Content uploaded by Melissa Fusari
Author content
All content in this area was uploaded by Melissa Fusari on Jan 16, 2015
Content may be subject to copyright.
Long-term Outcome after Inflammatory Abdominal Aortic Aneurysm Repair:
Case-matched Study
Luigi Bonati, M.D.,
1
Patrizia Rubini, M.D., Ph.D.,
1
Gioacchino G. Japichino, M.D.,
1
Alessandro Parolari, M.D., Ph.D.,
2
Sandro Contini, M.D.,
1
Roberto Zinicola, M.D.,
1
Melissa Fusari, M.D.,
2
Paolo Biglioli, M.D.
2
1
Institute of General Surgery and Organ Transplantation, University of Parma, Via Gramsci 14, 43100 Parma, Italy
2
Department of Cardiac Surgery, Centro Cardiologico Monzino, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), University of Milan, Via
Parea 4, 20138 Milano, Italy
Abstract. The purpose of this study was to compare early and late outcomes
after inflammatory and noninflammatory abdominal aortic aneurysm
(AAA) repair with emphasis on graft-related complications. Of 625 con-
secutive patients submitted to AAA repair, 18 were classified as having in-
flammatory AAAs (group 1). The results of this group were compared with
those of 54 patients (group 2) retrospectively drawn from patients who un-
derwent aortic replacement for noninflammatory AAAs. A computer-
assisted matching system was used to match patients according to date of
birth, gender, and surgical priority. All patients of both groups were fol-
lowed by periodic clinical and instrumental examinations. Patients in
group 1 complained more frequently of aneurysm-related symptoms (72%
vs. 20%; p= 0.0001), and their erythrocyte sedimentation rate was elevated
more often (78% vs. 19%; p< 0.0001). Surgical morbidity and mortality
rates were not different. The mean lengths of follow-up were 61 ± 47
months (group 1) and 71 ± 38 months (group 2). The 10-year overall sur-
vival rates did not differ significantly between the two groups (49.1% ±
16.9% for group 1 vs. 61.6% ± 13.8% for group 2; p= 0.26, log-rank test). In
contrast, the free from paraanastomotic aneurysm survival rates were sig-
nificantly lower in group 1 (57.3% ± 20.2% vs. 97.8% ± 2.5% at 10 years; p
= 0.025, log-rank test). Long-term outcomes showed a higher incidence of
graft-related complications in group 1. As inflammatory aneurysms might
represent a risk factor for the development of paraanastomotic aneurysms,
routine imaging surveillance of graft aortic healing after inflammatory
AAA repair is warranted.
Inflammatory (noninfectious) abdominal aortic aneurysms
(AAAs) [1] are characterized by marked thickness of the aortic
wall, with dense perianeurysmal fibrosis involving adjacent organs.
[2] It is not certain whether they have an independent pathogenesis
or simply represent the extreme end in the spectrum of inflamma-
tory changes present in all AAAs and even in atherosclerotic
plaques [2–5]. Nevertheless, they may be considered a distinct clini-
cal entity because of their histologic features and associated surgi-
cal problems [2, 6–9]. Almost all reports concerning late outcomes
after inflammatory AAA repair have focused on the evolution of
perianeurysmal fibrosis [10–13]. Imaging follow-up studies of graft-
related complications in comparison with those of noninflamma-
tory AAAs have rarely been reported [14–16]. Some experiences
using a clinical follow-up examination showed no significant differ-
ences in long-term survival rates between inflammatory and non-
inflammatory AAAs [6, 7, 16, 17].
This study is a case-control analysis of early and late outcomes of
18 patients who underwent repair of an inflammatory AAA during
the period January 1987 to December 1999. We included 54 control
patients operated on for noninflammatory aneurysms during the
same period, matched for gender, age, and surgical priority.
