Received: 22 July 2002Revised: 4 February 2003Accepted: 1 April 2003Published online: 17 June 2003© Springer-Verlag 2003

Abstract Aortic dissection is mostoften a catastrophic medical emer-gency which, if untreated, can be potentially fatal. The intention oftherapy in patients with aortic dis-section is to prevent aortic rupture or aneurysm formation as well as torelieve branch vessel ischaemia. Patients with aortic dissection are often poor candidates for anaesthesiaand surgery and the surgical proce-dure itself is challenging requiringthoracotomy, aortic cross clamping,blood transfusion as well as pro-longed hospital stay in some cases.Operative mortality is especiallyhigh in patients with critical mesen-teric or renal ischaemia. The past de-cade has experienced the emergenceof a number of interventional radio-logical or minimally invasive tech-niques which have significantly im-proved the management of patientswith aortic dissection. These includestent grafting for entry site closure toprevent aneurysmatic widening ofthe false lumen as well as percutane-

ous techniques such as balloon fenestration of the intimal flap andaortic true lumen stenting to alleviatebranch vessel ischaemia. False lumen thrombosis following entryclosure with stent grafts has been observed in 86–100% of patients,whereas percutaneous interventionsare able to effectively relieve organischaemia in approximately 90% ofthe cases. In the years to come, it isto be expected that these endolumi-nal techniques will become themethod of choice for treating mosttype-B dissections and will assist insignificantly reducing the number ofopen surgical procedures requiredfor type-A dissections. The intentionof this article is to provide an over-view of the current status of theseendoluminal techniques based on ourown experience as well as on a review of the relevant literature.

Keywords Aorta · Dissection · Aneurysm · Stent graft · Stent · Fenestration

Eur Radiol (2003) 13:2521–2534DOI 10.1007/s00330-003-1936-2 VA S C U L A R – I N T E RV E N T I O N A L

Ajay ChavanJoachim LotzFrank OelertMichael GalanskiAxel HaverichMatthias Karck

Endoluminal treatment of aortic dissection

Introduction

Aortic dissection is most often a catastrophic eventwhich, if untreated, can be potentially life threatening.Hypertension as a precipitating factor is present in70–90% of the patients. The peak incidence is betweenthe ages of 40 and 70 years with a male to female pre-dominance of 3:1. Less frequent causes of aortic dis-section, often in a younger age group are congenitalconnective tissue disorders such as the Marfan’s syn-

drome and the Ehlers Danlos syndrome as well as trau-ma [1].

The intention of therapy in patients with aortic dissec-tion is to prevent aortic rupture (either in the acute phaseor as a delayed complication of aneurysmatic wideningof the false lumen) as well as relief of branch vesselischaemia. Until approximately a decade ago, the man-agement of aortic dissection was almost exclusively sur-gical. The past 10–12 years have experienced the emer-gence of a number of interventional radiological or mini-

A. Chavan (✉) · J. Lotz · M. GalanskiDepartment of Diagnostic Radiology,Hannover Medical School,Carl Neuberg Strasse 1, 30625 Hannover, Germanye-mail: chavan.ajay@mh-hannover.deTel.: +49-51-15323354Fax: +49-51-15323885

F. Oelert · A. Haverich · M. KarckDepartment of Thoracic and Cardiovascular Surgery,Hannover Medical School,Carl Neuberg Strasse 1, 30625 Hannover, Germany

mally invasive techniques which have significantly im-proved the management of patients with aortic dissec-tion. These techniques include stent grafting (alsotermed endografting) for entry site closure to prevent an-eurysmatic widening of the false lumen [2, 3, 4] as wellas balloon fenestration with or without stenting of theaortic true lumen to alleviate branch vessel ischaemia [5,6, 7, 8, 9, 10]. The intention of this article is to providean overview of the current status of these techniques.

Pathomorphology of aortic dissection, definitions and classification

In aortic dissection, a tear in the intima leads to bloodfrom the true aortic lumen dissecting between the layersof the media, resulting in separation of the intimal layerfrom the outer adventitial layer. This gives rise to a falselumen between the intimal flap and the adventitia. As theouter wall of the false lumen consists merely of the ad-ventitia and a few layers of the media, it is at a higherrisk of rupture [1]. A further dreaded complication ofaortic dissection is the occurrence of branch vessel isch-aemia. This may be caused by a process of dynamic orstatic obstruction [5, 11]. Dynamic obstruction normallyaffects the vessels originating from the true lumen. Theexpanded false lumen may cause severe compression ofthe true lumen with resultant slow flow in this lumen. Inaddition, the intimal flap can be pressed against the ori-gins of the vessels arising from the true lumen, thus ob-structing blood flow in these vessels (Fig. 1). Static ob-struction is caused by extension of the dissection into thebranch vessels leading to the formation of a “blind sac”of the false lumen at the origins of these vessels. Higherpressures or thrombus formation in this blind sac lead tonarrowing of the true lumen (Fig. 2).

According to the Stanford classification, aortic dis-sections involving the ascending aorta are classified astype-A dissections, whereas those distal to the origin ofthe left subclavian artery are termed as type-B dissec-tions. The DeBakey classification differentiates the dis-sections involving the ascending aorta into type-I (in-volving the entire aorta) and type-II (restricted only tothe ascending aorta) dissections. The dissections exclu-sively involving the descending aorta are termed as type-III dissections (type IIIa: restricted only to the descend-ing thoracic aorta; type IIIb: involving the descendingthoracic as well as the abdominal aorta). The incidenceof Stanford type-A and type-B dissections is approxi-mately in the ratio of 2:1.

Borst et al. [1] classify dissections within 14 days ofthe acute episode as acute dissections; thereafter up to2 months is the sub-acute phase. All dissections beyond2 months following the acute episode are classified aschronic dissections.

Therapeutic strategy and treatment options

In order to prevent aortic rupture as well as to avoidcomplications, such as myocardial infarction or cardiactamponade, type-A aortic dissections are generally treat-ed with immediate surgical replacement of the proximalaorta [1, 3]. An elaboration of these surgical techniquesis beyond the scope of this article.

As opposed to the type-A aortic dissections, the type-B dissections have traditionally been treated conserva-tively; however, due to persistent flow in the false lu-men, rupture or aneurysmatic dilatation of the false lu-men may occur in approximately 20–50% of the conser-vatively managed patients within 1–5 years followingthe acute episode [12, 13]. This may necessitate surgicalreplacement of the descending aorta with thoracotomy,aortic cross clamping, blood transfusion as well as pro-longed hospital stay in some cases. Consequently, mini-mally invasive measures, such a trans-femorally placed

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Fig. 1 The ventrally placed true lumen has been compressed to athin sliver by the dilated false lumen dorsally, resulting in dynamicobstruction of the superior mesenteric artery arising from the truelumen

stent grafts (endografts) to close the proximal entry tearin the type-B dissections, appear to be justified.

