Original Cardiovascular
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Factors Affecting Anatomical Changes after Endovascular Abdominal Aortic Aneurysm Repair Keun-Myoung Park1 Kwang Bo Park2
Dong-Ik Kim1
Young-Wook Kim1
1 Division of Vascular Surgery, Sungkyunkwan University School of
Medicine, Samsung Medical Center, Seoul, Republic of Korea 2 Department of Radiology, Sungkyunkwan University School of Medicine, Samsung Medical Center, Seoul, Republic of Korea
Young-Soo Do2
Hong Suk Park2
Address for correspondence Dong-Ik Kim, MD, PhD, Division of Vascular Surgery, Sungkyunkwan University School of Medicine, Samsung Medical Center, 81 Irwon-Ro Gangnam-gu Seoul 135-710, Republic of Korea (e-mail: [email protected]).
Abstract
Keywords
► endoavascular aneurysm repair ► abdominal aortic aneurysm ► aneurysm sac size
Background The primary goal of endovascular aneurysm repair (EVAR) is to prevent death from aneurysm rupture. Regression of aortic sac size is believed to be a marker for success after EVAR. This study analyzes the changes in aneurysm sac size and the factors affecting sac regression after EVAR. Patients and Methods We retrospectively reviewed 121 patients with abdominal aortic aneurysm (AAA) who underwent elective treatment with EVAR at our institution from January 2005 to December 2011. In this study, 17 of the 121 patients were excluded due to loss during follow-up or for not having undergone a postoperative computed tomographic (CT) scan, and 3 patients were excluded due to an isolated iliac artery aneurysm. CT scans were scheduled at months 1, 6, and 12, and annually thereafter. Aneurysm size was defined by the minor axis on the largest axial cut of the aneurysm on a two-dimensional CT scan. Sac regression was defined as a reduction in the diameter of more than 5 mm. Results Sac regression was observed during follow-up in 39 of the 101 patients. There was 1 regression in 87 patients (1%) at 1 month, 18 in 62 patients at 6 months (29%), 26 regressions in 44 patients (59%) at 12 months, and 18 regressions in 34 patients (53%) at 24 months. After multivariate analysis, the absence of endoleaks was the only factor associated with sac regression (hazard ratio, 3.620; confidence interval, 1.692–7.747; p ¼ 0.001). Conclusion Sac regression over 5 mm is associated with current or previous endoleaks after EVAR. Continued surveillance is necessary in all patients after EVAR to prevent late complications.
Introduction Endovascular aneurysm repair (EVAR) is widely accepted as an alternative for open repair in treatment of abdominal aortic aneurysm (AAA). EVAR has proven to be a less-invasive procedure compared with conventional open repair surgery, with shorter procedure duration, reduced blood loss, shorter hospital stays, and a significantly lower 30-day mortality rate.1,2
received March 16, 2014 accepted after revision June 22, 2014 published online September 5, 2014
The primary goal of EVAR is to prevent death from aneurysm rupture. As EVAR continues to evolve, it is important to identify factors that predict long-term clinical success. Presently, many studies cite the regression of AAA size as the marker for successful repair.3–8 Regression of the aneurysm around the endograft is presumed to indicate exclusion of the aneurysm from the circulation and an absence of systemic pressure within the sac. Expansion implies persistent
© 2015 Georg Thieme Verlag KG Stuttgart · New York
DOI http://dx.doi.org/ 10.1055/s-0034-1387819. ISSN 0171-6425.
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Thorac Cardiovasc Surg 2015;63:139–145.
Factors Affecting Anatomical Changes after Endovascular AAA Repair pressurization and incomplete exclusion of the AAA sac and has been suggested as an indication for intervention with or without an endoleak. A recent study showed that an increase in sac enlargement after EVAR was attributable to liberalization of the Instructions For Use (IFU), which set guidelines for EVAR candidacy based on aortic neck diameter, aortic neck angle, and common iliac artery diameter.9 A recent report showed that young age, aortic neck quality, and neck calcification were associated with sac regression.10 However, there was no report about the factors associated with sac regression after EVAR under the IFU. The purpose of this investigation was to determine the change in aneurysm diameter and the factors affecting regression of the aneurysm sac after EVAR under anatomy inside the IFU.
Patients and Methods We performed a retrospective review of 121 patients with AAAs who underwent elective treatment with EVAR at our institution from January 2005 to December 2011. Out of the 121 eligible patients, 101 were included. Our indication of EVAR was aneurysm size over 5 mm, symptomatic aneurysm, saccular aneurysm, and ruptured aneurysm. The most indication of EVAR was aneurysm size. One patients was underwent EVAR although aneurysm size was below 5 mm with saccular aneurysm of Bechet disease. Out of all, 17 patients were excluded due to loss during follow-up or not having undergone a postoperative computed tomography (CT) scan, and 3 patients were excluded due to an isolated iliac artery aneurysm. All the AAAs were infrarenal. Isolated iliac artery aneurysms without a concurrent AAA were excluded. All aneurysms in our study were conservatively defined by Schanzer et al within the IFUs.9 All included patients had a technically successful EVAR. Technical success depends on periprocedural events that occur from the initiation of the procedure and extend through the first 24-hour postoperative period. Primary technical success is defined by an intention-to-treat basis and requires the successful introduction and deployment of the device in the absence of surgical conversion or death, type I or III endoleaks, or graft limb obstruction.