Patients and Methods
Patients
From January 1987 to December 1999 a total of 625 consecutive
patients underwent AAA repair. AAAs were defined as being in-
flammatory when macroscopic and microscopic findings were ob-
served as follows: (1) tomographic or intraoperative gross appear-
ance of marked thickening of the aneurysm wall with encasement
of surrounding retroperitoneal organs; and (2) adventitial fibrosis
together with inflammatory infiltrates of lymphocytes and plasma
cells, endarteritis obliterans, and fibrosis around nerves, as previ-
ously described in the literature [2, 3, 18]. Based on these criteria,
18 (2.8%) patients were considered to have an inflammatory AAA
(group 1). A control group (group 2) with noninflammatory AAAs
was retrospectively drawn from the remaining 607 patients who un-
derwent abdominal aortic replacement during the same period.
For each patient in group 1, three control patients were identified
using a computer-assisted matching system to match patients ac-
cording to date of birth, gender, and surgical priority (elective sur-
gery vs. emergent surgery).
Preoperative clinical features and cardiovascular risk factors
were compared in the two groups, and operative reports were re-
viewed to identify differences in the surgical technique and associ-
ated procedures. Postoperative (within 30 days after surgery) mor-
tality and morbidity, late survival rates, and graft-related
complications were compared.
This paper is dedicated to the memory of Prof. Giancarlo Botta, M.D.
Correspondence to: Patrizia Rubini, M.D., Ph.D.
WOR LD
Journal of
SURGERY
© 2003 by the Socie´te´
Internationale de Chirurgie
World J. Surg. 27, 539–544, 2003
DOI: 10.1007/s00268-003-6706-4
Surgical Procedure
A transperitoneal approach was used in all cases. In group 1 aortic
replacement was performed avoiding extensive dissections and by
the in-lay graft technique, according to Crawford et al. [6]. Dacron
polyester (woven or knitted) and polypropylene sutures were used
in all patients. A specimen of the aneurysmal aortic wall was rou-
tinely removed and sent for histopathologic evaluation in all cases.
Aneurysm repair was accomplished by experienced vascular sur-
geons certified in general and vascular surgery. Steroids were not
administered before or after operation.
Follow-up
Follow-up was routinely performed 6 months after operation by
clinical examination and laboratory tests and yearly by computed
tomography (CT) scanning. The last inquiry was made between
January 2000 and December 2000. The differentiation between
true and false aneurysms was performed on the basis of criteria
defined by Johnston et al. [1].
Statistical Analysis
All continuous data are expressed as means ± SD, and categorical
variables are reported as a percent. Commercial statistical software
(SPSS for Windows, version 8.0; SPSS, Chicago, IL, USA) has been
used for data analysis. Continuous data were compared by one-way
analysis of variance (ANOVA) and categorical data by the chi-
square test or Fisher’s exact test when indicated. Total survival and
“free from anastomotic pseudoaneurysm development” survival
rates of both patient populations were determined by Kaplan-
Meier survival analysis; the estimated survival proportions are re-
ported ± standard error of the estimates. Differences in survival
and “free from anastomotic pseudoaneurysm development” sur-
vival were compared by the log-rank test. A pvalue less than 0.05
was considered significant.
Results
Preoperative Risk Factors and Clinical Presentation
As expected from the selection criteria for the control group, the
two groups were similarly matched for age, gender, and surgical
priority. Differences between the groups were found regarding
clinical presentation and signs but not for preoperative risk factors
(Table 1). The incidence of symptoms was in fact significantly
higher in group 1 patients, who also had an elevated erythrocyte
sedimentation rate (ESR) more often. Abdominal and back pain
were the most common presenting symptoms in group 1 (11 cases,
65%); however, of these 11 patients, only 1 had a true rupture of the
aneurysm. Two more patients in group 1 were admitted to hospital
for symptoms referable to obstructive uropathy.
Operative Features
Inflammatory AAAs showed a typical white surface and dense peri-
aneurysmal fibrosis that entrapped the duodenum in all cases
(100%), the inferior vena cava and left renal vein in 10 (55.5%) and
8 (44.4%) cases, respectively, the ureters with varying degrees of
obstruction in 6 (33.3%), and the small bowel in 1 case (5.5%).
