the concept of interventional therapy in acute aortic syndrome

135

The Concept of Interventional Therapy in Acute Aortic Syndrome Hiiseyin Ince, M.D., and Christoph A. Nienaber, M.D.

Abteilung fur Kardiologie, Medizinische Klinik, Universitatsklinikum Rostock, Germany

Acute aortic syndrome (AAS) comprises an in- homogeneous group of patients with a poly- faceted clinical profile that ranges from penetrating atherosclerotic aortic ulcer and intramural aortic hematoma to the classic form of aortic dissection. AAS always represents a potentially life- threatening situation. Although great efforts have been made during the past decades in management of patients with AAS by new surgical techniques, postoperative morbidity and mortality re- main high. The afflicted population is usually of older age and characterized by a variety of co- morbidities with significant impact on postsurgi- cal outcome. Postoperative complications, such as paraplegia and renal insufficiency, contribute to prolonged hospital stays and higher medical costs if surgery is performed. Conversely, interventional stent-graft placement may be a promising nonsurgical strategy for the treatment of selected cases of AAS confined to the descending aorta. Endovascular stent-graft prosthesis are based on the concept of metal grids covered with graft material. Stent-grafts are intended to induce the natural healing process by sealing the proximal entry to a type B dissection, leading to remodeling of the aortic wall and consolidation of the false lumen.

SYMPTOMS

In the light of contemporary concepts in aortic pathology and considering the typical clinical

Address for correspondence: Prof. Dr. med. C. A. Nienaber, Abteilung fur Kardiologie, Universitatsklinikurn Rostock, Ernst- Heydemann-Str. 6, 18055 Rostock, Germany. Fax: + 49381 494 77 02; e-mail : christoph, nienaberQmed. uni-rostock.de

symptomatology of sudden onset crushing chest pain, AAS appears intuitively genuine for that sce- nario. AAS includes penetrating atherosclerotic aortic ulcer, intramural aortic hematoma, and classic aortic dissection.' The pathophysiological mechanism that precipitates the appearance of each of these entities, however, is different.

Typically, AAS is characterized clinically by aortic pain in a patient with a long history of hypertension. Likewise, in AAS, chest pain is charac- teristic and has been called "aortic pain." The recognition of pain associated with these pro- gressive aortic lesions is of paramount impor- tance. A severely intense, acute, searing or tear- ing, throbbing, and migratory chest pain denotes AAS. Anterior chest, neck, throat, and even jaw pain is related to involvement of the ascending aorta, whereas back and abdominal pain more often indicates an affected descending aorta. The pain description and clinical presentation of patients with penetrating aortic ulcer and intramural aortic hematoma can be confused with that of classic aortic dissection. Severe, acute chest pain consistent with AAS may even occur in patients with marked aortic dilatation but without histo- pathologic evidence of dissecting lesions. Aortic root stretching and distension are likewise mech- anisms for pain in these patients. However, aortic pain may be confused with that of ischemic syndromes. Moderate to severe hypertension is the most prevalent risk factor for the develop- ment of an AAS. Inheritable disorders such as Marfan's syndrome also predispose to the devel- opment of classic aortic dissection, as does pre- vious aortic valve surgery.2 Similarly, hypertension is the most common comorbid disease associated with penetrating aortic ulcer and intramural aortic hematoma or b ~ t h . ~ . ~

136 INCE AND NIENABER INTERVENTIONAL THERAPY IN AAS

J CARD SURG 2002; 17:135-142

PATHOLOGY OF AAS magnetic resonance (MR) imaging, or angiography

Ascending aortic dissection usually begins with a primary intimal tear. Tears occur primarily at fixa- tion sites where wall tension is more pronounced, i.e., at the sinobulbar junction and at the isthmus. About 60% of dissections involve the ascending aorta. The intimal tear is usually transverse, and the dissection progresses rapidly along the outer, thinner one-third of the media, which is precisely why rupture often occurs into the pericardial or pleural spaces through this outer wall. In ascending aortic dissections, the false lumen often occu- pies the right anterior aspects of the aorta, whereas the medial half usually remains intact.

In type A dissections, proximal extension of the dissection can cause distortion of the aortic com- missures and subsequent aortic insufficiency from prolapse of valvular leaflets. In addition, proximal extension of the dissection can also lead to dissection compromising the coronary arteries, and causes myocardial ischemia or infarction with the right coronary artery more frequently affected. As type A dissections progress proximally, rupture into the pericardial space may occur; tamponade is the most common cause of death in the first 2 weeks following type A dissection. Untreated type A dissection are associated with a very high mortality. During the first 24 to 48 hours, the mortality approximates 1-2% per hour. Therefore, patients with type A dissection must undergo urgent surgical repair.5-7

