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At least 19 recordsLinked to original sources
PubMed2005

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.

Animals↗
PubMed2003

Increased recognition of type II endoleaks using a modified intraoperative angiographic protocol: implications for intermittent endoleak and aneurysm expansion.

Retrograde arterial perfusion of the aneurysm sac (type II endoleak) may complicate endovascular abdominal aortic aneurysm (AAA) repair and may lead to AAA expansion and rupture. Aneurysm expansion may also occur in the absence of a demonstrable endoleak. Current intraoperative assessment techniques may underrepresent the incidence of type II endoleaks. This study evaluated the incidence and impact of previously unrecognized type II endoleaks using a modified intraoperative angiographic protocol. A total of 391 patients undergoing endovascular AAA repair were evaluated. In 264 patients standard completion angiograms were performed. In 127 patients a modified angiographic protocol was used to visualize collateral lumbar and inferior mesenteric arteries as well as the aneurysm sac. The modified protocol uses digital subtraction fluoroscopy continuously for 60 sec after injections of 20 mL iodinated contrast both in the pararenal aorta and within the endovascular graft. Postoperative CT scans were performed at 1, 6, and 12 months and annually thereafter. The average age was 73.3 years; 324 patients were men and 67 were women. Mean follow-up was 11.4 months (range, 1-60 months). Type II endoleaks were documented intraoperatively in a significantly increased proportion of patients in whom the modified angiographic protocol was used: modified, 53/127 = 41% vs. standard, 17/264 = 6%; p < 0.001. No significant difference in the incidence of type II endoleaks was present on CT scan at 6 or 12 months after surgery (6 months: modified, 6/72 = 8% vs. standard, 10/159 = 6%, p = NS; 12 months: modified, 2/36 = 5% vs. standard, 6/138 = 4%, p = NS). Forty-six type II endoleaks resolved spontaneously (10 in the standard cohort, 36 in the modified cohort). One patient had a 10-mm increase in AAA diameter after spontaneous thrombosis of a type II endoleak 18 months postoperatively. One patient had a type II endoleak intraoperatively and at 12 months after surgery but the endoleak was absent at 1 and 6 months. Thirteen patients from the standard protocol cohort and 1 from the modified protocol cohort developed newly visualized type II endoleaks during follow-up. These findings may imply intermittent patency of the artery supplying the type II endoleak. The overall morbidity rate was 14% and the perioperative mortality rate was 1.8%. Retrograde (type II) endoleaks originating from AAA side branches occur intraoperatively more frequently than is currently recognized. Intermittent patency and thrombosis of these vessels may also occur and may contribute to AAA expansion. The full significance of these previously unrecognized endoleaks with respect to risk of aneurysm rupture remains to be definitively determined.

Aged↗
PubMed2005

Recurrent endoleak detection and measurement of aneurysm size with CTA after coil embolization of endoleaks.

PURPOSE: The optimal modality for following aneurysm size and detecting endoleaks after endovascular aneurysm repair (EVAR) remains controversial. Computed tomographic angiography (CTA) has been widely employed but can be limited by metal artifact from stents, which is exacerbated by embolization coils placed during the treatment of type 2 endoleaks. The authors assessed interobserver agreement of CTA for measuring aneurysm size and presence of recurrent endoleak in patients with prior coil embolization of type 2 endoleaks. MATERIALS AND METHODS: A total of 65 CTAs were retrospectively reviewed in a cohort of 27 patients (25 men; two women; mean age, 77.4 years) who had prior endoleak embolization after EVAR. Endoleak embolizations included transarterial (n=8) and translumbar (n=19) approaches. In each patient, maximal aneurysm diameter and presence/absence of recurrent endoleak was measured independently by two observers. Cohen's Kappa statistic was used to assess interobserver agreement, as well as paired two-tailed Student t tests for aneurysm diameter. RESULTS: Recurrent type 2 endoleaks were detected with CTA in eight of 27 patients (30%) and on 13 of 65 CTAs (20%). A high degree of correlation (98.5%) was also seen between the two observers for presence of endoleak (Kappa=0.95). Mean aneurysm diameter for the entire cohort correlated closely between both observers: 54.8 mm+/-1.1 for observer A and 54.9 mm+/-1.1 for observer B (P=.66). There was a disagreement between the readers of greater than 2 mm regarding aneurysm size in 13.8% of the CTAs (nine of 65 CTAs). CONCLUSION: Despite the presence of streak artifact on CTA following coil embolization of type 2 endoleaks, CTA remains a useful study for following patients. The presence of embolization coils does not prevent CTA measurement of aneurysm diameter and detection of recurrent endoleak with a high degree of interobserver agreement.