Treatment of ureteral involvement depended on the degree of ure-
teral obstruction: Ureteral stenting and ureterolysis were per-
formed in two patients with severe bilateral obstruction, and the
remaining patients underwent aneurysm resection alone. None of
the noninflammatory AAAs had adjacent retroperitoneal organ
adhesion. Intraoperative factors—such as the site of clamping (be-
low or above renal arteries), type of graft replacement (straight or
bifurcated graft), incidence of left renal vein division, or associated
vascular and nonvascular procedures—were not different between
the two groups (Table 2).
Postoperative Outcomes
There were no perioperative deaths. In-hospital morbidity rates
and the various complications are shown in Table 3. No significant
differences were found between inflammatory and noninflamma-
tory AAAs.
Long-term Outcomes
The mean follow-up was 61 ± 47 months for group 1 and 71 ± 38
months for group 2 (p= 0.78). Cumulative survival rates (Fig. 1)
were lower, although not significantly so, for group 1 than for group
2 (49.1% ± 16.9% vs. 61.6% ± 13.8% at 10 years; p= 0.26); con-
versely, “free from paraanastomotic aneurysm” survival rates (Fig.
2) were significantly lower in group 1 (57.3% ± 20.2% vs. 97.8% ±
2.5% at 10 years; p= 0.025).
In detail, paraanastomotic aneurysms in group 1 occurred at the
aortic proximal anastomosis (two cases) and at the iliac anastomo-
sis (one case); the only complication of this type in group 2 occurred
at a femoral anastomosis. The first proximal paraanastomotic an-
eurysm of group 1 was detected 50 months after primary aortic re-
pair in a patient who had undergone ileal resection for volvulus on
postoperative day (POD) 8; it measured 5.4 cm in diameter. Surgi-
cal treatment was required 1 year later because of its enlargement.
At surgery a true aneurysm was seen to involve the aorta adjacent
to the suture line. Repair was accomplished by suprarenal cross-
Table 1. Preoperative risk factors and clinical presentation.
Variable
Group 1
patients
(n= 18)
Group 2
patients
(n= 54) p
Male gender 18 (100%) 54 (100%) 1.00
Age at intervention 67.0 ± 8.7 67.0 ± 9.4 1.00
Smokers 12 (66.6%) 37 (68.5%) 1.00
Chronic obstructive pulmonary
disease
4 (22.2%) 22 (40.7%) 0.26
Familiar history of aneurysms 1 (5.5%) 4 (7.4%) 1.00
Coronary artery disease 4 (22.2%) 23 (42.5%) 0.16
Serum creatinine increase
(± 2 mg/dl)
5 (27.7%) 7 (12.9%) 0.16
Hypertension 8 (44.4%) 29 (53.7%) 0.50
Diabetes 3 (16.7%) 8 (14.8%) 1.00
Hyperlipidemia 7 (38.8%) 31 (57.4%) 0.18
Peripheral arterial occlusive
disease
4 (22.2%) 20 (37.0%) 0.39
Symptomatic AAAs 13 (72.2%) 11 (20.4%) 0.0001
ESR elevation 14 (77.7%) 10 (18.5%) < 0.0001
Emergent operation 3 (16.7%) 9 (16.7%) 1
ESR: erythrocyte sedimentation rate; AAAs: abdominal aortic aneu-
rysms.
540 World J. Surg. Vol. 27, No. 5, May 2003
clamping and by placing a graft proximal to the old one. The patient
was discharged without complications, but 3 years later he devel-
oped a prosthetic-duodenal fistula, which was treated by duodenal
resection and aortic replacement with a cryopreserved homograft.
The patient died from a homograft rupture on POD 7. The second
patient with an aortic paraanastomotic aneurysm underwent emer-
gency operation because of rupture 70 months after the primary
repair; the rupture occurred at a focal bulging of the aortic wall at
the anastomotic site. Prosthetic replacement of the old graft was
carried out, but the patient died on POD 4 from multiple organ
failure. The third anastomotic aneurysm, located at an iliac anas-
tomosis, was discovered 88 months after the primary operation; it
measured 4.4 cm in diameter and was treated successfully by endo-
Table 2. Operative details and associated surgery.