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We reviewed preoperative, perioperative, and postoperative follow-up data from hospital records and radiology studies. Follow-up for all patients undergoing EVAR consisted of an office visit with the operating surgeon. Duplex or CT scans were scheduled at months 1, 6, and 12, and annually thereafter. Analysis of CT imaging was done using Centricity PACS viewer (GE Healthcare, Amersham, Buckinghamshire, UK). AAA size was defined as the minor axis on the largest axial cut of the aneurysm on a two-dimensional CT scan. AAA sac size change was determined by comparing the minor axis measurements between the preoperative and all subsequent imaging; major axis measurements were not used as they do not necessarily represent the true diameter of the AAA, since the AAA sac may not be parallel to the axis of the body. The minor axis was chosen for reproducibility and to prevent overestimation of AAA size due to tortuosity of the aorta. Neck angle was measured in sagittal (lateral angle) and coronal image (anteroposterior angle). All of the aneurysms were measured twice, and the size of the aneurysmal sac was considered the mean of both measurements. Thrombus in the aneurysm was measured by the proportion between the diameter of lumen and aneurysm in the long axis. On the basis of this measurement, we stratified the thrombi into three groups (below 50%, between 50% and 75%, and over 75%) (►Fig. 1). Significant sac regression was defined as > 5 mm.11 We used analysis of variance to analyze differences between the regression and nonregression groups. A chi-square test and t-test were performed. We considered a of p < 0 0.05 statistically significant. We used the standard definition of maximum diameter decrease over 5 mm without reintervention as longterm technical success for AAA sac regression. We used analysis of variance to analyze differences between the regression and nonregression groups. A chi square test and t test were performed. We considered a of p < 0 0.05 statistically significant. The primary end point of our study was sac regression rate without reintervention. The secondary end point was the factor affecting to longterm technical success. To determine risk factors related to sac regression, a multivariate analysis was conducted using logistic regression and the Cox proportional hazards model. Analysis of time-toevent occurrence of AAA sac regression without reintervention was performed with the Kaplan–Meier method, and
Fig. 1 Measurement of thrombus—three groups: (A) below 50%, (B) between 50 and 75%, and (C) over 75% were divided by the proportion between the diameter of the lumen and aneurysm in the long axis. Thoracic and Cardiovascular Surgeon
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group differences (stratified by endoleak) were compared using the log-rank test.
Results All patients had a baseline CT scan within 1 month before EVAR and at least one follow-up CT scan after EVAR. A total of 101 preoperative and 265 follow-up CTs were performed on 101 patients. The average preoperative AAA diameter was 55.04 7.38 mm (range, 35.7–91.4). Thrombus formation in the aneurysm (> 50% of the aneurysm diameter) in preoperative CT scan was observed in 81 patients. Mean follow-up was 24.10 15.17 months (range, 1–66), with an average of 2.62 1.45 postoperative CT scans available per patient for 5 years. At 1 month, 87 of 101 patients had a follow-up CT scan. At 6 months, 62 of 96 patients had a follow-up CT. At 12 months, 44 of 67 patients had a CT. At 24 months, 34 of 55 patients had a CT performed. There was no 30 days mortality and aneurysm-related death during follow-up. The presence of any type of endoleak during follow-up was documented in 48 patients for an overall incidence of 48%. Out of 48 patients, 4 had types I and III endoleaks. One type I and III were in initial aortogram. In cases of decreased amounts of leakage after balloon inflation, simple observation may be an alternative to repetitive procedures. But, endoleak did not appear in the 6-month follow-up CT. Type II endoleak was found in 44 patients [lumbar artery (LA) origin: 24 patients, inferior mesenteric artery (IMA) origin: 14 patients, LA þ IMA: 6 patients]. During followup, 20 patients of type II endoleak were discontinued within 6 months after EVAR. The remaining 24 patients of type II endoleak were continued more than 6 months after EVAR. The number of patients who experienced spontaneous resolving of type II endoleak at 1 month, 6 months, 1 year, and 2 years were nine patients, six patients, four patients, and one patient, respectively. The six patients with persistent type II endoleak over 6 months developed significant aneurysm sac increase. The 18 patients with persistent type II endoleak had same aneurysm sac comparing preoperative aneurysm size. Of the 48 patients who developed an endoleak, 8 patients developed significant aneurysm sac enlargements (> 5 mm). Six of eight patients underwent secondary interventions; five had embolization (type II endoleak 4, type I endoleak 1) and
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one patient had a stent graft placed (type III endoleak). Two patients without reintervention had persistent type II endoleak and under close observation due to there were no interval change in 1-year follow-up CT comparing 6 months follow-up CT. Sac regression was observed in 39 of 101 patients (39%) during the course of follow-up. After EVAR, there was one regression in 87 patients (1%) at 1 month, 18 in 62 patients at 6 months (29%), 26 regressions in 44 patients (59%) at 12 months, and 18 regressions in 34 patients (60%) at 24 months (►Table 1). There was no sac that was increasing after regression. Differences in patient demographics including age, sex, comorbidities, preoperative presence of thrombus within the AAA sac, mean maximal aneurysm diameter at baseline, neck and iliac artery anatomic factor (diameter and neck), or type of stent grafts were not statistically significant between the regression and no regression groups (►Table 2). In a multivariate analysis of factors associated with AAA regression, the most significant factor was the absence of an endoleak on any postoperative CT scan (hazard ratio, 3.620; confidence interval, 1.692–7.747). There was no relation between sac regression and other factors (►Table 3). ►Fig. 2 shows regression rates in the endoleak group versus the no endoleak group.
