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Clinical Research
Incidence of Post-Implantation Syndrome
with Different Endovascular Aortic
Aneurysm Repair Modalities and Devices
and Related Etiopathogenetic Implications
Ombretta Martinelli,
1
Alessia Di Girolamo,
1
Cristina Belli,
1
Roberto Gattuso,
1
Francesco Baratta,
2
Bruno Gossetti,
1
Alessia Alunno,
1
and Luigi Irace,
1
Rome, Italy
Background: Postimplantation syndrome (PIS) is a systemic inflammatory response occurring
in an early phase after abdominal aortic aneurysm (AAA) endovascular aneurysm repair
(EVAR).
The pathophysiology underlying PIS is still not well understood. It is speculated that the type of
the stent graft or the mural thrombus within the AAA may play a role in determining this inflam-
matory response. At present, there is no consensus about the influence of PIS on clinical out-
comes during follow-up.
The endovascular aneurysm sealing (EVAS) with the Nellix sac-anchoring endoprosthesis (Nel-
lix Endovascular, Palo Alto, CA) is a novel modality for AAA repair, which obliterates the sac,
thus preventing the new onset of thrombus in the aneurysm sac.
Our aim was to compare the incidence of postimplantation syndrome following EVAS and after
EVAR. Secondary aims were to assess the effect of endoskeleton AFX (Endologix) device
compared with other commercially available exoskeleton PTFE stent grafts on the inflammatory
response. Finally, we analyzed the potential association of PIS with clinical outcomes.
Methods: From January 2013 to June 2018, 60 AAA patients underwent EVAS (mean age
72 ±9 years), and 110 patients were submitted to EVAR: 56 AFX devices and 54 other
PTFE stent grafts (mean age 74 ±10 years) at a single center and were retrospectively
reviewed.
Results: EVAS with the Nellix system was associated with a lower incidence of PIS compared
to EVAR using both AFX device and other endografts (8.3, 30, 35%, respectively, P-
value ¼0.001). No statistically significant difference in PIS incidence was observed after endo-
skeleton AFX device deployment compared with other EVAR exoskeleton endografts. During
follow up, the major complications were proportionally but not significantly (P¼0.43) less
frequent after EVAS (10.3%) than after EVAR and after EVAR using AFX device (8.9%) than
after EVAR with other PTFE stent grafts (16.4%).
During follow up (mean 24 months), adverse outcome rates did not significantly differ in patients
with and without PIS (8.0 vs. 13.4% P¼0.43).
Conclusions: Our data confirm the lower risk of PIS following EVAS compared to EVAR. Most
importantly, this study highlights the role of new-onset mural thrombus in the genesis of PIS. The
lower inflammatory reaction observed after EVAS than after EVAR might be related to the
1
Vascular Surgery Department, ‘‘Sapienza’’ University of Rome,
Umberto I Hospital Rome, Rome, Italy.
2
Department of Medicine, ‘‘Sapienza’’ University of Rome, Umberto
I Hospital Rome, Rome, Italy.
Correspondence to: Ombretta Martinelli, MD, Department of
Vascular Surgery and Emergency Vascular Surgery, ‘‘Sapienza’’
University of Rome, Viale del Policlinico, 144 00161 Rome, Italy;
E-mail: ombretta.martinelli@uniroma1.it
Ann Vasc Surg 2019; -: 1–7
https://doi.org/10.1016/j.avsg.2019.08.095
Ó2019 Elsevier Inc. All rights reserved.
Manuscript received: June 12, 2019; manuscript accepted: August 13,
2019; published online: ---
1
endobags of the Nellix system, which completely seal the aneurysm sac, reducing the new onset
of mural thrombus.
The systemic inflammatory response does not significantly differ after endoskeleton AFX device
deployment compared with other EVAR exoskeleton stent grafts.
PIS does not seem to have any significant prognostic implications in terms of early major
adverse events.
INTRODUCTION
The postimplantation syndrome (PIS) may occur
shortly after endovascular aneurysm repair
(EVAR) in patients treated for abdominal aortic
aneurysm (AAA).
