Type II endoleak after endovascular abdominal aortic aneurysm repair: a conservative approach with selective intervention is safe and cost-effective

OBJECTIVES: The conservative versus therapeutic approach to type II endoleak after endovascular repair of abdominal aortic aneurysm (EVAR) has been controversial. The purpose of this study was to evaluate the safety and cost-effectiveness of the conservative approach of embolizing type II endoleak only when persistent for more than 6 months and associated with aneurysm sac growth of 5 mm or more. METHODS: Data for 486 consecutive patients who underwent EVAR were analyzed for incidence and outcome of type II endoleaks. Spiral computed tomography (CT) scans were reviewed, and patient outcome was evaluated at either office visit or telephone contact. Patients with new or late-appearing type II endoleak were evaluated with spiral CT at 6-month intervals to evaluate both persistence of the endoleak and size of the aneurysm sac. Persistent (>or=6 months) type II endoleak and aneurysm sac growth of 5 mm or greater were treated with either translumbar glue or coil embolization of the lumbar source, or transarterial coil embolization of the inferior mesenteric artery. RESULTS: Type II endoleaks were detected in 90 (18.5%) patients. With a mean follow-up of 21.7 +/- 16 months, only 35 (7.2%) patients had type II endoleak that persisted for 6 months or longer. Aneurysm sac enlargement was noted in 5 patients, representing 1% of the total series. All 5 patients underwent successful translumbar sac embolization (n = 4) or transarterial inferior mesenteric artery embolization (n = 4) at a mean follow-up of 18.2 +/- 8.0 months, with no recurrence or aneurysm sac growth. No patient with treated or untreated type II endoleak has had rupture of the aneurysm. The mean global cost for treatment of persistent type II endoleak associated with aneurysm sac growth was US dollars 6695.50 (hospital cost plus physician reimbursement). Treatment in the 30 patients with persistent type II endoleak but no aneurysm sac growth would have represented an additional cost of US dollars 200000 or more. The presence or absence of a type II endoleak did not affect survival (78% vs 73%) at 48 months. CONCLUSIONS: Selective intervention to treat type II endoleak that persists for 6 months and is associated with aneurysm enlargement seems to be both safe and cost-effective. Longer follow-up will determine whether this conservative approach to management of type II endoleak is the standard of care.     

Select early type IA endoleaks after endovascular aneurysm repair will resolve without secondary intervention

Objective

Although it is traditionally considered ominous, the natural history of early proximal attachment site endoleaks (IA) after endovascular aneurysm repair (EVAR) is not well known. Our aim was to identify risk factors for persistent type IA endoleaks and to determine their effect on long-term outcomes after EVAR.

Freedom from endoleak after endovascular aneurysm repair does not equal treatment success.

OBJECTIVE: To determine whether freedom from endoleak after endovascular repair of abdominal aortic aneurysm (EVAR) is a reliable guide to freedom from persistent or recurrent pressurisation of the aneurysm sac (endotension) and therefore freedom from risk of rupture. PATIENTS AND METHODS: The records of 55 patients followed for more than 3 months after EVAR were reviewed to correlate the presence or absence of endoleak on contrast-enhanced CT and/or angiography with changes in maximum aneurysm diameter (DMAX). RESULTS: in 22 (40%) patients there was no significant change in DMAX during follow-up. In 21 of these no endoleak was observed on CT or angiography. One patient developed a secondary side-branch endoleak which remains under observation. In 18 (33%) patients, DMAX decreased during follow-up. Thirteen of these remained free of endoleak. Four patients developed secondary endoleaks which were treated by secondary intervention. One patient with persistent primary endoleak suffered fatal aneurysm rupture three days before planned intervention. DMAX increased in 15 (27%) patients. In only five of these could an endoleak be identified on CT and/or angiography. One primary side-branch endoleak persists following failed embolisation. Four secondary endoleaks have been corrected by secondary intervention. Four of the remaining 10 patients died suddenly from unknown cause. All had DMAX greater than 65 mm at last follow-up. One patient underwent late conversion, which suggested continued pressurisation through thrombus at the site of a "sealed" primary proximal endoleak. Two patients are scheduled to undergo embolisation of patent side-branches revealed only by Levovist enhanced Duplex scanning and three patients remain under observation. CONCLUSION: Freedom from endoleak on conventional imaging incorrectly suggested freedom from endotension in 10 (18%) of our patients. Follow-up after endovascular repair must include regular measurement of DMAX and/or aneurysm sac volume to identify those patients who remain at risk of rupture.     

