Imaging Endoleaks: CT, US, MR or Angio?

5. Chuter TA, Wendt G, Hopkinson BR, et al. European expetience with a system for bifurcated stent-graft insertion. J Endovasc Surg 1997;4:1322. 6. Bemhard, VM, Mitchell RS, MatsumuraJS, et al. Ruptured abdominal aortic aneUlysm after endovascular repair. J Vasc Surg 2002;35:1155-62. 7. Harris PL, Vallabhaneni SR, Desgranges P, Becquemin JP, van Marrewijk C, Laheij RJF for the EDROSTAR Collaborators. Incidence and risk factors of late rupture, conversion, and death after endovascular repair of infrarenal aortic aneurysms: The EDROSTAR experience. J Vasc Surgely 2000;32(4);739748. 8. Resch T, Ivancev K, Brunkwall J, Nyman D, Malina M, Lindbald B. Distal migration of stent-grafts after endovascular repair of abdominal aortic aneurysms. ]VIR 1999;10:257-264. 9. Gould DA, Edwarcls RD, McWilliams RG, et al. Graft distortion after endovascular repair of abdominal aortic aneUlysm: Association with sac morphology and mid-term complications. Cardiovasc Intervent Radiol 2000;23:358-36310. Beebe HG, CronenwettJL, Katzen BT, Brewster DC, Green RM for the Vanguard Endograft Trial Investigators. J Vasc Surg 2001;33:S55-63. 11. Kareh LA, Hodgson KJ, Mattos MA, Bohannon WT, Ramsey DE, McLafferty RB. Management of ectatic, nonaneUlysmal iliac arteries during endoluminal aortic aneurysm repair. J Vasc Surg 2001 ;33:S33-8. 12. WolfYG, Hill BB, Lee WA, Corcoran CM, Fogarty TJ, Zarin CK. Eccentric stent graft compression: An indieator of insecure proximal fixation of aortic stent graft. J Vasc Surg 2001 ;33:481-7. 13. Carpenter JP, Neschis DG, Fairman RM, et al. Failure of endovascular abdominal aortic aneurysm graft limbs. J Vasc Surg 2001;33:296-303. 14. Becker G], Kovacs M, Mathison MN, et al. Risk stratification and outcomes of transluminal endografting for abdominal aortic aneurysm: 7-Year experience and long-term follow-up. J Vasc Interv Radiol 2001; 12:1033-1046. 15. Tillich M, Bell RE, Paik DS, Fleischmann D, Sofilos MC, Logan LJ, Rubin GD. Iliac arterial injuries after endovascular repair of abdominal aortic aneUlysms: Correlation with iliac curvature and diameter. Radiology 2001;219:129-136. 16. Carpenter JP, Baum RA, Barker CF, et al. Impact of exclusion criteria on patient selection for endovascular abdominal aortic aneurysm repair. J Vasc Surg 2001;34: 1050-1054. 17. Cao, P, Verzini F, Zannetti S, et al. Device migration after endoluminal abdominal aortic aneulysm repair: Analysis af 113 cases with a minimum follaw-up period of 2 years. J Vasc Surg 2002;35:229-235.

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18. Hovsepian DM, Hein AN, Pilgram TK, et al. Endovascular abdominal aortic aneurysm repair in 144 patients: Correlation of aneUlysm size, proximal aortic neck length, and procedure-related complications. J Vasc Interv Radiol 2001;12:1373-1382. 19. Parent III FN, GodziachviIi V, Meier GH, et al. Endograft limb occlusion and stenosis after ANCDRE endovascular abdominal aneUlysm repair. ] Vasc Surg 2002;35:686-690. 8:00 a.m. Imaging Endoleaks: CT, DS, MR or Angio? John A. KauJman, MD Dotter Interventional Institute Portland, OR

