Abstract Objective Penetrating atherosclerotic ulcer generally occurs in elderly patients with systemic atherosclerosis, predominantly in the descending thoracic aorta, and it is uncommon in the infrarenal aorta. We reviewed our experience of endovascular treatment of penetrating aortic ulcer in the infrarenal aorta. Methods In the last 4years, out of 348 patients who underwent abdominal aortic procedures, a total of 13 patients (12 men and 1 woman) were found to have an abdominal penetrating aortic ulcer, corresponding to an incidence of 3.7%. Mean age was 73±7years. All patients had hypertension. Three lesions were discovered incidentally and 10 were symptomatic. All patients underwent endovascular treatment in the operating room. Follow-up included CT-A control at 1, 4 and 12months after the intervention, and yearly thereafter. Results Primary technical success was 100%. No postoperative death was observed. Mean operative time was 100±29min. Mean blood loss was 168±133ml. No patient required intensive care unit stay. We observed one major complication (transient ischemic attack). Mean hospital stay was 4±1days. During a mean follow-up period of 26months no endoleak, aneurysm evolution or stent graft failure was recognized in any patient. One patient died 24months after the intervention after a stroke. Conclusions In our experience, endovascular or repair of infrarenal aortic ulcer appears feasible, and midterm results satisfactory

Chiara Lomazzi

Gabriele Piffaretti

Matteo Tozzi

Nicola Rivolta

Patrizio Castelli

Roberto Caronno

English

Open Access Repository

www. the i j s . comInternational Journal of Surgery (2007) 5, 172e175Endovascular repair of abdominal infrarenalpenetrating aortic ulcers: A prospectiveobservational studyGabriele Piffaretti*, Matteo Tozzi, Chiara Lomazzi, Nicola Rivolta,Roberto Caronno, Patrizio CastelliVascular Surgery, University of Insubria, Viale Borri 57, 21100 Varese, ItalyKEYWORDSAbdominal penetratingaortic ulcers;Endovascular repairAbstract Objective: Penetrating atherosclerotic ulcer generally occurs in elderly patientswith systemic atherosclerosis, predominantly in the descending thoracic aorta, and it is un-common in the infrarenal aorta. We reviewed our experience of endovascular treatment ofpenetrating aortic ulcer in the infrarenal aorta.Methods: In the last 4 years, out of 348 patients who underwent abdominal aortic procedures,a total of 13 patients (12 men and 1 woman) were found to have an abdominal penetrating aor-tic ulcer, corresponding to an incidence of 3.7%. Mean age was 73  7 years. All patients hadhypertension. Three lesions were discovered incidentally and 10 were symptomatic. Allpatients underwent endovascular treatment in the operating room. Follow-up included CT-Acontrol at 1, 4 and 12 months after the intervention, and yearly thereafter.Results: Primary technical success was 100%. No postoperative death was observed. Mean op-erative time was 100  29 min. Mean blood loss was 168  133 ml. No patient required inten-sive care unit stay. We observed one major complication (transient ischemic attack). Meanhospital stay was 4  1 days. During a mean follow-up period of 26 months no endoleak, aneu-rysm evolution or stent graft failure was recognized in any patient. One patient died 24 monthsafter the intervention after a stroke.Conclusions: In our experience, endovascular or repair of infrarenal aortic ulcer appearsfeasible, and midterm results satisfactory.ª 2006 Surgical Associates Ltd. Published by Elsevier Ltd. All rights reserved.* Corresponding author. Tel.: þ39 0332278226; fax: þ39 0332278581.E-mail address: gabriele.piffaretti@tiscali.it (G. Piffaretti).1743-9191/$ - see front matter ª 2006 Surgical Associates Ltd. Publdoi:10.1016/j.ijsu.2006.06.004IntroductionPenetrating atherosclerotic ulcer (PAU) of the aorta isdefined as atherosclerotic lesion with ulceration of theaortic intima and media, and rupture of the internal elasticished by Elsevier Ltd. All rights reserved.Endovascular repair of abdominal infrarenal PAU 173lamina.1e3 PAU occurs in elderly patients with systemic ath-erosclerosis, predominantly in the descending thoracicaorta, and it is uncommon in the infrarenal aorta.Although first described by Shennan in 1934,4 their nat-ural history still remains unclear and treatment is contro-versial; it may be complicated by aortic intramuralhematoma, adventitial pseudoaneurysm formation, or aor-tic rupture.5We reviewed the clinical features of PAU in the infrare-nal aorta and investigated the usefulness of endovascularrepair for this uncommon lesion.Materials and methodsIn the last 50 