Aged↗
PubMed2002

Type II endoleak: transperitoneal sacotomy and ligation of side branch endoleaks responsible for aneurysm sac expansion.

PURPOSE: To demonstrate aneurysm sac expansion in the face of a type II endoleak and its treatment with open ligation of multiple side branch endoleaks. CASE REPORT: An 81-year-old patient had undergone elective endovascular repair of a 6.3-cm infrarenal abdominal aortic aneurysm in September 1999. Routine spiral computed tomographic angiography at 10 months disclosed a type II endoleak; the aneurysm sac diameter had grown to 7.4 cm. Selective angiography revealed multiple lumbar endoleaks and a patent inferior mesenteric artery. Laparotomy and sacotomy was performed, confirming the presence of pulsatile type II endoleaks, which were ligated successfully. The patient made a full postoperative recovery. CONCLUSIONS: Type II endoleaks may cause aneurysm expansion. Open repair of multiple type II endoleaks is feasible and may be useful where endovascular or laparoscopic techniques are at high risk of procedural failure, such as multiple endoleak channels.

Aged↗
PubMed2000

Endoleak as a predictor of outcome after endovascular aneurysm repair: AneuRx multicenter clinical trial.

OBJECTIVE: The purpose of this study was to determine whether evidence of blood flow in the aneurysm sac (endoleak) is a meaningful predictor of clinical outcome after successful endovascular aneurysm repair. METHODS: We reviewed all patients in Phase II of the AneuRx Multicenter Clinical Trial with successful stent graft implantation and predischarge contrast computed tomographic (CT) imaging. The clinical outcome of patients with evidence of endoleak was compared with the outcome of patients without evidence of endoleak. The CT endoleak status before hospital discharge at 6, 12, and 24 months was determined by each clinical center as well as by an independent core laboratory. Endoleak status at 1 month was assessed with duplex scanning examination or CT at each center without confirmation by the core laboratory. RESULTS: Centers reported endoleaks in 152 (38%) of 398 patients on predischarge CT, whereas the core laboratory reported endoleaks in 50% of these patients (P <.001). The center-reported endoleak rate decreased to 13% at 1 month. Follow-up extended to 2 years (mean, 10 +/- 4 months). One patient had aneurysm rupture and underwent successful open repair at 14 months. This patient had a Type I endoleak at discharge but no endoleak at 1 month or at subsequent follow-up times. There were no differences between patients with and patients without endoleak at discharge in the following outcome measures: patient survival, aneurysm rupture, surgical conversion, the need for an additional procedure for endoleak or graft patency, aneurysm enlargement more than 5 mm, the appearance of a new endoleak, or stent graft migration. Despite a higher endoleak rate identified by the core laboratory, neither the endoleak rate reported by the core laboratory nor the endoleak rate reported by the center at discharge was significantly related to subsequent outcome measures. Patients with endoleak at 1 month were more likely to undergo an additional procedure for endoleak than patients without endoleaks. Patients with Type I endoleaks at discharge and patients with endoleak at 1 month were more likely to experience aneurysm enlargement at 1 year. However, there was no difference in patient survival, aneurysm rupture rate, or primary or secondary success rate between patients with or without endoleak. Actuarial survival of all patients undergoing endovascular aneurysm repair was 96% at 1 year and was independent of endoleak status. Primary outcome success was 92% at 12 months and 88% at 18 months. Secondary outcome success was 96% at 12 months and 94% at 18 months. CONCLUSIONS: The presence or absence of endoleak on CT scan before hospital discharge does not appear to predict patient survival or aneurysm rupture rate after endovascular aneurysm repair using the AneuRx stent graft. Although the identification of blood flow in the aneurysm sac after endovascular repair is a meaningful finding and may at times indicate inadequate stent graft fixation, the usefulness of endoleak as a primary indicator of procedural success or failure is unclear. Therefore, all patients who have undergone endovascular aneurysm repair should be carefully followed up regardless of endoleak status.