Thoraco-abdominal ischaemia complicating the typeA-dissections, if present, usually resolves after proximalaortic replacement [1, 14]. Post-operative persistence ofischaemia in the type-A dissections, or the presence ofsuch ischaemia in the type-B dissections may necessitatefurther measures downstream in 10–30% of the patients.Until a few years ago, such thoraco-abdominal malperfu-sion was treated by surgery or re-surgery [1, 15, 16, 17,18]. Surgical therapy was aimed at creating a re-entry inthe form of fenestration of the intimal flap or establish-ing bypasses to the ischaemic vessels [1]. Patients withorgan ischaemia are often poor candidates for anaesthe-sia and surgery. Surgical procedures may be technicallydifficult and operative mortality reported in literatureranges between 25 and 51%, mortality being higher inpatients with critical mesenteric or renal ischaemia [1,15, 16, 17]; thus, percutaneous measures for relief ofsuch ischaemia can significantly improve the prognosisin these patients. Over the past decade, successful reliefof such ischaemia using less invasive interventional ra-diological techniques has been reported with procedurerelated mortality ranging between 0 and 25% [5, 6, 7, 8,9, 10, 19, 20].

Stent grafts for proximal entry closure

Persistent flow in the false lumen through the proximalentry tear is responsible for aneurysmatic widening andpossible rupture of the false lumen. As opposed to this,type-B dissections with thrombosis of the false lumenshow a much better prognosis at long term follow-up[21, 22, 23]. The purpose of stent-graft implantation inthe true lumen is to close the proximal entry tear andthus initiate thrombosis of the false lumen and stabilizethe dissection [24] (Fig. 3). Furthermore, Chung et al.[25] were able to demonstrate in an experimental phan-tom simulating type-B aortic dissection, that the most ef-fective method to relieve true-lumen collapse was place-ment of a stent graft over the entry tear; thus, relief ofdistal ischaemia (especially in patients with dynamic ob-

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Fig. 2a–c Static obstruction. a False-lumen angiogram showingthe blind sacs of the false lumen extending into the origins of therenal arteries (arrows). Selective true-lumen angiograms of theb left and c right renal arteries showing the narrowing at the ori-gins caused by the blind pockets of the false lumen (arrowheads)

Fig. 3 The concept of proximal entry closure using stent grafts

struction) is another potential benefit which could be ex-pected from proximal entry closure with a stent graft.

Stent grafts consist of a metal endoskeleton coveredwith a polyester or polytetrafluroethylene (PTFE) mate-rial which is impermeable to blood. Although the firstgeneration devices were largely homemade ones withlarge and rigid introducer systems, they have been al-most completely replaced by commercially availablesystems [26]. At present in Europe, three devices areavailable in the market for the thoracic aorta, wherebythe Excluder device has been temporarily withdrawn.These devices are available either pre-mounted in asheath (Talent endograft, Medtronic, Santa Rosa, Calif.;Fig. 4) or on a catheter (Excluder endograft, Gore andAssociates, Flagstaff, Ariz.). The Endofit device (En-domed, Ariz.) is mounted in a cartridge and is introducedvia 22- to 24-F introducer sheaths.

Localization of proximal entry tear

For successful stent graft implantation, the precise local-ization of the proximal entry tear is of prime importance.The various diagnostic modalities used for this purposeinclude CT angiography (CTA), magnetic resonance im-aging (MRI), colour Doppler trans-oesophageal echocar-diography (TEE) as well as digital subtraction angiogra-phy (DSA). Whereas Nienaber et al. used MRI for thispurpose [4], most other authors use CTA as the pre-oper-ative diagnostic modality [3, 27, 28, 29]. Should the pre-cise localization of the entry tear not be possible by thesemeans, DSA in combination with TEE during the proce-dure generally reveals the site of entry. At DSA, an an-giogram of the iliac vessels is to be recommendedstrongly. The purpose is to choose an access vesselwhich is not dissected and to make sure that the diameterof the iliac vessels would allow the passage of the endo-graft system. As a rule, iliac diameters of at least 7 mmfor the 22-F systems, 8 mm for the 25-F systems and9 mm for the 27-F systems are necessary.

Stent graft implantation

For the stent-graft implantation, a femoral arteriotomy isnecessary. Although this is carried out under general an-aesthesia in most centres, the procedure can also be per-formed under local anaesthesia. In exceptional cases,surgical exposure of the iliac arteries may be necessary[4, 28]. In order to carry out control angiograms duringthe procedure, a pigtail catheter is introduced either fromthe right brachial or from the contralateral femoral ar-tery. It is advisable to have TEE handy in case difficultyis experienced in locating the proximal entry tear or de-termining the position of the guide wire and of the endo-graft system in the true lumen.

The stent-graft system is advanced over a super-stiffguide wire placed in the ascending aorta via the true lu-men. Just before releasing the stent graft, Nienaber et al.recommend reducing the systolic blood pressure to50 mm Hg with the help of a sodium nitroprusside infu-sion [4]. In their opinion, this reduces perfusion in thefalse lumen and thus possibly facilitates easy expansionof the stent graft in the true lumen. Such reduction ofblood pressure prior to endograft release is advocated byother authors also [28, 29]. In our experience, bloodpressure reduction also prevents “wind socking” andconsequent distal dislocation of the stent graft during re-lease. If the entry point is less than 15 mm distal to theorigin of the left subclavian artery, covering the origin ofthis vessel with the bare springs may become mandatory(Fig. 5b). Accidental or even intentional coverage of theorigin of the left subclavian artery with the stent-graftfabric is not always associated with arm ischaemia and issometimes even electively performed by some of the au-thors. Should such ischaemia occur, a surgical carotid–subclavian bypass can be carried out as a second-stageprocedure [28, 30].

The choice of correct endograft diameter may posedifficulties as the diameter of the entire aorta in the dis-sected portion is generally much larger than the diameterof the non-dissected aortic arch. The difficulty is com-pounded by the fact that the true lumen is compressedand narrowed in most cases. Dake et al. used the diame-

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Fig. 4 A Talent stent-graft con-sisting of a nitinol frameworkand a polyester covering. Theproximal 15 mm of the endo-grafts are comprised of baresprings. The endograft ismounted in a sheath and can bereleased by withdrawing thesheath over a ‘Pusher’

ter of the aortic arch as reference size for determiningcorrect endograft size [3]. Kato et al. chose an endograftdiameter which was 10–20% more than the diameter ofthe aortic arch where the endograft was to be anchored[2]. Hausegger et al. chose an endograft diameter ap-proximately 4 mm larger than the diameter of the non-diseased aortic segment [30]. If the diameter of the cho-sen endograft is too large as compared with the diameterof the non-dissected proximal aortic segment, the endo-graft may be extruded out of this segment and dislocatedistally during or after release. The mean length of theendografts used by Dake et al. was 69±15 mm; the meandiameter was 29.7±5.1 mm [3]. Nienaber et al. used stentgrafts with lengths varying between 43 and 150 mm anddiameters between 30 and 40 mm [4]. The lengths of theendografts varied between 50 and 120 mm as well as be-tween 50 and 75 mm in Czermak et al.’s [28] and Kato etal.’s [31] set of patients, respectively. In these patients,the diameters of the endografts were between 26 and42 mm [28] as well as between 30 and 36 mm, [31] re-spectively.