months, 348 patients underwent abdominalaortic procedures at our institution for atherosclerotic dis-ease (aneurysms (n Z 293), obstructive disease (n Z 55));overall, 251 patients were treated endovascularly, 97 withopen surgery. A total of 13 patients were found to havean abdominal PAU, corresponding to an incidence of 3.7%.They were analyzed in a retrospective manner: therewere 12 men and 1 woman in this series; mean age was73  7 years (range 56e84, median 77). All patients had hy-pertension (on anti-hypertensive medication); additionalco-morbidities and risk factors included peripheral obstruc-tive arterial disease (n Z 6), diabetes (n Z 5), chronicobstructive pulmonary disease (n Z 3), cerebrovascular in-sufficiency (n Z 3), chronic renal failure (n Z 2), hostileabdomen (n Z 2), coronary artery disease (n Z 2), andhyperlipidemia (n Z 1).Three lesions were discovered incidentally during aorto-iliac duplex ultrasound (US) screening examination andwere treated electively; of the 10 patients with symptoms,five had claudication and the presence of the PAU wassuspected during preliminary US, three had critical ische-mia of the lower extremities due to arterial embolism, andtwo complained of abdominal pain (one associated withsyncope that suggested a ruptured abdominal aorta).In every patient, PAU was diagnosed at computedtomography angiography (CT-A): on CT-A, PAU is recognizedas a contrast-filled, pouch-like aortic protrusion withouta dissection flap or false lumen (Fig. 1A,B). IntramuralFigure 1 Preoperative CT-angiography of an infrarenal PAUwith a 55 mm aortic expansion (A). Intraoperative angiogram(B) confirmed the presence of the PAU just above the aorto-iliac bifurcation and the ulceration (ring) of a plaque of theleft common iliac artery; both the lesions were excludedwith two abdominal ‘‘cuffs’’ and a ‘‘kissing’’-stent grafts(arrows) reconstruction of the aorto-iliac bifurcation (C).hematoma with aortic expansion, adventitial pseudoaneur-ysm formation without intramural hematoma, and con-tained ruptures with extra-aortic hematoma wererecognized. Because they were treated electively, it wasnot possible to obtain an histological diagnosis to supportthe CT diagnosis of PAU. CT-A also demonstrated associatedatherosclerotic arterial lesions in eight patients: stenosis ofan iliac artery (n Z 5; four bilateral, one unilateral), andstenosis of the internal carotid artery (n Z 2). CT also re-vealed thrombus in the abdominal aorta (n Z 5) and exten-sive aortic calcifications (n Z 4).All patients in this series underwent endovasculartreatment with stent graft (SG); the devices used werecuffs of Excluder (W.L. Gore and Associates, Flagstaff, AZ,USA), Zenith (Cook Inc., Bloomington, IN, USA), and Life-path (Edwards Lifesciences Corp., Irvine, CA, USA). Re-pairs were performed in the operating room with thepatient under loco-regional anesthesia (n Z 11), or generalanesthesia with endotracheal intubation (n Z 2); acell-saver system (Compact-Dideco; Modena, Italy) wasavailable in the event that surgical conversion was needed.Patients were prepared and draped for either femoral arte-riotomy and traditional transperitoneal approach. Everypatient received short-term antibiotic prophylaxis (vanco-mycin 1 g b.i.d.). The common femoral artery was exposedin standard fashion for device access in all patients. Com-pletion digital subtraction angiography (DSA) was routinelyperformed at the end of the procedure to confirm adequateposition of the SG, the complete exclusion of the lesion anddetect potential endoleaks (Fig. 1C).All patients underwent follow-up CT-A control, at 1, 4and 12 months after the intervention, and yearly thereaf-ter. Data for variables were expressed as mean values.Data were prospectively collected and analyzed in a retro-spective manner. Primary outcome measures were theexclusion of the PAU and patient survival.ResultsOverall, lesions were recognized as follows: PAU (n Z 6),pseudoaneurysm (n Z 6), and rupture (n Z 1). Deploymentof the SG was technically successful in all patients. No post-operative deaths occurred. A total of 17 SGs were used: tenpatients received one SG, two patients two SGs, and onepatients three SGs. Mean SG diameter was 25  3 (range20e28, median 24). Aortograms obtained after the proce-dure demonstrated complete exclusion of PAU and no endo-leak. Additional procedures included bilateral iliac arteriesPTA/stent (n Z 4), iliac artery PTA (n Z 1), and internalcarotid artery stenting (n Z 2). Mean operative time was100  29 min (range 60e150, median 80). Mean blood losswas 168  133 ml (range 50e500, median 120); blood trans-fusion (2 