relining with limbs only, but with the “advancing the bifurcation” technique (Fig 2). One patient underwent relining with an aortic cuff as well as iliac limbs. The procedure was performed using open femoral exposure in three patients and percutaneous techniques in two. Contrast was used to confirm the absence of endoleak, as it was not needed for device placement. Mean contrast use was 90 mL, fluoroscopy time, 26 minutes, and estimated blood loss, 190 mL. All patients went home on postoperative day 1 after overnight observation. No mortality or morbidity was reported during the hospital stay or at follow-up clinic visits (range, 7 to 24 months). No rupture, migration, endoleak, conversion, or other secondary intervention for endograft or aneurysm problems has occurred in any patient. Four procedures in this series were relatively recent and so far only have a CT scan at 1 month after relining. In three of these patients, both limbs were relined percutaneously, and in one patient both limbs and trunk were relined, using femoral exposure. One patient had concomitant hernia repair. Two patients each were discharged on postoperative day 1 or 2. Mean fluoroscopy time was 15 minutes, contrast volume was 40 mL (no longer using postrelining contrast after confirming no endoleak on pre-relining angiography), and estimated blood loss, 40 mL. At this early time point, all of these procedures also appear to have successfully arrested expansion by diameter and volume. Pattern of sac behavior A pattern of sac behavior was apparent in the patients who underwent relining. After primary EVAR, all of the patients had at least one CT scan demonstrating that the preoperative expansion of the AAA had stopped. Most AAAs initially showed significant decreases in size, with expansion typically starting in the 6-month to 12-month postoperative time period. Once expansion began, it did not stop spontaneously in any of these AAAs that were expanding without endoleak. A typical case is illustrated in Fig 3, demonstrating changes in aneurysm sac diameter and volume over time, categorized into “phases” both before and after relining. Expansion phase The pattern shown in Fig 3 is also apparent when examining size changes over time for the entire cohort, as presented in Table II. As might be expected, the first five AAAs that were relined had a more rapid rate of expansion than the four more recent relining cases (significant by both diameter and volume, Table II). Thus there was a trend for the latter four relining cases to have a longer duration of expansion before enlarging sufficiently to merit repair (P = .08), but ultimately, a similar amount of diameter and volume enlargement before relining. Of the patients yet to be relined (including those expanding by volume and not diameter), the four with the longest duration of expansion are also enlarging at a slower rate than the initial five relining patients (Table II). These patients have not been relined because of less total expansion than the others or serious comorbidities (one is elderly and recently diagnosed with lung cancer). Once expansion began, it has not stopped spontaneously in any of these 13 patients expanding without endoleak over a substantial period of time. The rate of expansion has been relatively linear for all patients, although in many cases the rate of expansion has tended to increase slightly over time, as shown in Fig 3. Relining phase Of the three groups listed in Table II, the relining phase is characterized well for the five patients with >6 months follow-up. In this group, over the entire mean 26-month duration of expansion, aneurysms expanded by 6.0 ± 1 mm/y diameter and by 12% ± 2%/y by 3D volume, despite the absence of endoleak by multiple imaging techniques. At a mean of 16 months’ follow-up after relining with another Excluder, the mean diameter decrease was 2.0 mm/y and the mean volume decrease was 2.6%/y (P < .03 and P < .01, respectively, compared with expansion phase, Table II). The graphic appearance is similar to Fig 3, with relatively linear growth followed by shrinking or