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PubMed2002

The incidence and natural history of type I and II endoleak: a 5-year follow-up assessment with color duplex ultrasound scan.

PURPOSE: The purpose of this study was the demonstration of the value of color duplex ultrasound (CDU) scanning in the detection of type I endoleak (T1EL) and type II endoleak (T2EL), the correlation of Doppler scan waveform pattern to endoleak persistence or seal, and the description of the natural history of endoleak. METHODS: The study was a retrospective review of 83 patients who underwent periodic CDU scan and computed tomographic (CT) scan surveillance of the endograft and aneurysm sac after insertion of an aortic endograft for abdominal aortic aneurysm (AAA). Forty-one patients (49%) with an endoleak at anytime in the follow-up period form the basis of this report. RESULTS: T1EL was detected in all five patients with CDU and CT scans. T2EL was detected in 36 patients with CDU scan as compared with 18 patients with CT scan. With CT scan, endoleak was not detected when CDU scan showed no endoleak. Conversely, all CT scan--detected endoleaks were found with CDU scanning. The T2EL source artery was identified with CT scan in seven patients, whereas the source was identified in all 36 patients with CDU scan. Endoleak source did not correlate with outcome (seal or persistence). However, a to/fro Doppler scan waveform pattern was associated with spontaneous T2EL seal in seven of 12 patients, and a monophasic or biphasic waveform was associated with endoleak persistence in 14 of 17 patients (P =.023, with chi(2) test). Thirteen of 36 T2ELs underwent spontaneous seal by 6.2 +/- 2.8 months. T2ELs without increasing AAA diameter were observed. Eight patients with persistent T2EL present for more than 12 months did not undergo treatment. However, two patients underwent T2EL obliteration with coils because of AAA sac enlargement. T1EL of the distal attachment site was the initial endoleak identified in five patients, but seven patients harboring T2ELs had subsequent T1ELs develop. For the entire 83 patients, the combined T1EL and T2EL prevalence rate was 20% of patients at a 6-month follow-up period, but this rate increased to 50% after 24 months. The incidence rate of newly detected endoleaks and of spontaneous sealing was 24.4% at 12 months and 12.5% in longer-term follow-up period. CONCLUSION: CDU scan is effective in the identification of the type of endoleak, the delineation of the vessel involved, and the hemodynamic information not available with any other testing method. Endoleaks have a dynamic natural history characterized by a variable onset with changing branch vessel involvement and spectral flow patterns. Periodic long-term endograft surveillance with CDU scanning is necessary for following existing endoleaks and for detecting new ones. Corroboration of these findings in larger multicenter prospective trials will be needed to determine whether CDU scan analysis of endoleaks would be predictive of long-term success in endovascular AAA repair.

Aortic Aneurysm, Abdominal↗
PubMed2002

Mechanism of failure in the treatment of type II endoleak with percutaneous coil embolization.

PURPOSE: Type II endoleak after endovascular abdominal aortic aneurysm repair is a failure of aneurysm sac exclusion with unknown long-term consequences. Elevated aneurysm sac pressures documented in these patients have led us to aggressively treat type II endoleaks with percutaneous transluminal coil embolization (PTCE). The purpose of this study was to evaluate the results and the mechanisms of failure of PTCE for type II endoleak. METHODS: One hundred ninety-one patients underwent endograft repair of infrarenal aortic aneurysms. Twenty-three of 28 patients with persistent primary (>3 months) or secondary (new-onset) endoleak underwent angiography; 14 of these patients had type II endoleaks. We reviewed our endovascular registry data, hospital charts, and radiologic studies of patients with type II endoleaks and analyzed the results in those treated with PTCE of the inflow vessel. RESULTS: All 14 patients with type II endoleaks were men, with a mean age of 76.7 years and a mean preoperative maximal aneurysm diameter of 5.7 +/- 1.0 cm. The type II endoleak was primary in 12 patients (86%) and secondary in two patients (14%) and iliolumbar in 11 patients (78%) and mesenteric in three patients (21%). Although a dominant affluent collateral channel (inosculation) was apparent in eight patients (57%), six patients (43%) showed a network of collateral vessels (retiform anastomosis). In six patients (43%), angiography revealed a second or "outflow" vessel indicative of a complex endoleak. In four patients with retiform iliolumbar type II endoleaks, PTCE was not attempted because of the retiform nature of the endoleak. The remaining 10 patients underwent PTCE, with coil deployment in all 10 and apparent initial technical success in nine patients. Follow-up computed tomographic scans revealed persistent endoleaks in six patients (60%). Mechanisms of failure included persistent flow through the coils in the treated vessel in two patients, development of a retiform anastomosis around the coiled vessel in three patients, and development of a new mesenteric endoleak after successful occlusion of an iliolumbar endoleak in one patient. Two patients underwent repeat PTCE with successful aneurysm sac exclusion in one. Internal iliac artery injury complicated one of the 12 PTCEs, and the resulting pseudoaneurysm was successfully treated with PTCE. Angiographic visualization of an outflow vessel (complex endoleak) was associated with PTCE failure (P =.008). CONCLUSION: PTCE of type II endoleaks has a high failure rate because of multiple anatomic mechanisms.