Variable
Group 1
patients
(n= 18)
Group 2
patients
(n= 54) p
Operative details
Straight graft 7 (38.8%) 15 (27.7%) 0.38
Graft diameter (mm) 19 ± 3 19 ± 2 0.73
Left renal vein division 2 (11.1%) 3 (5.5%) 0.59
Infrarenal clamping 15 (83.3%) 47 (87.0%) 0.70
Associated surgery
Vascular surgery 5 (27.7%) 9 (16.6%) 0.32
Lumbar sympathectomy 3 (16.6%) 4 (7.4%)
Renal artery angioplasty — 2 (3.7%)
Lower limb revascularization 2 (11.1%) 1 (1.8%)
Carotid endarterectomy — 2 (3.7%)
Nonvascular surgery 4 (22.2%) 21 (38.8%) 0.26
Cholecystectomy 1 (5.5%) 6 (11.1%)
Nephrectomy — 3 (5.5%)
Splenectomy — 1 (1.8%)
Hiatal hernia repair — 3 (5.5%)
Inguinal hernia repair 3 (16.6%) 8 (14.8%)
Table 3. Postoperative outcome.
Variable
Group 1
patients
(n= 18)
Group 2
patients
(n= 54) p
Cardiac 6 (33.3%) 22 (40.7%) 0.78
Arrhythmias 4 (22.2%) 11 (20.3%)
Ischemia 1 (5.5%) 7 (12.9%)
Congestive heart failure 1 (5.5%) 4 (7.4%)
Pulmonary 1 (5.5%) 3 (5.5%) 1.00
Prolonged ventilation (> 48 hours) 1 (5.5%) 1 (1.8%)
Pneumonia/severe atelectasis — 2 (3.7%)
Vascular 2 (11.1%) 4 (7.4%) 0.64
Acute lower limb ischemia 2 (11.1%) 1 (1.8%)
Deep vein thrombosis — 1 (1.8%)
Groin lymphatic leak — 2 (3.7%)
Renal 5 (27.7%) 12 (22.2%) 0.75
Serum creatinine rise 3 (16.6%) 5 (9.2%)
Urinary tract infections 2 (11.1%) 7 (12.9%)
Intestinal 3 (16.6%) 3 (5.5%) 0.16
Occlusion 2 (11.1%) 1 (1.8%)
Prolonged paralytic ileus 1 (5.5%) 1 (1.8%)
Ischemia — 1 (1.8%)
Other — 3 (5.5%) 0.57
Overall morbidity
a
8 (44.4%) 22 (40.7%) 1.00
Mortality 0 0 1.00
a
Some patients had more than one complication; for that reason the
sum of the complication rates in both groups does not give the exact rate of
overall morbidity.
Fig. 1. Time-related survival after abdominal aortic aneurysm (AAA) re-
placement in group 1 and 2 patients. Note the lack of significance between
groups (p= 0.26).
Fig. 2. Time-related “free from paraanastomotic aneurysm” survival after
AAA replacement in group 1 and 2 patients. There is a statistically signifi-
cant difference in survival (p= 0.025).
Table 4. Late outcome.
Variable
Group 1
patients
(n= 18)
Group 2
patients
(n= 54) p
Follow-up length (months) 61 ± 47 71 ± 38 0.78
Graft-unrelated complications 7 13
Cardiac 5 7
Neoplastic — 2
Cerebrovascular 1 4
Gastrointestinal 1 —
Graft-related complications 3 1
Aortic pseudoaneurysms 2 —
Iliac pseudoaneurysms 1 —
Femoral pseudoaneurysms — 1
Graft-related mortality 2 —
Aortic pseudoaneurysm rupture 1 —
Aortic homograft rupture 1 —
Graft-unrelated mortality 3 9
Cardiac 2 7
Cerebrovascular 1 —
Trauma — 1
Neoplastic — 1
541Bonati et al.: Inflammatory Aneurysm Repair
vascular stenting. In group 2 a patient with a femoral pseudoaneu-
rysm, detected 16 months after the primary operation, electively
underwent iliac-femoral graft replacement. Graft infection was not
found in cultures of any of the replaced grafts. The late complica-
tions of both groups are shown in Table 4.