Discussion The purpose of EVAR of an AAA is to modify the natural history of the AAA and prevent rupture-associated mortality. Many reports commented there was a relationship between clinical success and sac size.3–8 Aneurysm diameter is a major criterion of efficacy during the follow-up of EVAR.2,11,12 Koole et al commented that the risk of rupture in patients with an AAA enlargement of 8 mm after EVAR increased over 4 years.13 In the case of EVAR, the aneurysm sac persists after the intervention and fills with thrombus, which may act as a source of ongoing inflammation with the potential to alter neck morphology and lead to endoleak development, sac repressurization, and potentially, rupture. Sac shrinkage during follow-up is considered a representative marker of success, but little is known about the mechanisms behind this phenomenon.9 Schanzer et al reported that over a 10-year period, the incidence of AAA sac enlargement after EVAR was 41% at
Table 1 Changes in the size of the aneurysm sac over a 24-month period after EVAR Months
No. of patients with new regression
No. of patients with regressiona (%)
Changeb in sac (mean SD) mm
1 (n ¼ 87)
1
1 (1)
0.22 1.96
6 (n ¼ 62)
17
18 (29)
3.48 4.95
12 (n ¼ 44)
13
26 (59)
7.044 7.76
24 (n ¼ 34)
8
18 (60)
6.96 9.73
Abbreviation: SD, standard deviation. a Size decrease from baseline of > 5 mm. b Defined as sac size decrease. Thoracic and Cardiovascular Surgeon
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Factors Affecting Anatomical Changes after Endovascular AAA Repair
Factors Affecting Anatomical Changes after Endovascular AAA Repair
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Table 2 Comparison of demographic data and aneurysm characteristics between regression and no regression groups Patients
Regressiona (n ¼ 39)
No regression (n ¼ 62)
p
Age, y (mean SD)
70.1 6.3
71.3 6.0
0.601
Gender (male)
35 (90%)
58 (94%)
0.370
Hypertension
27 (69%)
45 (73%)
0.443
DM
10 (26%)
10 (16%)
0.181
Ischemic heart disease
13 (33%)
17 (27%)
0.339
COPD
5 (11%)
7 (13%)
0.526
Dyslipidemia
11 (28%)
24 (39%)
0.194
Smoking
14 (36%)
24 (39%)
Comorbidity
Indication
0.472 0.658
Size over 5 mm
35 (90%)
57 (91%)
Symptom or ruptured
3 (7%)
5 (9%)
Morphology
1 (3%)
0
53.5 5.10
55.1 10.49
Zenith (n ¼ 73)
35
38
0.081
Excluder (n ¼ 28)
4
24
0.157 0.600
Aneurysm size, mm (mean SD)
0.417
Graft material
Thrombusb > 50%
21 (54%)
35 (57%)
50–75%
12 (31%)
13 (21%)
< 75%
6 (15%)
14 (22%)
Endoleak
11 (28%)
37 (60%)
0.001
Diameter of aorta at renal ostium
23.3 4.45
22.6 5.32
0.642
Diameter of aorta at extent of aneurysm
21.5 3.10
20.1 2.89
0.485
Neck length (mm)
21.2 5.19
18.3 4.42
0.174
Max diameter of right CIA (mm)
9.9 1.32
10.9 1.32
0.588
Max diameter of left CIA (mm)
9.2 0.95
10.0 0.87
0.646
Neck angle (anteroposterior)
28.1 21.5
31.1 25.1
0.312
Neck angle (lateral)
38.5 23.7
37.1 21.5
0.492
Right CIA length
18.3 2.36
19.3 2.71
0.516
Left CIA length
21.3 1.92
20.7 1.85
0.394
Intern iliac artery embolization
10 (26%)
17 (27%)
0.524
Abbreviations: CIA, common iliac artery; COPD, chronic pulmonary obstructive disease; DM, diabetes mellitus; SD, standard deviation. a Size decrease from baseline of > 5 mm. b Thrombus was proportion between diameter of lumen and aneurysm in the long axis.
5 years. The increase in sac enlargement was attributed to liberalization of the IFU including aortic neck diameter, aortic neck angle, and common iliac artery diameter.9 However, our study excluded cases outside IFU and cases with technical failure. We have shown that after EVAR, the aneurysm diameter decreased at a mean rate of 0.58 mm/mo ( 0.64 mm/mo), similar to the rate of 0.41 to 0.50 mm/mo reported by Wolf et al14 and Broeders et al.15 Thoracic and Cardiovascular Surgeon
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The absence of an endoleak and a decrease in aneurysm size (at a rate of 0.28–0.35 mm/mo) are considered evidence of a successful and effective repair.9,16,17 In our study, we defined sac regression as > 5 mm, which is in line with definitions by The Society of Vascular Surgery.11 Sac regression was observed in 39 of 101 patients during the course of follow-up. After 12 months, the rate of regression was over 55%. Broker et al reported regression rates of 5 to 20% at 12 months after EVAR.7 However, Hogg et al reported
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Table 3 Associated factor analysisa for the regression of an aneurysm sac after EVAR HR (95% CI)
p
Age
0.953 (0.898–1.123)
0.102
Sex (male)
1.327 (0.387–4.952)
0.612
Hypertension
1.294 (0.564–2.789)
0.498
Diabetes mellitus
0.911 (0.423–2.009)
0.908
Ischemic heart disease
0.854 (0.379–1.895)
0.853
Aneurysm size
0.981 (0.932–1.050)
0.762
Device (Zenith)
1.142 (0.334–3.793)
0.765
Thrombus (> 75%)
0.841 (0.212–2.542)
0.812
No endoleak
3.712 (1.723–7.584)
0.001
Neck diameter
1.839 (0.654–4.239)
0.356
Neck angle (anteroposterior)
1.435 (0.324–7.392)
0.254
Initial artery embolization
0.982 (0.459–1.673)
0.893
Associated factor
Abbreviations: CI, confidence interval; EVAR, endovascular aneurysm repair; HR, hazard ratio. a Cox proportional hazard model.
rates similar to what we found, that is, 55, 66, and 60% at years 1, 2, and 3, respectively.8 Depending on the study period, the proportion of regression increased despite liberalization of the IFU. It was related to the progression of endografts such as Talent (Medtronics, Santa Rosa, California, United States) or the new Excluder low permeability endograft (ELPE; Gore & Associates INC, Flagstaff, Arizona, United States).8,18
Fig. 2 Regression rates and freedom rate form reintervention for endoleak and no endoleak groups over 3 years.