Aged↗
PubMed1998

Endoleaks after endovascular graft treatment of aortic aneurysms: classification, risk factors, and outcome.

PURPOSE: Incomplete endovascular graft exclusion of an abdominal aortic aneurysm results in an endoleak. To better understand the pathogenesis, significance, and fate of endoleaks, we analyzed our experience with endovascular aneurysm repair. METHODS: Between November 1992 and May 1997, 47 aneurysms were treated. In a phase I study, patients received either an endovascular aortoaortic graft (11) or an aortoiliac, femorofemoral graft (8). In phase II, procedures and grafts were modified to include aortofemoral, femorofemoral grafts (28) that were inserted with juxtarenal proximal stents, sutured endovascular distal anastomoses within the femoral artery, and hypogastric artery coil embolization. Endoleaks were detected by arteriogram, computed tomographic scan, or duplex ultrasound. Classification systems to describe anatomic, chronologic, and physiologic endoleak features were developed, and aortic characteristics were correlated with endoleak incidence. RESULTS: Endoleaks were discovered in 11 phase I patients (58%) and only six phase II patients (21%; p < 0.05). Aneurysm neck lengths 2 cm or less increased the incidence of endoleaks (p < 0.05). Although not significant, aneurysms with patent side branches or severe neck calcification had a higher rate of endoleaks than those without these features (47% vs 29% and 57% vs 33%, respectively), and patients with iliac artery occlusive disease had a lower rate of endoleaks than those without occlusive disease (18% vs 42%). Endoleak classifications revealed that most endoleaks were immediate, without outflow, and persistent (71% each), proximal (59%), and had aortic inflow (88%). One patient with a persistent endoleak had aneurysm rupture and died. CONCLUSIONS: Endoleaks complicate a significant number of endovascular abdominal aortic aneurysm repairs and may permit aneurysm growth and rupture. The type of graft used, the technique of graft insertion, and aortic anatomic features all affect the rate of endoleaks. Anatomic, chronologic, and physiologic classifications can facilitate endoleak reporting and improve understanding of their pathogenesis, significance, and fate.

Aged↗
PubMed2000

Experimental study of the influence of endoleak size on pressure in the aneurysm sac and the consequences of thrombosis.

BACKGROUND: This was an experimental study of endovascular aortic surgery, looking at the relationship between the size of an endoleak, pressure in the aneurysm sac and the effect of thrombosis produced by coagulation. METHODS: In three pigs, 16 saccular aneurysms were connected to the aorta by various side branches with different diameters and lengths ('endoleaks'). Mean and pulse pressures were measured in the systemic circulation as well as in the aneurysm sac during the experiment. Duplex ultrasonography was used to determine whether the endoleak and the aneurysm were patent or thrombosed. Thrombosis was influenced by systemic tranexamic acid, fibrinogen in the aneurysm sac, Gelfoam in both endoleak and aneurysm sac, and by Histoacryl glue in the endoleak. RESULTS: With an open endoleak, the mean pressure in the aneurysm and the aorta was identical. Mean aneurysm pressure was lower with a thrombosed endoleak and was related to the diameter of the endoleak. Pulse pressure was recorded in the aneurysm sac when there was an open endoleak and a non-thrombosed aneurysm, and was related to the diameter of the open endoleak. Thrombosed endoleaks never produced pulse pressure in the aneurysm. If Histoacryl and Gelfoam induced thrombosis of the endoleak, the decrease in mean aneurysm pressure was identical to that resulting from the spontaneous thrombosis of endoleaks. CONCLUSION: An open endoleak results in systemic arterial pressure in the aneurysm sac. Pulse pressure is detected if the aneurysm is patent, but absent if there is complete or partial thrombosis of the aneurysm. Endoleak thrombosis, either spontaneous or by embolization, is accompanied by a decrease in mean pressure and the absence of pulse pressure in the aneurysm sac. The extent to which these experimental findings are comparable to the clinical situation represents a field of further research.

