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Penetrating Atherosclerotic Ulcer: Presentation andManagement

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253

Early Management ofPAU

Initial management is directed at reducing radial, longitudinal and shear stresses on the aortic wall with medical therapy aimed at lowering systolic blood pressures and pulse pressures. In acute cases, with progression of a PAU towards intramural hematoma (IMH) or aortic dissection, the patient may present with unstable hemodynamics and urgent management is required. Medical management consists of using intravenous beta-blockers to target a heart rate of 60–80 beats per minute, a systolic pressure of 100–120mmHg and attempts to preserve end-organ perfusion [14, 15]. The main intravenous beta-blocking agents used in this setting are labetalol and esmolol. Esmolol is preferred by many physicians, because of its short duration of action. Additionally, effective pain control should be instituted to aid blood pressure management. In hemodynamically unstable patients, or patients with radiographic evidence of (contained) rupture, emergent surgical repair should be performed.

Treatment Options forType APAU

Since there is a higher risk of complications of PAU in the ascending thoracic aorta, and it is often associated with IMH, the management usually consists of surgical intervention (Fig.3). Open surgical repair is the mainstay of therapy [15, 16], similar to that seen in typical double barrel Type A dissection treatment.

Recently, there is an increasing interest in using thoracic endovascular aortic repair (TEVAR) as an alternative treatment paradigm. Several centers have reported successful endovascular treatment of aortic pathology, such as aneurysm and dissection, in the ascending aorta and transverse arch [17, 18]. Tsilimparis et al. reported on 10 patients undergoing ascending endograft placement. Four underwent cervical debranching, one received a fenestrated and one a branched endograft [17]. The technical success was 100%, the 30-day mortality was 10% and the stroke rate was 10%. Roselli etal. reported on 39 endovascular procedures with 35 stents having proximal and distal landing in Ishimaru zone 0, three occluder devices placed for pseudoaneurysms and one total arch endovascular procedure with an innominate side branch after cervical debranching [18]. Conversion to open surgery was performed in 10%, with the survival at 30days of 81% and the observed stroke rate of 10%. All patients had signicant associated comorbidities and were too high-risk for open surgery. This likely led to the relatively poor reported outcomes when compared to reports of open surgical repair. As only small cohorts of patients have been treated with this approach, and signicant complications are reported, endovascular treatment of the ascending aorta should be restricted to high risk patients who are deemed unsuitable for open surgical repair.

After successful repair of the aorta, imaging surveillance is mandatory to ensure there are no further aortic complications in either the treated, adjacent or

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remote aortic segments, particularly if endovascular therapy has been performed. Regular CT surveillance for endovascular procedures is performed at 1month, 3 months, 6 months, 12 months and annually after. Medical therapy is also required and typically consists of blood pressure management and control of lipids.

I. B. Houben et al.

Treatment Options forType B PAU

In patients with Type B PAU there are several options for management of the PAU (Fig.1). If a patient is hemodynamically stable, but symptomatic, medical therapy with intravenous beta-blocker and pain management is indicated. If the pain is recurrent or refractory, or there are other signs of impending rupture, repair should be performed urgently. If the patient can be stabilized and transitioned to oral antihypertensive medication and becomes asymptomatic, pre-operative planning can take place and the patient should be planned for early repair within 3months in select circumstances such as development of saccular aneurysms, or rapid expansion of aortic dimension.

TEVAR is an effective therapy for type B PAU and has evolved into the rst line strategy. The rate of endoleak and re-interventions are similar to those reported for TEVAR for other indications, and range from 0 to 13% and 0 to 20% respectively [14]. PAUs in patients with progressive disease are usually in more proximal aortic segments with the proximal descending thoracic aorta being the most common site [7]. In many cases, TEVAR needs to be performed in proximal landing is zone 2, and adjunctive left subclavian artery (LSA) management performed as per local practices.