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The factors associated with aneurysm size after EVAR are yet to be determined. In a recent study, the factors most closely associated with sac enlargement were age and a vessel anatomy outside IFU specifications (conical aortic neck, aortic neck diameter > 28 mm, aortic neck angle > 60, common iliac artery diameter > 20 mm), as well as the presence of an endoleak during follow-up.9 All cases in our study fell within the IFU guidelines and were technically successful. The most important factor associated with sac regression is the presence of an endoleak history during follow-up in our study like other reports.6,13,17 The anatomic factors not associated with the IFU (e.g., thrombus in aneurysm, sac size) were not associated with sac regression. We examined other anatomic factors (viz., diameter, length, angle, and calcification of neck and iliac artery), but there is no difference between regression and no regression group. Because we performed EVAR by IFU (Instruction For Use) of device, there were little anatomic variables between two groups. Several recent reports have shown that a change in aneurysm size after EVAR is device specific.6,7,18 Aneurysm shrinkage was greater with Talent endografts despite higher initial endoleak rates, but was lower with excluder graft.7 Others have reported that size changes in the presence of an endoleak are variable and unpredictable.6,17,19 In another study, the presence of an endoleak was associated with significantly less shrinkage at 1 year but not at 2 years.12 When endoleak occurs, management can be usually divided into five broad classifications: (1) conservative observation, (2) additional endoluminal graft, (3) embolization and other endovascular repair, (4) surgical correction of the aortic neck, and (5) conversion to open repair of aneurysm. Selection of the appropriate management depends on the severity of the endoleak, change of aneurysm sac size, the timing of detection, and the medical status of the patient. Type I and type III endoleaks signify incomplete exclusion of the aneurysm sac from systemic arterial pressure and therefore present a continued risk of aneurysm rupture and should be treated promptly. However, the treatment of type II endoleaks remains controversial. Although some type II endoleaks will resolve spontaneously, aneurysm expansion and even rupture can occur in the presence of a type II endoleak.20 Most cases of minor endoleak, and those detected only on early postoperative imaging studies will be treated initially by observation. This may include frequent imaging to determine aneurysm size and extent of the endoleak. In our institution, the indication of intervention for endoleak was enlargement of the AAA diameter of over 5 mm within 1 year after EVAR. The decision of management was made in collaboration between attending surgeons and radiologists. Patients who were selected for treatment of endoleaks underwent arteriography with selective injection of the internal iliac arteries and superior mesenteric artery to evaluate lumbar and IMA before embolization and stent grafting. Both the endoleak’s cavity and the associated artery were then embolized using coils and glue by a microcatheter.21 Additional grafting may be possible to close the endoleak. Embolization appears to be successful in obliterating the source of endoleak and Thoracic and Cardiovascular Surgeon
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Factors Affecting Anatomical Changes after Endovascular AAA Repair
Factors Affecting Anatomical Changes after Endovascular AAA Repair preventing enlargement of the aneurysm. The technique has been reserved primarily for endoleak associated with retrograde flow from collateral vessels such as internal iliac artery and LA, but there may also be applications for embolization of the aneurysm sac itself in cases of perigraft endoleak.22 Surgical banding or ligation may be possible to close a perigraft channel by placing ligation around the proximal aortic neck to reinforce and tighten the seal between the endoluminal graft-stent combination and the aortic wall. The disadvantage of this procedure is that it requires laparotomy, but this may be less stressful in high-risk patients because it does not require clamping or opening the aorta. Type I and type III endoleaks associated with adverse effect in many reports. And in our report, AAA sac regression seemed to be absent only in patients with current or previous endoleaks in our report. So that it is important to effort to lower the endoleak as to treat and follow-up endoleak. Recently, prophylactic intervention can be performed before EVAR (preoperatively) or during EVAR (intraoperatively and opinions have varied widely).23 Some reports advocated the use of prophylactic visceral artery and LA embolization, but a clear consensus has not been reached. Despite a lack of theoretical evidence, there were reports that statin or calcium channel blockers might abate the size of aneurysm after EVAR by inhibition of matrix metallopeptidase-9 (MMP-9). 24,25 This study is a retrospective study and involved several patients who were lost to follow-up, introducing a possible selection bias. We used the standard definition of maximum diameter decrease over 5 mm for AAA sac regression. Recent reports have suggested that changes in AAA sac volume may provide a more sensitive way to detect AAA sac growth. We only used the diameter as a measure of AAA regression, not volume. It was difficult to check AAA volume in our workstation. In our institution, volumetry is not a routine measurement. We could not correlate size change with rupture risk in this study. Our results have arisen from only 60% of the patients who met the primary end point at 2 years. In addition, the mean follow-up seems rather short in the light of the recruiting interval. Despite these limitations, our study showed the natural change of size and factors associated with sac regression after EVAR performed by a device within the IFU guideline with minimization of anatomic variable. AAA sac regression seemed to be absent only in patients with current or previous endoleaks. As with all EVAR patients, continued surveillance is necessary even in patients with stable or shrinking AAA sacs to better understand late performance and help prevent late complications.