The incidence of this disease has been varying
from 14 to 60% due to an underestimation of this
syndrome, which is not systematically reported.
1
Based on current evidence, this acute systemic
inflammatory response is defined as the presence
of fever (>38C) and leukocytosis (>12,000/mL) ac-
cording to the SIRS criteria without any evidence of
an infection. In addition, Vo^
ute et al.
2
also included
the elevated values of high sensitive serum C-reac-
tive protein (hs-CPR) level above serum C-reactive
protein in the definition of PIS syndrome since hs-
CRP may express more constantly and reliably the
intensity of inflammatory response to the endograft
deployment.
Although Velasquez first described the PIS in
1999,
3
its etiology is still unclear. It is conceivable
that the clinical and biochemical expression of this
inflammatory response is multifactorial. A hypothe-
sized cause of PIS is related to the amount of new-
onset thrombus within the aneurysm thrombus
and its release of tumor necrosis factor a(TNF- a),
interleukin-6 (IL- 6), and other cytokines within
the aortic aneurysm.
4
The endovascular aneurysm sealing (EVAS) sys-
tem with the Nellix sac-anchoring endoprosthesis
(Nellix Endovascular, Palo Alto, CA) is an alterna-
tive approach to the endovascular treatment of
AAA. Such a device provides an active aneurysm
sac management by means of 2 polymer-filled endo-
bags; these endobags form a cast of the flow lumen
of the aorta and iliac arteries, obliterating the sac
and preventing the new-onset of mural thrombus.
This novel EVAS device for abdominal aortic aneu-
rysm repair has shown a low incidence of endoleaks
and reintervention, comparable to conventional
EVAR with modern devices.
5,6
This study is aimed
at assessing whether the lack of new-onset
thrombus after EVAS may influence the incidence
of PIS compared to that after EVAR.
Different types of biomaterials may also provoke
varying inflammatory responses, activate white
blood cells
7
and platelets and promote the release
of inflammatory mediators such as cytokines.
8
Proof
of this, the severity of the postimplantation inflam-
matory reaction was different between patients
receiving different endografts with a stronger in-
flammatory reaction using polyester endovascular
grafts than PTFE devices.
Other factors, apart from stent graft material, may
have a role in the pathogenesis of PIS as the inci-
dence and severity of PIS may vary in patients
treated with the same type of endograft. Thus,
another aim of this study was to assess the role of
the endoskeleton and exoskeleton of EVAR stent
graft on the PIS.
Finally, we evaluated the association between
PIS and clinical complications, regardless of the
type of stent graft.
MATERIALS AND METHODS
This was a single-center, retrospective, observa-
tional study using data extracted from medical re-
cords. Informed consent for the study was
obtained from all patients, following the principles
outlined in the Declaration to Helsinki. Specific
ethical approval for this study was not required
because the analysis undertakes used data collected
for routine clinical care. All patients submitted to
elective AAA endovascular repair at our institution
from January 2013 to June 2018 were enrolled.
The exclusion criteria were clinical and/or labora-
tory evidence of a recent infection, ruptured AAA,
prior EVAR, complex endovascular procedures,
need for concomitant open surgical procedures
(e.g., vascular reconstruction), use of nonsteroidal
antiinflammatory drugs, corticosteroids or cyclo-
oxygenase-2 inhibitors.
The study sample included patients submitted to
EVAS with the Nellix system (Endologix, Irvine,
CA) and patients undergoing EVAR with devices
made from expanded polytetrafluoroethylene
(ePTFE). The EVAR cohort was further divided
into 2 groups with respect to the stent position of
the endograft used: group A, including modular de-
vices with nitinol exoskeleton (Gore Excluder and
Gore C3; W. L. Gore and Assoc, Flagstaff), group B
2Martinelli et al. Annals of Vascular Surgery
receiving a main bifurcated body with cobalt-
chromium endoskeleton (AFX Endologix, Irvine,
CA).
The morphological characteristics of the treated
aneurysms were similar. The choice of EVAS with
Nellix endosystem was determined by the presence
of at least 3 branches (lumbar arteries and/or infe-
rior mesenteric artery) with a high risk of type 2
endoleak. The indication for the use of AFX endog-
raft was linked to the presence of a tight aortic bifur-
cation diameter <20 mm, as well as to the presence
of branches emerging from the aneurysmal sac.