Learning objectives: As a result of attending session, the attendee should be able to: 1. Describe the types of persistent sac perfusion (endoleak) after aortic endograft placement. 2. Describe the different modalities used for detection of sac perfusion. 3. Describe the relative strengths and weaknesses of different imaging modalities for detection of sac perfusion. Successful insertion of a stent-graft for abdominal aortic aneurysm (AAA) is possible in more than 95% of procedures when patients are carefully selected and an appropriate device is utilized (1). The reported rates of immediate aneurysm exclusion range from 66%---87% (2). In the simplest of terms, a successful stent-graft procedure results in freedom from AAA rupture with long-term device patency. In the absence of long-term data in large numbers of patients using a stable endograft platform, decrease or stabilization of aneurysm dimensions is used as a surrogate for success (3). The visualization of flow in the anelllysm sac outside of the endograft but within the confines of the arterial wall has been termed "endoleak" (4). This phenomenon is not restricted to endografts, but can occur after surgical repair as well (5). The types of sac perfusion are described in Table 1. Systemic or near systemie pressures in the aneulysm sac have been measured in patients with persistent sac perfusion (6). The presence of sac perfusion is correlated with less reduction in the diameter of the sac and even slight enlargement (7). Type I and III perfusion are generally accepied as risk factors for late aneurysm rupture (8,9). Retrograde perfusion of the aneUlysm sac from branch vessels (Type II) is the most common etiology of perigraft flow. Though related to the number of patent branch vessels prior to endograft placement, type II perfusian remains a somewhat unpredietable event in terms of individual patients and timing of occurrence (2,10,11). Decrease in aneuIysm size (as measured by diameter, volume, or surface area) tends to be less in patients with type II endaleaks (12). Successful treatment of type II perfusion results in

Table 1 Classification of Sac Perfusion after Endograft Placement·

Type

Subtype

Definition Attachment

Il

Collateral VesseJ

!lI

Device

IV

Graft Fabric Porosity Unknown Immediate or less than 30 days post procedure Later than 30 days post procedure

V

Primaly Secondary

A: ProximaI B: Distal C: J1iac occluder A: Single vessel (imo blind space) B: Twa ar more vessels with inflow/outf1ow A: Modułar overlap B: Hole in fabric Minor: <2 mm Major: 2:2 mm Must be <30 days after graft placemem Sac enlargement wid10ut detectabłe endoJeak

._------------------------------------

• Adapted from references 4 and 18.

a significant deerease in aneulysm surface area when eompared to patients in whom treatment is unsueeessful 03-15). The risk of treatment failure (MA ruptlIre) in the presenee of Type II perfllsion is lInknown and eontroversial 06-18). There are several reports of rupture and open eonversion for inereasing anellJysm size due to Type II perfusion (9,19,20). Sae enlargement due to serolls fluid without perigraft flow has been reported in both endografts and surgieally repaired anellrysms (2]-23). Termed "sae hygromas", these are of unknown etiology but may be related to ultrafiltration of blood by graft fabrie (22). The presenee of sub-clinical endograft infection should always be eonsidered when sae hygroma is sllspeeted. Overt endograft infeetion resulting in endopyoma also results in sae enlargement without sae perfusion (24). The preeise sensitivity, specificity, and predietive values for deteetion or sae perfusion by different imaging modalities has not been determined for the. Operator skilI, knowledge, experience and interest greatly influence the reslllts. FUlthermore, the absenee of direet anatomie eorrelation for imaging in most eases as weB as reliable data on the long-term outeomes results in łarge amounts of eonjeeture. Fortunately, sae enlargement is readily deteeted by most eross-seetional imaging teehniques (25). Also helpful as a hint of sae perfusion is inereasing aneUlysm volume, which ean also be determined from CTA, MRA, and US. In most eenters, an enlarging aneurysm after endograft plaeemem triggers an intensive evaluation in seareh of a treatable eause (8,17,18,26). Helical CT is widely utilized in the follow-up of patients after endograft plaeement (27). This is due in part to the ready availability, simplieity, and reprodueibility of eTA, as well as the almost universal applieation of this modality for pre-endograft planning. The basic prineipies are a non-eontrast sean encompassing the abdomen and pelvis, folIowed by an arterial phase helical sean from the celiae artery to the groin with at least 3 rrun effective collimation or smal/er, and lastJy a delayed sean