units of packed red blood cells) was needed in thepatient with a ruptured PAU.Intensive care unit stay was never required; postope-rative course was uneventful in all but one patient.We observed a cerebrovascular event that spontaneouslyresolved in a patient who underwent simultaneous carotidstenting. Mean hospital stay after the operation was4  1 days (range 3e8, median 4).174 G. Piffaretti et al.During a mean follow-up period of 26 months (range 3e60, median 24) no endoleak, aneurysm evolution or SG fail-ure was recognized in any patient. In this series no patientwas lost to follow-up; one patient died 24 months after theintervention after a stroke.DiscussionPAU of the aorta was first identified by Shennan in 1934, butdescribed as a distinct clinical and pathologic entity byStanson in 1986.3,4 Stanson defines a PAU as an atheroscle-rotic lesion with an ulceration that penetrates the internalelastic lamina and the media of the aortic wall; subse-quently, hematoma formation may extend along the media,and in some cases hematoma extension causes stretching ofthe weakened aortic adventitia, forming a saccular pseu-doaneurysm. PAU generally affects elderly patients withadvanced atherosclerosis: as a result, PAU is associatedwith a high incidence of morbidity, such as hypertension,coronary artery disease, and carotid artery occlusive dis-ease.6 All patients in this series have received antihyper-tensive drugs, and three patients had multiple (carotid,coronary and peripheral) arterial disease. Of interest, interms of age we noted a significant difference betweenpatients with PAU if compared to patients who receivedaortic repair for peripheral obstructive disease (73  7 vs66  10, p < 0.05), but no statistical difference if com-pared to patients with aneurysmal disease (73  7 vs72  8, p Z NS).PAU typically involves the descending thoracic aorta,and it is comparatively rare that PAU develops in theinfrarenal abdominal aorta; few reports have dealt withendovascular stent grafting for treatment of PAU in theinfrarenal abdominal aorta.7e9 The true incidence of PAUhas yet to be determined. No literature study to date hasappropriately addressed this question. The incidence ofthoracic PAU varies from 2 to 7% while abdominal PAUhas been considered responsible for 1e5% of all aorticruptures.3,5e7 In our series abdominal PAU accounted for3.7% of all aortic procedures over almost 4-years.It has been reported that the incidence of these lesionsalso depends on the diagnostic method; in fact, mostcases reported in the medical literature regarding theimaging appearance of PAU or endovascular treatment donot have histologic proof and the diagnosis of atheroscle-rotic lesion is assumed but unconfirmed. Differentiation ofthese disease entities is sometimes difficult, and thereseems to be confusion regarding the concept of PAU.3,5,7,10For these reasons, Quint referred to these lesions as ‘‘ul-cerlike lesions’’ of the aorta rather than PAU. PAU may bediagnosed at CT, magnetic resonance imaging (MRI), andconventional aortography; a high degree of clinical suspi-cion is necessary for diagnosis of PAU. Extensive aortic cal-cification is often detected on plain CT scans, anddevelopment of intramural hematoma after PAU versus in-traluminal thrombus can be differentiated by the locationof calcified plaques in relation to the thrombus on plainCT scans. On contrast-enhanced CT scans, PAU is recog-nized as a contrast-filled, pouch-like aortic protrusionwithout a dissection flap or false lumen.2,5,11 An intramu-ral hematoma, advential pseudoaneurysm, and rupturewith extra-aortic hematoma may also be seen. We believeCT is more accurate, and is the most commonly used tech-nique. MRI appears more effective because it reduces therate of false negative diagnoses, but it is less availablethan CT; in our series, we detected six PAU, six pseudoa-neurysm, and one rupture.PAU are the subject of considerable controversy withrespect to definition as well as natural history. Thenatural history of abdominal PAU remains unclear andlittle information is available in the literature.5 The un-predictable course of PAU was previously emphasized; inparticular, some patients had distal ischemia caused byembolism from a PAU.3 Embolization from penetratingaortic ulcers has been considered rare, but lower limbembolisms were reported to be more frequent withabdominal PAU than with thoracic PAU.3,12,13 Harrisreported three patients with complicated forms of abdomi-nal PAU: two patients had distal ischemia caused by embo-lism, one of them with recurrent embolism that requiredamputation. Our series confirms that when