First experience in human beings with a permanently implantable intrasac pressure transducer for monitoring endovascular repair of abdominal aortic aneurysms

OBJECTIVES: Endovascular stent graft repair of abdominal aortic aneurysms (AAAs) prevents rupture by excluding the aneurysm sac from systemic arterial pressure. Current surveillance protocols after endovascular aneurysm repair (EVAR) follow secondary markers of sac pressurization, namely, endoleak and sac enlargement. We report the first clinical experience with the use of a permanently implantable, ultrasound-activated remote pressure transducer to measure intrasac pressure after EVAR. METHODS: Over 7 months, 14 patients underwent EVAR of an infrarenal abdominal aortic aneurysm with implantation of an ultrasound-activated remote pressure transducer fixed to the outside of the stent graft and exposed to the excluded aortic sac. Twelve patients received modular bifurcated stent grafts, and 2 patients received aortouniiliac devices. Intrasac pressures were measured directly with an intravascular catheter and by the remote sensor at stent-graft deployment. Follow-up sac pressures were measured with a remote sensor and correlated with systemic arterial pressure at every follow-up visit. Mean follow-up was 2.6 +/-1.9 months. RESULTS: Excellent concordance was found between catheter-derived and transducer-derived intrasac pressssure intraoperatively. Pulsatile waveforms were seen in all functioning transducers at each evaluation interval. One implant ceased to function at 2 months of follow-up. In 1 patient a type I endoleak was diagnosed on 1-month computed tomography (CT) scans; 3 type II endoleaks were observed. Those patients with complete exclusion of the aneurysm on CT scans had a significant difference in systemic and sac systolic pressures initially (P <.001) and at 1 month (P <.001). Initial sac diastolic pressures were higher than systemic diastolic pressures (P <.001). The ratio of systemic to sac systolic pressure increased over time in those patients with complete aneurysm exclusion ( P <.001). Four of 6 patients with no endoleak and greater than 1-month follow-up had diminution of sac systolic pressure to 40 mm Hg or less by 3 months. CONCLUSION: This is the first report of a totally implantable chronic pressure transducer to monitor the results of EVAR in human beings. Aneurysm exclusion leads to gradual diminution of sac pressure over several months. Additional clinical follow-up will be necessary to determine whether aneurysm sac pressure monitoring can replace CT in the long-term surveillance of patients after EVAR.     

Is a type II endoleak after EVAR a harbinger of risk? Causes and outcome of open conversion and aneurysm rupture during follow-up.

OBJECTIVE: There is still debate whether type II endoleaks represent a risk for the patient after EVAR. Treatment policies vary from fairly conservative to active intervention. In this analysis risk factors for type II endoleak and adverse events during follow-up were assessed. In addition, risk factors and causes for conversion to open repair and for rupture post-EVAR were studied. METHODS: The data of 3595 patients, who underwent operation between 1996 and 2002 in 114 European institutions that collaborated in the EUROSTAR Registry, were assessed. To accurately assess the influence of type II endoleaks patients with type I, III and combined endoleaks were excluded from the present study cohort. RESULTS: A combined adverse outcome event consisting of aneurysmal growth, transfemoral reintervention, and transabdominal secondary procedures (including laparoscopic branch vessel clipping) occurred in 55% in patients with type II endoleak at 3 years, compared to 15% in patients without any endoleak (p<0.0001). Conversion to open repair or post-EVAR rupture was not significantly associated with type II endoleaks. An independent association of device migration and expansion of the aneurysm with late conversion was observed. The cumulative incidence of aneurysm rupture at 3 years of follow-up was 1.2% for an annual rate of 0.4%. Variables that significantly and independently correlated with rupture were size of the aneurysm at preoperative measurement and device migration during follow-up. CONCLUSION: Endoleak type II may not be harmless as it was more frequently associated with enlargement of the aneurysm and reinterventions. Large aneurysms and migration of the device were the main risk factors for rupture. The clinical implications of these findings may involve more frequent surveillance visits for patients with type II endoleak. Aneurysm expansion is a clear indication for reintervention. Patients with large aneurysms, 65 mm or larger, may also benefit from a more comprehensive surveillance schedule.     

