The effect of endograft relining on sac expansion after endovascular aneurysm repair with the original-permeability Gore Excluder abdominal aortic aneurysm endoprosthesis

OBJECTIVE: Endovascular 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. METHODS: Patients who demonstrated sac expansion (>or=5 mm diameter, >or=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. RESULTS: AAA 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. CONCLUSIONS: It 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.     

Device-specific aneurysm sac morphology after endovascular aneurysm repair: evaluation of contemporary graft materials

OBJECTIVE: This study analyzed device-specific aneurysm sac morphology after endovascular aneurysm repair (EVAR) with low-permeability devices. METHODS: Between September 2004 and May 2006, 122 patients were treated with EVAR. Three different devices were implanted: 47 Zenith (Cook, Indianapolis, Ind), 46 AneuRx (Medtronic, Santa Rosa, Calif) with Resilient Dacron Graft Material, and 29 Excluder (W. L. Gore & Associates, Flagstaff, Ariz) with low-porosity polytetrafluoroethylene (PTFE). Patients were followed up at 1, 6, and 12 months and then biannually with computed tomography (CT) angiography. Standard axial two-dimensional CT measurements were obtained and compared with preoperative imaging. The preoperative scan served as a baseline, and the minor axis diameter, measured at the largest axial cut of the abdominal aortic aneurysm, was compared with the same measurement at follow-up. RESULTS: Patient age, sex, and preoperative aneurysm morphology were similar among groups. Patients receiving the Zenith endograft had a significantly larger neck diameter; however, there was no difference in the neck length between groups. The rate of type II endoleaks was similar for the Zenith (17%), AneuRx (17%), and Excluder (14%). At 1, 6, 12, and 18 months, all three grafts were associated with sac shrinkage. The resulting decreases in mean aneurysm size at 18 months and corresponding shrinkage were Zenith, 11%, 6.4 +/- 1.8 mm; AneuRx, 18.9%, 12.7 +/- 2.7 mm; and the Excluder, 5.5%, 3.3 +/- 0.9 (P < .05). The sac size in the 19 patients with a type II endoleak decreased 8.06% compared with a 15.43% decrease in sac size in patients without endoleak at 6 months. No significant sac expansion > or =5 mm has been observed among any of the groups to date. CONCLUSIONS: Sac regression with all devices appears to have been favorably influenced by the new generation of graft materials and is improved compared with published reports of older generation graft materials for the AneuRx and Excluder. However, there is a trend toward greater sac regression with devices using Dacron vs PTFE. The relationship of aneurysm morphology and long-term effects on aortic stent grafts is yet to be determined.     

Abdominal aortic aneurysm size regression after endovascular repair is endograft dependent

OBJECTIVE: This study was performed to determine whether abdominal aortic aneurysm (AAA) regression is different with various endografts after endovascular repair. METHODS: A four-center retrospective review of size change after endovascular AAA repair was performed. Consecutive patients with at least 1-year follow-up and available imaging studies were included. Three hundred ninety patients received either the Ancure, AneuRx, Excluder, or Talent endograft. AAA size and endoleak status were recorded from computed tomography (CT) scans at the initial postoperative follow-up visit and at 1 and 2 years thereafter. AAA size was defined as the minor axis of the infrarenal aorta on the largest axial section on the two-dimensional CT scan. A change in AAA size of 0.5 cm or greater from baseline was considered clinically significant. The effect of initial size, endoleak, and type of endograft on AAA regression was analyzed. RESULTS: Mean baseline size was significantly greater with Talent endografts and smaller with Excluder endografts. Clinically significant regression in AAA size occurred in nearly three fourths of patients with Ancure and Talent endografts at 2 years. Regression in AAA size was less frequent with the AneuRx (46%) and Excluder (44%) devices. Initial size, endoleak, and endograft type were significant predictors of regression at multivariate analysis at 1 year. However, by 2 years only endograft type was still an independent predictor of AAA shrinkage. CONCLUSIONS: Long-term morphologic changes after endovascular aneurysm repair depend on endograft type.     