there are nosigns suggesting a cardiac origin, discovery of lower limbembolism should prompt a search for an aortic cause, andin particular PAU.The treatment of PAU remains controversial too. Al-though some authors believe immediate surgical treatmentis not always required, because most PAU have a benignclinical course, early intervention has been recommendedwhen PAU is complicated with aneurysm expansion regard-less of size, rupture, embolic symptoms, or uncontrolledpain.1,2,5,10,11 Open surgical repair with graft interpositionhas been used traditionally, but patients with PAU are gen-erally not ideal candidates for open repair because ofadvanced age and poor general status.1,2,7e10 In fact, highoperative morbidity and mortality associated with open re-pair have been reported.7 Use of aortic SGs could probablychange the strategy for treatment of PAU. This less invasiveprocedure is suitable for high risk patients, and can also beused in cases of rupture.As a less invasive treatment for this disease, endovascularstent grafting was advocated and several reports of endo-vascular treatment of PAU have been published.7e9,13,14Early complications for abdominal PAU included endoleakmainly; peripheral embolization could be a potential intra-operative complication as well as in the post-operativecourse. We opted to use a SG in order to prevent potential de-bris migration or fragmentation from the original PAU duringthe positioning or deployment of the device, and to excludecompletely the potential aneurysm evolution of the PAU fromthe systemic flow. Review of all cases reported to date, in-cluding our own mid-term results, reveals that deploymentof the SGs was successful in all; thus, the lower morbidityand mortality after endovascular repair could also supporta more aggressive approach to this lesion, even in patientswithout symptoms.ConclusionsIn conclusion, this is the largest experience of stent grafttreatment for abdominal PAU. Infrarenal aortic lesionscaused by PAU are generally localized, and endovascularSG repair of this disease appears to be a feasible alternativeEndovascular repair of abdominal infrarenal PAU 175to surgical repair. Mid-term results of endovascular treat-ment of PAU are satisfactory; however, further investiga-tions of the long-term results of this procedure arenecessary.References1. Harris JA, Bis KG, Glover JL, Bendick PJ, Shetty A, Brown OW.Penetrating atherosclerotic ulcers of the aorta. J Vasc Surg1994;19:90e8.2. Coady MA, Rizzo JA, Hammond GL, Pierce JG, Kopf GS,Elefteriades JA. Penetrating ulcer of the thoracic aorta: whatis it? How do we recognize it? How do we manage it? J VascSurg 1998;27:1006e15.3. Stanson AW, Kazmier FJ, Hollier LH, et al. Ulcères athéromateuxpénétrant de l’aorte thoracique: histoire naturelle et corréla-tions anatomo-cliniques. Ann Chir Vasc 1985;1:15e23.4. Shennan T. Dissecting aneurysms. Medical Research SpecialCouncil Report Series 1934;193.5. Quint LE, Williams DM, Francis IR, et al. Ulcerlike lesions of theaorta: imaging features and natural history. Radiology 2001;218:719e23.6. Coady MA, Rizzo JA, Elefteriades JA. Pathologic variants of tho-racic aortic dissections. Penetrating atherosclerotic ulcers andintramural hematomas. Cardiol Clin 1999;17:637e57.7. Batt M, Haudebourg P, Planchard PF, Ferrari E, Hassen-Khodja R,Bouillanne PJ. Penetrating atherosclerotic ulcers of the infrare-nal aorta: life-threatening lesions. Eur J Vasc Endovasc Surg2005;29:35e42.8. Tsuji Y, Tanaka Y, Kitagawa A, et al. Endovascular stent-graftrepair for penetrating atherosclerotic ulcer in the infrarenalabdominal aorta. J Vasc Surg 2003;38:383e8.9. Moriyama Y, Yamamoto H, Hisatomi K, et al. Penetrating athero-sclerotic ulcers in an abdominal aortic aneurysm: report ofa case. Surg Today 1998;28:105e7.10. Cho KR, Stanson AW, Potter DD, et al. Penetrating atheroscle-rotic ulcer of the descending thoracic aorta and arch. J ThoracCardiovasc Surg 2004;127:1393e401.11. Brittenden J, McBride K, McInnes G, et al. The use of endovas-cular stents in the treatment of penetrating ulcers of thethoracic aorta. J Vasc Surg 1999;30:946e9.12. Goldstein DJ, Flores RM, Todd GJ. Rupture of a non-aneurys-mal atherosclerotic infrarenal aorta. J Vasc Surg 1997;26:700e3.13. Farooq MM, Kling K, Yamini D, Gelabert HA, Baker JD,Freischlag JA. Penetrating ulceration of the infrarenal aorta:case reports of an embolic and an asymptomatic lesion. AnnVasc Surg 2001;15:255e9.14. Eggebrecht H, Baumgart D, Herold U, et al. Multiple penetrat-ing atherosclerotic ulcers of the abdominal aorta: treatmentby endovascular stent graft placement. Heart 2001;85:526.