Evolution of Fibrosis in Group 1 Patients
Symptoms and elevated ESRs disappeared within 12 to 18 months
after aneurysm repair. Hydronephrosis regressed within the same
period in patients treated by ureterolysis as well as in those who
underwent aneurysm repair alone; neither recurrence nor progres-
sion of ureteral obstruction was detected. CT scanning follow-up
showed complete regression of retroperitoneal fibrosis in 11 pa-
tients (61.1%) and partial regression in 7 (38.8%) at an average
follow-up of 61 ± 47 months.
Discussion
Imaging follow-up studies evaluating aortic-graft healing after an-
eurysm repair are infrequent in the literature. Therefore the true
rate of false aneurysm development is still undefined not only for
inflammatory AAAs but also after noninflammatory AAA repair.
The wide range of rates previously reported is probably due to the
various procedures, prosthetic materials, length of follow-up, and
methods of detection as well as the aggressiveness with which these
lesions have been sought [19–22]. Edwards et al. followed up with
yearly sonographic examination 111 patients who underwent aortic
bypass grafting for AAA or occlusive disease; they documented a
paraanastomotic aneurysm rate of 27% at 15 years [23]. Hallett et
al., in a population-based study, evaluated graft-related complica-
tions after AAA repair by ultrasonography, CT scanning, or both.
They reported that 3% of patients showed anastomotic aneurysms
(1% at the aortic anastomosis) at a median follow-up of 6.1 years
[24]. More recently, Kalman et al. performed CT scan follow-up 8
to 9 years postoperatively in a cohort of patients enrolled in the
Canadian Aneurysm Group and documented a 7.5% rate of proxi-
mal false aneurysms [25].
Late surveillance of aortic graft healing after inflammatory AAA
repair using routine CT scans or sonographic follow-up examina-
tions has been reported even more rarely. Nitecki et al., in a case-
control study using CT or ultrasound scans for follow-up, reported
similar 5-year survival rates for inflammatory and noninflamma-
tory AAAs, without any occurrence of pseudoaneurysms in inflam-
matory AAAs [15]. A review of the literature concerning graft-
related complications after inflammatory AAA repair is reported
in Table 5 [10, 12, 14, 15].
Our single-institution case-matched study showed that inflam-
matory AAA repair is associated with a higher incidence of anas-
tomotic aneurysms than noninflammatory AAA repair despite
early outcomes and late cumulative survival rates that were not sig-
nificantly different. It should be noted that the number of patients
in this study is fairly small because of the strict criteria adopted to
define the inflammatory AAA; our prevalence is in fact relatively
low (2.8%) compared with other previously reported experiences
[2, 3, 7, 8, 17]. However, the selection procedure allowed us to ob-
tain two groups with similar preoperative risk factors followed by
periodic instrumental examination and to make the groups strictly
comparable.
Patients with symptoms due to the aneurysm and ESR elevation
were found more frequently among those with inflammatory AAAs
according to data reported in most surgical series [6–8, 10, 15–17,
26]. Nevertheless, different preoperative results have been de-
scribed in other studies. Similar incidences of symptomatic patients
regarding inflammatory and noninflammatory AAAs have been re-
ported by Johnston and Scobie in a multicenter study of 666 pa-
tients with nonruptured AAAs [27]; iatrogenic lesions in surround-
ing organs and increased postoperative complications in
inflammatory AAA patients have been noted by others [7–9, 15,
27–29].
Late evolution of periaortic fibrosis in inflammatory AAAs is
still controversial. Some reports showed regression after graft re-
pair in almost all patients, [6, 7, 10, 17, 26], whereas more recent
studies have shown partial or no regression of the fibrotic process
[11–13, 15]. Certainly, the length and the methods of follow-up vary
among papers, and some observations are sporadic. A literature
review revealed that complete fibrosis regression was noted in 23%
to 53% of cases, partial regression in 21% to 57%, and no change or
progression of inflammation in 0 to 38% and 0 to 3.8%, respectively
[11–13, 15]. The overall mean follow-up in these reports is about 2
years. In our study, most patients showed regression of the fibrotic
process after about 5 years. Thus it can be hypothesized that regres-
sion of fibrosis can take several years to complete, and that such a
process is not necessarily related to normalization of the ESR,
which occurs much earlier during the follow-up of these patients.