stabilization of size, or both. At the last CT measurement a mean 16 months after relining, all AAAs were smaller by diameter, volume, or both after relining, and exceeded SVS thresholds defining shrinkage in two of these five patients. No rupture, migration, endoleak, conversion, or other secondary intervention for endograft or aneurysm problems has been reported in any patient. Discussion  Multiple studies have suggested that sac expansion in the absence of endoleak is not uncommon after EVAR, especially with the original Excluder device.3, 4, 5, 7, 9, 12, 23, 24 This has been attributed to material permeability, leading to a modification of the Excluder graft fabric to make it essentially impermeable.8, 25 Recent work by our group has demonstrated that sac behavior after EVAR with this newer low-permeability Excluder endoprosthesis is significantly improved compared with the original-permeability Excluder endoprosthesis, and the low-permeability endografts may have eliminated this problem.8 The issue of sac expansion with the original Excluder remains, however, with 15,000 to 30,000 devices distributed worldwide3 and ≥33% of treated AAAs enlarging at 4 years.3, 5, 7 Notably, the original Excluder device has no greater incidence of endoleak than other devices,26 but as indicated in our series and others with the original-permeability Excluder device, expansion without endoleak is at least as common as expansion with endoleak.3, 7, 9 Treatment options for sac expansion after EVAR without apparent endoleak (endotension) are difficult, owing to the combination of an uncertain natural history for endotension and the treatment options. Before this report, the only treatment that appeared to be effective for endotension was conversion to open repair.9 Given the apparently low complication rate for expansion owing to endotension, open repair may be difficult to recommend for many patients from a risk/benefit standpoint. Less invasive options, such as laparoscopic fenestration with resection of the aneurysm wall, opening the abdomen with tight wrapping of the aneurysm wall around the graft, and repeated punctures with aspiration of fluid, have all been attempted, but ultimately were unsuccessful due to rapid recurrence.15 In this study, however, we found that sac expansion without endoleak after EVAR with the original-permeability Excluder can be arrested by relining the endograft with another Excluder endoprosthesis. It is important to note that our data indicate a pattern of initial sac shrinkage, then sac expansion, as shown in Fig 3. The importance of noting this shrinkage-or-stable phase is to demonstrate that good results at 6 or 12 months with the original-permeability Excluder do not imply freedom from late expansion, even in the absence of endoleak. The initial shrinkage is typically followed by a later expansion phase, with expansion typically starting between 12 and 36 months by diameter and 6 to 18 months by 3D volume, as noted in this series and larger series.7, 8, 27 Once expansion began, no patient in our series experienced spontaneous cessation of expansion over the long periods of follow-up summarized in Table II. Fortunately, this sac expansion appears to be arrested by relining the original permeability device with low-permeability Excluder endoprosthesis components. Nonetheless, the very nature of the original expansion pattern makes one hesitate to declare the relining procedure a permanent solution at this point. Whether the initial success will persist probably depends on the low-permeability fabric, which is dramatically different in tests that make the original material wet out immediately.8 It is encouraging that at a mean follow-up of 16 months (range, 7 to 24 months), none of the patients in our series have significant AAA expansion by diameter or volume. Notably, if the expansion rates before relining had persisted after relining, all five patients with expansion during 6 months of follow-up would already have exceeded the threshold for clinically significant expansion. When should relining of an original permeability