Endovascular repair of abdominal infrarenal penetrating aortic ulcers: a prospective observational study.

AbstractObjectivePenetrating atherosclerotic ulcer generally occurs in elderly patients with systemic atherosclerosis, predominantly in the descending thoracic aorta, and it is uncommon in the infrarenal aorta. We reviewed our experience of endovascular treatment of penetrating aortic ulcer in the infrarenal aorta.MethodsIn the last 4years, out of 348 patients who underwent abdominal aortic procedures, a total of 13 patients (12 men and 1 woman) were found to have an abdominal penetrating aortic ulcer, corresponding to an incidence of 3.7%. Mean age was 73±7years. All patients had hypertension. Three lesions were discovered incidentally and 10 were symptomatic. All patients underwent endovascular treatment in the operating room. Follow-up included CT-A control at 1, 4 and 12months after the intervention, and yearly thereafter.ResultsPrimary technical success was 100%. No postoperative death was observed. Mean operative time was 100±29min. Mean blood loss was 168±133ml. No patient required intensive care unit stay. We observed one major complication (transient ischemic attack). Mean hospital stay was 4±1days. During a mean follow-up period of 26months no endoleak, aneurysm evolution or stent graft failure was recognized in any patient. One patient died 24months after the intervention after a stroke.ConclusionsIn our experience, endovascular or repair of infrarenal aortic ulcer appears feasible, and midterm results satisfactory

Piffaretti, Gabriele

Tozzi, Matteo

Lomazzi, Chiara

Rivolta, Nicola

Caronno, Roberto

Castelli, Patrizio

Elsevier - Publisher Connector 

Endovascular repair of abdominal infrarenal penetrating aortic ulcers: A prospective observational study 