The higher incidence of paraanastomotic aneurysms after in-
flammatory AAA repair in our study raises the question of whether
they have specific features predisposing to the development of this
complication. Histopathologic changes of the aortic wall could play
a pathogenetic role in the development of these complications. Flo-
gistic infiltrates and endarteritis obliterans with subsequent isch-
emic aortic wall damage could induce arterial weakness leading to
pseudoaneurysmal degeneration. Recent studies investigating the
extracellular matrix modifications by immunoelectron microscopy
and immunohistochemical techniques have shown that elastin
depletion and collagen fiber alterations are more extensive in in-
Table 5. Late outcome: literature review.
No. of patients
Study
No. of patients
followed Methods of detection
Graft-related
complications (%) Infection
Aortoenteric
fistula
Paraanastomotic
aneurysms
Follow-up length
(months)
Lindblad [10] 35 CT, US, urography 8.5% 2 1 — 12–96
Nitecki [15] 19 CT, US 5.2% 1 — — 12.9 ± 1.7 (mean)
Koch [14] 54 CT 9.2% — 1 4 30 (mean)
Von Fritschen [12] 26 CT — — — — 36 (median) (10–91)
CT: computed tomography; US: ultrasonography.
542 World J. Surg. Vol. 27, No. 5, May 2003
flammatory AAAs than in noninflammatory AAAs [30]. It is likely
that these or other unidentified defects affect the resistance of the
aortic wall, predisposing to late anastomotic aneurysm develop-
ment.
Conclusions
Our study suggests that inflammatory AAAs constitute a risk factor
for late paraanastomotic aneurysm development. Large series with
imaging follow-up are warranted to detect the true incidence of late
graft pathology in this type of aneurysm and to confirm the ten-
dency for anastomotic aneurysms to develop more frequently with
inflammatory AAAs than with noninflammatory AAAs.
Résumé. Le but de cette étude a été de comparer l’évolution précoce et
tardive de la cure d’anévrisme de l’aorte abdominale (AAA), en distinguant
entre les AAA inflammatoire et non-inflammatoire et en insistant sur les
complications en rapport avec le greffon. De 625 patients consécutifs ayant
eu une cure de leur AAA, 18 ont été classés comme inflammatoires (groupe
1). Les résultats de ce groupe ont été comparés à ceux de 54 patients
(groupe 2), tirés rétrospectivement parmi les patients qui ont eu un
remplacement de l’aorte pour AAA non inflammatoire. Un système
d’appariement assisté par ordinateur a été utilisé pour apparier les
patients selon la date de naissance, le sexe et le degré d’urgence de la
chirurgie. Tous les patients ont été suivis par un examen périodique
clinique et paraclinique. Les patients du groupe 1 se sont plaints plus
souvent de symptômes en rapport avec l’anévrysme (72% vs. 20%, p=
0.0001) et avaient une vitesse de sédimentation plus élevée (78% vs. 19%, p
< 0.0001). La morbidité et mortalité chirurgicales n’étaient pas
différentes. Le suivi moyen a été de 61 ± 47 mois dans le groupe 1 et de 71
± 38 mois dans le groupe 2. La survie à 10 ans ne différait pas de façon
significative entre les deux groupes (49.1% ± 16.9% pour le groupe 1 vs.
61.6% ± 13.8% pour le groupe 2, p= 0.26, test du log-rank) alors que la
survie sans anévrysme para-anastomotique a été significativement moins
élevée dans le groupe 1 (57.3% ± 20.2% vs. 97.8% ± 2.5% à 10 ans, p=
0.025, test de log-rank). L’évolution à long terme a montré une incidence
plus élevée de complications en rapport avec le greffon dans le groupe 1.
Comme l’inflammation pourrait représenter un facteur de risque pour le
développement de faux anévrysmes para-anastomotique, on conseille une
surveillance régulière de la cicatrisation après cure d’AAA inflammatoire.