Secondary interventions following endovascular repair of abdominal aortic aneurysm

Endovascular aneurysm repair (EVAR) of the abdominal aortic aneurysms is an attractive alternative to open surgery with significantly improved perioperative outcomes. However, EVAR is accompanied by a higher rate of graft-related complications and secondary interventions. Therefore, life-long surveillance and management of secondary treatment is essential for successful EVAR. Endoleaks are one of the most crucial problems after EVAR. Persistent endoleaks are classified into five types and its management depends on the type and severity. Most persistent endoleaks are detectable by contrast-enhanced computed tomography; however, in some cases, two different endoleak types may coexist. Determining whether an endoleak requires any treatment or not is an important consideration. Most if not all type I and III endoleaks require prompt and definitive secondary treatment. While type II endoleaks are most commonly encountered during follow-up, not all type II endoleaks require invasive treatment. When secondary treatment is required, it can be treated endovascularly in most cases, even if there is no endoleak. Following EVAR, due to the decompression of the sac, the integrity of the aneurysmal wall strength reduces. Therefore, sudden sac expansion/rupture may occur when an endoleak is encountered following a period of complete aneurysmal exclusion. If diagnosed promptly most late complications can be treated in a less invasive manner, but it could lead to catastrophic event if it is missed. Therefore, adequate and life-long radiographic follow-up is as important as the appropriate patient and device selection as well as the EVAR procedure itself.     

Type II endoleaks: predictable,preventable, and sometimes treatable?

OBJECTIVE: The purpose of this study was to evaluate the effect of preoperative coil embolization of lumbar and inferior mesenteric arteries on the incidence of type II endoleak after endovascular abdominal aortic aneurysm repair. METHODS: The subjects were consecutive patients who underwent EVAR between January 1996 and January 2001. Patent aortic side branches were identified with preprocedural spiral computed tomographic scanning and calibrated angiography. Coil embolization was performed before EVAR. Patients were followed up with plain radiographs and ultrasound and dual phase spiral computed tomographic scans. Digital subtraction angiography was performed when endoleak was suspected. The outcome measures were the incidence of type II endoleaks and changes in maximum aortic sac diameter (Dmax). RESULTS: Forty patients underwent EVAR, with a median duration of follow-up of 24 months (range, 3 to 48 months). Before surgery, the inferior mesenteric artery was patent in 16 patients (45%) and the lumbar arteries in 21 patients (53%). Inferior mesenteric artery embolization was successful in 13 of 16 patients (81%). Lumbar embolization was attempted in 13 patients and was successful in eight (62%). During EVAR, successful sac exclusion was achieved in 38 patients (95%). None of the patients who underwent embolization before EVAR had type II endoleak develop, eight of 13 patients (62%) with patent lumbar arteries had endoleaks develop (P =.006), and three of these patients subsequently underwent successful coil embolization. Type II endoleak was associated with a 2.0-mm median increase in Dmax (P =.045). A 3.0-mm median reduction in Dmax was seen in the absence of type II endoleak (P =.002). CONCLUSION: Type II endoleaks are predictable, preventable, and sometimes treatable. Significant sac shrinkage occurs in the absence of lumbar endoleak but not in the presence of type II endoleak.     