Aortic Aneurysm, Abdominal↗
PubMed2006

Endoleaks after endovascular repair of thoracic aortic aneurysms.

OBJECTIVE: Endoleaks are one of the unique complications seen after endovascular repair of thoracic aortic aneurysms (TEVAR). This investigation was performed to evaluate the incidence and determinants of endoleaks, as well as the outcomes of secondary interventions in patients with endoleaks, after TEVAR. METHODS: Over a 6-year period, 105 patients underwent TEVAR in the context of pivotal Food and Drug Administration trials with the Medtronic Talent (n = 64) and Gore TAG (n = 41) devices. The medical and radiology records of these patients were reviewed for this retrospective study. Of these, 69 patients (30 women and 39 men) had follow-up longer than 1 month and were used for this analysis. The patients were evaluated for the presence of an endoleak, endoleak type, aneurysm expansion, and endoleak intervention. RESULTS: The mean follow-up in this patient cohort was 17.3 +/- 14.7 months (range, 3-71 months). Endoleaks were detected in 29% (20/69) of patients, of which 40% (8/20) were type I, 35% (7/20) were type II, 20% (4/20) were type III, and 5% (1/20) had more than one type of endoleak. Patients without endoleaks experienced greater aneurysm sac regression than those with endoleaks (-2.89 +/- 9.1 mm vs -0.13 +/- 7.2 mm), although this difference was not statistically significant (P = .232). All but 2 endoleaks (90%; 18/20) were detected on the initial postoperative computed tomographic scan at 30 days. Two endoleaks (10%; 2/20) developed late. The endoleak group had more extensive aneurysms with significantly larger aneurysms at the time of intervention (69.4 +/- 10.5 mm vs 60.6 +/- 11.0 mm; P = .003). Factors predictive of endoleak included male sex (P = .016), larger aneurysm size (P = .003), the length of aorta treated by stent grafts (P = .0004), and an increasing number of stents used (P < .0001). No open conversions were performed for treatment of endoleaks. Four (50%) of the eight type I endoleaks were successfully repaired by using endovascular techniques. None of the type II endoleaks was treated by secondary intervention. During follow-up, the maximum aneurysm diameter in the type II endoleak patients increased a mean of 2.94 +/- 7.2 mm (range, -4.4 to 17 mm). Spontaneous thrombosis has occurred in 29% (2/7) of the type II endoleaks. Patients with type III endoleaks experienced a decrease in mean maximal aneurysm diameter of 0.78 +/- 3.1 mm during follow-up. CONCLUSIONS: Endoleaks are not uncommon after TEVAR. Many type I endoleaks may be treated successfully by endovascular means. Short-term follow-up suggests that observational management of type II endoleaks is associated with continued sac expansion, and these patients should be monitored closely.

Adult↗
PubMed2004

Effectiveness of coiling in the treatment of endoleaks after endovascular repair.