Results: stent grafts for proximal entry closure

Stent-graft deployment is generally possible in all caseswith successful entry closure in 86–100% of the patients[3, 4, 27, 28, 29, 30, 31]. Both Nienaber [4] and Hausegger[30] have treated dissections with entries 5 mm or moreaway from the origin of the left subclavian artery. Tosuccessfully occlude the entry site, the left subclavian or-igin had to be covered by the endograft fabric in 4 of the5 patients treated by Hausegger et al. [30]. Only one ofthese patients required a carotid–subclavian bypass. Inthe other 3 patients collateral circulation via the circle ofWillis provided for adequate blood supply to the left arm

[30]. As opposed to this, Kato et al. treated dissectionswith entries less than 2 cm distal to the left subclavianorigin using a trans-thoracic approach [2].

In all the 12 patients with sub-acute or chronic type-Bdissections treated by Nienaber et al., thrombosis withshrinkage of the false lumen was observed. The MRAwas the imaging modality used for follow-up. They rec-ommend stent grafting in selected patients without com-plicating distal ischaemia [4]. Similarly, partial or com-plete thrombosis and shrinkage of the thoracic false lu-men with significant widening of the true lumen was ob-served in 6 of 7 patients reported by Czermak et al. [28],and in all 19 patients reported by Dake et al. [3] as wellas in all 10 patients reported by Kato et al. [31]. Whereasthrombosis of the false lumen could be observed at thelevel of the stent graft, the lumen continued to be per-fused further distally. Thrombosis was particularly pro-nounced in dissections which were not older than6 months [2]. Apart from Nienaber et al. [4], the otherauthors used CTA as the follow-up modality.

Whereas the fate of the two lumina in the abdominalaorta have not been mentioned in the report by Nienaberet al.[4], the abdominal false lumen remained patent inall but one of Dake et al.’s 19 patients [3]. Similarly, inthe 5 patients reported by Hausegger et al., the abdomi-nal aortic false lumen remained unchanged in 3 patients[30]. Thrombosis of the false lumen of the abdominalaorta was not observed in any of the patients reported byCzermak et al. [28].

Of particular interest in the 19 patients reported byDake et al. was the thrombosis of the false lumen of theascending aorta in 4 patients with retrograde type-A dis-sections with a mean reduction in diameter of the as-cending aorta from 41 to 34 mm [3]. More recently, Katoet al. presented their experience with stent grafting in 10patients with acute or sub-acute type-A dissections who

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Fig. 5a, b Oblique sagittalmultiplanar reconstructions ofCT angiograms of a patientwith type-B aortic dissectiona before and b 12 months afterstent-graft implantation. Thebare springs of the stent grafthave been placed across the origin of the left subclavian artery. At follow-up, a markedwidening of the true lumen isnoticeable. The thrombosedfalse lumen is barely recogniz-able (arrowheads). No intimalflap was visible in the abdomi-nal aorta

had primary entry tears in the descending aorta. All ini-tially perfused false lumina in the ascending and the de-scending thoracic aorta thrombosed following stentgrafting [31].

Complications: stent grafts for proximal entry closure

Paraplegia as a complication of stent grafting for aorticdissection has not been reported. Whereas Nienaber et al.observed no serious complications in their set of patientswith sub-acute or chronic dissections [4], a mortality of16% was noted by Dake et al. [3], however in a settingof acute dissections with over half the patients sufferingfrom symptomatic branch vessel ischaemia. Two of thesedied of aortic rupture despite stent grafting, whereas onedied of persistent thoraco-abdominal ischaemia. Five ofthe 11 patients with symptomatic branch vessel isch-aemia required additional interventions further down-stream for effective relief of ischaemia [3]. Of the 6 pa-tients treated trans-femorally by Kato et al., one died ofaortic rupture, also in the acute phase [2]. In 7 patientsreported by Czermak et al. [28], access vessel rupture ordissection occurred in 2 patients which was correctedsurgically. For satisfactory relief of ischaemia, 1 of 2 pa-tients with distal ischaemia required surgical endarterec-tomy and flap fixation despite stent grafting. In 1 patient,retrograde conversion of the dissection to a type-A dis-section was observed which had to be treated by proxi-mal aortic replacement [28]. In our experience with 15patients, we have observed one retrograde ascending aor-tic dissection following stent grafting. Post-operative ac-cess site bleeding necessitating surgical evacuation wasobserved in 1 of 7 patients reported by Sailer et al. also[27]. A minor stroke in 1 of 10 patients has been report-ed by Kato et al. [31].

A further complication worthy of mention is the oc-currence of saccular aneurysms either proximal or distalto the stent graft in the follow-up period. This has beenobserved in one of five patients reported by Hausegger etal. [30] and four of Kato et al.’s 14 patients [29]. Most ofthem were treated by additional stent grafts in the fol-low-up period. All patients had been primarily treatedfor acute dissections.

Current status: stent grafts for proximal entry closure

The patient numbers in the studies thus far are small andthe follow-up periods are short. Based on the experiencein these patients, it is obvious that successful entry clo-sure using stent grafts initiates partial or completethrombosis with shrinkage of the false lumen in the tho-racic aorta (Fig. 5), especially if treatment is carried out

within 6 months of the acute episode. The expansion ofthe true lumen is caused not only by the radial force ex-erted by the stent graft, but also due to pressure reduc-tion in and shrinkage of the false lumen. The complica-tion rate as well as the procedure time for stent grafts(1.6±0.4 h) in Nienaber et al.’s study were markedlylower as compared with those of conventional descend-ing aortic surgery (8.0±2 h) [4].

The mortality of the procedure is quoted to be be-tween 0 and 16% and was observed only in acute dissec-tions. Causes of death were aortic rupture or persistentbranch vessel ischaemia [2, 3]. As the false lumen re-quires some time to thrombose (possibly due to persis-tent retrograde perfusion via further entries in the distalthoracic or abdominal aorta), it is imaginable that rupturein the acute phase cannot be prevented merely by proxi-mal entry closure. Whether the incidence of this compli-cation can be reduced by using longer stent grafts withmore radial force is still an unanswered question.

Furthermore, the fate of organs supplied exclusivelyby the false lumen at long-term follow-up will have to beawaited. Especially with regard to the kidneys, a gradualloss of function in one of the two kidneys (arising fromthe false lumen), caused by thrombosis of the false lu-men, may not become clinically apparent in the earlystages and thus go clinically unnoticed, until significantloss of organ function has occurred.

Symptomatic thoraco-abdominal ischaemia is re-lieved (especially in the acute dissections) in only halfthe patients treated with stent grafts. Consequently, thetreating interventionist should be prepared to carry outadditional interventions (such as balloon fenestration ofthe intimal flap or stenting of the true aortic lumen) fur-ther distally to effectively relieve persistent ischaemia.

Percutaneous relief of branch vessel ischaemia

Ischaemia involving the spinal, coeliac, mesenteric, andrenal or lower extremity vessels occurs in approximately10–30% of the patients with aortic dissection [15, 16,17]. In 1988, Shimshak et al. first reported relief of clau-dication following balloon angioplasty of the true lumenof the abdominal aorta [32]. The first percutaneous bal-loon fenestration of the intimal flap was performed byWilliams et al. in 1990 [19]. Since then, these techniquesfor relief of ischaemia have been further developed andsupplemented by true lumen stenting and thrombolysis.