Symptomatic sac enlargement and rupture due to seroma after open abdominal aortic aneurysm repair with polytetrafluoroethylene graft: Implications for endovascular repair and endotension

OBJECTIVE: We report 5 patients in whom a symptomatic perigraft seroma developed within the aortic sac, without vascular endoleak, after open repair of an abdominal aortic aneurysm (AAA) with a polytetrafluoroethylene (PTFE) graft. We also discuss possible relationships of this phenomenon to endovascular repair of AAAs. PATIENTS AND METHODS: Over 18 years, 1156 patients underwent repair of an AAA by one of the authors (B.M.B.). Of these, 1084 underwent open repair, 256 with PTFE grafts. Five patients in the PTFE group (2.3%) returned at a mean of 4.5 years with acute abdominal or back pain and enlargement of the aortic sac. Mean diameter of the aneurysms was 5.9 cm preoperatively and 8.1 cm at readmission. There was no evidence of vascular endoleak on computed tomography scans, but 1 patient had a retroperitoneal hematoma. RESULTS: Laparotomy in 4 patients disclosed a seroma containing firm rubbery gelatinous material under tension, histologically identified as amorphous eosinophilic material containing thrombus and degenerate blood cells in all cases. Rupture of the sac was confirmed in the patient with a retroperitoneal hematoma. The sac contents were evacuated and the integrity of the underlying grafts and anastomoses was confirmed before sac reduction, with imbricating sutures, and closure was performed. One patient died at 8 months of an unrelated cause; the other 3 patients remain well at mean follow-up of 12 months. The fifth patient received conservative treatment and remains asymptomatic 3 years after acute presentation. CONCLUSIONS: These findings of sac enlargement without vascular endoleak after open AAA repair are reminiscent of sac enlargement in the absence of endoleak after endovascular AAA repair. This has been referred to as endotension. The comparatively benign outcome in 5 patients with symptomatic sac enlargement, including 2 patients with rupture, after open AAA repair provides data to support a circumspect approach to endotension, especially in patients with asymptomatic disease, which has been reported as occurring in almost half of patients who received a PTFE Excluder endograft.     

Endovascular conversion with femorofemoral bypass as a treatment of endotension and aneurysm sac enlargement

We report a case of a patient treated with a Gore Excluder endograft for AAA in November 2003 with subsequent aneurysm sac enlargement in the absence of an identified endoleak. The patient had a Type I endoleak treated with a Palmaz stent at the neck and later developed a Type II endoleak treated with translumbar coil embolization. This was successful with absence of pressure in the sac after the procedure and stable aneurysm size over the next nine months. Surveillance of the patient with both CT and ultrasound then revealed an increase in the aortic sac diameter in the absence of endoleak. A Cook Zenith converter was used to reline this PTFE endograft. Subsequently, imaging showed aneurysm sac shrinkage. This is a report of endotension with aneurysm expansion following Gore Excluder placement which was treated successfully with a dacron endograft.     

Open surgical treatment of aneurysmal sac expansion following endovascular abdominal aneurysm repair: solution for an unresolved clinical dilemma

The advantages of endovascular aneurysm repair (EVAR) are probably related to the avoidance of the three major physiological insults associated with open abdominal aortic aneurysm (AAA) repair: laparotomy, aortic cross-clamping and ischemia reperfusion injury. Continuing aneurysm expansion indicates a failure to exclude the AAA from the circulation. We describe our experience with open surgery of post-EVAR sac expansion. A consecutive series of 68 EVAR patients was followed up. Endovascular and minimally invasive procedures were the initial treatment option. Failure of these attempts to curtail AAA sac expansion or type 2 large endoleaks (EL) resulted in opening of the aneurysm sac. The procedure includes positioning of a deflated occlusion balloon proximal to the stent graft (SG). Laparotomy with opening of the eneurysm sac was then performed. The thrombus was removed and backbleeding vessels oversewn. The aneurysm sac was then plicated over the SG. Four patients (5.9%) were diagnosed as having either persistent large type 2 EL or sac enlargement. In all patients the procedure was accomplished successfully. One patient died from acute myocardial infarction perioperatively. Three patients recovered uneventfully and follow-up computed tomography confirmed the absence of endoleak and a disappearance of the AAA. We believe that whenever EVAR fails to exclude the aneurysm from the circulation, open exploration without graft replacement should be considered.     