Long-term follow-up on PAU post TEVAR is sparse. The current two longest reported clinical series had a mean follow-up of 51 and 53months. Demers etal. included 26 descending TEVARs and showed relatively low aortic event related mortality of 4% and an equally low aortic reintervention rate of 4% [19]. Mestres etal. included 22 PAUs and showed a similar aortic event related mortality rate 5% and a higher aortic reintervention rate of 14% [20]. The overall range of follow-up, mortality and reintervention rate ranged from 9–53 months, 0–13% and 0–20% respectively (Table1). These numbers suggest that at least in the rst 2 years after repair, TEVAR compares well to open repair mortality and that attention is needed on the durability of TEVAR.Patel etal. performed a comparison between descending thoracic open repair and TEVAR and found excellent results with the endovascular approach [35]. Early outcomes from descending TEVAR case series over the last two decades can be found in Table2. Similar to those patients who presented with type A PAU, statin therapy, in addition to blood pressure control and long term imaging surveillance is indicated for the long-term management of these patients (Fig.4).

Penetrating Atherosclerotic Ulcer: Presentation andManagement

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Table 1 Late outcomes of contemporary clinical series (n>5) of descending endovascular repair of penetrating aortic ulcers

References Year N Endoleak Reintervention

Schoder etal. [ Kos etal. [ Eggebrecht etal.

[23] Demers etal. [ Brinster etal. [24] 2005 21 0 0 0 14 Eggebrecht etal.

[25] Dalainas etal. [ Pauls etal. [27] 2007 12 8% 0 0 28 Geisbüsch etal.

[28] Botta etal. [ Girn etal. [30] 2009 11 9% – 18% 32 D’Souza etal. [31] 2009 20 15% 5% 0 24 Patel etal. [13] 2010 37 11% 16% 8% 33 Czerny etal. [32] 2011 72 4% 1% 1% 42 Palombo etal. [33] 2012 16 6% 0 13% 16 Mestres etal. [20] 2012 22 14% 14% 5% 53 Jánosi etal. [34] 2016 63 6% 19% 0 45

21] 2002 8 13% 0 13% 14

22] 2002 10 20% – 10% 9

2003 10 10% 20% 0 24

19] 2004 26 14% 4% 4% 51

2006 22 5% 9% 0 27

26] 2007 18 6% 0 0 41

2008 48 23% 8% – 31

29] 2008 18 17% 11% 0 22

Related mortality

Follow-up (months)

255

Follow Up

Patients with a history of PAU and atherosclerotic aorta should be kept under lifelong CT-surveillance. The guidelines for the rst period after surgery or diagnosis are CT angiography at 1, 3, 6 and 12months and hereafter annually [12, 15, 16]. If the patient remains asymptomatic and the aorta does not grow more than 5 millimeters per year the interval can be increased. It should be noted that aggressive blood pressure control and lifestyle management are critically important to prevent complications during follow-up. PAU should be considered a chronic disease that necessitates lifelong treatment and surveillance.

Conclusion

PAU is a disease of the arterial wall and is mostly asymptomatic. If a patient develops symptoms, they largely overlap with the other causes of AAS (AD and IMH). The management of PAU closely resembles the two other pathologies in acute aortic syndrome. Initial control consists of blood pressure management and pain

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Table 2 Early outcomes of contemporary clinical series (n > 5) of descending thoracic endovascular repair of penetrating aortic ulcers

PAU location

References Year N

Schoder etal. [

Kos etal. [

22]

Eggebrecht etal. [

Demers etal. [

Brinster etal. [

Eggebrecht etal. [

Dalainas etal. [

Pauls etal. [

27]

Geisbüsch etal. [

Botta etal.

29]

[ Girn etal.

[

30]

D’Souza etal. [

Patel etal. [

13]

Czerny etal. [

Palombo etal. [33]

Mestres etal. [20]

Jánosi etal. [34]

PAU penetrating atherosclerotic ulcer, SCI spinal cord ischemia

In-hospital or 30-day mortality

2002 8 100% 0 0 0 0 0 13%

21]

2002 10 100% 0 0 – 0 0 10%

2003 10 80% 20% 0 0 0 0 0

23]

2004 26 100% 0 0 4% 12% 4% 0

19]

2005 21 100% 0 0 0 0 0 0

24]

2006 22 73% 9% 18% 0 0 5% 0

25]

2007 18 89% 11% 0 0 0 0 0

26]

2007 12 100% 0 0 0 0 0 0

2008 48 71% 25% 4% – 6% 4% 0

28]

2008 18 100% 0 0 5% 11% 0 0

2009 11 100% 0 0 0 18% 0 9%

2009 20 100% 0 0 5% 0 0 0

31]