www. the i j s . com
International Journal of Surgery (2007) 5, 172e175Endovascular repair of abdominal infrarenal
penetrating aortic ulcers: A prospective
observational study
Gabriele Piffaretti*, Matteo Tozzi, Chiara Lomazzi, Nicola Rivolta,
Roberto Caronno, Patrizio Castelli
Vascular Surgery, University of Insubria, Viale Borri 57, 21100 Varese, Italy
KEYWORDS
Abdominal penetrating
aortic ulcers;
Endovascular repair
Abstract Objective: Penetrating atherosclerotic ulcer generally occurs in elderly patients
with systemic atherosclerosis, predominantly in the descending thoracic aorta, and it is un-
common in the infrarenal aorta. We reviewed our experience of endovascular treatment of
penetrating aortic ulcer in the infrarenal aorta.
Methods: In the last 4 years, out of 348 patients who underwent abdominal aortic procedures,
a total of 13 patients (12 men and 1 woman) were found to have an abdominal penetrating aor-
tic ulcer, corresponding to an incidence of 3.7%. Mean age was 73  7 years. All patients had
hypertension. Three lesions were discovered incidentally and 10 were symptomatic. All
patients underwent endovascular treatment in the operating room. Follow-up included CT-A
control at 1, 4 and 12 months after the intervention, and yearly thereafter.
Results: Primary technical success was 100%. No postoperative death was observed. Mean op-
erative time was 100  29 min. Mean blood loss was 168  133 ml. No patient required inten-
sive care unit stay. We observed one major complication (transient ischemic attack). Mean
hospital stay was 4  1 days. During a mean follow-up period of 26 months no endoleak, aneu-
rysm evolution or stent graft failure was recognized in any patient. One patient died 24 months
after the intervention after a stroke.
Conclusions: In our experience, endovascular or repair of infrarenal aortic ulcer appears
feasible, and midterm results satisfactory.
ª 2006 Surgical Associates Ltd. Published by Elsevier Ltd. All rights reserved.* Corresponding author. Tel.: þ39 0332278226; fax: þ39 03322
78581.
E-mail address: gabriele.piffaretti@tiscali.it (G. Piffaretti).1743-9191/$ - see front matter ª 2006 Surgical Associates Ltd. Publ
doi:10.1016/j.ijsu.2006.06.004Introduction
Penetrating atherosclerotic ulcer (PAU) of the aorta is
defined as atherosclerotic lesion with ulceration of the
aortic intima and media, and rupture of the internal elasticished by Elsevier Ltd. All rights reserved.
Endovascular repair of abdominal infrarenal PAU 173lamina.1e3 PAU occurs in elderly patients with systemic ath-
erosclerosis, predominantly in the descending thoracic
aorta, and it is uncommon in the infrarenal aorta.
Although first described by Shennan in 1934,4 their nat-
ural history still remains unclear and treatment is contro-
versial; it may be complicated by aortic intramural
hematoma, adventitial pseudoaneurysm formation, or aor-
tic rupture.5
We reviewed the clinical features of PAU in the infrare-
nal aorta and investigated the usefulness of endovascular
repair for this uncommon lesion.
Materials and methods
In the last 50 months, 348 patients underwent abdominal
aortic procedures at our institution for atherosclerotic dis-
ease (aneurysms (nZ 293), obstructive disease (nZ 55));
overall, 251 patients were treated endovascularly, 97 with
open surgery. A total of 13 patients were found to have
an abdominal PAU, corresponding to an incidence of 3.7%.
They were analyzed in a retrospective manner: there
were 12 men and 1 woman in this series; mean age was
73  7 years (range 56e84, median 77). All patients had hy-
pertension (on anti-hypertensive medication); additional
co-morbidities and risk factors included peripheral obstruc-
tive arterial disease (nZ 6), diabetes (nZ 5), chronic
obstructive pulmonary disease (nZ 3), cerebrovascular in-
sufficiency (nZ 3), chronic renal failure (nZ 2), hostile
abdomen (nZ 2), coronary artery disease (nZ 2), and
hyperlipidemia (nZ 1).
Three lesions were discovered incidentally during aorto-
iliac duplex ultrasound (US) screening examination and
were treated electively; of the 10 patients with symptoms,
five had claudication and the presence of the PAU was
suspected during preliminary US, three had critical ische-
mia of the lower extremities due to arterial embolism, and
two complained of abdominal pain (one associated with
syncope that suggested a ruptured abdominal aorta).
In every patient, PAU was diagnosed at computed
tomography angiography (CT-A): on CT-A, PAU is recognized
as a contrast-filled, pouch-like aortic protrusion without
a dissection flap or false lumen (Fig. 1A,B). Intramural
Figure 1 Preoperative CT-angiography of an infrarenal PAU
with a 55 mm aortic expansion (A). Intraoperative angiogram
(B) confirmed the presence of the PAU just above the aorto-
iliac bifurcation and the ulceration (ring) of a plaque of the
left common iliac artery; both the lesions were excluded
with two abdominal ‘‘cuffs’’ and a ‘‘kissing’’-stent grafts