at least 90 to 120 seconds after the initial eontrast injeetion (28). With ultrafast 06+ deteetor row) seanners, the delay before the last acqllisition may need to be even longer. The non-eontrast scan is crucial to avoid confusing pre-existing calcium or even contrast within the thromblls with sac perfusion. Type I perfusion tends to appear early with density equal to eontrast in the vessel lumen, and adjaeenL to the ends of the endograft. Type II perfusion may be early or late, but generally is less dense than type I, and has identifiable branch vessels feeding into it. Type III appears early and with equal density to the intravasclllar contrast. Type IV is lIsually lower in density than I or m, appears late, and without focality in relation to the endograft or branch vessels. CTA remains an integral part of post-endograft surveillance. Color flow DS, without Ol' with eontrast, performs at least as well as CTA for detection of sac perfusion in some eenters (29,30). However, this is by no means consistent among institutions (3]). Direction of flow in branch vessels such as the IMA and lumbar arteries can be determined. The addition of a contrast agent may substantially improve visualization of peri-endagraft flow (32). Identification af morion of the wall of aneurysm sae after endograft placement has not proved to be helpful in assessing sac pressurization (33). Impoltant limitations of this modaJity are operator skUl, patiem size, and bowel gas. Contrast-enhaneed MRl and MRA appears to have excellent sensitivity for sae perfusion despite the presence of metallic endograft components. In particular, nitinol based fully suppolted endografts and unsllpported deviees are suited for /\tIR imaging (2] ,28,34-36). Administration of gadolinium and delayed aequisitions through the sac are essential to detect peri-graft flow. A eonU'ast enhanced MRA using a 3-D volllme proscribed to cover from the renal arteries to the iliac alteries can be repeated several times (well imo the venous phase) to reveal sac perfusion. This will allow identification of early type I or m, or sJower type II perfusion. Delayed

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(5-10 minutes) axial SPGR or Tl-weighted or images obtained through the sac after contrast administration are also useful. In the near future blood pool contrast agents may prove advantageous for this purpose, Conventional angiography is usually reserved for patients undergoing an intervention of an abnormality detected with other imaging modalities, lnjection with adequate volumes of contrast is essential. A compJete study may require injection at the proximal and distal attachment sites, folIowed by selective injection of the SMA and hypogastric arteries, Balloon occlusion of a limb with retrograde injection at the distal attachment site may be necessary to identify a distal source of type I perfusion, or a pinhole in the graft material (type III), Failure of visualization by conventional angiography does not exclude the presence of sac perfusion, Plain fJlms remain an integral part of endograft follow-up, Although not directly able to assess for aneurysm sac perfusion, they are essential to detect subtle derangements of endograft elements, or component migration (24,28). Nuclear medicine flow studies have not proved reliable in detection of perigraft flow (37). Enzymatic evidence consistent with ongoing aneurysmai activity in the aortic wall has been documented in patients with type II perfusion when compared to surgical controls and patients with endografts but no visible sac perfusion (38,39), Of equal concern, evidence suggestive of aortic wall atrophy following exclusion from the circulation raises the possibility t11at mpture may be more likely in the event of delayed sac re-pressurization (40), In the future, serum markers combined with minimai imaging may prove most influential in de termining which patients with persistent sac perfusion after endograft placement require intervention (38,39,41-45). The nature of the intervention may change as well, with targeting of the underlying aortic wall physiology rather than the branch vessels (46,47). Currently, most patients are folIowed with plain fJlms and CTA after endograft placement. A baseline exam at one month, with follow-up at 6 month, 12 months, then yearly is suffJcient for patients with no documented sac perfusion Ol' stable/shrinking sacs, Patients with a suspected type I or III perfusion are not folIowed but undergo angiography and intervention at the time of diagnosis in our practice,

References 1. Becker, G" et al., Risk stratmcation and outcomes of transluminal endografting for abdominal aortic aneurysm: 7-year experience and long-term follow-up, J Vasc lnterv Radiol, 2001; 12(9):1033-46, 2, Parent, F., et al., The inciclence and naturai histolY of type l and II endoleak: a 5-year follow-up assessment with color duplex ultrasound scan, J Vasc Surg, 2002; 35(3):474-81. 3, Gilling-Smith, G" et al., Freedom from endoleak after endovascular aneurysm repair does not equaJ