2010 37 100% 0 0 27% 5% 5% 5%

2011 72 96% 1% 3% 35% 4% 3% 1%

32]

2012 16 81% 19% 0 25% 6% 0 6%

2012 22 100% 0 0 27% 5% 0 5%

2016 63 86% 0 14% 5% 8% 0 0

Adjunctive debranching

Early mortality

Stroke SCIThoracic Abdominal Both

management. Type A PAU necessitates urgent or early elective repair, depending on the hemodynamic stability and symptoms of the patient. Type B lesions are preferably medically managed when asymptomatic and are managed by endovascular repair when symptoms or complications are present. Future advances in endovascular technology may extend the patient population who benets from the less invasive approach.

Penetrating Atherosclerotic Ulcer: Presentation andManagement

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Confirmed

PAU on imaging

257

Type A

open repair

Yes

BP management + pain

control (if present)

e.g. Saccular aneurysm,

Refractory pain, Extensive IMH

Yes

-Unsuitable anatomy for TEVAR

open repair

BP management and surveillance at 1 month, 3 months, 6 months, 12 months and annually

-Suitable anatomy for TEVAR

Hemodynamically

stable?

Type B

Symptoms?

BP management and

CT surveillance at 3

months, 6 months, 12

months and annually

TEVAR

IV BP management

<120 mmHg systolic with end-organ

perfusion + IV pain control

Type A

Emergent/Urgent

open repair

Emergent/Urgent

open repair

Type

Emergent/

Urgent

TEVAR

Fig. 4 Flowchart for treatment decision-making in a patient with penetrating aortic ulcer

References

1. Vilacosta I, San Roman JA.Acute aortic syndrome. Heart. 2001;85(4):365–8.

2. Stanson AW, Kazmier FJ, Hollier LH, Edwards WD, Pairolero PC, Sheedy FC, et. al. Penetrating atherosclerotic ulcers of the thoracic aorta: natural history and clinicopathologic correlations. Ann Vasc. Surg. 1986;1:15–23.

3. Coady MA, Rizzo JA, Hammond GL, Pierce JG, Kopf GS, Elefteriades JA.Penetrating ulcer of the thoracic aorta: What is it? How do we recognize it? How do we manage it? J Vasc Surg. 1998;27(6):1006–16.

4. Cho KR, Stanson AW, Donald Potter D, Cherry KJ, Schaff HV, Sundt TM III.Penetrating atherosclerotic ulcer of the descending thoracic aorta and arch. J Thorac Cardiovasc Surg. 2004;127(5):1393–9.

5. Nathan DP, Boonn W, Lai E, Wang GJ, Desai N, Woo EY, etal. Presentation, complications, and natural history of penetrating atherosclerotic ulcer disease. J Vasc Surg. 2012;55(1):10–5.

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6. Quint LE, Williams DM, Francis IR, Monaghan HM, Sonnad SS, Patel S, et al. Ulcerlike lesions of the aorta: Imaging features and natural history. Radiology. 2001;218(3):719–23.

7. Ganaha F, Craig Miller D, Sugimoto K, Do YS, Minamiguchi H, Saito H, etal. Prognosis of aortic intramural hematoma with and without penetrating atherosclerotic ulcer: a clinical and radiological analysis. Circulation. 2002;106(3):342–8.

8. Tittle SL, Lynch RJ, Cole PE, Singh HS, Rizzo JA, Kopf GS, et al. Midterm follow-up of penetrating ulcer and intramural hematoma of the aorta. J Thorac Cardiovasc Surg. 2002;123(6):1051–9.

9. Wooley CF, Sparks EH, Boudoulas H.Aortic pain. Prog Cardiovasc Dis. 1998;40(6):563–89.

10. Toda R, Moriyama Y, Iguro Y, Matsumoto H, Masuda H, Ueno T.Penetrating atherosclerotic ulcer. Surg Today. 2001;31(1):32–5. https://doi.org/10.1007/s005950170216.

11. Gifford SM, Duncan AA, Greiten LE, Gloviczki P, Oderich GS, Kalra M, et al. The natural history and outcomes for thoracic and abdominal penetrating aortic ulcers. J Vasc Surg. 2016;63(5):1182–8.