All patients were submitted to preoperative
computed tomography (CT) scans or magnetic reso-
nance imaging (MRI) to plan the endovascular
treatment based on the aortoiliac morphology. The
diameters of the AAA and flow-lumen were calcu-
lated using a multiplanar reconstruction (MPR)
method on both the MRI images and the CT scans.
All measurements of the aneurysm were performed
using automatic 3-dimensional sizing software
(EndoSize; Therenva SAS, Rennes, France). The
volume of both the aneurysm sac and mural
thrombus was measured using a dedicated software
OsiriX MD; Pixmeo Labs, Geneva, Switzerland).
Preoperative thrombus volume was calculated
from the difference between AAA volume and
flow lumen volume.
The choice of the device to use was based on the
anatomical characteristics of the aortic neck and of
the iliac arteries, aneurysm sac configuration, the
presence of thrombus or calcification and the num-
ber of patent arteries emerging from the aneurysmal
sac. All stent grafts were used at the discretion of the
surgeon for the duration of the study.
All patients received prophylactic antibiotics
before the procedure and 5.000 International Units
of unfractionated heparin before insertion of the
stent graft deployment system.
Local or general anesthesia was selected at the
discretion of the anesthesiological team.
PIS should fulfill at least 2 of the following
criteria: persisting body temperature >38C lasting
for >1 day, leukocyte count >12,000/mL, and hs-
CPR >10 mg/L. These parameters were serially
assessed before EVAR and during hospitalization.
We also measured the erythrocyte sedimentation
rate (ESR) as an additional marker of inflammation.
Hospital duration of stay was also recorded for
each patient.
All patients received antiplatelet therapy imme-
diately after the endovascular procedure and
continued throughout the follow-up.
Follow-up surveillance included visits and
Duplex ultrasound scanning (DUS) examination at
1 month after discharge, at 3, 6, and 12 months after
the procedure, and annually thereafter. CT scans or
MRIs were performed at 1 and 12 months after the
procedure and, then, based on DUS results. The vol-
ume of new-onset thrombus after EVAR was calcu-
lated using the formula: volume of the endografte
preoperative luminal volume ¼volume of the
new-onset thrombus (provided there were no endo-
leak), whereas the post-EVAS thrombus volume
was calculated from the difference between AAA
volume and the volume of the Nellix endobags,
including the balloon-expandable stents.
The major complications included adverse car-
diovascular events (myocardial infarction and tran-
sient or permanent cerebral ischemia), bowel
ischemia, renal dysfunction (increase in serum
creatinine of 1.5 times than preoperative level), res-
piratory failure, stroke, and paraplegia.
STATISTICAL ANALYSIS
Categorical variables are reported as apercentage
(%), and continuous variables were expressed as
mean ± SD. Differences were tested using Fisher’s
exact test. A multivariable logistic regression anal-
ysis was built to investigate the factors associated
with PIS in the whole study population. Variables
used for PIS definition were excluded from the
model.
Only Pvalues <0.05 were considered as statisti-
cally significant. Analyses were performed using
computer software packages (SPSS-25.0, SPSS Inc.)
RESULTS
The study included 169 patients (86% males, mean
age 72 ± 9 years) 58 patients (34.2%) underwent
EVAS with Nellix system and of the 111 patients
(65.8%) were submitted to EVAR using modular de-
vices made from expanded polytetrafluoroethylene
(ePTFE) and a nitinol exoskeleton (Excluder, Gore
C3) in 55 cases of group A and Chromium-Cobalt
endoskeleton (AFX) in 56 cases of group B,
respectively.
The stent grafts were inserted through percuta-
neous femoral access in 44% of cases and with sur-
gical femoral cutdown in the remaining 56% based
on morphological features of the femoral arteries.
The baseline characteristics and procedure data
were comparable between groups as shown in
Table I.
Postoperative data about PIS are summarized in
Table II. PIS occurred in 50 cases of all the studied
populations (29.6%).