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treatment success, Eur J Vasc Endovasc Surg, 2000; 19(4):421-5, 4, White, G" et al., Endoleak as a complication of endoluminal grafting of abdominal aOltic aneurysms: classmcation, incidence, diagnosis, and management. J Endovasc Surg, 1997; 4(2): 152- 68, 5, Chan, C, et al., Endoleaks following conventional open abdominal aortic aneurysm repair. Eur J Vasc Endovasc Surg, 2000; 19(3):313-7, 6, Baum, R., et al., Aneurysm sac pressure measurements after endovascular repair of abdominal aortic aneUlysms. J Vasc Surg, 2001; 33(1):32-41. 7, Zarins, C, et al., Endoleak as a predictor of outcome after endovascular aneurysm repair: AneuRx multicenter clinical trial. J Vasc Surg, 2000; 32(1):90-107, 8, Harris, p" et al., Incidence and risk factors of late rupture, conversion, and death after endovascular repair of infrarenaJ aortic aneurysms: the EUROSTAR experience, European Collaborators on Stentlgraft techniques for aortic aneurysm repair. J Vasc Surg, 2000; 32(4)739-49, 9, Dattilo, ]., et al., Clinical failures of endovascular abdominal aortic aneurysm repair: incidence, causes, and management. J Vasc Surg, 2002; 35(6): 1137-44, 10, Fan, C, et al., Endovascular stent-graft in abdominal aortic aneurysms: the relationship between patent vessels that arise from the aneurysmai sac and early endoleak. Radiology, 2001; 218: 176-182, 11, Parry, D" et al., Type II endoleaks: predictable, preventable, and sometimes treatable? J Vasc Surg, 2002; 36(1):105-10, 12, Arko, F" et al., Type-II endoleaks following endovascular AAA repair: preoperative predictors and long-term effects, J Endovasc Ther, 2001; 8(5):50310, 13, Liewald F, E,e, Gorich J, Halter G, Scharrer-Pamler R, Sunder-PLassmann L, Influence of treatment of Type II endoJeaks on aneurysm surface area, Eur J Vasc Endovasc Surg, 2001; 21:339-343, 14, Amesur, N" et al., Embolotherapy of persistent endoleaks after endovascular repair of abdominal aortic aneurysm with the ancure-endovascular technologies endograft system. J Vasc Interv Radiol, 1999; 10(9): 1175--82, 15, Haulon, S" et al., Embolization of type II endoleaks after aOltic stent-graft implantation: technique and immediate results, J Vasc Surg, 2001; 34(4):600-5, 16, Tuerff, S" et al., Are type II (branch vessel) endoleaks really benign?, Ann Vasc Surg, 2002; 16(1): 50-4 17, Buth,]., p, Harris, and M, van, Causes and outcomes of open conversion and aneurysm rupture after en-

dovaseular abdominal aortie aneulysm repair: ean type II endoleaks be dangerous? ] Aro Coli Surg, 2002; 194(1 Suppl):S98-102. 18. Veith, F., et al., Nature and signifIeanee of endoleaks and endotension: summary of opinions expressed at an international eonferenee.] Vase Surg, 2002; 35(5): 1029-35. 19. Hinehliffe, R., et al., Rupture of an abdominal aortie aneurysm seeondary to type II endoleak. Eur] Vasc Endovasc Surg, 2001; 22(6):563-5. 20. White, R., et al., Failed AAA endograft exclusion due to type II endoleak: explant analysis. ] Endovasc Ther, 2001; 8(3):254-61. 21. Kato, N., et al., Aneurysm expansion after stent-graft plaeement in the absenee of endoleak. ] Vase Interv Radiol, 2002; 13(3):321-6. 22. WUliams, G., The management of massive ultrafiltration distending the aneurysm sae after abdominal aortie aneurysm repair with a polytetraf)uoroethylene aortobiiJiae graft. ] Vase Surg, 1998; 28(3):551-5. 23. Risberg, B., et al., Aneurysm sae hygroma: a eause of endotension.] Endovase Ther, 2001; 8(5):447-53. 24. Kaufman, J., et al., Endovaseular repair of abdominal aortie aneulysms: euerent status and future direetions. A]R Am] Roentgenol, 2000; 175(2):289-302.