12. Writing Committee, Riambau V, Böckler D, Brunkwall J, Cao P, Chiesa R, et al. Editor’s choice– management of descending thoracic aorta diseases: clinical practice guidelines of the European Society for Vascular Surgery (ESVS). Eur J Vasc Endovasc Surg. 2017;53(1):4–52.

13. Patel HJ, Williams DM, Upchurch GR, Dasika NL, Deeb GM.The challenge of associated intramural hematoma with endovascular repair for penetrating ulcers of the descending thoracic aorta. J Vasc Surg. 2010;51(4):829–35.

14. Oderich GS, Kärkkäinen JM, Reed NR, Tenorio ER, Sandri GA.Penetrating aortic ulcer and intramural hematoma. Cardiovasc Intervent Radiol. 2019;42(3):321–34.

15. Erbel R, Aboyans V, Boileau C, Bossone E, Di Bartolomeo R, Eggebrecht H, etal. 2014 ESC guidelines on the diagnosis and treatment of aortic diseases. Russ J Cardiol. 2015;123(7):7–72.

16. Hiratzka LF, Bakris GL, Beckman JA, Bersin RM, Carr VF, Casey DE, etal. 2010 ACCF/ AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients with Thoracic Aortic Disease: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. A Circulation. 2010;121(13):e266–369.

17. Tsilimparis N, Debus ES, Oderich GS, Haulon S, Terp KA, Roeder B, etal. International experience with endovascular therapy of the ascending aorta with a dedicated endograft. J Vasc Surg. 2016;63(6):1476–82.

18. Roselli EE, Idrees JJ, Johnston DR, Eagleton MJ, Desai MY, Svensson LG.Zone zero thoracic endovascular aortic repair: a proposed modication to the classication of landing zones. J Thorac Cardiovasc Surg. 2018;155(4):1381–9.

19. Demers P, Miller DC, Mitchell RS, Kee ST, Chagonjian L, Dake MD.Stent-graft repair of penetrating atherosclerotic ulcers in the descending thoracic aorta: mid-term results. Ann Thorac Surg. 2004;77(1):81–6.

20. Mestres G, Rodríguez R, García-Madrid C, Montañà X, Burrel M, Cruz LF, etal. Endovascular treatment of penetrating aortic ulcers: mid-term follow-up. Rev Española Cardiol (Engl Ed). 2012;65(1):54–9.

21. Schoder M, Grabenwöger M, Hölzenbein T, Domanovits H, Fleischmann D, Wolf F, et al. Endovascular stent-graft repair of complicated penetrating atherosclerotic ulcers of the descending thoracic aorta. J Vasc Surg. 2002;36(4):720–6.

22. Kos X, Bouchard L, Otal P, Chabbert V, Chemla P, Soula P, etal. Stent-graft treatment of penetrating thoracic aortic ulcers. J Endovasc Therapy. 2002;9(Suppl 2):II25–31.

23. Eggebrecht H, Baumgart D, Schermund A, von Birgelen C, Herold U, Wiesemes R, etal. Endovascular stent-graft repair for penetrating atherosclerotic ulcer of the descending aorta. Am J Cardiol. 2003;91(9):1150–3.

24. Brinster DR, Wheatley GH, Williams J, Ramaiah VG, Diethrich EB, Rodriguez-Lopez JA.Are penetrating aortic ulcers best treated using an endovascular approach? Ann Thorac Surg. 2006;82(5):1688–91.

I. B. Houben et al.

Penetrating Atherosclerotic Ulcer: Presentation andManagement

https://t.me/med1917

25. Eggebrecht H, Herold U, Schmermund A, Lind AY, Kuhnt O, Martini S, etal. Endovascular stent-graft treatment of penetrating aortic ulcer: results over a median follow-up of 27 months. Am Heart J. 2006;151(2):530–6.

26. Dalainas I, Nano G, Medda M, Bianchi P, Casana R, Ramponi F, etal. Endovascular treatment of penetrating aortic ulcers: mid-term results. Eur J Vasc Endovasc Surg. 2007;34(1):74–8.

27. Pauls S, Orend KH, Sunder-Plassmann L, Kick J, Schelzig H.Endovascular repair of symptomatic penetrating atherosclerotic ulcer of the thoracic aorta. Eur J Vasc Endovasc Surg. 2007;34(1):66–73.