(arrows) reconstruction of the aorto-iliac bifurcation (C).hematoma with aortic expansion, adventitial pseudoaneur-
ysm formation without intramural hematoma, and con-
tained ruptures with extra-aortic hematoma were
recognized. Because they were treated electively, it was
not possible to obtain an histological diagnosis to support
the CT diagnosis of PAU. CT-A also demonstrated associated
atherosclerotic arterial lesions in eight patients: stenosis of
an iliac artery (nZ 5; four bilateral, one unilateral), and
stenosis of the internal carotid artery (nZ 2). CT also re-
vealed thrombus in the abdominal aorta (nZ 5) and exten-
sive aortic calcifications (nZ 4).
All patients in this series underwent endovascular
treatment with stent graft (SG); the devices used were
cuffs of Excluder (W.L. Gore and Associates, Flagstaff, AZ,
USA), Zenith (Cook Inc., Bloomington, IN, USA), and Life-
path (Edwards Lifesciences Corp., Irvine, CA, USA). Re-
pairs were performed in the operating room with the
patient under loco-regional anesthesia (nZ 11), or general
anesthesia with endotracheal intubation (nZ 2); a
cell-saver system (Compact-Dideco; Modena, Italy) was
available in the event that surgical conversion was needed.
Patients were prepared and draped for either femoral arte-
riotomy and traditional transperitoneal approach. Every
patient received short-term antibiotic prophylaxis (vanco-
mycin 1 g b.i.d.). The common femoral artery was exposed
in standard fashion for device access in all patients. Com-
pletion digital subtraction angiography (DSA) was routinely
performed at the end of the procedure to confirm adequate
position of the SG, the complete exclusion of the lesion and
detect potential endoleaks (Fig. 1C).
All patients underwent follow-up CT-A control, at 1, 4
and 12 months after the intervention, and yearly thereaf-
ter. Data for variables were expressed as mean values.
Data were prospectively collected and analyzed in a retro-
spective manner. Primary outcome measures were the
exclusion of the PAU and patient survival.
Results
Overall, lesions were recognized as follows: PAU (nZ 6),
pseudoaneurysm (nZ 6), and rupture (nZ 1). Deployment
of the SG was technically successful in all patients. No post-
operative deaths occurred. A total of 17 SGs were used: ten
patients received one SG, two patients two SGs, and one
patients three SGs. Mean SG diameter was 25  3 (range
20e28, median 24). Aortograms obtained after the proce-
dure demonstrated complete exclusion of PAU and no endo-
leak. Additional procedures included bilateral iliac arteries
PTA/stent (nZ 4), iliac artery PTA (nZ 1), and internal
carotid artery stenting (nZ 2). Mean operative time was
100  29 min (range 60e150, median 80). Mean blood loss
was 168  133 ml (range 50e500, median 120); blood trans-
fusion (2 units of packed red blood cells) was needed in the
patient with a ruptured PAU.
Intensive care unit stay was never required; postope-
rative course was uneventful in all but one patient.
We observed a cerebrovascular event that spontaneously
resolved in a patient who underwent simultaneous carotid
stenting. Mean hospital stay after the operation was
4  1 days (range 3e8, median 4).
174 G. Piffaretti et al.During a mean follow-up period of 26 months (range 3e
60, median 24) no endoleak, aneurysm evolution or SG fail-
ure was recognized in any patient. In this series no patient
was lost to follow-up; one patient died 24 months after the
intervention after a stroke.
Discussion
PAU of the aorta was first identified by Shennan in 1934, but
described as a distinct clinical and pathologic entity by
Stanson in 1986.3,4 Stanson defines a PAU as an atheroscle-
rotic lesion with an ulceration that penetrates the internal
elastic lamina and the media of the aortic wall; subse-
quently, hematoma formation may extend along the media,
and in some cases hematoma extension causes stretching of
the weakened aortic adventitia, forming a saccular pseu-
doaneurysm. PAU generally affects elderly patients with
advanced atherosclerosis: as a result, PAU is associated
with a high incidence of morbidity, such as hypertension,
coronary artery disease, and carotid artery occlusive dis-
ease.6 All patients in this series have received antihyper-
tensive drugs, and three patients had multiple (carotid,
coronary and peripheral) arterial disease. Of interest, in
terms of age we noted a significant difference between
patients with PAU if compared to patients who received
aortic repair for peripheral obstructive disease (73  7 vs
66  10, p < 0.05), but no statistical difference if com-
pared to patients with aneurysmal disease (73  7 vs
72  8, pZ NS).
PAU typically involves the descending thoracic aorta,
and it is comparatively rare that PAU develops in the
infrarenal abdominal aorta; few reports have dealt with
endovascular stent grafting for treatment of PAU in the
infrarenal abdominal aorta.7e9 The true incidence of PAU
has yet to be determined. No literature study to date has
appropriately addressed this question. The incidence of
thoracic PAU varies from 2 to 7% while abdominal PAU