BACKGROUND: Persistent endoleaks are a common problem following endovascular repair of abdominal aortic aneurysms, and the best method of treatment has been an issue of debate. Some experimental evidence has suggested that coiling may not be an effective method because it allows transmission of pressure across the coils with continued expansion of the sac. We reviewed our experience with endoleak coiling to assess the degree of clinical success of this treatment. METHODS: A retrospective review of patients with type I or type II endoleaks treated solely by coiling over a 7-year period (1997-2003) was performed. All endoleaks had been observed for at least 6 months prior to intervention to detect spontaneous resolution. All coils were delivered by selective catheterization of the endoleaks. For Type II endoleaks, the branches were all coiled at their junction with the sac when feasible and the endoleak cavity was packed. Clinical success was defined as cessation of endoleak on follow-up computed tomography as well as no further aneurysmal growth (> or =5mm minor axis). RESULTS: Twenty-eight patients had their endoleaks treated only with coils. There were 22 Ancure, 2 Excluder, 2 AneuRx, and 2 Lifepath endografts in this patient cohort. Procedural morbidity was 0%. Mean follow-up after coiling for all patients was 18 months (range, 1-60 months) while mean follow-up for patients with a type I endoleak was 24 months. Clinical success was achieved in 15 of 19 (79%) patients with type II endoleaks and 8 of 9 (89%) patients with type I. Three patients, all with type I endoleak, required more than 1 episode of coiling, while 2 others, both with type II lumbar endoleaks, required repeat angiography due to inability to access the leak during the first attempt. There were 2 proximal and 6 distal type I endoleaks (2 aortic, 6 iliac) successfully treated while the type II successes included 8 inferior mesenteric artery and 7 sole lumbar endoleaks. Five patients continued to show evidence of endoleak over time: 2 endoleaks were associated with aneurysm growth leading to conversion in 1 patient, 2 patients with type II endoleaks are stable, and the sole type I endoleak with continued perigraft flow has shown significant shrinkage of the sac and continues to be observed 18 months later. No ruptures were noted during follow-up. CONCLUSION: Coiling as the sole method of endoleak management may be a suitable treatment option in selected patients. Clinical success can be expected in over 80% of patients with type II and select type I endoleaks, with minimal morbidity.

Angioplasty↗
PubMed2003

Management of endoleak after endovascular aneurysm repair: cuffs, coils, and conversion.

OBJECTIVE: The effectiveness of endovascular treatment of abdominal aortic aneurysm (AAA) may be limited by persistent perfusion of the aneurysm sac (endoleak). Endoleak that results in persistent systemic pressurization of the aneurysm or in continued AAA expansion is believed to require treatment to prevent rupture. This report describes the results of three techniques used to treat endoleak. METHODS: Endovascular repair of AAA was performed in 597 patients between January 1996 and September 2002. Seventy-three endoleaks that required treatment developed in 70 patients (11.7%). These involved the graft attachment site (type I) or the graft junction site (type III) or originated from collateral side-branch vessels (type II) and were associated with an increase in aneurysm size. Endoleak type was confirmed at angiography in all cases. Average time between the initial endovascular procedure and endoleak treatment was 14.5 +/- 5.7 months. The techniques used for endoleak treatment were deployment of an endovascular extension graft or cuff (n = 44), coil embolization (n = 24,) and conversion to conventional open repair (n = 5). Configurations of endovascular grafts in which endoleak developed were bifurcated (n = 44), aortouniiliac (n = 15), and aortoaortic-tube (n = 11). Mean follow-up after endoleak treatment was 24.5 +/- 12.2 months (range, 1-60 months). RESULTS: Endovascular extension grafts or cuffs were used to treat 41 attachment site endoleaks and 3 graft junction endoleaks, with overall technical success rate of 97%. Embolic coils were used to treat 16 retrograde side-branch endoleaks and 8 attachment site endoleaks, with overall technical success rate of 87%. Conversion to open surgery was performed in 4 patients with attachment site endoleaks and 1 patient with a graft junction site endoleak, and was successful in all cases. After endoleak treatment, aneurysm size decreased (>5 mm) in 38% of patients, stabilized in 58% of patients, and increased (>5 mm) in 4% of patients. Major morbidity occurred in 7.0%, with no perioperative deaths. CONCLUSIONS: Endovascular extension grafts, coil embolization, and conversion to open surgery each may be used to effectively repair endoleak. Selection of the treatment method used is determined by the anatomic characteristics of the endoleak and the patient's ability to tolerate conventional repair. Conversion to open repair was uniformly successful. Deployment of an extension cuff was successful when complete closure of the endoleak was achieved. Embolic coils were effective for retrograde endoleaks and provided stabilization of AAA size in selected patients with attachment site endoleaks in limited follow-up.