Volume -,-2019 EVAS and EVAR postimplantation syndrome 3
The incidence of PIS was significantly lower after
EVAS than after EVAR (13.8 vs. 38.7%, P¼0.001).
Although less frequent after AFX stent graft implan-
tation, there was no statistically significant differ-
ence in PIS incidence among group A and group B
of EVAR cohort (46.6 vs. 33.29%, P¼0.333).
No significant differences in PIS duration were
recorded among the 3 groups (P¼0.06).
With respect to the maximum value for each
outcome during the 72-hour post-procedural
period.
EVAS group had lower values of all 3 major
indices of inflammation than the EVAR cohort
(Table III).
As regards the thrombus behavior, we observed
an average reduction of 2% of thrombus-filled vol-
ume immediately after EVAS in 4 patients (6.9%)
and an average decrease of 15% at 1 year in 10 cases
(17.2%), comparing equivalent postoperative im-
ages. No significant new-onset of mural thrombus
occurred following EVAS.
After EVAR, an average new-onset thrombus of
21 and 14% were found in the patients of group A
and group B, respectively.
From a multivariate analysis considering the
characteristics of PIS patients of all the studied pop-
ulations, the use of the Nellix device was the only in-
dependent factor in inverse correlation with the PIS
(Table IV).
As depicted in Figure 1 by Kaplan-Meier analysis,
there were no significant differences in freedom from
early complications between device groups. During a
mean follow-up period of 24 months (ranging from 12
to 60 months), major adverse events were proportion-
ally but not statistically significant less frequent after
EVAS (10.3%) than after EVAR (16.4%).
In the EVAR cohort, the incidence of complica-
tions was also lower in group B (8.9%) than in
group A (16.4%), but this difference also was not
statistically significant (P¼0.43).
The adverse outcomes rates did not significantly
differ in patients with and without PIS (8.0 vs.
Table I. Baseline characteristics and procedure data of the study population
Variable
Whole
(n¼169)
EVAS
(n¼58)
EVAR group A
(n¼55)
EVAR group B
(n¼56) P
Age (years) 73.7 ± 7.5 72.5 ± 8.5 74.1 ± 7.1 74.7 ± 6.6 0.278
Blood hypertension (%) 66.3 62.1 76.4 60.7 0.154
Atrial Fibrillation (%) 8.3 8.6 9.1 7.1 0.927
Renal dysfunction (%) 12.4 10.3 14.5 12.5 0.795
Diabetes (%) 15.4 12.1 14.5 19.6 0.522
Dyslipidaemia (%) 41.4 48.3 27.3 48.2 0.035
Procedure characteristics
Duration, min 100 ± 28.1 132 ± 21.2 120 ± 55 0.56
Contrast material volume, mL 180 ± 34 185 ± 30 80 ± 55 0.07
Table II. Incidence rate of postimplantation syndrome
Incidence rate of PIS Whole (n¼169) EVAS (n¼58) EVAR (n¼111) P
EVAS vs EVAR (%) 29.6 13.8 38.7 0.001
Incidence rate of PIS Whole (n¼111) EVAR (n¼55) AFX (n¼56) P
Other EVAR devisces vs AFX device (%) 29.6 46.6 33.9 0.333
Table III. Inflammatory markers of PISby endovascular procedure
PIS markers EVAS (n¼58) EVAR (n¼111) P
Postprocedural fever >38.5 (%) 8.6 34.5 0.004
Postprocedural leukocytosis >13,000/mL (%) 12.1 20.8 0.456
Postprocedural high-sensitivity C-reactive
protein elevation >10 mg/L (%)
46.6 72.7 0.015
4Martinelli et al. Annals of Vascular Surgery
13.4% P¼0.43). Postoperative hospital stay was
longer for patients with PIS than without PIS (7
vs. 4 days).
DISCUSSION
With the growing application of the endovascular
repair of abdominal aortic aneurysm, many issues
related to this treatment option are becoming
crucial, and PIS is one of these issues. The true path-
ophysiology and the clinical significance of this in-
flammatory response following EVAR are still
largely unknown.