Predicting aneurysm enlargement in patients with persistent type II endoleaks

OBJECTIVE: The clinical significance of type II endoleaks is not well understood. Some evidence, however, indicates that some type II endoleaks might result in aneurysm enlargement and rupture. To identify factors that might contribute to aneurysm expansion, we analyzed the influence of several variables on aneurysm growth in patients with persistent type II endoleaks after endovascular aortic aneurysm repair (EVAR). METHODS: In a series of 348 EVARs performed during a 10-year period, 32 patients (9.2%) developed type II endoleaks that persisted for more than 6 months. Variables analyzed included those defined by the reporting standards for EVAR (SVS/AAVS) as well as other endoleak characteristics. Univariate, receiver operating characteristic curve, and Cox regression analyses were used to determine the association between variables and aneurysm enlargement. RESULTS: The median follow-up period was 26.5 months (range, 6-88 months). Thirteen patients (41%) had aneurysm enlargement by 5 mm or more (median increase in diameter, 10 mm), whereas 19 (59%) had stable or shrinking aneurysm diameter. Univariate and Cox regression analyses identified the maximum diameter of the endoleak cavity, ie, the size of the nidus as defined on contrast computed tomography scan, as a significant predictor for aneurysm enlargement (relative risk, 1.12; 95% confidence interval, 1.04-1.19; P =.001). The median size of the nidus was 23 mm (range, 13-40 mm) in patients with aneurysm enlargement and 8 mm (range, 5-25 mm) in those without expansion (Mann-Whitney U test, P <.001). Moreover, receiver operating characteristic curve and Cox regression analyses showed that a maximum nidus diameter greater than 15 mm was particularly associated with an increased risk of aneurysm enlargement (relative risk, 11.1; 95% confidence interval, 1.4-85.8; P =.02). Other risk factors including gender, smoking history, hypertension, need of anticoagulation, aneurysm diameter, type of endograft used, and number or type of collateral vessels were not significant predictors of aneurysm enlargement. CONCLUSIONS: In patients with persistent type II endoleaks after EVAR, the maximum diameter of the endoleak cavity or nidus is an important predictor of aneurysm growth and might indicate the need for more aggressive surveillance as well as earlier treatment.     

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.     

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.     

Long-term outcomes after endovascular abdominal aortic aneurysm repair: the first decade

OBJECTIVE: The proper role of endovascular abdominal aortic aneurysm repair (EVAR) remains controversial, largely due to uncertain late results. We reviewed a 12-year experience with EVAR to document late outcomes. METHODS: During the interval January 7, 1994 through December 31, 2005, 873 patients underwent EVAR utilizing 10 different stent graft devices. Primary outcomes examined included operative mortality, aneurysm rupture, aneurysm-related mortality, open surgical conversion, and late survival rates. The incidence of endoleak, migration, aneurysm enlargement, and graft patency was also determined. Finally, the need for reintervention and success of such secondary procedures were evaluated. Kaplan-Meier and multivariate methodology were used for analysis. RESULTS: Mean patient age was 75.7 years (range, 49-99 years); 81.4% were male. Mean follow-up was 27 months; 39.3% of patients had 2 or more major comorbidities, and 19.5% would be categorized as unfit for open repair. On an intent-to-treat basis, device deployment was successful in 99.3%. Thirty-day mortality was 1.8%. By Kaplan-Meier analysis, freedom from AAA rupture was 97.6% at 5 years and 94% at 9 years. Significant risk factors for late AAA rupture included female gender (odds ratio OR, 6.9; P = 0.004) and device-related endoleak (OR, 16.06; P = 0.009). Aneurysm-related death was avoided in 96.1% of patients, with the need for any reintervention (OR, 5.7 P = 0.006), family history of aneurysmal disease (OR, 9.5; P = 0.075), and renal insufficiency (OR, 7.1; P = 0.003) among its most important predictors. 87 (10%) patients required reintervention, with 92% of such procedures being catheter-based and a success rate of 84%. Significant predictors of reintervention included use of first-generation devices (OR, 1.2; P < 0.01) and late onset endoleak (OR, 64; P < 0.001). Current generation stent grafts correlated with significantly improved outcomes. Cumulative freedom from conversion to open repair was 93.3% at 5 through 9 years, with the need for prior reintervention (OR, 16.7; P = 0.001) its most important predictor. Cumulative survival was 52% at 5 years. CONCLUSIONS: EVAR using contemporary devices is a safe, effective, and durable method to prevent AAA rupture and aneurysm-related death. Assuming suitable AAA anatomy, these data justify a broad application of EVAR across a wide spectrum of patients.     