Indications and contraindications for intervention:branch-vessel ischaemia

Indications for intervention include hepatic, intestinal,renal, lower extremity or acute spinal ischaemia. A deci-sion to intervene is taken only in the presence of positive

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symptomatology and laboratory parameters associatedwith corresponding morphological findings as seen withCTA, MRI or DSA. Intervention is rarely warrantedpurely on the basis of CT, MR or angiographic findingsin the absence of clinical symptomatology. Gastro-intes-tinal ischaemia is indicated by acute intractable abdomi-nal pain, absent bowel sounds, bloody stools, abdominalangina, a rise in serum lactate values above 2.4 mmol/lor a more than threefold rise in serum transaminase val-ues. Renal ischaemia requires intervention in cases ofacute anuria with dialysis dependence, sudden sustainedrise in serum creatinine values above 93 µmol/l, acuteonset of uncontrollable hypertension and typical pain inthe renal area. Cold, painful, pulseless lower extremities,claudication as well as acute paraplegia or paraparesisalso warrant treatment. In view of the relatively highmortality and morbidity in such patients, there are sel-dom any contraindications to intervention [11].

Patient preparation

The CT examination which is normally carried out to es-tablish the diagnosis should be performed as a CTA. Thisis extremely helpful in planning the intervention. It en-ables identification of the two lumina and the vesselswhich arise from them. The orientation of the intimalflap at the level one wishes to fenestrate can be deter-mined. Presence of thrombus and extension of the dis-section into the branch vessels can also be reliably de-tected. At present, due to the difficulties associated withexamining emergency patients with MRI, this cannot berecommended as a standard investigation in the pre-interventional planning, especially of patients with acutedissections. Angiography is carried out only if interven-tion is necessary or is under consideration.

Except in patients who are already intubated at admis-sion, the procedures are normally carried out under localanaesthesia. If the patient is restless or in severe pain, i.v.Propofol (1–3 mg/kg h−1) as continuous infusion may beused for sedation. As with all other complicated inter-ventions, an i.v. injection of 5000 IU heparin is advisableat the outset of the procedure [11].

Percutaneous balloon fenestration of the intimal flap

The rationale behind fenestrating the dissection flap is toequalize pressures in the two lumina as well as to im-prove blood flow to the ischaemic vessels. We prefer tocarry out the interventions under intravascular ultra-sound (IVUS) guidance (Fig. 6) [9]. IVUS has been usedby other groups as well [5, 6, 7, 8]. One of the advanta-ges of IVUS is that all catheter manipulations can be car-ried out from one single lumen without necessarily hav-

ing to gain access to both lumina [5]. Secondly, after per-forating the intimal flap with the needle-catheter combi-nation, the entry of the catheter from one lumen into theother can be well visualized with IVUS by merelysweeping the IVUS catheter up and down the aorta. Anangiogram is not necessarily required for this purpose [5,9, 11]. Thirdly, dynamic obstructions are best visualizedwith IVUS [11]; however, balloon fenestrations havealso been carried out under fluoroscopy without IVUS[8, 33, 34]. In such cases, angiograms in multiple projec-tions may be necessary. To assist safe puncture of the in-timal flap under fluroscopy, balloon catheters or Dormiabaskets placed in the false lumen may be used as targetsat which one may aim with the puncturing needle [5, 8].

A bilateral femoral approach is necessary. Althoughfemoral pulses may be poorly palpable or totally absentas a consequence of the dissection, it is almost alwayspossible to gain percutaneous femoral access [33, 35,36]. A point to bear in mind is that the flow through theneedle after puncturing may not be as pulsatile as in nor-mal vessels. In our personal experience with over 45 pa-tients, bilateral femoral catheterization was possible inall cases; we have thus far never been forced to adopt abrachial approach.

Initially, diagnostic angiograms are carried out to clar-ify the vascular anatomy of the ischaemic vessels. Theangiograms along with CTA help in identifying whichvessels arise from which lumen as well as the nature ofthe obstruction—whether dynamic or static. It is desir-able, but not absolutely necessary, to have angiograms ofboth lumina at the outset of the intervention. If access to

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Fig. 6 Intravascular ultrasound catheter in the false lumen. Theneedle catheter combination used to perforate the intimal flap is inthe crumpled and compressed true lumen (arrowheads) with the tipof the needle placed against the centre of the intimal flap (arrow)

one of the two lumina is difficult, manipulation with ahydrophilically coated guide wire at the level of the iliacvessels often helps in accessing the desired lumen.

Following the angiograms, pressure measurements inthe two lumina are carried out. If access to the false lu-men is not possible, measurement of false-lumen pres-sure can be carried out after puncturing the intimal flapbut before carrying out the balloon fenestration.

The IVUS catheter is introduced from the contralater-al femoral artery. In order to image the entire aorta,IVUS catheters with lower frequencies between 10 and12.5 MHz are preferable to those with higher frequen-cies. In which lumen the IVUS catheter is placed is oflittle consequence (Fig. 6) [11].

For perforating the intimal flap, various combinationsof catheters and guide wires or transseptal needles havebeen used [8, 19, 33, 34, 35, 36]. We prefer to use the so-called TIPSI set (Rösch-Uchida trans-jugular liver accessset, William Cook Europe, Bjaeverskov, Denmark) forthis purpose. It consists of a 10-F guiding catheter with acoaxial stiffening cannula angulated at the tip and a 5-Fcatheter carrying a protruding flexible stylet (0.038 in.)which can be advanced through the stiffening cannula.The guiding catheter with inner stiffening cannula areadvanced to the desired level over a super-stiff guidewire (Amplatz Super Stiff, Boston Scientific Corpora-tion, Watertown, Mass.). Using IVUS guidance the tip ofthe guiding catheter (with stiffening cannula) is placedagainst the intimal flap such that it does not point to-wards the aortic wall. This normally produces a tentingof the dissection flap (Fig. 6). The 5-F catheter carryingthe flexible stylet is then introduced up to the tip of thestiffening cannula. Using a quick short thrust, this cathe-ter–stylet combination is advanced through the intimalflap from one lumen into the other. As far as possible,the puncture of the intimal flap should be performedfrom the true lumen. As this lumen is narrower than thefalse lumen, the tip of the stylet enters the wider of thetwo lumina after piercing the intimal flap (Fig. 6). Thisreduces the risk of perforating the free aortic wall by thestylet tip [5, 11]. The stylet is replaced by the super-stiffguide wire over which a 5-mm balloon catheter is posi-tioned across the intimal flap to pre-dilate the perfora-tion. This enables the larger diameter balloons (whichalso have a larger profile) to easily pass through theopening created in the dissection flap. Following this,18- to 20-mm balloons are used for fenestration, as useof smaller balloons may lead to insufficient decompres-sion of the false lumen and may render further fenestra-tions necessary [37]. In sub-acute and chronic dissec-tions, a “waisting” of the balloon at the level of the inti-mal flap is often recognizable (Fig. 7) [9]. This may notalways be the case in acute dissections [11].