Aortic Dissection↗
PubMed2006

Type II endoleak after endoaortic graft implantation: diagnosis with helical CT arteriography.

PURPOSE: To retrospectively assess endoleak shapes and locations within aneurysms to differentiate type II from type I and type III endoleaks. MATERIALS AND METHODS: The institutional review board granted an exemption for this HIPAA-compliant study; patient informed consent was not required. A retrospective review of arterial phase helical computed tomographic (CT) studies and medical records was performed for 39 patients (29 men, 10 women; age range, 60-89 years; mean, 78.5 years) who had an endoleak after endoaortic graft implantation for treatment of abdominal aortic aneurysm and who subsequently underwent angiography (n = 25), surgery (n = 8), or long-term follow-up (n = 6) to classify their endoleak into a specific type. At CT, endoleak shape (tubular or nontubular) and location (central or peripheral) were recorded. An endoleak was classified as type II if it contained a peripheral tubular component (PTC) near the aortic wall, with or without an identifiable feeding vessel. Endoleaks without these features were classified as type I or III. The Fisher exact test was used to assess associations between CT findings and endoleak type. RESULTS: There were 22 type II and 17 type I or III endoleaks. CT enabled correct identification of 22 (100%) of 22 type II endoleaks, all of which contained a PTC. Of 17 type I or III endoleaks, only two (12%) contained a PTC and were misclassified as type II endoleaks; the remaining 15 (88%) were correctly classified. Overall, CT enabled correct identification of endoleaks as type II or type I or III in 37 (95%) of 39 patients. PTCs were significantly more common (P < .001) in type II than in type I or III endoleaks, with a sensitivity, specificity, accuracy, negative predictive value, and positive predictive value of 100%, 88.2%, 94.9%, 100%, and 91.7%, respectively. CONCLUSION: A PTC is a statistically significant predictor of type II endoleak in most patients.

Aged↗
PubMed2004

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.

Aortic Aneurysm, Abdominal↗
PubMed2006

An 8-year experience with type II endoleaks: natural history suggests selective intervention is a safe approach.

OBJECTIVE: The treatment of type II endoleaks remains controversial because little is known about their long-term natural history and impact on changes in aneurysm morphology. This study reviews type II endoleaks occurring in patients after endovascular abdominal aortic aneurysm repair (EVAR) at a single-institution over an 8-year period. METHODS: All patients undergoing EVAR who had type II endoleaks documented on follow-up imaging studies at our institution between January 1997 and March 2005 were reviewed. Data regarding patient demographics in addition to aneurysm size, device type, operative complications, and secondary interventions were reviewed. Outcomes evaluated included the rate of spontaneous sealing, freedom from secondary intervention, and aneurysm enlargement, rupture, or conversion. RESULTS: Type II endoleaks were present in 154 of 965 patients (16.0%) undergoing EVAR. Mean follow-up time was 22.0 months (range, 1 to 72 months). Fifty-five patients (35.7%) with type II endoleaks sealed spontaneously in a mean time of 14.5 months. According to Kaplan-Meier analysis, approximately 75% of type II endoleaks sealed spontaneously within a 5-year period. Nineteen patients (12.3%) with type II endoleaks were treated at a mean time of 19.9 months at the operating surgeon's discretion, including 13 with sac enlargement >5 mm. Kaplan-Meier analysis estimated that approximately 65% of the patients remained free of intervention after a period of 4 years. Thirteen patients (8.4%) experienced aneurysm sac enlargement >5 mm. Kaplan-Meier analysis estimated that approximately 80% of patients with type II endoleaks remained free of sac enlargement >5 mm over a 4-year period. No patients with type II endoleaks experienced rupture or required conversion to open repair during their follow-up. Cox regression analysis showed that cancer, coronary artery disease, and chronic obstructive pulmonary disease were associated with earlier spontaneous closure of the type II endoleaks (P < .05). CONCLUSIONS: We observed that type II endoleaks have a relatively benign course, and in the absence of sac expansion, can be followed for a prolonged course of time without the need for intervention. The rate of spontaneous seal continues to increase with time and, therefore, close follow-up of patients with type II endoleaks who show no signs of aneurysm expansion is a safe approach. For patients in whom the exact etiology of their endoleak is in question, dynamic imaging should be used to exclude the presence of a type I endoleak.