Aged↗
PubMed2004

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.

Anastomosis, Surgical↗
PubMed2006

Fate of endoleaks detected by CT angiography and missed by color duplex ultrasound in endovascular grafts for abdominal aortic aneurysms.

PURPOSE: To analyze the clinical implications of endoleaks documented by computed tomographic angiography (CTA) and missed by color duplex ultrasound (CDU). METHODS: During a recent 5-year period, 232 patients underwent endovascular aortic reconstruction (EVAR) and were followed according to a protocol that included CTA and CDU at 1 month and every 6 months thereafter. CTA was the gold standard for determining the presence of endoleaks. The size of the AAA sac at the latest postoperative follow-up was compared to the preoperative size and correlated to the type of endoleak and clinical outcome. This study analyzed only patients with endoleak documented by CTA and CDU and specifically analyzed the outcome of patients with false negative CDU studies for endoleaks. RESULTS: Thirty-nine endoleaks were documented in 35 (15%) of 232 patients using CTA. Four patients had both early and late endoleaks. The mean follow-up was 25 months (range 1-64). CDU was more helpful in detecting type I endoleaks than type II endoleaks (89% versus 58%, p<0.05). There were 18 (46%) type I endoleaks (12 early, 6 late) detected by CTA; 16 (89%) of these were detected by CDU (2 late endoleaks missed). Nineteen (49%) type II endoleaks (16 early, 3 late) were diagnosed using CTA, 11 (58%) of which were detected by CDU (6 early and 2 late missed). Of the 2 (5%) early type IV endoleaks found on CTA, 1 (50%) was missed by CDU. Overall, CDU failed to identify endoleak in 11 (28%) of 39 endoleaks [2 late type I, 8 type II (6 early, 2 late), and 1 early type IV]. Consequences to treatment occurred in 2 (20%): 1 type I endoleak required treatment and 1 type II endoleak would have missed treatment. CONCLUSION: CDU has a lower sensitivity in detecting endoleak, particularly type II; therefore, EVAR surveillance should not be based solely on CDU. Although a significant number of type II endoleaks resolved spontaneously, intervention can be offered for type II endoleaks if associated with an increasing sac size.

Aged↗
PubMed2003

Intrasac flow velocities predict sealing of type II endoleaks after endovascular abdominal aortic aneurysm repair.