Compliance of abdominal aortic aneurysms before and after stenting with tissue doppler imaging: evolution during follow-up and correlation with aneurysm diameter

Usual imaging after endovascular aneurysm repair (EVAR) of abdominal aortic aneurysm (AAA) consists of AAA diameter monitoring and endoleak detection. Among additional predictor parameters previously proposed to help clinicians in better identifying subgroups of AAA still at risk of rupture, AAA wall motion after EVAR has been studied, but its value was not clearly established. Tissue Doppler imaging (TDI) is an ultrasonographic modality which allows wall motion measurements along an arterial segment. The aim of the current study was to analyze AAA wall motion with TDI before and after EVAR and to describe its evolution in patients with more than 1 month of follow-up. Twenty-five consecutive patients undergoing EVAR between February 2005 and June 2007 gave informed consent to be prospectively investigated with the TDI system before EVAR and at each visit during follow-up. The mean (SD) follow-up was 13.7 (9.7) months. Maximum mean segmental dilation (MMSD), segmental compliance, dilation at maximum diameter, pressure strain elastic modulus (Ep), and stiffness were compared between three periods (before stenting, before discharge, and at last follow-up), and their relation with AAA diameter was analyzed. A significant decrease in AAA compliance was immediately observed after successful EVAR and remained stable during later follow-up. On the other hand, AAA diameter progressively decreased along time and was statistically lower at the last control compared to the initial value. MMSD, segmental compliance, and dilation at maximum diameter were positively related to AAA diameter. This means that the larger the AAA diameter after stenting, the higher the value for these parameters can be expected. On the contrary, percentage of AAA diameter decrease and percentage of MMSD decrease were not related after successful EVAR. There was no parallelism between loss in compliance and diameter decrease along time, and there is not a unique pattern of AAA diameter and compliance evolution after EVAR. Even if comparison between patients without and with endoleak was weak due to the small sample of the latter group (five patients with endoleak), compliance tended to be greater in case of endoleak. AAA wall motion after successful EVAR reflects complex interactions between all the components of the stented aneurysm which evolve over time, including true compliance of the aneurysm wall itself; intra-aneurysm sac pressure with possible different effects for peak, mean, and pulse pressures; remodeling of the thrombus; stiffness characteristics of the graft; and systemic pressure. Combining simultaneous MMSD records with actual intrasaccular pressure measurements in patients with and without endoleak would improve our understanding of the clinical pulsatility mechanism within AAA after EVAR.     

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.     

Intermediate Follow-Up after Endovascular Aneurysm Repair: Can We Forgo CT Scanning in Certain Patients?

Current recommendations for follow-up after endovascular repair of abdominal aortic aneurysms (EVAR) include yearly computed tomographic (CT) scans after the first year. We hypothesize that this is unnecessary for patients who have aneurysm sacs that are stable or shrinking at 1 year and no evidence of endoleak. To explore this hypothesis, we reviewed the records of all patients undergoing EVAR at our institution who were implanted with grafts that are currently commercially available and had a minimum of 18 months' follow-up. Of 415 patients who underwent EVAR over an 8-year period, 93 met the entry criteria. At a mean follow-up of approximately 3 years, secondary interventions were required in 13%, 39%, and 25% of patients undergoing EVAR with Zenith, AneuRx, and Excluder devices, respectively, and secondary interventions after the first year were required in 3%, 22%, and 8% of such grafts, respectively. Seventy-one patients (76%) had aneurysm sacs that were stable or shrinking at 1 year and no endoleak. Only two of these patients subsequently required reintervention. Both patients had AneuRx grafts, and both problems could have easily been identified without CT scanning. Our data support the hypothesis that patients who meet these criteria at 1 year are unlikely to have problems that cannot be identified by ultrasound and/or clinical evaluation alone and, thus, that CT scans are not necessary after this point, especially in patients with Zenith or reengineered Excluder devices.     