endoprosthesis be considered? First, the AAA should demonstrate significant and persistent sac expansion on high-quality imaging studies, with expansion meeting the SVS definition of expansion on two successive studies ≥6 months apart. Second, additional investigation for endoleak should be performed. In a review of the explants for the Gore Pivotal trials, Kong et al9 found that eight of 16 conversions to open repair were for expansion without endoleak, but two of these were found to be missed endoleak (7 of 16 truly had endoleak).9 Thus, at least one study such as delayed-contrast CT, delayed contrast MR, or angiography should be performed to evaluate for slow or low-flow endoleak.20, 28, 29, 30 Three-dimensional CT volume studies are the most sensitive and accurate for detecting size change, but specialized MR techniques appear more sensitive than CT for detecting endoleak.7, 20, 27, 29, 30, 31, 32 For persistent expansion in the absence of endoleak by multiple modalities, endovascular relining should be considered. Logically, the relining procedure only needs to involve the components that are exposed to the aneurysm sac itself, as illustrated in Fig 2. With this strategy, any portion of the endograft in contact with the sac is relined using the minimal number of components and the smallest possible delivery system. We have used this strategy to treat nine patients, with minimal morbidity and percutaneous technique in most cases. Of course, some will argue that nothing needs to be done about aneurysms undergoing expansion in the absence of endoleak. Exploration of the aneurysm sac in these patients usually does not reveal blood, but rather a hygroma or gelatinous substance.1, 9, 10, 15 Anecdotal reports suggest rupture in these cases may be managed successfully without operation in selected patients, although at least one such rupture may have been associated with fatal bowel obstruction.10 Certainly, reports of significant complications from endotension are uncommon at this point. Despite this, at least one consensus conference of prominent practitioners in the field suggested that, “An enlarging aneurysm after EVAR mandates surgical or interventional treatment,” and a number of open conversions have been performed for this problem.9, 23 We believe sac expansion in the absence of endoleak merits consideration of intervention. Sac expansion is associated with problems, including rupture, pain, open operative exploration, or conversion to open aneurysm repair. Even if these events are rare, they can cause significant morbidity. Expansion without endoleak has caused a progressively decreasing seal zone within the proximal neck at least once in our series with the original Excluder device,8 and at least once in the 38 patients enlarging at 4 years in the Excluder Pivotal trial.7 In each case, this problem was only detected with serial 3D imaging, suggesting that this problem may be under-reported. Finally, even in the absence of complications, there is the cost of increased patient visits, time for patient counseling about the issue, more frequent imaging, and more extensive imaging. Conclusion  Our method of relining offers a minimally invasive and seemingly effective option in the surgical management of sac expansion in the absence of endoleak. Longer-term follow-up will demonstrate the efficacy of this strategy (or lack thereof), but if it remains successful in the long term, it offers the potential benefits of less frequent follow-up and reduction in the risk of complications such as rupture or loss of proximal fixation. Author contributions  Conception and design: MF Analysis and interpretation: PG, MF Data collection: PG, MF Writing the article: PG, MF Critical revision of the article: PG, MF Final approval of the article: PG, MF Statistical analysis: PG, MF Obtained funding: MF Overall responsibility: MF PG and MF contributed equally to this work.  We acknowledge the contributions of Jack Cronenwett, MD, for his help and guidance throughout the abstract and manuscript process. We also thank and acknowledge co-investigators Christopher Alessi, MD, Jack Cronenwett, MD, Brian Nolan, MD, Richard Powell, MD, Eva Rzucidlo, MD, Daniel Walsh, MD, Mark Wyers, MD, and Robert Zwolak, MD for contributing their clinical experience, care, and follow-up of patients within the study, as well as review of the manuscript. References  1. 1Matsumura JS, Brewster DC, Makaroun MS, Naftel DC. A multicenter controlled clinical trial of open versus endovascular treatment of abdominal aortic aneurysm. J Vasc Surg. 2003;37:262–271. Abstract |