The improvement of flow between the two luminafollowing balloon fenestration may be a localized phe-nomenon; consequently, the fenestration should be as

close to the ischaemic vessels as possible so that thesevessels benefit maximally from the opening created inthe intimal flap [5, 9, 25]. Two or three fenestrationsmay be necessary to attain satisfactory results, especiallyin patients with ischaemia involving multiple vascularterritories. It should be borne in mind that the true lumenmay become wider and the intimal flap less taut after thefirst fenestration (due to decompression of the false lu-men) especially in the acute dissections; consequently,care should be taken during subsequent punctures of theflap, as the needle tip may not have as much leeway inthe false lumen as during the first puncture [11].

The result of the fenestration may be controlled bypressure measurements in the two lumina, angiographyas well as with IVUS. A fall in the pressure gradient be-tween the two lumina signifies a satisfactory result [5].This is often visible angiographically as improved flowespecially in the true lumen and in the previously isch-aemic vessels (Fig. 8). If the intimal flap lies in the coro-

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Fig. 7 The “waisting” of the balloon at the level of the intimalflap, indicating a correct position of the balloon catheter across theintimal flap

nal plane at the level of the fenestration, angiographicdocumentation may be difficult as the two lumina areprojected onto each other. In such cases IVUS is usefulin documenting the result [11]. A millilitre of air agitatedwith approximately 10 ml of normal saline injected rap-idly into the aorta produces excellent ultrasound contrastfor visualizing flow of blood through the fenestration. Ifafter a maximum of three fenestrations satisfactory re-sults are not obtained, further fenenstrations are general-ly not helpful. Such attempts may even lead to an insta-bility or change in orientation of the intimal flap with re-sultant loss of blood flow to vital organs [38, 39]. Thesecases normally require stents, mostly in the true lumen,to hold the lumen open [5]. Balloon fenestration oftenhas to be supplemented by measures such as stent im-plantation, thrombolysis or angioplasty to obtain satis-factory results [5, 6, 7, 8, 9, 10].

Stent implantation

Stents can be implanted in the true lumen of the aorta orof the branch vessels. In the aorta, stents may be implant-ed primarily or may become necessary following fenes-tration of the dissected flap. They help in widening andholding open the narrowed true lumen. Furthermore, dueto decompression of the false lumen following balloonfenestration, the intimal flap may sometimes become laxand change orientation thus occluding origins of vitalvessels. In such cases, stents may help in preserving flowto these vessels by keeping the flap away from the vesselorigin. We normally carry out a balloon fenestration of

the intimal flap as the first step. If, despite fenestration,persistent low flow to the ischaemic vessels is observedon the angiograms carried out from both lumina, we pro-ceed to stent implantation in the true aortic lumen be-tween the site of fenestration and the ischaemic vessel inorder to improve blood flow to the vessel (Fig. 9). Thereasons for this approach are twofold. Firstly, in our ex-perience, balloon fenestration combined with stents in theaffected branch vessels produce satisfactory relief ofischaemia in most cases. Thus far, in over 45 cases treat-ed by us, stent implantation in the aorta has been neces-sary in merely four patients. Secondly, recompression ordislocation of aortic stents in the chronic phase has beendescribed [5, 40] and the long-term sequelae of such oc-currences are unknown. Consequently, it may be judi-cious to hold the number of stents in the aorta to a mini-mum. An exception to this rule is a compression of thetrue aortic lumen caused by a thrombosed false lumen. Insuch cases, widening of the true lumen or improvementof blood flow from the false into the true lumen is not tobe expected after fenestration and hence one could pro-ceed directly to stent implantation. As far as possible oneshould attempt not to cover vessel origins with suchstents, but in difficult situations, such “overstenting” ofvessels is not contraindicated and may even be necessary[5, 8]. The most frequently used stents are the Palmaz(Johnson and Johnson, Warren, N.J.) or the Wallstents(Schneider, Europe GmbH, Bülach, Switzerland) [5, 6, 7,8, 9, 10]. The Wallstents require smaller sheaths (up to10 F) but have a maximum diameter of 16 mm. The Pal-maz stents can be expanded to a diameter of 25 mm butrequire sheaths as large as 14 F.

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Fig. 8 a True-lumen angio-gram showing severe compres-sion of this lumen with veryslow flow (large arrows). Thesuperior mesenteric artery(small arrows) and the right re-nal artery (arrowheads) arisefrom this lumen. b Obliquetrue-lumen angiogram follow-ing fenestration at the level ofthe coeliac tru0nk as well asabove the aortic bifurcation.Note the marked widening ofthe true lumen and the opacifi-cation of the false lumenthrough the fenestration (arrow). Satisfactory opacifica-tion of all visceral vessels

As opposed to stents in the aorta, stenting of branchvessels per se are established procedures for which long-term results are available. Stent dislocation even at long-term follow-up is rare. Stents are implanted in dissectedaortic branch vessels most often to relieve static obstruc-tion of these vessels. While selecting the stent size, itmust be borne in mind that the diameter of dissected ves-sels is often a little larger than the diameter of normalvessels [11].

Stents are helpful not only in the acute phase but alsoin chronic dissections. Narrowed or occluded true aorticlumina can also be recanalized and stented leading to ef-fective alleviation of symptoms (Fig. 9) [9, 40]. They havealso been used successfully in traumatic dissections [20].

Thrombolysis

Thrombus formation in the false lumen is not uncom-mon. If this occurs in the blind sacs in the branch vessels(such as in the renal or iliac vessels) or the distal abdom-

inal aorta, this distended and thrombosed false lumencauses static obstruction of the true lumen. There is littleexperience in the literature with local thrombolysis in thefalse lumen to relieve such obstruction of the true lumen.Such cases are generally managed by stent implantationin the true lumen of the affected vessel [5].

As opposed to thrombosis of the false lumen, throm-bus formation in the true lumen is less frequent. It isgenerally appositional thrombus at the level of maximalcompression. Distal to this level the true lumen normallytends to remain patent either due to collateral circulationor due to persistent blood flow past the thrombus in thetrue lumen. Following fenestration of the intimal flap,despite widening of the true lumen, the thrombus maystill hamper flow in the true lumen or potentially causedistal embolization. In addition to heparin, which is nor-mally injected at the outset of the intervention, injectionof 4–10 mg of recombinant tissue plasminogen activator(rTPA, Actilyse, Boehringer Ingelheim Pharma, Ingel-heim, Germany) directly into the thrombus before or af-ter fenestration normally results in effective thromboly-sis (Fig. 10) [10]. Such thrombolysis is generally neces-sary in acute dissections. There is little reported experi-ence in literature regarding thrombolysis in chronic dis-sections.