Adult↗
PubMed1999

Algorithm for the diagnosis and treatment of endoleaks.

BACKGROUND: Endoluminal grafting of abdominal aortic aneurysms (AAA) has shown promising early results. However, endoleaks present a new and challenging obstacle to successful aneurysm exclusion. We report our experience with primary, persistent endoleaks and provide an algorithm for their diagnosis and management. METHODS: Over a 19-month period, 73 patients underwent endoluminal repair of their AAAs using a modular bifurcated endograft as part of a US FDA Investigational Device Exemption trial. Spiral computed tomography (CT) scanning was performed prior to discharge after repair to evaluate for complete aneurysm exclusion. If no endoleak was present on that initial CT scan, color-flow duplex scanning was performed at 1 month, with repeat CT scanning at 6 months and 1 year. If the initial CT scan revealed the presence of an endoleak, repeat CT scanning was performed at 2 weeks, 1 month, and 3 months, or until the endoleak resolved. Any patient with an endoleak that persisted beyond 3 months underwent angiographic evaluation to localize the source of the leak. RESULTS: At 1 month, 62 patients (85%) had successful aneurysm exclusion. The remaining 11 patients (15%) had primary endoleaks, 8 (11%) of which persisted beyond 3 months, prompting angiographic evaluation. In 2 patients the endoleak was related to a graft-graft or graft-arterial junction. One was from the endograft terminus in the common iliac artery and was successfully embolized, along with its outflow lumbar artery. The other required placement of an additional endograft component across a leaking graft-graft junction to successfully exclude the aneurysm. The remaining six endoleaks were due to collateral flow through the aneurysm sac. In 4 cases this was lumbar to lumbar flow fed by hypogastric artery collaterals to the inflow lumbar artery. In the remaining 2 patients the endoleak was found to be due to flow between a lumbar and inferior mesenteric artery. Resolution of the endoleak by coil embolization of the feeding hypogastric artery branch in 1 patient was unsuccessful due to rapid recruitment of another hypogastric branch. Two of the six collateral flow endoleaks have resolved spontaneously without treatment, while the remaining cases have been followed up without evidence of aneurysm expansion. CONCLUSION: Systematic postoperative surveillance facilitates proper diagnosis and treatment of endoleaks. This involves serial CT scans to detect the presence of endoleaks, followed by angiography to determine their etiology and guide treatment, if clinically indicated.

Algorithms↗
PubMed2002

Potential impact of therapeutic warfarin treatment on type II endoleaks and sac shrinkage rates on midterm follow-up examination.