28. Geisbüsch P, Kotelis D, Weber TF, Hyhlik-Dürr A, Kauczor HU, Böckler D.Early and midterm results after endovascular stent graft repair of penetrating aortic ulcers. J Vasc Surg. 2008;48(6):1361–8.

29. Botta L, Buttazzi K, Russo V, Parlapiano M, Gostoli V, Di Bartolomeo R, etal. Endovascular repair for penetrating atherosclerotic ulcers of the descending thoracic aorta: early and midterm results. Ann Thorac Surg. 2008;85(3):987–92.

30. Girn HRS, McPherson S, Nicholson T, Mavor AID, Homer-Vanniasinkam S, Gough MJ.Short series of emergency stent-graft repair of symptomatic penetrating thoracic aortic ulcers (PTAU). Vasc Med. 2009;14(2):123–8.

31. D’Souza S, Duncan A, Aguila F, Oderich G, Ricotta J, Kalra M, et al. TEVAR for nonaneurysmal thoracic aortic pathology. Catheter Cardiovasc Interv. 2009;74(5):783–6.

32. Czerny M, Funovics M, Sodeck G, Dumfarth J, Schoder M, Juraszek A, etal. Results after thoracic endovascular aortic repair in penetrating atherosclerotic ulcers. Ann Thorac Surg. 2011;92(2):562–7.

33. Palombo D, Lucertini G, Robaldo A, Pane B, Spinella G.Treatment of penetrating aortic ulcer by endoprosthesis: A single center experience. Int Angiol. 2012 Feb;31(1):54–61.

34. Jánosi RA, Gorla R, Tsagakis K, Kahlert P, Horacek M, Bruckschen F, etal. Thoracic endovascular repair of complicated penetrating aortic ulcer: an 11-year single-center experience. J Endovasc Ther. 2016;23(1):150–9.

35. Patel HJ, Sood V, Williams DM, Dasika NL, Diener AC, Deeb GM.Late outcomes with repair of penetrating thoracic aortic ulcers: the merits of an endovascular approach. Ann Thorac Surg. 2012;94(2):516–23.

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Endovascular Treatment ofType AAortic

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Dissections

MaximilianKreibich andFriedhelmBeyersdorf

Abbreviation

TEVAR Thoracic endovascular aortic repair

Introduction

Patients with acute type A aortic dissection require an immediate surgical intervention to survive [1, 2]. Yet survival after such surgery remains unacceptably low in patients with severe organ malperfusion and/or shock [2, 3], despite considerably improved surgical techniques [3], individualized organ protection and cannulation strategies [4] and integrated, standardized surgical management strategies [5]. In fact, while the predicted mortality of patients with acute type A aortic dissection without shock or malperfusion remains well below 10% even in the elderly, outcomes in older patients presenting shock and malperfusion are dismal, with predicted mortality rates exceeding 50% [2]. Moreover, even in specialized high-volume centers, up to 8% of all patients with an acute type A aortic dissection are deemed inoperable [6].

Thoracic endovascular aortic repair (TEVAR) has signicantly improved the perioperative results in the treatment of acute complicated dissections of the descending aorta compared to conventional open surgery [7]. Yet TEVAR’s use in the more proximal aortic segments, specically the ascending aorta, remains experimental and is limited to high-volume aortic centers with specialized aortic teams. In fact, although TEVAR in the ascending aorta remains the subject of only case reports and small case series [8], the rising numbers of successful TEVARs in the ascending aorta highlight this therapy’s feasibility. In patients with acute type A aortic dissection and a dismal perioperative risk, TEVAR may help to signicantly improve peri- und postoperative outcomes [2, 8, 9]. Nevertheless, four frontiers

M. Kreibich (*) · F. Beyersdorf Department of Cardiovascular Surgery, Heart Centre Freiburg University, Freiburg, Germany

Faculty of Medicine, University of Freiburg, Freiburg, Germany e-mail: maximilian.kreibich@universitaets-herzzentrum.de

J. S. Coselli et al. (eds.), Aortic Dissection and Acute Aortic Syndromes,

https://doi.org/10.1007/978-3-030-66668-2_18

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currently restrict the routine application of ascending aortic TEVAR to treat acute type A aortic dissection, namely, a physiologic, anatomic, medical, and technical frontier.