Angioplasty

Atherosclerotic stenoses of branch vessels may be ob-served as associated findings in patients with aortic dis-section. As in patients without dissection, these stenoses

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Fig. 9 Left anterior oblique true-lumen angiograms of a patientwith chronic type-A dissection presenting with claudication. Fen-estration alone at the level of the renal arteries (arrow) performedthrough a small pre-existing re-entry from the abrupted left renalartery did not adequately decompress the false lumen and a Pal-maz stent below the fenestration was necessary to restore satisfac-tory blood flow to the lower extremities. The stent was not fullyexpanded in order to preserve blood flow to the left lower pole re-nal artery. Fenestration was performed prior to stent implantationto ensure blood flow to the two left renal arteries which arosefrom the false lumen

can be treated with balloon angioplasty using standardtechniques [11, 38].

Results: percutaneous interventions for branch vessel ischaemia

Over the past 10–12 years, successful relief of thoraco-abdominal malperfusion following percutaneous inter-ventions in aortic dissection has been reported by manyauthors [5, 6, 7, 8, 9, 10, 33, 34, 35, 36, 37, 38]. Exceptfor isolated case reports on stent implantation in dissect-ed carotid arteries, there is little experience in the litera-ture on interventional radiological treatment of malper-fusion involving the supra-aortic vessels [41]. Malperfu-sion resolves in 85–93% of the cases following interven-tion alone [5, 8, 10]; however certain points need to beemphasized.

In acute dissections, therapy should be initiated assoon as possible. This is especially true for mesentericand lower limb ischaemia. Severe bowel ischaemia last-ing more than 12 h is often associated with intestinal ne-crosis. Even after successful restoration of blood flow tothe ischaemic vessels, such patients should be closelymonitored after the intervention for signs of bowel ne-crosis. Surgical resection of necrotic bowel is necessaryin some cases. In acute lower limb ischaemia, if satisfac-tory restoration of blood flow to the iliac vessels cannotbe documented after the intervention, surgical measuressuch as an aorto-iliac or aorto-femoral Y-graft, or a fe-moro-femoral bypass graft may be necessary. Such oper-ations are required in approximately 8–13% of patients[5, 8, 10].

Acute ischaemic renal failure as old as 14 days maybe reversible after successful intervention. Consequently,

even if a patient presents several days after acute onsetof renal failure, intervention should be carried out as itoften assists in taking the patient off dialysis [11]. Al-though little experience exists in literature regarding thebenefit of such interventions in acute paraplegia, bothcases in our experience showed partial recovery of motorfunction following balloon fenestration [10].

Complications: percutaneous interventions for branch-vessel ischaemia

Procedure-related complications are encounterd in ap-proximately 10–20% of the cases, approximately half ofwhich can be treated percutaneously during the proce-dure [5, 6, 7, 8, 9, 10]. Following balloon fenestration,due to slackening of the intimal flap, the flap may hanglike a curtain over some vessel origins and obstruct or-gan perfusion. Although this can mostly be treated bystent implantation, surgery may be necessary in rarecases. Perforation of the aortic wall by the puncturingneedle has been described, but all four reported cases inthe literature have shown no clinical sequelae [5, 10, 34].In patients with mesenteric ischaemia lasting over10–12 h, restoration of blood flow to the ischaemic ves-sels may cause flushing out of endotoxins from necroticbowel resulting in circulatory collapse and even death[5]. Isolated cases of pseudo-aneurysm formation at thefemoral puncture site, paraplegia following stenting ofthe infra-renal true lumen, stent dislocation, stent throm-bosis and peripheral emboli have also been described [5,8, 38]. Procedure-related mortality ranges between 0 and25%. The deaths reported in the literature have been onlyin patients with acute dissection, whereas those with sub-acute or chronic dissections recovered after therapy [5,

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Fig. 10 a True-lumen angio-gram after fenestration belowthe renal arteries (not shown)showing opacification of bothlumina and thrombus in thetrue lumen of the left commoniliac artery (arrows). b Well-opacified true lumen after suc-cessful thrombolysis

6, 7, 8, 9, 10]. Prognosis was largely governed by isch-aemic damage suffered before the intervention and bythe occurrence of aortic rupture despite successful reliefof ischemia [5, 8, 10].

Current status: percutaneous interventions for branch vessel ischaemia

Percutaneous interventions (combined with judicioussurgery such as resection of necrotic bowel in approxi-mately 10% of the cases) are effective in relieving tho-raco-abdominal ischaemia in approximately 90% of thepatients. Most often, a combination of balloon fenestra-tion of the intimal flap and true lumen stenting is neces-sary for optimal results. In occasional cases, thromboly-sis of clot in the true lumen or angioplasty may be neces-sary to enhance the results.

On the basis of the scanty data available in literatureconcerning effects of stent grafting in branch vessel isch-aemia, stent grafting for proximal entry closure is able torelieve thoraco-abdominal malperfusion only in approxi-mately half the patients. The others require further inter-ventions or surgical measures downstream for effectiverelief of ischaemia. This holds true especially for symp-tomatic branch vessel compromise in acute dissections.Consequently, at the present, stent grafting and percuta-neous interventions to relieve branch-vessel ischaemiashould be considered as measures which complimenteach other in obtaining optimal results.

Future prospects

The results of stent grafting for proximal entry closureare encouraging. In a recent retrospective analysis, Bernardet al. were able to prove that patency of descending aor-tic false lumen was one of the predictors of late mortali-ty. It is responsible for progressive aortic dilation [42].This suggests that more aggressive treatment of type-Bdissections (e.g. with stent grafting) may be indicated iffalse lumen perfusion persists; however, most of the re-ported studies so far concerning stent grafting in aorticdissections have been uncontrolled, non-randomizedstudies largely in patients with type-B dissections. Ran-domized studies to prove the superiority of this methodover conservative medical therapy are indicated.

All the commercially available stent-graft devices atpresent require an arteriotomy. The large size as well asthe rigidity of the delivery device can cause complica-tions in the access vessel. Furthermore, certain endo-grafts may be difficult to release especially in cases oftortuosity or angulation of the distal aortic arch and theproximal descending aorta [30]. Thinner and more flexi-ble stent-graft systems which could overcome these dif-ficulties are necessary. Successful percutaneous occlu-

sion of the proximal entry tear in six patients using a so-called separating stent graft introduced via 12-F intro-ducer sheaths has been recently reported by Kang et al.[43]. Such endeavours are likely to be supported by com-mercially available percutaneous suture devices for clos-ing the puncture site.

Intramural haematomas (IMH) constitute a distinctclinical entity which is classified by some as a sub-groupof aortic dissection possibly with a smaller intimal tear.In a total of 124 patients with IMH who were treatedconservatively, Song and colleagues [44] were able todemonstrate a high rate of spontaneous resorption (67%in the proximal and 78% in the distal type). Seven per-cent of the patients with proximal — and 1% of thosewith distal IMH — died. Twenty-five percent of the pa-tients with the proximal IMH developed classical aorticdissections, whereas 16% of the patients with distal IMHdeveloped purely localized dissections [44]. Against thisbackdrop, it is difficult at present to suggest a definitivetreatment strategy for such patients. If the initial encour-aging results of stent grafting for type-B dissections areconfirmed by prospective randomized studies in the fu-ture, it is imaginable that distal IMHs which develop intolocalized dissections would be treated in future by stentgrafting. As opposed to this, there are few endoluminaltherapy options at present for patients with proximalIMH.