OBJECTIVE: Successful endovascular aortic aneurysm repair depends on exclusion and spontaneous thrombosis of the aneurysm sac. The need for chronic postoperative anticoagulation therapy could limit the applicability of this technology with delay or prevention of sac thrombosis resulting in endoleak formation and altered remodeling of the aneurysm sac. The purpose of this study was the determination of whether chronic therapeutic anticoagulation therapy with warfarin was associated with an increased incidence rate of early or delayed postoperative endoleaks or altered rates of reduction in aneurysm sac maximum diameter. METHODS: Two hundred thirty-two consecutive patients underwent abdominal aortic endografting during a 32-month period. The data were recorded prospectively with a current mean follow-up period of 18 months. The patients with endoleaks identified with 30-day postoperative computed tomographic scan angiograms subsequently underwent selective arteriography to characterize the source. The patients who underwent chronic warfarin therapy that resulted in a therapeutic internationalized normalized ratio comprised the study group. The control group was defined as all the patients with healthy coagulation profiles. RESULTS: Thirty-six patients (15%) were undergoing warfarin therapy after surgery, and their conditions were chronically maintained with a therapeutic international normalized ratio. Forty-three patients (18%) had endoleaks on 30-day computed tomographic scan angiographic results. There were 39 patients with type II endoleaks and four patients with type I endoleaks. None of the type I endoleaks occurred in patients who were undergoing warfarin therapy, and all endoleaks were repaired with either proximal or distal covered extensions. At 30 days, seven patients (19.4%) undergoing chronic warfarin therapy had type II endoleaks as compared with 36 controls (18.4%; P =.798). Four patients had delayed type II endoleaks develop, two in the control group and two in the warfarin group (P =.3). Ten control individuals (31%) had spontaneous resolution of type II endoleaks develop, whereas spontaneous endoleak thrombosis was not observed in the warfarin group (P =.33). Aneurysm sac remodeling assessed with mean percent reduction in maximum sac diameter at 12 months revealed a statistical difference between the control group (17.5%) and the warfarin group (7.6%; P =.04). CONCLUSION: Warfarin treatment is not associated with an increase in the incidence rate of early or delayed postoperative endoleaks. However, the rate of reduction in maximum aneurysm sac diameter after aortic endografting is slower in patients who undergo therapeutic warfarin therapy at 1-year follow-up examination, a statistically significant difference from the control group. In addition, type II endoleaks may be less likely to undergo spontaneous thrombosis in patients who undergo warfarin therapy.

Anticoagulants↗
PubMed2004

Proximal type I endoleak after endovascular abdominal aortic aneurysm repair: predictive factors.

Proximal type I endoleaks after endovascular abdominal aortic aneurysm repair (EVAR) are associated with a high risk of rupture. Risk factors for developing this complication are not fully elucidated. We aimed to define preoperative predictors for proximal type I endoleak and describe its clinical outcome. From a consecutive series of 257 patients who underwent EVAR, we selected 202 who had available pre- and postoperative CT scan studies. Proximal neck diameter, length, angulation, calcification, thrombus load (thickness, percentage of neck circumference coverage, percentage of neck area occupancy), and maximum aneurysm diameter were evaluated on preoperative CT scans. All postoperative CT and duplex ultrasound scans, supplemented with angiograms in selected cases, were reviewed for the presence or absence of endoleak. Device overlap and oversizing (relative to the proximal neck) were also determined. Type I proximal endoleak rates were estimated using the Kaplan-Meier method. The associations between the variables listed above and proximal type I endoleak were evaluated by use of Cox proportional hazards models. Proximal type I endoleak occurred in eight patients, corresponding to a 3-year incidence rate of 4% (SE = 1.5%). The median follow-up was 340 days (range, 22-1954). Univariate analyses found significant associations between proximal type I endoleak and the following variables: percentage of calcified neck circumference (hazards ratio = 2.19 for a 25% increase, p = 0.019), aneurysm maximum diameter (hazards ratio = 1.98 for a 1-cm increase, p = 0.006) and proximal neck and device overlap (hazards ratio = 0.53 for a 5-mm increase, p = 0.007). The mean overlap among cases with and without type I proximal endoleak was 15.6 mm and 29.3 mm, respectively. When these variables were included in a multivariate model, all remained statistically significant. No significant association could be documented for neck thrombus-related variables. Thirty-nine (19.3%) patients had a beta neck angle inferior to 120 degrees . There was a trend toward a higher incidence of proximal type I endoleaks in these patients (p = 0.057). Device oversize relative to proximal neck diameter did not affect the probability of this type of endoleak. One patient survived an emergency open repair of a ruptured aneurysm after significant expansion. Six patients underwent endovascular reinterventions (4 additional proximal cuff placements, 2 proximal angioplasties). The mean interval for reintervention was 389 days. Distal migration (>or=5 mm) was identified in four cases (50%). Proximal type I endoleak is a rare complication after EVAR, but it is associated with a high number of reinterventions and potentially serious consequences. Patients with short and heavily calcified aneurysmal necks and large aneurysms are at increased risk of proximal type I endoleaks.