Full-Text PDF (254 KB)
|
CrossRef
2. 2van Marrewijk CJ, Leurs LJ, Vallabhaneni SR, Harris PL, Buth J, Laheij RJFEUROSTAR collaborators. Risk-adjusted outcome analysis of endovascular abdominal aortic aneurysm repair in a large population: how do stent-grafts compare?. J Endovasc Ther. 2005;12:417–429. MEDLINE |
CrossRef
3. 3WL Gore & Associates. Excluder Bifurcated Endoprosthesis Annual Clinical Update. Available at: www.gore.com. Accessed, February 1, 2006. 4. 4Bertges DJ, Chow K, Wyers MC, Landsittel D, Frydrych AV, Stavropoulos W, et al. Abdominal aortic aneurysm size regression after endovascular repair is endograft dependent. J Vasc Surg. 2003;37:716–723. Abstract | Full Text |
Full-Text PDF (103 KB)
|
CrossRef
5. 5Cho J, Dillavou E, Rhee R, Makaroun M. Late abdominal aortic aneurysm enlargement after endovascular repair with the Excluder device. J Vasc Surg. 2004;39:1236–1241. Abstract | Full Text |
Full-Text PDF (277 KB)
|
CrossRef
6. 6van der Laan M, Prinssen M, Bertges D, Makaroun M, Blankensteijn J. Does the type of endograft affect AAA volume change after endovascular aneurysm repair?. J Endovasc Ther. 2003;10:406–410. MEDLINE |
CrossRef
7. 7Fillinger M. Three-dimensional analysis of enlarging aneurysms after endovascular abdominal aortic aneurysm repair in the Gore Excluder Pivotal clinical trial. J Vasc Surg. 2006;43:888–895. Abstract | Full Text |
Full-Text PDF (981 KB)
|
CrossRef
8. 8Tanski WJ, Fillinger MF. Outcomes of original and low permeability Gore Excluder endoprosthesis for endovascular aaa repair. J Vasc Surg. 2007;42:227–235. Abstract | Full Text |
Full-Text PDF (173 KB)
|
CrossRef
9. 9Kong LS, MacMillan D, Kasirajan K, Milner R, Dodson TF, Salam AA, et al. Secondary conversion of the Gore Excluder to operative abdominal aortic aneurysm repair. J Vasc Surg. 2005;42:631–638. Abstract | Full Text |
Full-Text PDF (190 KB)
|
CrossRef
10. 10Mennander A, Pimenoff G, Heikkinen M, Partio T, Zeitlin R, Salenius J-P. Nonoperative approach to endotension. J Vasc Surg. 2005;42:194–199. Abstract | Full Text |
Full-Text PDF (249 KB)
|
CrossRef
11. 11Thoo C, Bourke B, May J. Symptomatic sac enlargement and rupture due to seroma after open abdominal aortic aneurysm repair with polytetrafluoroethylene graft: implications for endovascular repair and endotension. J Vasc Surg. 2004;40:1089–1094. Abstract | Full Text |
Full-Text PDF (730 KB)
|
CrossRef
12. 12Gilling-Smith GL, Martin J, Sudhindran S, Gould DA, McWilliams RG, Bakran A, et al. Freedom from endoleak after endovascular aneurysm repair does not equal treatment success. Eur J Vasc Endovasc Surg. 2000;19:421–425. Abstract |
Full-Text PDF (150 KB)
|
CrossRef
13. 13Lipsitz E, Ohki T, Veith F, Suggs W, Wain R, Rhee S, et al. Delayed open conversion following endovascular aortoiliac aneurysm repair: partial (or complete) endograft preservation as a useful adjunct. J Vasc Surg. 2003;38:1191–1198. Abstract | Full Text |
Full-Text PDF (363 KB)
|
CrossRef
14. 14Risberg B, Delle M, Eriksson E, Klingenstierna H, Lonn L. Aneurysm sac hygroma: a cause of endotension. J Endovasc Ther. 2001;8:447–453. MEDLINE |
CrossRef
15. 15Risberg B, Delle M, Lonn L, Syk I. Management of aneurysm sac hygroma. J Endovasc Ther. 2004;11:191–195. MEDLINE |
CrossRef
16. 16Chaikof EL, Blankensteijn JD, Harris PL, White GH, Zarins CK, Bernhard VM, et al.Ad Hoc Committee for Standardized Reporting Practices in Vascular Surgery of The Society for Vascular Surgery/American Association for Vascular Surgery Reporting standards for endovascular aortic aneurysm repair. J Vasc Surg. 2002;35:1048–1060. Abstract | Full Text |