Thus far, the use of endoluminal techniques in type-Aaortic dissections has been limited. Surgical treatment ofsuch dissections in most centres still consists of aorticroot reconstruction, replacement of the ascending aortaand revision of the aortic arch. Whenever large tears inthe aortic arch are present, total arch replacement may beadvisable, including placement of an “elephant trunk” in-to the descending aorta. A subsequent, second-stage op-eration may become necessary in patients with pro-nounced dilatation of the descending aorta. This proce-dure entails a lateral or dorso-lateral thoracotomy forgraft replacement of the descending aorta which is thenanastomosed proximally to the “elephant trunk”. Kato etal. describe a combined open repair of the ascending aor-ta with endoluminal stent-graft placement in the de-scending aorta [2]. More recently, Karck et al. [45] de-scribed the use of a novel prototype endograft (Curative,Dresden, Germany) for treating complex combined pa-thologies of the ascending and descending thoracic aorta.The Chavan-Haverich (CH) endograft used by them con-sists of a surgical dacron graft with stainless steel stentsaffixed to its distal end. It can be introduced antegradelyinto the descending aorta. After deploying the stentedportion into the descending aorta, the proximal non-stented dacron graft was used to reconstruct the aorticarch or was anastomosed to a proximal aortic graft. Theadvantages of this approach are obvious: the patient isspared the second lateral thoracotomy. Should a distalextension be necessary, this can be carried out transfe-

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morally. Although at present the reported patient num-bers are small, the results are very encouraging. Morework is expected in the future using such hybrid endo-grafts which could reduce the multiple surgeries requiredfor type-A aortic dissections to a one-step procedure.

In the years to come, it is expected that endoluminaltechniques will become the method of choice for treatingmost type-B dissections and will assist in significantlyreducing the number of open surgical procedures re-quired for type-A dissections.

Present therapeutic strategy at our institution

In our centre, the acute type-A dissections are treatedwith immediate proximal aortic replacement. Shouldthoraco-abdominal ischaemia persist post-operatively,this is generally managed using transfemoral percutane-ous interventional techniques. Chronic type-A dissec-tions are treated using the “frozen elephant trunk” tech-nique described by Karck et al. which combines openproximal aortic replacement with endoluminal placementof the CH endograft in the descending aorta [45].

Uncomplicated type-B dissections are worked up forenrollment in the INSTEAD study (prospective random-

ized multi-centre study comparing stent grafting withconservative medical therapy). If contained or impend-ing rupture is suspected, a treatment decision (whetherstent grafting or open surgical replacement of the de-scending aorta) is reached by interdisciplinary consensuson a “case-to-case” basis. In patients with critical bowelor lower limb ischaemia, the first endeavour is to relievethe ischaemia as soon as possible using a combination ofballoon fenestration and true lumen stenting. Similarly,true lumen stenting is carried out as a primary measurein patients in whom the ischaemia results from static ob-struction caused by a dilated thrombosed false lumencompressing the true lumen. In patients with non-criticalischaemia, we would tend to attempt stent grafting as thefirst measure followed by further interventions down-stream, should the ischaemia not resolve after stent graft-ing.

Intramural haematomas in stable patients are treatedconservatively, but with close surveillance. In patientswith proximal IMHs who are haemodynamically unsta-ble, in whom the pericardial effusion or the aortic diame-ter increases or in whom a frank aortic dissection devel-ops, surgery with proximal aortic replacement is carriedout. A similar constellation in patients with distal IMHswould be treated by stent grafting.

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References1. Borst HG, Heinemann MK, Stone CD

(eds) (1996) Surgical treatment of aor-tic dissection. Churchill Livingstone,New York

2. Kato M, Matsuda T, Kaneko M, Kuratani T, Mizushima T, Seo Y, Uchida H, Kichikawa K, Maeda M,Ohnishi K (1998) Outcomes of stent-graft treatment of false lumen in aorticdissection. Circulation 98:305–312

3. Dake MD, Noriyuki Kato, Mitchell RS,Semba CP, Razavi MK, Shimono T,Hirano T, Takeda K, Yada I, Miller DC(1999) Endovascular stent-graft place-ment for the treatment of acute aorticdissection. N Engl J Med340:1546–1552

4. Nienaber CA, Fattori R, Lund G, Dieckmann C, Wolf W, Kodolitsch Yvon, Nicolas V, Pierangeli A (1999)Nonsurgical reconstruction of thoracicaortic dissection by stent-graft place-ment. N Engl J Med 340:1539–1545

5. Williams DM, Lee DY, Hamilton BH,Marx MV, Narasimham DL, KazanjianSN, Prince MR, Andrews JC, Cho KJ,Deeb GM (1997) The dissected aorta:percutaneous treatment of ischemiccomplications: principles and results. J Vasc Interv Radiol 8:605–625

6. Slonim SM, Nyman U, Semba CP,Miller DC, Mitchell SR, Dake MD(1996) Aortic dissection: percutaneousmanagement of ischaemic complica-tions with endovascular stents and bal-loon fenestration. J Vasc Surg23:241–253

7. Slonim SM, Nyman U, Semba CP,Miller DC, Mitchell SR, Dake MD(1996) True lumen obliteration in com-plicated aortic dissection: endovasculartreatment. Radiology 201:161–166

8. Slonim SM, Miller DC, Mitchell RS,Semba CP, Razavi MK, Dake MD(1999) Percutaneous balloon fenestra-tion and stenting for life-threateningischaemic complications in patientswith acute aortic dissection. J ThoracCardiovasc Surg 117:1118–1127

9. Chavan A, Hausmann D, Dresler C, Rosenthal H, Jaeger K, Haverich A,Borst HG, Galanski M (1997) Intravas-cular ultrasound-guided percutaneousfenestration of the intimal flap in the dis-sected aorta. Circulation 96:2124–2127

10. Chavan A, Kutschka I, Rosenthal H,Goehde SC, Haverich A, Galanski M(1999) Percutaneous management ofischemic complications of aortic dis-section. Radiology 213 (Suppl):S477

11. Chavan A, Galanski M, Pichlmaier M(2000) Minimal invasive therapiean-sätze bei der aortendissektion. FortschrRöntgenstr 172:576–586

12. Doroghazi RM, Slater EE, DesanctisRW, Buckley MJ, Austen WG, Rosenthal S (1984) Long-term survivalof patients with treated aortic dissec-tion. J Am Coll Cardiol 3:1026–1034

13. Wheat MW Jr (1987) Acute dissectionof the aorta. Cardiovasc Clin17:241–262

14. Miller DC (1988) Vascular complica-tions associated with spontaneous aor-tic dissection (discussion). J Vasc Surg7:208–209

15. Heinemann MK, Buehner B, SchaefersHJ, Jurmann MJ, Laas J, Borst HG(1994) Malperfusion of the thoracoab-dominal vasculature in aortic dissec-tion. J Card Surg 9:748–757

16. Cambria RP, Brewster DC, Gertler J,Moncure AC, Gusberg R, Tilson D,Darling RC, Hammond G, MegermanJ, Abbott WM (1988) Vascular compli-cations associated with spontaneousaortic dissection. J Vasc Surg7:199–209