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Conflict of Interest There is no conflict of interest.
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References
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Factors Affecting Anatomical Changes after Endovascular Abdominal Aortic Aneurysm Repair Keun-Myoung Park1 Kwang Bo Park2
Dong-Ik Kim1
Young-Wook Kim1
1 Division of Vascular Surgery, Sungkyunkwan University School of
Medicine, Samsung Medical Center, Seoul, Republic of Korea 2 Department of Radiology, Sungkyunkwan University School of Medicine, Samsung Medical Center, Seoul, Republic of Korea
Young-Soo Do2
Hong Suk Park2
Address for correspondence Dong-Ik Kim, MD, PhD, Division of Vascular Surgery, Sungkyunkwan University School of Medicine, Samsung Medical Center, 81 Irwon-Ro Gangnam-gu Seoul 135-710, Republic of Korea (e-mail: [email protected]).
Abstract
Keywords
► endoavascular aneurysm repair ► abdominal aortic aneurysm ► aneurysm sac size
Background The primary goal of endovascular aneurysm repair (EVAR) is to prevent death from aneurysm rupture. Regression of aortic sac size is believed to be a marker for success after EVAR. This study analyzes the changes in aneurysm sac size and the factors affecting sac regression after EVAR. Patients and Methods We retrospectively reviewed 121 patients with abdominal aortic aneurysm (AAA) who underwent elective treatment with EVAR at our institution from January 2005 to December 2011. In this study, 17 of the 121 patients were excluded due to loss during follow-up or for not having undergone a postoperative computed tomographic (CT) scan, and 3 patients were excluded due to an isolated iliac artery aneurysm. CT scans were scheduled at months 1, 6, and 12, and annually thereafter. Aneurysm size was defined by the minor axis on the largest axial cut of the aneurysm on a two-dimensional CT scan. Sac regression was defined as a reduction in the diameter of more than 5 mm. Results Sac regression was observed during follow-up in 39 of the 101 patients. There was 1 regression in 87 patients (1%) at 1 month, 18 in 62 patients at 6 months (29%), 26 regressions in 44 patients (59%) at 12 months, and 18 regressions in 34 patients (53%) at 24 months. After multivariate analysis, the absence of endoleaks was the only factor associated with sac regression (hazard ratio, 3.620; confidence interval, 1.692–7.747; p ¼ 0.001). Conclusion Sac regression over 5 mm is associated with current or previous endoleaks after EVAR. Continued surveillance is necessary in all patients after EVAR to prevent late complications.
Introduction Endovascular aneurysm repair (EVAR) is widely accepted as an alternative for open repair in treatment of abdominal aortic aneurysm (AAA). EVAR has proven to be a less-invasive procedure compared with conventional open repair surgery, with shorter procedure duration, reduced blood loss, shorter hospital stays, and a significantly lower 30-day mortality rate.1,2
received March 16, 2014 accepted after revision June 22, 2014 published online September 5, 2014
The primary goal of EVAR is to prevent death from aneurysm rupture. As EVAR continues to evolve, it is important to identify factors that predict long-term clinical success. Presently, many studies cite the regression of AAA size as the marker for successful repair.3–8 Regression of the aneurysm around the endograft is presumed to indicate exclusion of the aneurysm from the circulation and an absence of systemic pressure within the sac. Expansion implies persistent
© 2015 Georg Thieme Verlag KG Stuttgart · New York
DOI http://dx.doi.org/ 10.1055/s-0034-1387819. ISSN 0171-6425.
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Thorac Cardiovasc Surg 2015;63:139–145.
Factors Affecting Anatomical Changes after Endovascular AAA Repair pressurization and incomplete exclusion of the AAA sac and has been suggested as an indication for intervention with or without an endoleak. A recent study showed that an increase in sac enlargement after EVAR was attributable to liberalization of the Instructions For Use (IFU), which set guidelines for EVAR candidacy based on aortic neck diameter, aortic neck angle, and common iliac artery diameter.9 A recent report showed that young age, aortic neck quality, and neck calcification were associated with sac regression.10 However, there was no report about the factors associated with sac regression after EVAR under the IFU. The purpose of this investigation was to determine the change in aneurysm diameter and the factors affecting regression of the aneurysm sac after EVAR under anatomy inside the IFU.
Patients and Methods We performed a retrospective review of 121 patients with AAAs who underwent elective treatment with EVAR at our institution from January 2005 to December 2011. Out of the 121 eligible patients, 101 were included. Our indication of EVAR was aneurysm size over 5 mm, symptomatic aneurysm, saccular aneurysm, and ruptured aneurysm. The most indication of EVAR was aneurysm size. One patients was underwent EVAR although aneurysm size was below 5 mm with saccular aneurysm of Bechet disease. Out of all, 17 patients were excluded due to loss during follow-up or not having undergone a postoperative computed tomography (CT) scan, and 3 patients were excluded due to an isolated iliac artery aneurysm. All the AAAs were infrarenal. Isolated iliac artery aneurysms without a concurrent AAA were excluded. All aneurysms in our study were conservatively defined by Schanzer et al within the IFUs.9 All included patients had a technically successful EVAR. Technical success depends on periprocedural events that occur from the initiation of the procedure and extend through the first 24-hour postoperative period. Primary technical success is defined by an intention-to-treat basis and requires the successful introduction and deployment of the device in the absence of surgical conversion or death, type I or III endoleaks, or graft limb obstruction.