Resumen. El objetivo del trabajo fue comparar los resultados precoces y
tardíos del tratamiento quirúrgico de aneurismas de la aorta abdominal
(AAAs) de etiología inflamatoria. En el estudio se enfatiza sobre las
complicaciones relacionadas con el injerto. De 625 pacientes tratados por
AAA, 18 fueron clasificados en el grupo AAA inflamatorio (grupo 1)
comparándose con 54 pacientes (grupo 2) elegidos retrospectivamente por
padecer un AAA no inflamatorio. Mediante un sistema computerizado se
conformaron grupos homologables por lo que a la fecha de nacimiento,
sexo y urgencia quirúrgica se refiere. Los pacientes del grupo 1
presentaban con más frecuencia síntomas relacionados con el aneurisma
(72% vs. 20% p= 0.0001). La velocidad de sedimentación también estaba
más elevada (78% vs. 19% p< 0.0001). Sin embargo, las tasas de
morbi-mortalidad no fueron diferentes. El seguimiento medio fue de 61 ±
47 (grupo 1) y 71 ± 38 meses (grupo 2). La supervivencia global a los 10
años fue similar (49.1 ± 16.9% grupo 1 y 61.6% ± 13.8% grupo 2; log rank
test p= 0.26). Sin embargo, el porcentaje de supervivencia sin aneurismas
para-anastomóticos fue significativamente menor en el grupo 1 (57.3 ±
20.2% frente al 97.8% ± 2.5% a los 10 años, p= 0.025). Los resultados
tardíos revelaron un mayor número de complicaciones dependientes del
injerto en los pacientes del grupo 1. Dado que los aneurismas inflamatorios
tienen más riesgo de desarrollar aneurismas para-anastomóticos, la
vigilancia rutinaria mediante pruebas de imagen es obligatoria tras el
tratamiento quirúrgico de los AAA inflamatorios.
References
1. Johnston KW, Rutherford RB, Tilson MD, et al. Suggested standards
for reporting on arterial aneurysms. J. Vasc. Surg. 1991;13:452–458
2. Walker DI, Bloor K, Williams G, et al. Inflammatory aneurysms of the
abdominal aorta. Br. J. Surg. 1972;59:609–614
3. Rose AG, Dent DM. Inflammatory variant of abdominal atheroscle-
rotic aneurysm. Arch. Pathol. Lab. Med. 1981;105:409–413
4. Schwartz CJ, Mitchell JRA. Cellular infiltration of the human arterial
adventitia associated with atheromatous plaques. Circulation 1962;26:
73–78
5. Rasmussen TE, Hallett JW. Inflammatory aortic aneurysms: a clinical
review with new perspectives in pathogenesis. Ann. Surg. 1997;225:
155–164
6. Crawford JL, Stowe CL, Safi HJ, et al. Inflammatory aneurysm of the
aorta. J. Vasc. Surg. 1985;2:113–124
7. Pennel RC, Hollier LH, Lie JT, et al. Inflammatory abdominal aortic
aneurysms: a thirty-year review. J. Vasc. Surg. 1985;2:859–869
8. Goldstone J, Malone JM, Moore WS. Inflammatory aneurysms of the
abdominal aorta. Surgery 1978;83:425–430
9. Downs AR, Lye CR. Inflammatory abdominal aortic aneurysm. Can. J.
Surg. 1986;29:50–53
10. Lindblad B, Almgren B, Berqvist D, et al. Abdominal aortic aneurysm
with perianeurysmal fibrosis: experience from 11 Swedish vascular cen-
ters. J. Vasc. Surg. 1991;13:231–239
11. Stella A, Gargiulo M, Faggioli GL, et al. Postoperative course of in-
flammatory abdominal aortic aneurysms. Ann. Vasc. Surg. 1993;7:229–
238
12. Von Fritschen U, Malzfeld E, Clasen A, et al. Inflammatory abdominal
aortic aneurysm: a postoperative course of retroperitoneal fibrosis. J.