Multiple factors have been proposed as a trigger
of this postimplantation syndrome.
Some authors suggest that the endograft material
is associated with the release of proinflammatory
markers involved in PIS development.
9
The type of fabric used in manufacturing endovas-
cular stent grafts has proven to play a material role in
the development of postimplantation syndrome
10
In this respect, Moulakakis demonstrated that the
polyester stent grafts can induce a higher postoper-
ative inflammatory response than PTFE devices.
11
Arnaoutoglou et al. confirmed this finding in a later
report showing a 10 times higher risk for an inflamma-
tory response in patients with polyester endograft.
12
Based on this evidence of the influence of poly-
ester in the determinism of PIS after EVAR, patients
receiving conventional polyester stent grafts were
excluded from the current study, which was aimed
to assess the real incidence of PIS following EVAS
with Nellix platform compared to EVAR using
PTFE devices.
Among the EVAR cases, the incidence and
severity of PIS may vary in patients treated with
the same type of endograft. Thus, apart from stent
graft material, other factors, such as the stent graft
design, may have a role in the pathogenesis of PIS.
Most of the currently available endografts share
similar design features, such as a bifurcated fabric stent
construct, and have an exoskeleton except for the
AFX device (Endologix) which has an endoskeleton.
It is conceivable that the endoskeleton of the AFX
device may stimulate a different inflammatory
response than the standard EVAR with exoskeleton.
Our findings showed that the incidence of PIS
was lower with EVAR using AFX devices than
with other EVAR devices, but this difference was
not statistically significant even if the low number
of the 2 samples may have been affected the data.
Our data showed that the use of the Nellix system
resulted in a less frequent inflammatory response in
comparison to EVAR PTFE endograft.
Accordingly, by retrospectively studying 41 pa-
tients after the use of Nellix, Berg et al.
13
have found
that EVAS is associated with a mild systematic in-
flammatory response compared with EVAR.
The lower incidence of PIS observed after implan-
tation of the Nellix stents with exoskeleton
compared to the AFX implantation confirms that
the position of the stent does not significantly influ-
ence the genesis of this syndrome.
There may be other differences between stent
grafts, unrelated to graft material and design, which
can be involved in the postimplant inflammatory
reaction.
Some authors suggest that manipulations with
large introducers, sheaths, and catheters within
the femoroiliac arterial lumen and inside the aorta
might be the source of ILs and other inflammation
mediators released during the AAA endovascular
repair.
14
Our findings seem to controvert this theory
because the procedure with AFX stent graft has al-
ways implied the minor manipulations and the use
of lower profile device while having an incidence
of PIS greater than EVAS with Nellix platform
even in cases of complex procedures combined
with chimney.
15
Table IV. Multivariable associations: Nellix system was the only predictor independently and inversely
associated postimplantation syndrome in PIS patients
PIS patients (n¼50) POR
95% CI for OR
Lower Upper
Age 0.422 0.980 0.934 1.029
Atrial fibrillation 0.360 0.511 0.122 2.148
Blood hypertension 0.359 0.700 0.327 1.500
Renal dysfunction 0.378 1.599 0.563 4.545
Coronary heart disease 0.252 0.639 0.297 1.375
Diabetes 0.232 0.510 0.169 1.537
Dyslipidaemia 0.634 0.831 0.388 1.780
Nellix 0.000 0.196 0.079 0.490
Volume -,-2019 EVAS and EVAR postimplantation syndrome 5
The multivariate analysis considering the charac-
teristics of all PIS patients of our series showed that
EVAS with Nellix device was the only independent
factor inversely related with the PIS.
A full explanation of this finding cannot be
formulated due to the multifactorial and still uncer-
tain etiology of PIS. However, a plausible hypothesis
for this lower incidence of PIS involves the amount
of new-onset mural thrombus observed after EVAR
and EVAS. Several investigations tried to correlate
PIS with thrombus inside the aneurysm sac that
might be the source of ILs and other mediators of
the systemic inflammatory response released during
the endovascular procedure. Swartbol et al.