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We reviewed preoperative, perioperative, and postoperative follow-up data from hospital records and radiology studies. Follow-up for all patients undergoing EVAR consisted of an office visit with the operating surgeon. Duplex or CT scans were scheduled at months 1, 6, and 12, and annually thereafter. Analysis of CT imaging was done using Centricity PACS viewer (GE Healthcare, Amersham, Buckinghamshire, UK). AAA size was defined as the minor axis on the largest axial cut of the aneurysm on a two-dimensional CT scan. AAA sac size change was determined by comparing the minor axis measurements between the preoperative and all subsequent imaging; major axis measurements were not used as they do not necessarily represent the true diameter of the AAA, since the AAA sac may not be parallel to the axis of the body. The minor axis was chosen for reproducibility and to prevent overestimation of AAA size due to tortuosity of the aorta. Neck angle was measured in sagittal (lateral angle) and coronal image (anteroposterior angle). All of the aneurysms were measured twice, and the size of the aneurysmal sac was considered the mean of both measurements. Thrombus in the aneurysm was measured by the proportion between the diameter of lumen and aneurysm in the long axis. On the basis of this measurement, we stratified the thrombi into three groups (below 50%, between 50% and 75%, and over 75%) (►Fig. 1). Significant sac regression was defined as > 5 mm.11 We used analysis of variance to analyze differences between the regression and nonregression groups. A chi-square test and t-test were performed. We considered a of p < 0 0.05 statistically significant. We used the standard definition of maximum diameter decrease over 5 mm without reintervention as longterm technical success for AAA sac regression. We used analysis of variance to analyze differences between the regression and nonregression groups. A chi square test and t test were performed. We considered a of p < 0 0.05 statistically significant. The primary end point of our study was sac regression rate without reintervention. The secondary end point was the factor affecting to longterm technical success. To determine risk factors related to sac regression, a multivariate analysis was conducted using logistic regression and the Cox proportional hazards model. Analysis of time-toevent occurrence of AAA sac regression without reintervention was performed with the Kaplan–Meier method, and
Fig. 1 Measurement of thrombus—three groups: (A) below 50%, (B) between 50 and 75%, and (C) over 75% were divided by the proportion between the diameter of the lumen and aneurysm in the long axis. Thoracic and Cardiovascular Surgeon
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group differences (stratified by endoleak) were compared using the log-rank test.
Results All patients had a baseline CT scan within 1 month before EVAR and at least one follow-up CT scan after EVAR. A total of 101 preoperative and 265 follow-up CTs were performed on 101 patients. The average preoperative AAA diameter was 55.04 7.38 mm (range, 35.7–91.4). Thrombus formation in the aneurysm (> 50% of the aneurysm diameter) in preoperative CT scan was observed in 81 patients. Mean follow-up was 24.10 15.17 months (range, 1–66), with an average of 2.62 1.45 postoperative CT scans available per patient for 5 years. At 1 month, 87 of 101 patients had a follow-up CT scan. At 6 months, 62 of 96 patients had a follow-up CT. At 12 months, 44 of 67 patients had a CT. At 24 months, 34 of 55 patients had a CT performed. There was no 30 days mortality and aneurysm-related death during follow-up. The presence of any type of endoleak during follow-up was documented in 48 patients for an overall incidence of 48%. Out of 48 patients, 4 had types I and III endoleaks. One type I and III were in initial aortogram. In cases of decreased amounts of leakage after balloon inflation, simple observation may be an alternative to repetitive procedures. But, endoleak did not appear in the 6-month follow-up CT. Type II endoleak was found in 44 patients [lumbar artery (LA) origin: 24 patients, inferior mesenteric artery (IMA) origin: 14 patients, LA þ IMA: 6 patients]. During followup, 20 patients of type II endoleak were discontinued within 6 months after EVAR. The remaining 24 patients of type II endoleak were continued more than 6 months after EVAR. The number of patients who experienced spontaneous resolving of type II endoleak at 1 month, 6 months, 1 year, and 2 years were nine patients, six patients, four patients, and one patient, respectively. The six patients with persistent type II endoleak over 6 months developed significant aneurysm sac increase. The 18 patients with persistent type II endoleak had same aneurysm sac comparing preoperative aneurysm size. Of the 48 patients who developed an endoleak, 8 patients developed significant aneurysm sac enlargements (> 5 mm). Six of eight patients underwent secondary interventions; five had embolization (type II endoleak 4, type I endoleak 1) and
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one patient had a stent graft placed (type III endoleak). Two patients without reintervention had persistent type II endoleak and under close observation due to there were no interval change in 1-year follow-up CT comparing 6 months follow-up CT. Sac regression was observed in 39 of 101 patients (39%) during the course of follow-up. After EVAR, there was one regression in 87 patients (1%) at 1 month, 18 in 62 patients at 6 months (29%), 26 regressions in 44 patients (59%) at 12 months, and 18 regressions in 34 patients (60%) at 24 months (►Table 1). There was no sac that was increasing after regression. Differences in patient demographics including age, sex, comorbidities, preoperative presence of thrombus within the AAA sac, mean maximal aneurysm diameter at baseline, neck and iliac artery anatomic factor (diameter and neck), or type of stent grafts were not statistically significant between the regression and no regression groups (►Table 2). In a multivariate analysis of factors associated with AAA regression, the most significant factor was the absence of an endoleak on any postoperative CT scan (hazard ratio, 3.620; confidence interval, 1.692–7.747). There was no relation between sac regression and other factors (►Table 3). ►Fig. 2 shows regression rates in the endoleak group versus the no endoleak group.