33, Schurink, G., et al., Pulsatile wall motion and blood pressure in aneUlysms with open and thrombosed endoleaks-comparison of a wall track system and M-mode ultrasound seanning: an in vitro and animai study, ] Vase Surg, 2000; 32(4):795-803, 34. Hilfiker, P., T. Pfammatter, and M, Laehat, Depietion of an endoleak after abdominal aortie stent-grafting with eontrast-enhaneed three-dimensional MR angiography. A]R Aro] Roentgenol, 1999; 172(2):558. 35. Haulon, S., et al., Diagnosis and treatment of type II endoleak after stent placement for exclusion of an abdominal aortie aneurysm. Ann Vase Surg, 2001; 15(2):148-54, 36. Haulon, S" et al., Prospective evaluation of magnetie resonanee imaging after endovaseular treatment of infrarenal aortie aneurysms. Eur ] Vasc Endovase Surg, 2001; 22(1):62-9. 37, Hovsepian, D" et al., Te-99m sulfur colloid scintigraphy for deteeting perigraft f)ow following endovaseular aortie aneurysm repair: A feasibility study. Cardiovase Intervent Radiol, 1999; 22(6):447-51. 38. Lorelli, D" et al., Response of plasma matrix metal10proteinase-9 to eonventional abdominal aortie aneUlysm repair or endovaseular exclusion: implieations for endoleak. ] Vase Surg, 2002; 35(5):916-22.

25. Thompson, M., et al., Comparison of computed tomography and duplex imaging in assessing aortie morphology following endovaseular aneurysm repair. Br] Surg, 1998; 85(3):346-50.

39. Sangiorgi, G., et al., Plasma levels of metalloproteinases-3 and -9 as markers of sueeessful abdominal aortie aneUlysm exclusion after endovaseular graft treatment. Cireulation, 2001; 104(12 Su ppl 1):128895.

26. Kareh, L., et al., Algorithm for the diagnosis and treatment of endoleaks. Aro] Surg, 1999; 178(3):22531.

40. Vorp, D., et al., Association of intraluminal thrombus in abdominal aortie aneurysm with local hypoxia and wall weakening.] Vase Surg, 2001; 34(2):291-9,

27. Tummala, S. and A. Powell, Imaging of endoleaks. Teeh Vase Interv Radiol, 2001; 4(4):208-12.

41. Annabi, B" et al., Differential regulation of matrix metaJloproteinase aetivities in abdominal aortie aneUlysms. ] Vase Surg, 2002; 35(3):539-46,

28. Thurnher, S. and M. Cejna, Imaging of aoltic Stentgrafts and endoleaks. Radiol Clin North Aro, 2002; 40(4):799-833. 29. Wolf, Y., et al., Duplex ultrasound seanning versus computed tomographie angiography for postoperative evaluation of endovaseular abdominal aortic aneurysm repair.] Vase Surg, 2000; 32(6):1142-8. 30. MeLafferty, R., et al., The use of color-f)ow duplex sean for the deteetion of endoleaks. ] Vase Surg, 2002; 36(1):100-4. 31. MeWilliams, R., et al., Detection of endoleak with enhaneed ultrasound imaging: eomparison with biphasie eomputed tomography. ] Endovase Ther, 2002; 9(2): 170-9. 32. MeWilliams, R., et al., Use of eontrast-enhaneed ultrasound in follow-up after endovaseular aortie aneurysm repair. ] Vase 1nterv Radiol, 1999; 10(8): 1107-14.