has been considered responsible for 1e5% of all aortic
ruptures.3,5e7 In our series abdominal PAU accounted for
3.7% of all aortic procedures over almost 4-years.
It has been reported that the incidence of these lesions
also depends on the diagnostic method; in fact, most
cases reported in the medical literature regarding the
imaging appearance of PAU or endovascular treatment do
not have histologic proof and the diagnosis of atheroscle-
rotic lesion is assumed but unconfirmed. Differentiation of
these disease entities is sometimes difficult, and there
seems to be confusion regarding the concept of PAU.3,5,7,10
For these reasons, Quint referred to these lesions as ‘‘ul-
cerlike lesions’’ of the aorta rather than PAU. PAU may be
diagnosed at CT, magnetic resonance imaging (MRI), and
conventional aortography; a high degree of clinical suspi-
cion is necessary for diagnosis of PAU. Extensive aortic cal-
cification is often detected on plain CT scans, and
development of intramural hematoma after PAU versus in-
traluminal thrombus can be differentiated by the location
of calcified plaques in relation to the thrombus on plain
CT scans. On contrast-enhanced CT scans, PAU is recog-
nized as a contrast-filled, pouch-like aortic protrusion
without a dissection flap or false lumen.2,5,11 An intramu-
ral hematoma, advential pseudoaneurysm, and rupturewith extra-aortic hematoma may also be seen. We believe
CT is more accurate, and is the most commonly used tech-
nique. MRI appears more effective because it reduces the
rate of false negative diagnoses, but it is less available
than CT; in our series, we detected six PAU, six pseudoa-
neurysm, and one rupture.
PAU are the subject of considerable controversy with
respect to definition as well as natural history. The
natural history of abdominal PAU remains unclear and
little information is available in the literature.5 The un-
predictable course of PAU was previously emphasized; in
particular, some patients had distal ischemia caused by
embolism from a PAU.3 Embolization from penetrating
aortic ulcers has been considered rare, but lower limb
embolisms were reported to be more frequent with
abdominal PAU than with thoracic PAU.3,12,13 Harris
reported three patients with complicated forms of abdomi-
nal PAU: two patients had distal ischemia caused by embo-
lism, one of them with recurrent embolism that required
amputation. Our series confirms that when there are no
signs suggesting a cardiac origin, discovery of lower limb
embolism should prompt a search for an aortic cause, and
in particular PAU.
The treatment of PAU remains controversial too. Al-
though some authors believe immediate surgical treatment
is not always required, because most PAU have a benign
clinical course, early intervention has been recommended
when PAU is complicated with aneurysm expansion regard-
less of size, rupture, embolic symptoms, or uncontrolled
pain.1,2,5,10,11 Open surgical repair with graft interposition
has been used traditionally, but patients with PAU are gen-
erally not ideal candidates for open repair because of
advanced age and poor general status.1,2,7e10 In fact, high
operative morbidity and mortality associated with open re-
pair have been reported.7 Use of aortic SGs could probably
change the strategy for treatment of PAU. This less invasive
procedure is suitable for high risk patients, and can also be
used in cases of rupture.
As a less invasive treatment for this disease, endovascular
stent grafting was advocated and several reports of endo-
vascular treatment of PAU have been published.7e9,13,14
Early complications for abdominal PAU included endoleak
mainly; peripheral embolization could be a potential intra-
operative complication as well as in the post-operative
course.Weopted to use a SG in order to prevent potential de-
bris migration or fragmentation from the original PAU during
the positioning or deployment of the device, and to exclude
completely thepotential aneurysmevolutionof thePAU from
the systemic flow. Review of all cases reported to date, in-
cluding our own mid-term results, reveals that deployment
of the SGs was successful in all; thus, the lower morbidity
and mortality after endovascular repair could also support
a more aggressive approach to this lesion, even in patients
without symptoms.
Conclusions
In conclusion, this is the largest experience of stent graft
treatment for abdominal PAU. Infrarenal aortic lesions
caused by PAU are generally localized, and endovascular
SG repair of this disease appears to be a feasible alternative
Endovascular repair of abdominal infrarenal PAU 175to surgical repair. Mid-term results of endovascular treat-
ment of PAU are satisfactory; however, further investiga-
tions of the long-term results of this procedure are
necessary.
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Endovascular repair of abdominal infrarenal penetrating aortic ulcers: a prospective observational study.

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