Discussion The purpose of EVAR of an AAA is to modify the natural history of the AAA and prevent rupture-associated mortality. Many reports commented there was a relationship between clinical success and sac size.3–8 Aneurysm diameter is a major criterion of efficacy during the follow-up of EVAR.2,11,12 Koole et al commented that the risk of rupture in patients with an AAA enlargement of 8 mm after EVAR increased over 4 years.13 In the case of EVAR, the aneurysm sac persists after the intervention and fills with thrombus, which may act as a source of ongoing inflammation with the potential to alter neck morphology and lead to endoleak development, sac repressurization, and potentially, rupture. Sac shrinkage during follow-up is considered a representative marker of success, but little is known about the mechanisms behind this phenomenon.9 Schanzer et al reported that over a 10-year period, the incidence of AAA sac enlargement after EVAR was 41% at
Table 1 Changes in the size of the aneurysm sac over a 24-month period after EVAR Months
No. of patients with new regression
No. of patients with regressiona (%)
Changeb in sac (mean SD) mm
1 (n ¼ 87)
1
1 (1)
0.22 1.96
6 (n ¼ 62)
17
18 (29)
3.48 4.95
12 (n ¼ 44)
13
26 (59)
7.044 7.76
24 (n ¼ 34)
8
18 (60)
6.96 9.73
Abbreviation: SD, standard deviation. a Size decrease from baseline of > 5 mm. b Defined as sac size decrease. Thoracic and Cardiovascular Surgeon
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Table 2 Comparison of demographic data and aneurysm characteristics between regression and no regression groups Patients
Regressiona (n ¼ 39)
No regression (n ¼ 62)
p
Age, y (mean SD)
70.1 6.3
71.3 6.0
0.601
Gender (male)
35 (90%)
58 (94%)
0.370
Hypertension
27 (69%)
45 (73%)
0.443
DM
10 (26%)
10 (16%)
0.181
Ischemic heart disease
13 (33%)
17 (27%)
0.339
COPD
5 (11%)
7 (13%)
0.526
Dyslipidemia
11 (28%)
24 (39%)
0.194
Smoking
14 (36%)
24 (39%)
Comorbidity
Indication
0.472 0.658
Size over 5 mm
35 (90%)
57 (91%)
Symptom or ruptured
3 (7%)
5 (9%)
Morphology
1 (3%)
0
53.5 5.10
55.1 10.49
Zenith (n ¼ 73)
35
38
0.081
Excluder (n ¼ 28)
4
24
0.157 0.600
Aneurysm size, mm (mean SD)
0.417
Graft material
Thrombusb > 50%
21 (54%)
35 (57%)
50–75%
12 (31%)
13 (21%)
< 75%
6 (15%)
14 (22%)
Endoleak
11 (28%)
37 (60%)
0.001
Diameter of aorta at renal ostium
23.3 4.45
22.6 5.32
0.642
Diameter of aorta at extent of aneurysm
21.5 3.10
20.1 2.89
0.485
Neck length (mm)
21.2 5.19
18.3 4.42
0.174
Max diameter of right CIA (mm)
9.9 1.32
10.9 1.32
0.588
Max diameter of left CIA (mm)
9.2 0.95
10.0 0.87
0.646
Neck angle (anteroposterior)
28.1 21.5
31.1 25.1
0.312
Neck angle (lateral)
38.5 23.7
37.1 21.5
0.492
Right CIA length
18.3 2.36
19.3 2.71
0.516
Left CIA length
21.3 1.92
20.7 1.85
0.394
Intern iliac artery embolization
10 (26%)
17 (27%)
0.524
Abbreviations: CIA, common iliac artery; COPD, chronic pulmonary obstructive disease; DM, diabetes mellitus; SD, standard deviation. a Size decrease from baseline of > 5 mm. b Thrombus was proportion between diameter of lumen and aneurysm in the long axis.
5 years. The increase in sac enlargement was attributed to liberalization of the IFU including aortic neck diameter, aortic neck angle, and common iliac artery diameter.9 However, our study excluded cases outside IFU and cases with technical failure. We have shown that after EVAR, the aneurysm diameter decreased at a mean rate of 0.58 mm/mo ( 0.64 mm/mo), similar to the rate of 0.41 to 0.50 mm/mo reported by Wolf et al14 and Broeders et al.15 Thoracic and Cardiovascular Surgeon
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The absence of an endoleak and a decrease in aneurysm size (at a rate of 0.28–0.35 mm/mo) are considered evidence of a successful and effective repair.9,16,17 In our study, we defined sac regression as > 5 mm, which is in line with definitions by The Society of Vascular Surgery.11 Sac regression was observed in 39 of 101 patients during the course of follow-up. After 12 months, the rate of regression was over 55%. Broker et al reported regression rates of 5 to 20% at 12 months after EVAR.7 However, Hogg et al reported
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Table 3 Associated factor analysisa for the regression of an aneurysm sac after EVAR HR (95% CI)
p
Age
0.953 (0.898–1.123)
0.102
Sex (male)
1.327 (0.387–4.952)
0.612
Hypertension
1.294 (0.564–2.789)
0.498
Diabetes mellitus
0.911 (0.423–2.009)
0.908
Ischemic heart disease
0.854 (0.379–1.895)
0.853
Aneurysm size
0.981 (0.932–1.050)
0.762
Device (Zenith)
1.142 (0.334–3.793)
0.765
Thrombus (> 75%)
0.841 (0.212–2.542)
0.812
No endoleak
3.712 (1.723–7.584)
0.001
Neck diameter
1.839 (0.654–4.239)
0.356
Neck angle (anteroposterior)
1.435 (0.324–7.392)
0.254
Initial artery embolization
0.982 (0.459–1.673)
0.893
Associated factor
Abbreviations: CI, confidence interval; EVAR, endovascular aneurysm repair; HR, hazard ratio. a Cox proportional hazard model.
rates similar to what we found, that is, 55, 66, and 60% at years 1, 2, and 3, respectively.8 Depending on the study period, the proportion of regression increased despite liberalization of the IFU. It was related to the progression of endografts such as Talent (Medtronics, Santa Rosa, California, United States) or the new Excluder low permeability endograft (ELPE; Gore & Associates INC, Flagstaff, Arizona, United States).8,18
Fig. 2 Regression rates and freedom rate form reintervention for endoleak and no endoleak groups over 3 years.