Aged↗
PubMed2004

Intrasac pressure waveforms after endovascular aneurysm repair (EVAR) are a reliable marker of type I endoleaks, but not type II or combined types: an experimental study.

PURPOSE: To ascertain the nature of the pressure wave transmitted through aneurysm thrombus and the changes produced after endovascular repair and the development of type I and II endoleaks. METHODS: A 25 mm Talent endovascular graft was deployed in a latex model of an abdominal aortic aneurysm, which was incorporated in a pulsatile flow unit. The graft was surrounded by thrombus analogue to simulate conditions in vivo. Pressure waveforms in the sac were captured over 5s at 1000 Hz in these settings: (i) no endoleaks (baseline), after introduction of (ii) type I (iii) type II and (iv) combined type I and II endoleaks. The arterial blood pressure settings used were 140/100 and 130/90 mmHg, denoted the high and low settings, respectively. ANOVA in Minitab 13 was applied for statistical analysis. RESULTS: Pulsatile waveforms were transmitted through the thrombus. Intrasac pressure after stent-grafting reduced to 110/107, 99/96 mmHg (p<0.001) (high, low settings, respectively). Introduction of a type I endoleak caused this to rise to 120/112, 115/107 mmHg (p<0.001, vs. baseline); after producing a type II endoleak these were 101/98, 91/88 mmHg (p<0.001, vs. baseline). A combined type I and II endoleak produced intrasac pressures identical to that of a type I endoleak. CONCLUSIONS: Intrasac pressure waveforms following EVAR are easily defined following a type I endoleak. Waveforms obtained following type II endoleak simulation resemble the baseline waveform in an attenuated form. Intrasac pressures are, therefore, a reliable marker for type I, but not a type II endoleak. In the case of a combined endoleak, the type I endoleak waveform effectively masks that of the type II. Intrasac thrombus faithfully transmits intrasac pressures.

Aortic Aneurysm, Abdominal↗
PubMed2005

Type II lumbar endoleaks: hemodynamic differentiation by contrast-enhanced ultrasound scanning and influence on aneurysm enlargement after endovascular aneurysm repair.

OBJECTIVE: The objective of this study was to differentiate type II lumbar endoleaks on the basis of dynamic features identified by contrast-enhanced ultrasound scanning (CUS) and to evaluate the role of this differentiation in detecting abdominal aortic aneurysm (AAA) enlargement > or =1 mL/mo. METHODS: Eighteen male patients (mean age, 71.8 years) with type II lumbar endoleak suspected at CUS underwent computed tomography angiography (CTA) and digital subtraction angiography (DSA). On CTA, AAA volumes and endoleak visualization and volume were assessed. At CUS, performed after a bolus of 1.5 to 2.4 mL of a second generation blood pool contrast agent, the following parameters were evaluated: presence of contrast material within the aneurysmal sac (endoleak), delay of endoleak detection (wash-in) and disappearance (washout) from the beginning of contrast injection, visualization of inflow and outflow vessels, and presence of cavity filling. Statistical analysis was performed regarding endoleak features at CUS, endoleak detection at CTA, and rate of AAA enlargement. RESULTS: DSA confirmed all the endoleaks. Mean +/- standard deviation wash-in and washout times were 121.9 +/- 132.6 and 337.2 +/- 193.7 seconds, respectively; a significant relation was observed between these two parameters (P < .01, analysis of variance). By Youden plots, endoleaks were classified as hyperdynamic when wash-in was <100 seconds (n = 10, 55.5%) and/or washout was <520 seconds (n = 13, 72.2%). A slower washout was associated with nonvisualized outflow (66.7%) and/or inflow arteries (66.7%) ( P < .05). Eight endoleaks (44.4%) were missed at CTA; it occurred in hypodynamic endoleaks, absence of detectable inflow or outflow vessels, and absence of cavity filling at CUS (P < .05). Overall mean AAA volume increase rate was 1.1 +/- 1.7 mL/mo. By multiple logistic regression model, the washout time > or = 520 seconds was the only independent predictor of AAA volume increase > or = 1 mL/mo (8 patients, 44.4%). CONCLUSION: Type II lumbar endoleaks show different hemodynamic features at CUS, which might influence the rate of aneurysm enlargement, addressing the need for treatment.