PURPOSE: The purpose of this study was to determine whether intrasac spectral Doppler flow velocities can predict whether or not a type II endoleak will spontaneously seal and to relate intrasac flow to preoperative branch vessel anatomy. METHODS: Between October 1996 and June 2002, 265 patients with abdominal aortic aneurysms underwent endovascular repair. Patients with less than 24 months of follow-up and type I endoleaks were excluded. Type II endoleaks were confirmed with duplex scan and computed tomographic angiography. Two groups were identified: 14 patients with sealed endoleaks (<6 months) without intervention and 16 patients with persistent endoleaks greater than 6 months and without resolution. Spectral Doppler flow velocities were recorded from endoleaks within the aneurysm sac. RESULTS: The two groups were similar in age, demographics, and aneurysm morphology. The mean follow-up times were 29.9 +/- 7.9 months for sealed endoleaks and 30.2 +/- 8.6 months for persistent endoleaks (P = not significant). Spectral Doppler velocities were significantly lower in patients with sealed endoleaks compared with persistent endoleaks (75.5 +/- 78.8 cm/s versus 138.2 +/- 36.2 cm/s; P <.01). Patients with sealed endoleaks and low (<100 cm/s) intrasac Doppler velocities had significantly fewer patent inferior mesenteric arteries (43% versus 81%; P <.01), a smaller inferior mesenteric artery (5.6 +/- 1.8 mm versus 7.2 +/- 1.3 mm; P <.01), and fewer paired lumbar arteries (1.3 +/- 0.8 versus 2.4 +/- 0.6; P <.0001) compared with those with persistent endoleaks and high (>100 cm/s) intrasac flow velocities. Three patients with sealed endoleaks had Doppler velocities of 200 cm/s or greater. However, the diameter of the inferior mesenteric artery in these patients was 4 mm or less with no visualized lumbar arteries before surgery. Aneurysm diameter(-4.6 +/- 5.6 mm) and volume (-0.9 +/- 45.2 mL) decreased in patients with sealed endoleaks. Aneurysm diameter (1.8 +/- 4.9 mm) and volume (18.5 +/- 33.9 mL) increased slightly in patients with persistent endoleaks (P <.05). No ruptures or conversions occurred in any patient. Secondary interventions to treat type II endoleaks were unsuccessful in six of 16 patients (38%) with persistent endoleaks. CONCLUSION: Intrasac Doppler velocities can be used to predict whether a type II endoleak will spontaneously seal. High-velocity type II endoleaks are related to preoperative large branch vessel diameter and number and are resistant to endovascular treatment.

Aortic Aneurysm, Abdominal↗
PubMed2004

Late-onset type II endoleaks and the incidence of secondary intervention.

Type II endoleaks are a recognized complication of endoluminal treatment of abdominal aortic aneurysms. In order to better understand the natural history of type II endoleaks and their influence on secondary procedures, we examined our experience with patients who developed isolated type II endoleaks 6 months or more after their original procedure. We conducted a retrospective review of patients who underwent endoluminal repair of infrarenal abdominal aortic aneurysms with bifurcated endoluminal devices at a single institution from June 1996 to June 2000. Endoleak surveillance was performed on all patients by using a defined CT angiogram protocol. Patients with definitive and isolated type II endoleaks on CT angiogram were identified. Patients with indeterminate endoleaks or a combination of different types of endoleaks were excluded. Data were analyzed on the basis of early (<6 months) or late occurrence of isolated type II endoleak. Fifty patients were identified with isolated type II endoleaks. Of these patients, 20 (40%) had endoleaks discovered before the 6-month follow-up interval whereas the majority (60%) had new type II leaks discovered at least 6 months after their initial procedure. The timing of endoleak occurrence did not significantly influence the rate of spontaneous endoleak resolution between the early- (<6 months) and late-onset (>6 months) groups, which was nearly identical (40% vs. 43%). Ten patients in the early group and seven of the late-onset group required secondary intervention for treatment of type II endoleak (50% vs. 23%; NS). Three patients in the early group underwent surgical conversion (vs. 0 patients in the late-onset group). The mortality rate was not significantly different between groups (15% vs. 7%). Most isolated type II endoleaks in this patient population occurred 6 months or more after initial endoluminal repair of infrarenal abdominal aortic aneurysm. Timing of type II endoleak occurrence did not significantly affect the rates of spontaneous resolution or mortality. Although differences were observed in the number of patients receiving secondary interventions, these findings did not reach statistical difference. All patients who required surgical conversion had early type II endoleaks. There were no observed ruptures in patients with increased aneurysm size treated with secondary intervention or those with stable aneurysm volumes who were followed without intervention. The continued development of type II endoleaks beyond the perioperative period supports the need for continued endoleak surveillance.

Aged↗
PubMed2005

Use of CT angiography to classify endoleaks after endovascular repair of abdominal aortic aneurysms.