42. Carrell, T., et al., Stromelysin-l (matrix metalloproteinase-3) and tissue inhibitor of metalloproteinase-3 are overexpressed in the wall of abdominal aortic aneurysms. Cireulation, 2002; 105(4):477-82. 43, Ferrans, V., New insights into the world of matrix metalloproteinases. Circulation, 2002; 105(4):405-7. 44, Goodall, S., et al., Ubiquitous elevation of matrix metalloproteinase-2 expression in the vaseulature of patients with abdominal aneurysms. Cireulation, 2001; 104(3):304-9, 45. Petersen, E" F, Wagberg, and K. Angquist, Proteolysis of the abdominal aortic aneulysm wall and the assoeiation with rupture, Eur] Vasc Endovase Surg, 2002; 23(2):153-7. 46, Curci, J., et al., Preoperative treatment with doxyeyc1ine reduees aortie wall expression and aetivation of matrix metalloproteinases in patients with abdom-

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inal aortic aneurysms. J Vasc Surg, 2000; 31(2):32542. 47. Mosorin, M., et al., Use of doxycycline to decrease the growth rate of abdominal aortic aneurysms: a randomized, double-blind, placebo-controlled pilot study. J Vasc Surg, 2001; 34(4):606-10.

8:15 a.m. Endoleaks and Endotension: When Do You Intervene? Richard A. Baum., MD Brigham. and Wom.en's Hospital Boston, A1A 8:30 a.m. Next Wave of Stent GraftDevices Chieh-Min Fan, MD Massachusetts Geneml Hospital Boston, k1A

8:45 a.m. Featured Speaker: Radiation Safety Stephen BalteJ~ PhD New York, NY 9:00 a.m. Thoracie Aneurysms: Seleetion Criteria, Devices, and Outeomes to Date Michael D. Dake, MD Stan/ord University Hospital Palo AILO, CA

9:15 a.m. Stent Grafts for Aortic Dissection: Which Patients Will Benefit? David M. Williams, MD University Hospital Ann Arbol~ MI

Renovascular Disease

Tuesday, April 1, 2003 10:00 a.m.-12:00 p.m. Moderatol~·

Alan H. Matsumoto, MD

10:00 a.m. Natural History of Atherosclerotie Renal Artery Stenosis Marc Pohl, MD Cleveland Clinic Cleveland, OH

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10:17 a.m. Noninvasive Sereening Tests for Renal Artery Stenosis: Are There Reliable Predietors of Outeomes? john H Rundback, MD Columbia Presbyterian Medical Center New York, NY 10:34 a.m. Atherosclerotie Renat Artery Stenosis: Does Revaseularization Alter Patient Outeomes? StepheJl Chas Textor, MD lvIayo Clinic RochesteJ~ MN Few areas of vascular intelvention have been associated wit h more controversy" than endovascular procedures for renal artelY stenosis. Intuitively, restoration of the blood supply to the kidney ought to improve the functional disturbances produced by renal artery lesions. It should be emphasized that when applied to the right patients, revascularization of the kidney can, in fact, provide major improvements in both blood pressure and recovelY of renal function. Why, then, is there any ąuestion as to its widespread application? Most clinicians recognize that revascularization is a "double-edged sword". AIrhough most procedures can be achieved with excellent technical success, the risks of atheroemboli, arterial dissection and clinical failure are genuine. Sometimes they produce catasrrophic conseąuences leading ro end-srage renal failure. As a resuJt, it is more important than ever to balance the potential benefits with the potential risks for each patient. The purpose of this discussion is to highlight reasons for ambiguity in this area. Changing Population Demographics The lasr several decades have been characrerized by longer Iifespan. This is likely the resulr of several factors, including major declines in mortality related to stroke and cardiovascular disease. Population groups above age 65 are now among the most rapidly growing segments in the United States (1). One conseąuence of lower mortality from coronary and cerebrovascular events is the delayed appearance of vascular disease affecting other bed~, such as the aorta and kidneys (2). As a result, clinical manifestations of renal altelY stenosis are appearing in older individuals, often combinecl with other comorbid diseases. These features change the clinical presentation and affect the risk/benefit considerations inherent in deciding whether to consider renal revascularization. Series with renal artelY intelvention now routinely include average age values above 70 years, whereas a decade ago the mea n age was between 61 and 63 years and series from the 1970s reported a mean age in the 50s (3,4). Changing Medical Therapy Since the early 1980s, new classes of antihypertensive agents have become available and widely used. These