Persistent type 2 endoleak after endovascular repair of abdominal aortic aneurysm is associated with adverse late outcomes

OBJECTIVE: Type 2 endoleak occurs in up to 20% of patients after endovascular aneurysm repair (EVAR), but its long-term significance is debated. We reviewed our experience to evaluate late outcomes associated with type 2 endoleak. METHODS: During the interval January 1994 to December 2005, 873 patients underwent EVAR. Computed tomography (CT) scan assessment was performed < or =1 month of the operation and at least annually thereafter. Sequential 6-month CT scan follow-up was adopted for those patients with persistent type 2 endoleaks, and reintervention was limited to those with sac enlargement >5 mm. Study end points included overall survival, aneurysm sac growth, reintervention rate, conversion to open repair, and abdominal aortic aneurysm (AAA) rupture. Preoperative variables and anatomic factors potentially associated with these endpoints were assessed using multivariate analysis. RESULTS: We identified 164 (18.9%) patients with early (at the first follow-up CT scan) type 2 endoleaks. Mean follow-up was 32.6 months. In 131 (79.9%) early type 2 endoleaks, complete and permanent leak resolution occurred < or =6 months. Endoleaks persisted in 33 patients (3.8% of total patients; 20.1% of early type 2 endoleaks) for >6 months. Transient type 2 endoleak (those that resolved < or =6 months of EVAR) was not associated with adverse late outcomes. In contrast, persistent endoleak was associated with several adverse outcomes. AAA-related death was not significantly different between patients with and without a type 2 endoleak (P = .78). When evaluating patients with no early endoleak vs persistent endoleak, freedom from sac expansion at 1, 3, and 5 years was 99.2%, 97.6%, and 94.9% (no leak) vs 88.1%, 48.0%, and 28.0% (persistent) (P < .001). Patients with persistent endoleak were at increased risk for aneurysm sac growth vs patients without endoleak (odds ratio [OR], 25.9; 95% confidence interval [CI] 11.8 to 57.4; P < .001). Patients with a persistent endoleak also had a significantly increased rate of reintervention (OR, 19.0; 95% CI, 8.0 to 44.7); P < .001). Finally, aneurysm rupture occurred in 4 patients with type 2 endoleaks. Freedom from rupture at 1, 3, and 5 years for patients with a persistent type 2 endoleak was 96.8%, 96.8%, and 91.1% vs 99.8%, 98.5%, and 97.4% for patients without a type 2 endoleak. Multivariate analysis demonstrated persistent type 2 endoleak to be a significant predictor of aneurysm rupture (P = .03). CONCLUSIONS: Persistent type 2 endoleak is associated with an increased incidence of adverse outcomes, including aneurysm sac growth, the need for conversion to open repair, reintervention rate, and rupture. These data suggest that patients with persistent type 2 endoleak (>6 months) should be considered for more frequent follow-up or a more aggressive approach to reintervention.     