PURPOSE: Accurate endoleak detection and classification is critical for the follow-up of patients who have undergone endovascular aneurysm repair (EVAR). This determination is often made with computed tomography angiography (CTA). This investigation was performed to determine the accuracy of CTA in the classification of endoleaks in patients who have undergone EVAR. MATERIALS AND METHODS: Thirty-six patients with endoleaks underwent both CTA and conventional contrast digital subtraction angiography (DSA) to determine endoleak etiology. Two independent radiologists determined the source of the endoleak based on a retrospective review of the CTA. The results of the CTA-based endoleak classification were compared to the reference standard, contrast DSA. RESULTS: There was agreement regarding endoleak classification between CTA and DSA on 86% of the patients (31 of 36 patients). Correlation between the CTA reading of the two readers was 94% (34 of 36 patients), yielding a kappa statistic of 0.8. In three patients, the CTA reading incorrectly classified endoleaks as type 2 when the endoleaks were actually type 1 endoleaks on DSA. One patient was incorrectly classified as having a type 1 endoleak on CTA when it was a type 2 endoleak on DSA. Finally, one patient had a type 1 endoleak on DSA that was incorrectly classified as a type 3 endoleak on CTA. The change in CTA endoleak classification based on the DSA resulted in a significant change in patient management in four of the 36 patients (11%). CONCLUSIONS: Endoleak classification based on CTA correlates fairly well with DSA findings. However, optimal endoleak management requires performance of selective angiograms with DSA to classify endoleaks that are detected on CTA.

Angiography↗
PubMed2006

Are type II endoleaks after endovascular aneurysm repair endograft dependent?

PURPOSE: Most clinical end points after endovascular aneurysm repair (EVAR) are endograft-specific, but type II endoleaks have been assumed to be an unavoidable consequence of the repair method and independent of the type of endograft used. Some recent data have suggested that the rate of type II endoleaks may also be graft-dependent. We reviewed a large clinical experience with six endografts to determine the behavior of type II endoleaks and whether they are graft-specific. METHODS: All elective EVAR cases from five university institutions from 1996 to 2003 were retrospectively analyzed. Endografts used in <50 patients were excluded. Endoleaks were diagnosed and classified from contrast-enhanced computed tomography (CT) scans by the treating surgeons. Results of angiography and interventions for endoleaks were tracked. The rate of type II endoleaks was compared among endografts at 1, 6, and 12 months, and yearly thereafter. Statistical significance was defined as P < .05. RESULTS: During the study period, 1909 patients underwent elective EVAR and had an adequate imaging follow-up at one of the specified time points. At 1 month, the overall rate of type II endoleak was 14.0% (range, 9.8% to 25.2%.) The Excluder had a significantly higher incidence of type II endoleaks at 1 month but was similar to most other grafts during longer follow-up. At 6 months, the overall rate of type II endoleak was 16.3% (range, 8.3% to 16.8%). The Talent and Lifepath had an apparent lower initial rate of type II leaks, but this was only significant for the Talent at 6 months compared with Excluder, Zenith, and Ancure, and at 1 year compared with Excluder and Zenith. No graft had a long-term statistically significant difference in the rate of type II endoleak formation. Intervention rates varied by institution and graft type but in general were quite low. Of 25 successful interventions (Ancure, 12; AneuRx, 8; Excluder, 2; Lifepath, 2; Zenith, 1; Talent, 0), 21 were performed during the first year. Interim spontaneous resolution, defined as a negative CT scan after a CT positive for endoleak, was high, especially in the first year. Resolution of type II endoleaks occurred in 54 (33%) of 164 between 1 and 6 months, in 37 (33%) of 112 between 6 and 12 months, in 20 (35%) of 57 from 12 to 24 months, and in 5 (20%) of 25 between 24 and 36 months. The various grafts had a nearly identical pattern, but the rates were highest for the Talent. Late appearing endoleaks, defined as a positive CT after a negative CT, were frequent. At 6 months, 44 (30%) of 147 type II endoleaks were newly diagnosed. The rates were 37 (35%) of 107 at 12 months, 15 (27%) of 56 at 2 years and 5 (25%) of 20 at 3 years. No conversions to open repair for type II endoleaks were noted in the first 4 years. The thrombus burden could not be determined in this analysis. CONCLUSIONS: Type II endoleaks occur in nearly 15% of patients treated by EVAR. The early incidence varies only slightly with graft type. The long-term prevalence and clinical significance are masked by different treatment patterns, spontaneous resolution, newly evident endoleaks, and aneurysm size at initial treatment.