Velocities of type II endoleaks on Doppler ultrasonography predict outcome

ObjectiveWe sought to determine whether flow velocities measured using Doppler ultrasonography after endovascular aortic aneurysm repair (EVAR) can predict for resolution of type II endoleaks without intervention. We also assessed the relationship of the flow velocities to sac growth and the need for intervention. We hypothesized that hemodynamic properties suggesting low flow velocity would predict for resolution of type II endoleaks.MethodsThe data from 23 patients with type II endoleaks identified on Doppler ultrasonography after EVAR from January 2014 to December 2017 were retrospectively analyzed. The 23 patients with type II endoleaks were split into two groups. Group 1 included the 13 patients with resolved endoleaks or shrinking sac size and group 2, the 10 patients with an increasing sac size or those requiring intervention to seal the endoleak because of an increased sac size. We analyzed the velocities of the endoleak nidus.ResultsDoppler ultrasound velocities were significantly lower in patients with resolved type II endoleaks and those with a shrinking aneurysm sac size compared with those demonstrating an increase in aneurysm sac size (42.6 ± 25.2 cm/s vs 219.5 ± 84.1 cm/s; P < .0001). Of the 10 patients in group 2, nine had required intervention with either translumbar embolization or transarterial embolization, with only two experiencing complete resolution of the type II endoleak, despite the intervention. All patients in group 2 had had ≥1 duplex ultrasound scan with endoleak nidus velocities >100 cm/s. In contrast, no patient in group 1 had had any duplex ultrasound scan with endoleak nidus velocities >100 cm/s.ConclusionsThe Doppler ultrasound velocities of type II endoleaks might be able to predict for spontaneous resolution of type II endoleaks or increased sac growth. Type II endoleaks on Doppler ultrasonography with endoleak nidus velocities >100 cm/s can persistent, even with attempted treatment.     

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.     

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. Presented at the Thirteenth Annual Winter Meeting of the Peripheral Vascular Surgery Society, Snowmass, CO, January 31-February 2, 2003. Faries et al. Intraoperative angiographic protocol for type II endoleaks     

Volumetric analysis of effectiveness of embolization for preventing type II endoleaks following endovascular aortic aneurysm repair

ObjectiveThe presence of endoleak was associated with the failure of endovascular aortic aneurysm repair (EVAR) treatment. The key to eliminating type II endoleak has shifted from reintervention to prevention. This study aimed to evaluate the effectiveness and safety of applying fibrin sealant to prevent type II endoleak in conjunction with EVAR.MethodsAll patients with abdominal aortic aneurysm who underwent EVAR from June 2019 to July 2021 were reviewed. Patients were grouped as Group A: standard EVAR with preemptive embolization and Group B: standard EVAR alone. The primary endpoint was the incidence of type II endoleak. The secondary endpoints were aneurysm sac regression, the inferior mesenteric artery patency, the numbers of patent lumbar arteries, and all-cause mortality.ResultsA total of 104 patients were included in Group A, and 116 were included in Group B. Technical success rate was 100%. The overall incidence of type II endoleak in Group A was significantly lower than that in Group B (4.8% vs 19.0%). The mean time of freedom from type II endoleak was 22.71 months for Group A (95% confidence interval, 21.59-23.83 months) and 19.89 months for Group B (95% confidence interval, 18.08-21.70 months). The Kaplan-Meier estimate of freedom from type II endoleak showed a significantly longer duration of freedom from type II endoleak in Group A (81.0% vs 95.2%). Group A showed a continuous sac regression tendency. In Group B, the sac volume decreased within 12 months but increased by 3.07 cm³ at 24 months. No complications were noted in both groups.ConclusionsNonselective preemptive embolization with porcine fibrin sealant during EVAR was safe and effective in preventing type II endoleak in the short and mid-term. Preemptive embolization can lead to a significantly higher sac regression rate. Larger patient populations and longer follow-ups with randomized control designed trials are expected to verify the long-term effectiveness and safety of preemptive embolization in preventing type II endoleak.     

The significance and management of different types of endoleaks

Development of endovascular abdominal aortic aneurysm repair (EVAR) has been accompanied by previously unencountered complications. The most challenging but least understood of these complications is the incomplete seal of the endovascular graft (endoleak), a phenomenon that has a variety of causes. An important consequence of endoleakage may be persistent pressurization of the aneurysm sac, which may ultimately lead to post-EVAR rupture. Data of 110 European centers were recorded in a central database (EUROSTAR). Patient, anatomic characteristics, and operative and device details were correlated with the occurrence of different types of endoleaks. Outcome events during follow-up, particularly expansion of the aneurysm, incidence of conversion to open repair, and post-EVAR rupture were assessed in the different categories of endoleaks and in a group of patients without any endoleak. Type I and III endoleak were associated with an increased frequency of open conversions or risk of rupture of the aneurysm. Device-related endoleaks also correlated with an increased need for secondary interventions. These types of endoleaks need to be treated without delay, and when no other possibilities are present, an open conversion to avert the risk of rupture should be considered. Type II endoleaks do not pose an indication for urgent treatment. However, they may not be harmless, because there was a frequent association with enlargement of aneurysm and reinterventions. Our findings suggest that more frequent surveillance examinations are indicated than in patients without collateral endoleak. The indication for intervention is primarily dictated by documented expansion of the aneurysm.     