高危复杂腹主动脉瘤腔内修复术临床分析

目的 评估应用多种腔内技术治疗高危复杂腹主动脉瘤的可行性.方法 2001年1月至2010年12月,共138例腹主动脉瘤患者接受腹主动脉腔内修复术(EVAR),其中9例患者为高危复杂性腹主动脉瘤.男性8例,女性1例,年龄26～87岁,平均67岁.其中2例近肾腹主动脉假性动脉瘤,5例近肾腹主动脉瘤,1例腹主动脉瘤合并双髂总动脉瘤及左侧髂内动脉瘤,1例EVAR术后右髂内动脉瘤.所采用的腔内技术包括:主动脉支架开窗技术和扇形技术2例,烟囱技术5例,球囊辅助下髂内动脉瘤腔内治疗1例和球囊辅助反转支架技术1例.结果 所有腔内技术均获得成功.术中支架释放后即刻发现内漏4例,其中1例患者为Ⅰ型和Ⅲ型内漏,经大动脉球囊扩张后内漏消失;2例Ⅰ型内漏,其中1例行弹簧栓栓塞成功,另1例行近端裸支架成功.1例Ⅱ型内漏,经随访瘤腔直径未增大,未处理.随访4～79个月,平均25.9个月.无动脉瘤破裂,动脉瘤瘤体直径均有不同程度的缩小.随访过程中7例患者的靶血管(肾动脉、肠系膜上动脉和髂内动脉)均保持通畅.1例髂内动脉重建支架术后18个月血栓形成,但无盆腔缺血等症状.结论 对于不能耐受手术的高危复杂腹主动脉瘤患者,选择合适的腔内技术可以增加EVAR术的成功率,近、中期效果满意.     

Rupture of abdominal aortic aneurysm previously treated by endovascular stentgraft

We describe a case of abdominal aortic aneurysm (AAA) with rupture 16 months after treatment by an endograft. A 76-year-old patient on Coumadin after aortic valve replacement had initially successful exclusion by stentgraft. There was no evidence of an endoleak seven months after stentgraft repair, although a computed tomography scan detected an enlargement of the aneurysm sac. Sixteen months after initial endograft surgery, rupture of the aneurysm occurred and we performed open emergency surgery. We treated the aneurysm by conventional technique, and the patient survived the rupture. This case emphasized the fact that patients after endograft AAA repair require a close follow-up. An expansion of the aneurysm sac after the procedure should signal failed exclusion, even if a computed tomography scan does not demonstrate an endoleak. Anticoagulation can be an important factor in failure after endoluminal graft treatment. Supravisceral aortic cross clamping is helpful in dealing with a stented aorta. (J Vasc Surg 1998;28:184-7.)     

Fenestrated and branched stent-grafting after previous surgery provides a good alternative to open redo surgery.

OBJECTIVE: To present our experience using fenestrated and branched endoluminal grafts for Para-anastomotic aneurysms (PAA) following prior open aneurysm surgery, and after previous endovascular aneurysm repair (EVAR) complicated by proximal type I endoleak. METHODS: Fenestrated and/or branched EVAR was performed on eleven patients. Indications included proximal type I endoleak after EVAR and short infrarenal neck (n=4), suprarenal aneurysm after open AAA (n=4), distal type I endoleak after endovascular TAA (n=1), proximal anastomotic aneurysm after open AAA (n=1), and an aborted open AAA repair due to bleeding around a short infrarenal neck. RESULTS: The operative target vessel success rate was 100% (28/28) with aneurysm exclusion in all patients. Mean hospital stay was 6.0 days (range 2-12 days, SD 3.5 days). Thirty day mortality was 0%. All cause mortality during 18 months mean follow-up (range 5-44 months, SD 16.7 months) was 18% (2/11) with no deaths from aneurysm rupture. Cumulative visceral branch patency was 96% (27/28) at 42 months. Average renal function remained unchanged during the follow-up period. CONCLUSIONS: Our report highlights the potential of fenestrated and branched technology to improve re-operative aortic surgical outcomes. The unique difficulties of increased graft on graft friction hindering placement, short working distance, and increased patient co-morbidities should be recognized.     

Total robotic ligation of inferior mesenteric artery for type II endoleak after endovascular aneurysm repair

We present a case of totally robotic ligation of the inferior mesenteric artery (IMA) for treatment of a persistent endoleak from the IMA into the aneurysm sac after endovascular aneurysm repair (EVAR). An 84-year-old male underwent EVAR with a Gore Excluder stent graft for an asymptomatic infrarenal abdominal aortic aneurysm. Follow-up computed tomographic (CT) scan showed persistent type II endoleak from the IMA, with progressive enlargement of the aneurysm sac from 5 to 6.1 cm over an 18-month period. In this case, the patient underwent ligation of the IMA using the da Vinci Surgical System for the treatment of retrograde flow into the aneurysm sac. The total operating time was 249 min; of this, the robotic assistance time was approximately 180 min. No intraoperative complications occurred. The estimated blood loss was 50 mL and the urine output 650 mL. The patient was extubated immediately after the procedure and tolerated a regular diet the following day. He was discharged home with a urinary catheter on postoperative day 2. CT scan postoperatively and at 3-month follow-up demonstrated an occluded IMA and stabilization of the aneurysm sac size.     