Adult↗
PubMed2003

Use of cine magnetic resonance angiography in quantifying aneurysm pulsatility associated with endoleak.

OBJECTIVE: Persistent aneurysm perfusion or endoleak is associated with pulsatility of abdominal aortic aneurysm (AAA) after endovascular repair. However, the resultant pulsatile change in aneurysm diameter may be difficult to quantify, and therefore its significance is unknown. In this study cine magnetic resonance angiography (MRA) was used to quantify aneurysm wall motion during the cardiac cycle and to correlate it with the presence and type of endoleak. METHODS: Cine MRA was performed in 16 patients undergoing endovascular repair of AAA. A 1.5 T magnet and post-processing with GEMS 4.0 Fiesta computerized video image analysis software were used to calculate maximum aortic diameter during systole and diastole. Changes in aortic diameter were determined from these measurements. Cine MRA was performed on aneurysms before treatment and in patients with and without endoleak after endovascular repair. Type of endoleak was confirmed at angiography in all cases. Four patients had antegrade (type I) endoleak, and eight patients had retrograde (type II) endoleak; no endoleak was present in four patients. Endovascular grafts with stent support throughout the entire length of the graft (Talent) were used in all cases (14 bifurcated grafts, 2 tube grafts). RESULTS: Cine MRA demonstrated significantly greater wall motion and resultant change in aneurysm diameter in patients with type I endoleak compared with patients without endoleak (type I, 2.14 +/- 1.28 mm vs no endoleak, 0.12 +/- 0.09 mm, P =.001). Change in aneurysm diameter in patients with type II endoleak was not significantly greater than in patients with no endoleak (type II, 0.26 +/- 0.21 mm vs no endoleak, 0.12 +/- 0.09 mm, P = NS). Untreated aneurysms demonstrated the greatest change in diameter during the cardiac cycle (3.51 +/- 0.79 mm). CONCLUSION: Cine MRA may be used to accurately quantify AAA wall motion before and after endovascular stent-graft treatment. The extent of change in diameter corresponds to the type of endoleak, with antegrade (type I) endoleak generating greater pulsatile change in diameter than retrograde-collateral (type II) endoleak or no endoleak. Cine MRA may provide a noninvasive means of assessing the success of endovascular treatment of AAA. Further studies will be necessary to confirm the utility and efficacy of cine MRA in postoperative assessment of endovascular aneurysm repair.

Aged↗
PubMed2001

[Diagnosis and management of endoleak after endovascular repair of abdominal aortic aneurysm].

OBJECTIVE: To determine the diagnosis and management of endoleak after endovascular repair of abdominal aortic aneurysm (AAA). METHODS: We analysed retrospectively the data of 37 cases of infrarenal AAA treated by endovascular repair and investigated the reasons, managements, results and prognosis of endoleaks. RESULTS: Of 13 patients with endoleak at stent-graft deployment, 6 developed type I endoleak, 3 type II endoleak, 2 type III endoleak, 1 type IV endoleak, and 1 unknown reason. Type I and III endoleaks disappeared after management with additional techniques. The primary endoleak rate was 13.5%(5/37). Three sealed endoleak, 2 persistent endoleaks and 2 secondary endoleaks were found during follow up. The late endoleak rate was 10.8% (4/37). CONCLUSIONS: Endoleak is a chief complication after endovascular repair of infrarenal AAA. The influencing factors for endoleak include neck morphology, distance, angulation, calcification, stent-graft selection and side branching arteries. Additional procedure and follow up are very important. Techniques to find endoleak include CTA, Duplex and MRA after operation. Endoleak with enlarged aneurysm should be treated actively.

Aortic Aneurysm, Abdominal↗