Static sac size with a type II endoleak post-endovascular abdominal aortic aneurysm repair: surveillance or embolization?

A best evidence topic was written according to a structured protocol. The question addressed was whether embolization is superior to surveillance for a type II endoleak associated with a static sac size post-endovascular abdominal aortic aneurysm repair (EVAR). Four hundred and sixty-one papers were identified, of which 10 papers presented the best evidence to answer the clinical question. The author, journal, date and country of publication, patient group studied, study type, and relevant outcomes and results are tabulated. A review of the available literature suggests that most type II endoleaks are innocuous and will seal spontaneously during the long-term follow-up, even when they persist for more than 6 months. An analysis of the large European Collaborators on Stent-Graft Techniques for Aortic Aneurysm Repair (EUROSTAR) registry that includes prospective data on 2463 patients from 87 European hospitals showed that type II endoleaks were not associated with an increased risk of rupture; this correlates well with the large single-centre studies included in this review. Based on the available evidence, we conclude that the management of most isolated type II endoleaks should be conservative-with close radiological follow-up-even when persistent, with intervention restricted to theoese associated with sac enlargement >5?mm over a 6-month period or >10?mm when compared with pre-EVAR diameter.     

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.     

Long-term freedom from aneurysm-related mortality remains favorable after endovascular abdominal aortic aneurysm repair in a 15-year multicenter registry

ObjectiveEndovascular aneurysm repair (EVAR) has become the preferred approach to abdominal aortic aneurysm (AAA) because of lower early morbidity and mortality than open repair. However, the ability of EVAR to prevent long-term aneurysm-related mortality (ARM) has been questioned in light of recent trial data. We have updated our long-term EVAR experience in a large multicenter registry to further examine this issue.MethodsBetween 2000 and 2010, 1736 patients with AAA underwent EVAR in a large integrated regional healthcare system. We extended follow-up in this previously reported cohort through 2015 and identified predictors associated with ARM and need for major reintervention. The primary outcome was ARM. Secondary outcomes were all-cause mortality, delayed aneurysm rupture, major adverse event, major reintervention, sac growth of more than 5 mm, and type I or III endoleak. End points were analyzed for the whole cohort and compared for patients who underwent EVAR during the earlier (2000-2005) and latter (2006-2010) halves of the enrollment period to assess for changes in outcomes over time of repair.ResultsThe overall follow-up rate was 96.3%, and median follow-up was 5.5 years (interquartile range, 2.8-7.7 years). During the study period, 958 patients died, of whom 63 experienced ARM (6.6%). Overall crude rate of freedom from ARM was 96.4%. Delayed aneurysm rupture was seen in 1.3% (n = 23), with a median time to event of 4.1 years (interquartile range, 1.7-7.2 years). Major adverse events occurred in 12.4% of patients, and major reintervention was performed in 10.3%. Overall freedom from major adverse event or major reintervention was seen in 84.0%. Significant predictors of ARM included female sex, age 80 to 89 years, urgent EVAR, and any major reintervention. The unadjusted cumulative probability of all-cause survival was significantly higher in the late group than the early group at 5 years (66.8% vs 59.8%; P = .01, log-rank test); however, freedom from ARM at 5 years was not significantly different (96.5% and 97.1%, respectively; P = .67, log-rank test).ConclusionsOur results demonstrate favorable long-term freedom from major adverse event or major reintervention after EVAR and extremely low rates of ARM and delayed rupture. Our findings support EVAR as a safe, long-term solution for managing patients with AAA and provide insight into clinical parameters that can be used to stratify patients' post-EVAR surveillance and need for reintervention.