16
sug-
gested that fresh thrombi may be more prone to
cause reactions and release of cytokines than orga-
nized thrombi. To confirm this, Kakisis et al.
17
indi-
cated that PIS is related to filling the excluded
aneurysm sac, rather than the chronic mural
thrombus.
In line with these observations, the lower inci-
dence of PIS following the Nellix implantation
may be related to the lack of new-onset mural
thrombus, reducing the release of various proin-
flammatory cytokines. We have even observed a
reduction of thrombus-filled volume inside the
AAA after EVAS comparing equivalent preoperative
images.
18
This reduction may be related to the
squeezing of the most fluid parts of the intramural
thrombus into patent lumbar arteries and the infe-
rior mesenteric artery due to endobag inflation.
As a further confirmation of this hypothesis, the
smaller amount of new-onset thrombus following
AFX implantation than after other conventional
stent grafts may explain the proportional, although
not significant, lower incidence of PIS observed after
EVAR with AFX stent graft compared to EVAR with
other PTFE devices.
The Relation of PIS with Patient’s
Outcomes is Still a Concern
Some authors assert that the release of pro-
inflammatory cytokines, leukocyte activation, and
proliferation due to PIS may be associated with
increased postoperative complications and mortal-
ity, especially in high-risk patients. In a prospective
study, Arnaoutoglou showed that the magnitude of
inflammation (measured by the maximum value of
high sensitivity CRP) correlated with adverse car-
diovascular events within 30 days after the proced-
ure.
19
In other studies, PIS has been considered a
transient and harmless condition, although it may
lead to prolonged hospitalization. Moulakakis
et al.
20
showed that postimplantation inflammatory
syndrome was not associate with early clinical
adverse events. Kwon et al.
21
observed that patients
with and without PIS had similar long-term overall
survival rates and other clinical outcomes. Accord-
ingly, our group found no association between the
development of PIS and the occurrence of major car-
diovascular events.
There were several limitations to this study. First,
the relatively limited sample size. Second, due to the
retrospective design of the study, we could not
assess some important inflammatory markers, such
as interleukins and tumor necrosis factors; we
were also unable to check an asymptomatic
Fig. 1. Major complication rates following the deployment of Nellix device, AFX endografts, and other ePTFE devices.
6Martinelli et al. Annals of Vascular Surgery
elevation of myocardial ischemia markers and its
relation to PIS. Another limitation concerns the
methodology for measuring the preoperative and
follow-up thrombus burden of the aneurysmal sac
based on CTA images since we used the maximum
recorded thickness, which may be less accurate.
Given these limitations, our data confirm the
lower risk of PIS following EVAS compared to
EVAR. Most importantly, this study highlights the
association between the occurrence of PIS and the
different amounts of new-onset mural thrombus
observed after EVAR and EVAS. The stent graft
design seems not to influence the postimplant in-
flammatory reaction.
CONCLUSIONS
Finally, we did not find any significant interrelation-
ship between PIS and the incidence of early major
complications, although there is no evidence of
this in the long term. Anyhow, PIS prolongs the
postoperative hospital stay with inherent economic
and management implications. A prospective design
of the studies with a larger number of patients
would be required for more complete results.
REFERENCES
1. Arnaoutoglou E, Kouvelos G, Milionis H, et al. Post-implan-
tation syndrome following endovascular abdominal aortic
aneurysm repair: preliminary data. Interact Cardiovasc
Thorac Surg 2011;12:609e14.
2. Vo^
ute MT1, Bastos Gonc
¸alves FM, van de Luijtgaarden KM,
et al. Stent graft composition plays a material role in the
postimplantation syndrome. J Vasc Surg 2012;56:1503e9.
3. Vel
azquez OC, Carpenter JP, Baum RA, et al. Perigraft air,
fever, and leukocytosis after endovascular repair of abdom-
inal aortic aneurysms. Am J Surg 1999;178:185e9.
4. Ferreira V, Machado R, Martins J, et al. Post-implantation
syndromeeretrospective analysis of 52 patients. Angiol Cir
Vasc 2015;11:204e8.