M. Kreibich and F. Beyersdorf

Physiologic Frontier

The ascending aorta’s motion pattern is uniquely different from the more distal aortic segments such as the tubular, straight descending aorta. In fact, the ascending aorta’s ow and motion are signicantly inuenced by its non-planar curvature, specic inlet ow conditions from the aortic valve, radial expansion-contraction, and transational movement secondary to being attached to the beating heart [10]— effects that result in its substantial deformation, rotation, and craniocaudal movement [11]. The precise implantation of the stent-graft may be perioperatively feasible through rapid over-pacing, halting the heart’s ejection and the movement within the ascending aorta. However, when returning to a normal cardiac cycle, the interaction between a dissected, exible, and highly mobile ascending aorta and stiff tubular stent-graft remains unclear and the potential risk for stent-graft dislocation and other stent-graft induced complications is very high.

Stable xation to prevent stent-graft dislocation or migration can be ensured by oversizing the stent-graft in comparison to the native aorta. However, particularly in a dissected aorta, oversizing also signicantly increases the risk for stent-graft induced new entries and aortic rupture [12]. If we consider a stent-graft’s potentially unequal pressure distribution in the ascending aorta’s small and large curvature, the risk for stent-graft-induced complications may even be higher in the ascending aorta than in the straight, tubular aortic segments.

Lastly, two small studies, have recently suggested negative aortic remodeling entailing reduced biventricular function following the use of TEVAR in the descending aorta [13, 14]. The impact of stiff endovascular grafts in more proximal aortic segments, particularly the ascending aorta compared with the native exible aortic wall, and elimination of the Windkessel effect need to be considered when performing ascending aortic TEVAR.

Anatomic Frontier

The length of any stent-graft is dened as the distance between the proximal and distal landing zone. When using short stent-grafts, the landing zone should at least comprise 20mm to ensure the stent-graft’s durable xation and stabilization [15]. In addition, there must be no entry tear in either of the two landing zones [15]. In this respect, the length of an ascending aortic stent-graft is very limited by the need

Endovascular Treatment ofType AAortic Dissections

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for proximal and distal landing zons, each measuring at least 20mm, as well as by the short distance between the aortic sinus with the coronary arteries’ offspring and the brachiocephalic trunk with the cerebral arteries’offspring. Because of these preconditions, high quality feasibility studies addressing the application of ascending aortic TEVAR with a straight stent-graft in patients with type A aortic dissection have identied just 32–46% of all patients as being potential candidates suitable for a conventional straight endovascular tube graft because the entry tear would need to be average length of 30–40mm in the mid ascending aorta for a straight stent-graft to adequately cover it [9, 16, 17]. Therefore, to treat more patients with ascending aortic TEVAR, shorter stent-graft landing zones seem inevitable, yet without additional stent-graft anchorage, the risk for stent-graft-induced complications such as its migration would increase considerably. In addition, a perpendicular angle between the sinotubular junction and distal ascending aorta can further compromise the precise implantation of a straight stent-graft [18].

263

Medical Frontier

A substantial number of patients with type A aortic dissection develop cardiac tamponade and/or moderate to severe aortic regurgitation [19]. The latter can be a major limitation for isolated ascending aortic TEVAR, while cardiac tamponade may be alleviated by simultaneous pericardial drainage or by transapical, antegrade stentgraft implantation. Antegrade implantation would both remove any pericardial effusion and simplify stent-graft implantation: true lumen wire placement would be simpler, the aortic arch’s steep curvature would be avoided, the risk for dissection membrane perforation would be reduced, and accurate and precise stent-graft deployment would be easier because of the shorter distance to the ascending aorta.

Technical Frontier

Currently and commercially available stent-grafts may not be ideal for deployment within a dissected ascending aorta, because most patients presenting an acute type A aortic dissection would require tapered stent-grafts because of signicantly different sizes between the proximal and distal landing zones [9]. Moreover, stentgraft dislocation due to the jump phenomenon remains an issue during TEVAR deployment, and even slight displacements of the stent-graft in the short ascending aorta can have devastating consequences because of the high risk for coronary or cerebral malperfusion [20]. The stent-graft’s wedge apposition in the ascending aorta is another potential factor limiting durable stent-graft deployment within the ascending aorta as it can also raise the risk for stent-graft-induced complications.

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