Nonoperative approach to endotension

OBJECTIVE: The necessity of operative treatment of endotension after endovascular grafting of abdominal aortic aneurysms (endovascular aneurysm repair; EVAR) is under debate. The proposed causes of endotension and related treatment protocols are controversial. We report the outcome of a nonoperative approach to five patients with endotension after EVAR. METHODS: From February 1997 to August 2004, 160 patients who underwent EVAR of an infrarenal abdominal aortic aneurysm were evaluated for the incidence of endotension. According to the endovascular protocol, plain radiographs, spiral computed tomography, and angiography were performed before and after surgery for follow-up. To detect endotension, spiral computed tomography was performed by using a delayed imaging technique after the infusion of contrast medium. Endotension was defined as an aneurysm sac enlargement after EVAR without evidence of endoleak. Aneurysm sac rupture was defined as discontinuity of the calcific rim of the aneurysmal sac and the presence of intra-aneurysmal fluid outside the sac. RESULTS: We found five (3.1%) patients with endotension. Three of these experienced aneurysmal sac rupture. Only one of the three was underwent operation on experiencing sudden intestinal occlusion due to intra-abdominal adhesions. This patient had no intra-abdominal or retroperitoneal bleeding or hematoma but died after intensive care as a result of non-aneurysm-related problems. Four patients with endotension are still being closely followed up according to our surveillance protocol, and they are doing clinically well. After rupture, clear shrinking of the aneurysm sac was seen in two patients. CONCLUSIONS: Endotension after EVAR may cause subsequent aneurysm rupture. Endotension is evidently not associated with endoleak I to III provided that the endovascular graft is maintained in appropriate position and that free endovascular flow is observed. We propose to consider a nonoperative approach in the clinically asymptomatic patient with aneurysm enlargement after EVAR if endoleak is excluded by well-performed imaging techniques.     

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.     

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.     

Successful treatment of endotension and aneurysm sac enlargement with endovascular stent graft reinforcement

Abdominal aortic aneurysm (AAA) enlarges after successful endovascular repair because of endoleak, which is persistent blood flow within the aneurysm sac. In the absence of detectable endoleak, AAA may still expand, in part because of endotension, which is persistent pressurization within the excluded aneurysm. We report three patients who underwent successful endovascular AAA repair using the Excluder device (W. L. Gore & Associates, Flagstaff, Ariz). Although their postoperative surveillance showed an initial aneurysm regression, delayed aneurysm enlargement developed in all three, apparently due to endotension. Endovascular treatment was performed in which endograft reinforcement with a combination of aortic cuff and iliac endograft extenders were inserted in the previously implanted stent grafts. The endograft reinforcement procedure successfully resulted in aneurysm sac regression in all three patients. Our study underscores the significance of increased graft permeability as a mechanism of endotension and delayed aneurysm enlargement after successful endovascular AAA repair. In addition, our cases illustrate the feasibility and efficacy of an endovascular treatment strategy when endotension and aneurysm sac enlargement develops after endovascular AAA repair.     

Postoperative initial 2-day blood pressure management facilitates the shrinkage of abdominal aortic aneurysm after endovascular aneurysm repair by reducing the incidence of type II endoleak

Objective

The aim of this study was to evaluate the effect of initial 2-day blood pressure management (BPM) after endovascular aneurysm repair (EVAR) for the incidence of subsequent type II endoleak (T2E) and shrinkage of abdominal aortic aneurysm (AAA) sac diameter.

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.