Full-Text PDF (102 KB)
|
CrossRef
17. 17Chaikof EL, Fillinger MF, Matsumura JS, Rutherford RB, White GH, Blankensteijn JD, et al. Identifying and grading factors that modify the outcome of endovascular aortic aneurysm repair. J Vasc Surg. 2002;35:1061–1066. Full Text |
Full-Text PDF (86 KB)
|
CrossRef
18. 18WL Gore & Associates. Gore Excluder Bifurcated Endoprosthesis Instructions for Use. Available at: http://www.goremedical.com/en/ifu/AH0312_EN.pdf. Accessed May 31, 2006. 19. 19Fillinger MF. Utility of spiral CT in the preoperative evaluation of patients with abdominal aortic aneurysms. Adv Vasc Surg. 1997;5:115–131. 20. 20Fillinger MF. Postoperative imaging after endovascular AAA repair. Semin Vasc Surg. 1999;12:327–338. MEDLINE 21. 21Wyers MC, Fillinger MF, Schermerhorn ML, Powell RJ, Rzucidlo EM, Walsh DB, et al. Endovascular repair of abdominal aortic aneurysm without preoperative arteriography. J Vasc Surg. 2003;38:730–738. Abstract | Full Text |
Full-Text PDF (291 KB)
|
CrossRef
22. 22Whittaker DR, Dwyer J, Fillinger MF. Prediction of altered endograft path during endovascular abdominal aortic aneurysm repair with the Gore Excluder. J Vasc Surg. 2005;41:575–583. Abstract | Full Text |
Full-Text PDF (348 KB)
|
CrossRef
23. 23Veith FJ, Baum RA, Ohki T, Amor M, Adiseshiah M, Blankensteijn JD, et al. Nature and significance of endoleaks and endotension: summary of opinions expressed at an international conference. J Vasc Surg. 2002;35:1029–1035. Abstract | Full Text |
Full-Text PDF (101 KB)
|
CrossRef
24. 24White GH. What are the causes of endotension?. J Endovasc Ther. 2001;8:454–456. MEDLINE |
CrossRef
25. 25Trocciola SM, Dayal R, Chaer RA, Lin SC, DeRubertis B, Ryer EJ, et al. The development of endotension is associated with increased transmission of pressure and serous components in porous expanded polytetrafluoroethylene stent-grafts: characterization using a canine model. J Vasc Surg. 2006;43:109–116. Abstract | Full Text |
Full-Text PDF (533 KB)
|
CrossRef
26. 26Sheehan MK, Ouriel K, Greenberg R, McCann R, Murphy M, Fillinger M, et al. Are type II endoleaks after endovascular aneurysm repair endograft dependent?. J Vasc Surg. 2006;43:657–661. Abstract | Full Text |
Full-Text PDF (210 KB)
|
CrossRef
27. 27Wever JJ, Blankensteijn JD, Th M, Mali WP, Eikelboom BC. Maximal aneurysm diameter follow-up is inadequate after endovascular abdominal aortic aneurysm repair. Eur J Vasc Endovasc Surg. 2000;20:177–182. Abstract |
Full-Text PDF (201 KB)
|
CrossRef
28. 28Fillinger M. Endovascular abdominal aortic aneurysm repair. In: Cronenwett J, Rutherford R editor. Decision making in vascular surgery. Philadelphia, PA: WB Saunders; 2001;p. 120–126. 29. 29Faries P, Agarwal G, Lookstein R, Bernheim J, Cayne N, Cadot H, et al. Use of cine magnetic resonance angiography in quantifying aneurysm pulsatility associated with endoleak. J Vasc Surg. 2003;38:652–656. Abstract | Full Text |
Full-Text PDF (106 KB)
|
CrossRef
30. 30van der Laan MJ, Bakker CJ, Blankensteijn JD, Bartels LW. Dynamic CE-MRA for endoleak classification after endovascular aneurysm repair. Eur J Vasc Endovasc Surg. 2006;31:130–135. Abstract | Full Text |
Full-Text PDF (235 KB)
|
CrossRef
31. 31Pitton MB, Schweitzer H, Herber S, Schmiedt W, Neufang A, Kalden P, et al. MRI versus helical CT for endoleak detection after endovascular aneurysm repair. AJR Am J Roentgenol. 2005;185:1275–1281.
CrossRef
32. 32van der Laan MJ, Bartels LW, Viergever MA, Blankensteijn JD. Computed tomography versus magnetic resonance imaging of endoleaks after EVAR. Eur J Vasc Endovasc Surg. 2006;32:361–365. Abstract | Full Text |
Full-Text PDF (217 KB)
|
CrossRef
Section of Vascular Surgery, Dartmouth-Hitchcock Medical Center, Lebanon, NH. Correspondence: Mark Fillinger, MD, Dartmouth-Hitchcock Medical Center, 1 Medical Center Dr, Lebanon, NH 03766.
Competition of interest: Dr Fillinger receives grant and research support from WL Gore, M2S, Medtronic, and Lombard. PII: S0741-5214(06)02261-0 doi:10.1016/j.jvs.2006.12.025 © 2007 The Society for Vascular Surgery. Published by Elsevier Inc. All rights reserved. | |
|