Aged↗
PubMed2005

Influence of type II endoleak volume on aneurysm wall pressure and distribution in an experimental model.

OBJECTIVE(S): We have previously shown that type II endoleak size is a predictor of aneurysm growth after aortic endografting. To better understand this observation, we investigated the influence of endoleak size on pressure transmitted to the aneurysm wall and its distribution within the aneurysm sac. METHODS: In an ex vivo model, an artificial aneurysm sac was incorporated within a mock circulation comprised of rubber tubing and a pulsatile pump. Three strain-gauge pressure transducers were placed in the aneurysm wall at different locations, including the site of maximum aneurysm diameter. The aneurysm was filled with either human aneurysm thrombus or dough that mimicked thrombus and simulated type II endoleaks of varying volumes (1 to 10 mL) were created. Aneurysm wall pressure (AWP) measurements were recorded at mean arterial pressures (MAPs) of 60, 80, and 100 mm Hg. Correlation coefficients ( r ) and analysis of variance were used to assess the relationship between endoleak volume and AWP. RESULTS: Increasing endoleak volume '3 cm 3 resulted in proportionally increased AWP at all levels of MAP and at all sites, with highest pressures recorded at the site of the maximum aneurysm diameter (r = 0.83 when MAP = 100 mm Hg; r = 0.85 when MAP = 80 mm Hg; r = 0.88 when MAP = 60 mm Hg; P < .001). AWP plateaued when the endoleak volume was >3 cm 3 . Pressure distribution within the sac was not uniform. Although the difference was within +/-10%, statistically significant higher AWPs were observed at the site of maximum aneurysm diameter (P <.001). AWP also correlated with MAP. CONCLUSIONS: Increasing type II endoleak volume results in proportionally higher AWP, which is greatest at the site of maximum aneurysm diameter. This study confirms the clinical observation that type II endoleak volume and MAP may be important predictors of aneurysm expansion. CLINICAL RELEVANCE: Our experimental model of a type II endoleak revealed that endoleak size is a significant factor that influences the magnitude of pressure transmission into the aneurysm wall. Increasing volume of the endoleak nidus was associated with proportionally higher aneurysm sac pressures. This mechanism may, in fact, account for the increased risk of aneurysm expansion observed in our clinical experience, thereby suggesting the need for more aggressive surveillance and possibly earlier intervention for patients with larger endoleaks.

Aneurysm↗
PubMed2000

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.

Aged↗
PubMed2000

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

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

Aortic Aneurysm, Abdominal↗
PubMed2001

Endoleak after endovascular repair of abdominal aortic aneurysm.

PURPOSE: We sought to assess the role of endovascular techniques in the management of perigraft flow (endoleak) after endovascular repair of an abdominal aortic aneurysm. METHOD: We performed endovascular repair of abdominal aortic aneurysm in 114 patients, using a variety of Gianturco Z-stent-based prostheses. Results were evaluated with contrast-enhanced computed tomography (CT) at 3 days, 3 months, 6 months, 12 months, and every year after the operation. An endoleak that occurred 3 days after operation led to repeat CT scanning at 2 weeks, followed by angiography and attempted endovascular treatment. RESULTS: Endoleak was seen on the first postoperative CT scan in 21 (18%) patients and was still present at 2 weeks in 14 (12%). On the basis of angiographic localization of the inflow, the endoleak was pure type I in 3 cases, pure type II in 9, and mixed-pattern in 2. Of the 5 type I endoleaks, 3 were proximal and 2 were distal. All five resolved after endovascular implantation of additional stent-grafts, stents, and embolization coils. Although inferior mesenteric artery embolization was successful in 6 of 7 cases and lumbar embolization was successful in 4 of 7, only 1 of 11 primary type II endoleaks was shown to be resolved on CT scanning. There were no type III or type IV endoleaks (through the stent-graft). Endoleak was associated with aneurysm dilation two cases. In both cases, the aneurysm diameter stabilized after coil embolization of the inferior mesenteric artery. There were two secondary (delayed) endoleaks; one type I and one type II. The secondary type I endoleak and the associated aneurysm rupture were treated by use of an additional stent-graft. The secondary type II endoleak was not treated. CONCLUSIONS: Type I endoleaks represent a persistent risk of aneurysm rupture and should be treated promptly by endovascular means. Type II leaks are less dangerous and more difficult to treat, but coil embolization of feeding arteries may be warranted when leakage is associated with aneurysm enlargement.