5. Reijnen MMPJ, Holden A. Status of endovascular aneurysm
sealing after 5 Years of commercial use. J Endovasc Ther
2018;25:201e6.
6. Gossetti B, Martinelli O, Ferri M, et al., IRENE Group Investi-
gators. Preliminary results of endovascular aneurysm sealing
from the multicenter Italian Research on Nellix Endoprosthe-
sis (IRENE) study. J Vasc Surg 2018;67:1397e403.
7. Swartbol P, Norgren L, Parsson H, et al. Endovascular
abdominal aortic aneurysm repair induces significant alter-
ations in surface adhesion molecule expression on donor
white blood cells exposed to patient plasma. Eur J Vasc
Endovascular Surg 1997;14:48e59.
8. Syk J, Brunkwall J, Ivancev K, et al. Postoperative fever,
bowel ischaemia and cytokine response to abdominal aortic
aneurysm repairda comparison between endovascular and
open surgery. Eur J Vasc Endovascular Surg 1998;15:
398e405.
9. Gerasimidis T, Sfyroeras G, Trellopoulos, et al. Impact of
endograft material on the inflammatory response after elec-
tive endovascular abdominal aortic aneurysm repair. Angi-
ology 2005;56:743e53.
10. Lee JH, Choi JH, Kim EJ. Volume of mural thrombus plays a
role in the elevation of inflammatory markers after endovas-
cular aortic repair. J Cardiothorac Surg 2018;13:27.
11. Kadoglou NP, Moulakakis KG, Papadakis I, et al. Differential
effects of stent-graft fabrics on arterial stiffness in patients
undergoing endovascular aneurysm repair. J Endovasc
Ther 2014;21:850e8.
12. Arnaoutoglou E, Kouvelos G, Papa N, et al. Regarding ‘‘the
impact of endograft type on inflammatory response after
endovascular treatment of abdominal aortic aneurysm’’. J
Vasc Surg 2013;58:570.
13. Berg P, Stroetges RA, Miller LE, et al. Propensity score-
matched analysis of inflammatory response with endovas-
cular aneurysm sealing vs endovascular aneurysm repair. J
Endovasc Ther 2017;24:670e4.
14. Espinosa G, Marchiori E, Silva LF, et al. Initial results of
endovascular repair of abdominal aortic aneurysms with a
self-expanding stent-graft. J Vasc Interv Radiol 2002;13:
1115e23.
15. MalajA,MartinelliO,FresilliM,etal.Treatmentofa
juxtarenal aneurysm with a parallel graft in the left
renal artery and polymer-based technology to seal
the entire aneurysmal. Sac Ann Vasc Surg 2015;29:
1662.e19e22.
16. Swartbol P, Truedsson L, Norgren L. Adverse reactions dur-
ing endovascular treatment of aortic aneurysms may be trig-
gered by interleukin 6 release from the thrombotic content.
J Vasc Surg 1998;28:664e8.
17. Kakisis JD, Moulakakis KG, Antonopoulos CN, et al. Volume
of new-onset thrombus is associated with the development
of postimplantation syndrome after endovascular aneurysm
repair. J Vasc Surg 2014;60:1140e5.
18. Gossetti B, Malaj A, Alunno A, et al. Early and mid-
term outcomes of a novel Endovascular Aneurysm Seal-
ing (EVAS) system in patients with infrarenal abdom-
inal aortic aneurysms. J Cardiovasc Surg 2019;60:
66e72.
19. Arnaoutoglou E, Kouvelos G, Papa, et al. Prospective evalu-
ation of post-implantation inflammatory response after
EVAR for AAA: influence on patients’ 30 day outcome.
Eur J Vasc Endovasc Surg 2015;49:175e83.
20. Moulakakis KG, Alepaki M, Sfyroeras GS, et al. The impact
of endograft type on inflammatory response after endovas-
cular treatment of abdominal aortic aneurysm. J Vasc Surg
2013;57:668e77.
21. Kwon H, Ko GY, Kim MJ, et al. Effects of postimplantation
systemic inflammatory response on long-term clinical out-
comes after endovascular aneurysm repair of an abdominal
aortic aneurysm. Medicine 2016;95:4532.
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