Vasc. Surg. 1999;30:1090–1098
13. Bitsch M, Norgaard HH, Roder O, et al. Inflammatory aortic aneu-
rysms: regression of fibrosis after aneurysm surgery. Eur. J. Vasc. En-
dovasc. Surg. 1997;13:371–374
14. Koch JA, Poll L, Klinger G, et al. Intraoperative findings and postop-
erative computer tomographic follow up of inflammatory aortic aneu-
rysm. Rofo Fortschr. Geb. Rontgenstr. Neuen. Bildgeb. Verfahr. 1998;
169:140–145
15. Nitecki SS, Hallett JW, Stanson AW, et al. Inflammatory abdominal
aortic aneurysms: a case-control study. J. Vasc. Surg. 1996;23:860–869
16. Sasaki S, Yasuda K, Takigami K, et al. Inflammatory abdominal aortic
aneurysms and atherosclerotic abdominal aortic aneurysms: compari-
sons of clinical features and long-term results. Jpn. Circ. J. 1997;61:231–
235
17. Sterpetti AV, Hunter WJ, Feldhaus RJ, et al. Inflammatory aneurysms
of the abdominal aorta: incidence, pathologic, and etiologic consider-
ations. J. Vasc. Surg. 1989;9:643–650
18. McMahon JN, Davies JD, Sott DJA, et al. The microscopic features of
inflammatory abdominal aortic aneurysms: discriminant analysis. His-
topathology 1990;16:557–564
19. Szilagyi DE, Smith RF, Elliott JP, et al. Anastomotic aneurysms after
vascular reconstruction: problems of incidence, etiology, and treat-
ment. Surgery 1975;78:800–816
20. Plate G, Hollier LA, O’Brien P, et al. Recurrent aneurysms and late
vascular complications following repair of abdominal aortic aneurysms.
Arch. Surg. 1985;120:590–594
21. Dennis JW, Littooy FN, Greisler HP, et al. Anastomotic pseudoaneu-
rysms: a continuing late complication of vascular reconstructive proce-
dures. Arch. Surg. 1986;121:314–317
22. Johnston KW. Canadian Society for Vascular Surgery Aneurysm Study
Group. Nonruptured abdominal aortic aneurysm: six-year follow-up
results from the multicenter prospective Canadian aneurysm study. J.
Vasc. Surg. 1994;20:163–170
23. Edwards JM, Teefey SA, Zierler RE, et al. Intraabdominal paraanas-
tomotic aneurysms after aortic bypass grafting. J. Vasc. Surg. 1992;15:
344–353
24. Hallet JW, Marshall DM, Petterson TM, et al. Graft-related complica-
tions after abdominal aortic aneurysm repair: reassurance from a 36-
year population-based experience. J. Vasc. Surg. 1997;25:277–286
25. Kalman PG, Rappaport DC, Merchant N, et al. The value of late com-
puted tomographic scanning in identification of vascular abnormalities
after abdominal aortic aneurysm repair. J. Vasc. Surg. 1999;29:442–450
26. Leseche G, Schaetz A, Arrive L, et al. Diagnosis and management of 17
consecutive patients with inflammatory abdominal aortic aneurysm.
Am. J. Surg. 1992;164:39–44
27. Johnston KW, Scobie TK. Multicenter prospective study of nonrup-
543Bonati et al.: Inflammatory Aneurysm Repair
tured abdominal aortic aneurysms. I. Population and operative man-
agement. J. Vasc. Surg. 1988;7:69–81
28. Sultan S, Duffy S, Madhavan P, et al. Fifteen-year experience of trans-
peritoneal management of inflammatory abdominal aortic aneurysms.
Eur. J. Vasc. Endovasc. Surg. 1999;18:510–514
29. Lacquet JP, Lacroix H, Nevelsteen A, et al. Inflammatory abdominal
aortic aneurysms: a retrospective study of 110 cases. Acta Chir. Belg.
1997;97:286–292
30. Cenacchi G, Guiducci G, Pasquinelli G, et al. The morphology of elas-
tin in non-specific and inflammatory abdominal aortic aneurysms: a
comparative transmission, scanning and immunoelectron microscopy
study. J. Submicrosc. Cytol. Pathol. 1995;27:75–81
544 World J. Surg. Vol. 27, No. 5, May 2003