Aortic Aneurysm, Abdominal↗
PubMed2006

Detection of endoleaks after endovascular aneurysm repair with use of technetium-99m sulfur colloid and (99m)Tc-labeled red blood cell scans.

PURPOSE: This study was performed to determine whether endoleaks could be detected after endovascular aneurysm repair (EVAR) with use of technetium-99m sulfur colloid and (99m)Tc-labeled red blood cell (RBC) nuclear medicine scans. MATERIALS AND METHODS: There were 13 patients enrolled in this study: nine with endoleaks seen on computed tomographic (CT) angiography and four with no endoleak on CT angiography. All patients underwent regularly scheduled surveillance CT angiography examination after EVAR to evaluate for endoleak. Endoleak detection was then attempted in each patient with two nuclear medicine scans: a (99m)Tc sulfur colloid scan and a (99m)Tc-labeled RBC scan. Flow images (5 seconds per frame) were obtained for 1 minute after intravenous administration of 555 MBq (15 mCi) (99m)Tc sulfur colloid. Sequential dynamic images were then obtained every minute for 30 minutes. Next, a (99m)Tc-labeled RBC study was performed after the intravenous administration of 370-1,073 MBq (10-29 mCi) in vitro labeled (99m)Tc RBCs. Flow images were obtained, followed by sequential dynamic images obtained every minute for 30 minutes. Single photon emission CT images of the abdomen were then acquired. The nuclear medicine scans were evaluated for the presence or absence of endoleak independent of the CT angiography findings. RESULTS: Of the nine patients with endoleaks on CT angiography, seven (78%) had them detected by nuclear medicine examinations. Two of the nine endoleaks seen on CT angiography (22%) were not seen on either scintigraphic examination. All patients with no endoleak on CT angiography had their nuclear medicine scans correctly interpreted as showing no endoleak present (n = 4; 100%). No complications occurred as a result of the nuclear medicine scans. CONCLUSIONS: Endoleaks can be detected with (99m)Tc sulfur colloid and (99m)Tc-labeled RBC nuclear medicine scans. This initial work suggests that the sensitivities of these scintigraphic scanning methods for endoleak detection are lower than that of CT angiography.

Aortic Aneurysm, Abdominal↗
PubMed2004

Endoleak following endovascular abdominal aortic aneurysm repair: implications for duration of screening.

OBJECTIVE: Endovascular abdominal aortic aneurysm repair (EAR) requires long-term surveillance for endoleak or increase in aneurysm diameter. We analyzed the natural history of and risk factors for endoleak development. SUMMARY BACKGROUND DATA: Endoleak is a common complication of EAR that can lead to aneurysm enlargement and even rupture. Following EAR, imaging studies are used to identify leaks since patients with endoleak may require additional endovascular interventions or conversion to open repair. No criteria currently exist for cessation or reduction in frequency of screening imaging studies. METHODS: Data on 220 patients undergoing EAR were retrospectively reviewed. Kaplan-Meier survival analysis and Cox proportional hazards regression were used with the end point being new endoleak development. Potential risk factors included preoperative aneurysm diameter, number of negative surveillance studies, and postoperative increase in diameter. RESULTS: A total of 52 patients (24%) who underwent EAR had endoleak detected during postoperative follow-up, which averaged 19 months (range, 0.4-101 months). One, 6-, 12-, and 24- month endoleak-free survival was 90%, 80%, 77%, and 73%, respectively. Three leaks occurred after year 2, at postoperative months 24, 48, and 85. Increasing number of negative screening studies was negatively associated with risk for endoleak development (B = -3.122, P < 0.001), while increase in aneurysm diameter was positively associated with risk for endoleak (B = 0.072, P = 0.04). CONCLUSION: Risk for endoleak declines as the number of negative postoperative scans increases, but new endoleaks are identified as late as 7 years following EAR. Reduction in screening frequency cannot be uniformly recommended at this time. Patients with documented aneurysm expansion should be monitored carefully and endoleak should be suspected.

Adult↗