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The factors associated with aneurysm size after EVAR are yet to be determined. In a recent study, the factors most closely associated with sac enlargement were age and a vessel anatomy outside IFU specifications (conical aortic neck, aortic neck diameter > 28 mm, aortic neck angle > 60, common iliac artery diameter > 20 mm), as well as the presence of an endoleak during follow-up.9 All cases in our study fell within the IFU guidelines and were technically successful. The most important factor associated with sac regression is the presence of an endoleak history during follow-up in our study like other reports.6,13,17 The anatomic factors not associated with the IFU (e.g., thrombus in aneurysm, sac size) were not associated with sac regression. We examined other anatomic factors (viz., diameter, length, angle, and calcification of neck and iliac artery), but there is no difference between regression and no regression group. Because we performed EVAR by IFU (Instruction For Use) of device, there were little anatomic variables between two groups. Several recent reports have shown that a change in aneurysm size after EVAR is device specific.6,7,18 Aneurysm shrinkage was greater with Talent endografts despite higher initial endoleak rates, but was lower with excluder graft.7 Others have reported that size changes in the presence of an endoleak are variable and unpredictable.6,17,19 In another study, the presence of an endoleak was associated with significantly less shrinkage at 1 year but not at 2 years.12 When endoleak occurs, management can be usually divided into five broad classifications: (1) conservative observation, (2) additional endoluminal graft, (3) embolization and other endovascular repair, (4) surgical correction of the aortic neck, and (5) conversion to open repair of aneurysm. Selection of the appropriate management depends on the severity of the endoleak, change of aneurysm sac size, the timing of detection, and the medical status of the patient. Type I and type III endoleaks signify incomplete exclusion of the aneurysm sac from systemic arterial pressure and therefore present a continued risk of aneurysm rupture and should be treated promptly. However, the treatment of type II endoleaks remains controversial. Although some type II endoleaks will resolve spontaneously, aneurysm expansion and even rupture can occur in the presence of a type II endoleak.20 Most cases of minor endoleak, and those detected only on early postoperative imaging studies will be treated initially by observation. This may include frequent imaging to determine aneurysm size and extent of the endoleak. In our institution, the indication of intervention for endoleak was enlargement of the AAA diameter of over 5 mm within 1 year after EVAR. The decision of management was made in collaboration between attending surgeons and radiologists. Patients who were selected for treatment of endoleaks underwent arteriography with selective injection of the internal iliac arteries and superior mesenteric artery to evaluate lumbar and IMA before embolization and stent grafting. Both the endoleak’s cavity and the associated artery were then embolized using coils and glue by a microcatheter.21 Additional grafting may be possible to close the endoleak. Embolization appears to be successful in obliterating the source of endoleak and Thoracic and Cardiovascular Surgeon
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Factors Affecting Anatomical Changes after Endovascular AAA Repair preventing enlargement of the aneurysm. The technique has been reserved primarily for endoleak associated with retrograde flow from collateral vessels such as internal iliac artery and LA, but there may also be applications for embolization of the aneurysm sac itself in cases of perigraft endoleak.22 Surgical banding or ligation may be possible to close a perigraft channel by placing ligation around the proximal aortic neck to reinforce and tighten the seal between the endoluminal graft-stent combination and the aortic wall. The disadvantage of this procedure is that it requires laparotomy, but this may be less stressful in high-risk patients because it does not require clamping or opening the aorta. Type I and type III endoleaks associated with adverse effect in many reports. And in our report, AAA sac regression seemed to be absent only in patients with current or previous endoleaks in our report. So that it is important to effort to lower the endoleak as to treat and follow-up endoleak. Recently, prophylactic intervention can be performed before EVAR (preoperatively) or during EVAR (intraoperatively and opinions have varied widely).23 Some reports advocated the use of prophylactic visceral artery and LA embolization, but a clear consensus has not been reached. Despite a lack of theoretical evidence, there were reports that statin or calcium channel blockers might abate the size of aneurysm after EVAR by inhibition of matrix metallopeptidase-9 (MMP-9). 24,25 This study is a retrospective study and involved several patients who were lost to follow-up, introducing a possible selection bias. We used the standard definition of maximum diameter decrease over 5 mm for AAA sac regression. Recent reports have suggested that changes in AAA sac volume may provide a more sensitive way to detect AAA sac growth. We only used the diameter as a measure of AAA regression, not volume. It was difficult to check AAA volume in our workstation. In our institution, volumetry is not a routine measurement. We could not correlate size change with rupture risk in this study. Our results have arisen from only 60% of the patients who met the primary end point at 2 years. In addition, the mean follow-up seems rather short in the light of the recruiting interval. Despite these limitations, our study showed the natural change of size and factors associated with sac regression after EVAR performed by a device within the IFU guideline with minimization of anatomic variable. AAA sac regression seemed to be absent only in patients with current or previous endoleaks. As with all EVAR patients, continued surveillance is necessary even in patients with stable or shrinking AAA sacs to better understand late performance and help prevent late complications.
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Conflict of Interest There is no conflict of interest.
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References
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