17. Fann JI, Sarris GE, Mitchell RS,Shumway NE, Stinson EB, Oyer PE,Miller CD (1990) Treatment of patientswith aortic dissection presenting withperipheral vascular complications. AnnSurg 212:705–713

18. Elefteriades JA, Hammond GL, Gusberg RJ, Kopf GS, Baldwin JC(1990) Fenestration revisited: a safeand effective procedure for descendingaortic dissection. Arch Surg125:786–790

19. Williams DM, Brothers TE, MessinaLM (1990) Relief of mesenteric isch-emia in type III aortic dissection withpercutaneous fenestration of the aorticseptum. Radiology 174:450–452

20. Vernhet H, Marty-Ané CH, Lesnik A,Chircop R, Serres-Cousiné O, PicardE, Mary H, Senac JP (1997) Dissectionof the abdominal aorta in blunt trauma:management by percutaneous stentplacement. Cardiovasc Interv Radiol20:473–476

21. Erbel R, Oelert H, Meyer J et al.(1993) For the European cooperativestudy group on echocardiography: ef-fect of medical and surgical therapy onaortic dissection evaluated by trans-esophageal echocardiography. Implica-tions for prognosis and therapy. Circu-lation 87:1064–1615

22. Williams DM, Andrews JC, Marx V,Abrams GD (1993) Creation of reentrytears in aortic dissection by means ofpercutaneous balloon fenestration:gross anatomic and histologic consid-erations. J Vasc Interv Radiol 4:75–83

23. Ergin MA, Phillips RA, Galla JD et al.(1994) Significance of distal false lu-men after type A dissection repair. AnnThorac Surg 57:820–825

24. Vlahakes GJ (1999) Catheter-basedtreatment of aortic dissection. N Engl JMed 340:1585–1586

25. Chung JW, Elkins C, Sakai T, Kato N,Vestring T, Semba CP, Slonim SM,Dake MD (2000) True-lumen collapsein aortic dissection. Part II: evaluationof treatment methods in phantoms withpulsatile flow. Radiology 214:99–106

26. Dake MD (2001) Endovascular stent-graft management of thoracic aorticdiseases. Eur J Radiol 39:42–49

27. Sailer J, Peloschek P, Rand T, Grabenwöger M, Thurnher S, LammerJ (2001) Endovascular treatment ofaortic type B dissection and penetratingulcer using commercially availablestent-grafts. AJR 177:1365–1369

28. Czermak BV, Waldenberger P, Fraedrich G, Dessl AH, Roberts KE,Bale RJ, Perkmann R, Jaschke WR(2000) Treatment of Stanford type Baortic dissection with stent-grafts: preliminary results. Radiology217:544–550

29. Kato N, Hirano T, Kawaguchi T, IshidaM, Shimono T, Yada I, Takeda K(2001) Aneurysmal degeneration of theaorta after stent-graft repair of acuteaortic dissection. J Vasc Surg34:513–518

30. Hausegger KA, Tiesenhausen K,Schedlbauer P, Oberwalder P, Tauss J,Rigler B (2001) Treatment of acuteaortic type B dissection with stent-grafts. Cardiovasc Intervent Radiol24:306–312

31. Kato N, Shimono T, Hirano T, IshidaM, Yada I, Takeda K (2001) Translu-minal placement of endovascular stent-grafts for the treatment of type A aorticdissection with an entry tear in the descending thoracic aorta. J Vasc Surg34:1023–1028

32. Shimshak TM, Giorgi LV, Hartzler GO(1988) Successful percutaneous angio-plasty of an obstructed abdominal aortasecondary to a chronic dissection. AmJ Cardiol 61:486–487

33. Saito S, Arai H, Kim K, Aoki N, Tsurugida M (1992) Percutaneous fenestration of dissecting intima with atransseptal needle: a new therapeutictechnique for visceral ischaemia com-plicating acute aortic dissection. CathetCardiovasc Diagn 26:130–135

34. Cowling MG, Redwood D, BuckenhamTM (1995) Case report: critical limbischaemia due to aortic dissection re-lieved by percutaneous transfemoralfenestration. Clin Radiol 50:654–657

35. Faykus MH, Hiette P, Koopot R (1992)Percutaneous fenestration of type I aor-tic dissection for relief of lower ex-tremity ischaemia. Cardiovasc Inter-vent Radiol 15:183–185

36. Kato N, Sakuma H, Takeda K, HiranoT, Nakagawa T (1993) Relief of acutelower limb ischaemia with percutane-ous fenestration of intimal flap in a pa-tient with type III aortic dissection: acase report. Angiology 44:755–759

37. Schild HH, Düber C, Grebe P, Hake U,Oelert H, Thelen M, Meyer J (1994)Transvaskuläre fensterung eines disse-ziierenden aortenaneurysmas. FortschrRöntgenstr 2:164–167

38. Manke C, Strotzer M, Seitz J, LenhartM, Aebert H, Kasprzak P, Kaiser B,Feurbach ST (1999) Ischämische komplikationen bei aortendissektion:perkutane behandlung mit ballon-fensterung und stentimplantation.Fortschr Röntgenstr 198–204

39. Lookstein RA, Mitty H, Falk A, GullerJ, Scott-Nowakowski F (2001) Aorticintimal dehiscence: a complication ofpercutaneous balloon fenestration foraortic dissection. J Vasc Interv Radiol12:1347–1350

40. Nyman U, Ivancev K, Gottsäter A, Lindblad B, Lindh M, Uher P (1999)Chronic aortic dissection: stenting ofaortic true lumen obliteration with latedynamic variations of both lumens.Cardiovasc Interv Radiol 22:135–149

41. Müller-Lung U, König M, Heidrich M,Sivitanidis E, Heuser L (1998) Stentimplantation bei akuter zerebralerischämie infolge einer dissektion derarteria carotis communis im rahmeneiner thorakalen aortendissektion.Fortschr Röntgenstr 4:447–449

42. Bernard Y, Zimmermann H, ChocronS, Litzler J-F, Kastler B, Etievent J-P,Meneveau N, Schiele F, Bassand J-P(2001) False lumen patency as a pre-dictor of late outcome in aortic dissec-tion. Am J Cardiol 87:1378–1382

43. Kang S-G, Lee DY, Maeda M, Kim ES,Choi D, Kim B-O, Yoon HK, SungKB, Song H-Y (2001) Aortic dissec-tion: percutaneous management with aseparating stent-graft: preliminary re-sults. Radiology 220:533–539

44. Song J-K, Kim H-S, Song J-M, KangD-H, Ha J-W, Rim S-J, Chung N, KimKS, Park SW, Kim YJ, Sohn DW(2002) Outcomes of medically treatedpatients with aortic intramural hemato-ma. Am J Med 113:181–187

45. Karck M, Chavan A, Hagl C, FriedrichH, Galanski M, Haverich A (2003) The“frozen elephant trunk technique”: anew treatment for thoracic aortic aneu-rysms. J Thorac Cardiovasc Surg125:1550-1553

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