Aortic intramural hematoma represents a re- cently described variant of dissection characterized by the absence of an entry tear *r9 and insanguina- tion of the aortic media layers from rhexis of the vasa vasorum. In some patients a tiny intimomedial entrance tear could be present but not visualized by the current imaging techniques. In these cases, intramural hematoma would not be decompressed by an exit tear, and therefore no flowing blood is de- tected within the aortic wall. The entrance tear can be absent or, if present, must be very small.10 On histology, a hematoma disrupting the aortic media is well documented. In some patients echolucent zones may be identify by TEE within the aortic wall, probably representing areas of liquefaction of the intramural hematoma; with such lacunae directly beneath the intimomedial layer, dissection can rapidly develop. A thickened aortic wall does not generally show enhancement with contrast admin- istration on computed tomography (CT) scanning,

since there is no inflow through an entry tear. Char- acteristically, aortic intramural hematoma displays dynamic behavior and a crescent-shaped or circular aortic wall thickness of > 7 mm along the aortic wall that may vary with time.’ The mechanism of rapid regression of the aortic hematoma has not been fully understood. In other cases this segmental noncommunicating aortic dissection can progress to a typical dissection. Increased perme- ability of the aortic wall leading to pericardial, pleural, and mediastinal hemorrhage, and progres- sion to an aortic rupture has also been reported. Aortic intramural hematoma may also originate from ulceration in an atherosclerotic aortic plaque; in these cases, the ulcerated aortic plaque practi- cally functions as an entry tear. The term “penetrating atherosclerotic aortic ulcer“ describes the condition in which ulceration of an aortic atherosclerotic lesion penetrates the internal elastic lam- ina into the media. This lesion may precipitate intramural hemorrhage or even dissection. In most patients intramural hematoma is localized, but oc- casionally involves the entire descending thoracic aorta. Ulcers may also be complicated by aneurysm formation by rupture into the periaortic space or by pseudoaneurysm. Concomitant aneurysms of the descending or abdominal aorta are com- monly found.3 Aortic ulcers are usually focal lesions most frequently located in the descending thoracic aorta. On the contrary, intramural hematoma and classic aortic dissection are more ex- tensive lesions. In contrast to classic dissection, aortic dissection secondary to an aortic ulcer is shorter in extension, away from classic entry tears, and have a thicker, calcified and static flap. This type of dissection, in an area of gross atheroscle- rosis, is usually limited by neighboring fibrosis and calcification.

DIAGNOSIS

The common denominator in all scenarios of AAS is its unpredictable nature with often an unfa- vorable outcome. Therefore, early diagnosis and appropriate treatment are essential. The most important diagnostic imaging modalities in AAS are transesophageal echocardiography, contrast- enhanced computed tomography, magnetic resonance imaging, and contrast angiography.’*~’~ There is growing interest and use of magnetic

J CARD SURG 2002:17:135-142

INCE AND NIENABER 137 INTERVENTIONAL THERAPY IN AAS

resonance and CT imaging due to high sensitivity to identify entries and reentries or the nature of the false lumen, and most important, unrestricted image orientation, especially with three-dimensional (3D) magnetic resonance angiography (MRA) tech- nology. Computer-enhanced 3D reconstruction of the aorta can serve as a blueprint for surgical or interventional reconstructive procedures. Exact morphometry of the aorta and side branches al- lows individual endovascular prostheses to be constructed.

MATERIALS AND METHODS

Endovascular stent-graft placement

The stent-graft prosthesis (Talent, World Med- ical Manufacturing, Sunrise, FLA, USA) is a self- expanding endoprosthesis consisting of circum- ferential nitinol stent springs arranged as a tube and covered on its exterior with a Dacron graft; the tube was customized with respect to width, length, and the configuration of each end (as a bare spring or a covered web for optimal conformance with the aorta) and is compressed in a 22-to-27- French polytetrafluoroethylene (Teflon) sheath; the nitinol rings are interconnected by a longitudinal wire to ensure stabilization and separation of all the rings and to prevent twisting. Each device is custom-made according to morphometric measurements obtained from each patient’s MRI scan.

Imaging protocol

All the patients underwent spin-echo (anatomical) MRI and three-dimensional MRA after the in- jection of a bolus of gadolinium-diethylenetriamine pentaacetic acid (gadolinium-DTPA; Magnevist, Schering, Berlin, Germany). The use of gadolinium- DTPA during data acquisition produces contrast- induced T,-shortening effects and eliminates saturation problems due to slow flow or turbulence- induced signal voids. With the use of ultrafast gradients, acquisition was performed with the patients holding their breath. A FLASH (fast low- angle shot) three-dimensional sequence was used with or without intravenous contrast material to create maximal-intensity projections; echo and repetition times were as short as 1.9 and 4.0 msec, respectively. With a field of view of 390 to 450 mm, a 512-by-512 matrix provided an in- plane resolution of 1 .l-by-1.6 mm. Slice thick-

ness varied from 2 to 4 mm; a flip angle of 30E was selected. Imaging of 64 interpolated con- tiguous slices with half-k-space data acquisition in the phase-encoding direction took 20 to 28 seconds.

Images were obtained with a 1.5-T magnetic resonance scanner (Magnetom Vision, Siemens Medical Systems, Erlangen, Germany) equipped with an ultrafast-gradient system; a body-array coil was used for signal transmission and recep- tion. Optimal image quality was ensured by individual tracking of the bolus before the infusion of 0.25 mmol of gadolinium-DTPA per kilogram of body weight over a period of 10 to 14 seconds (approximately half the acquisition time). With subvolume multiplanar reconstruction, the dissecting lamella (the exact site of a communication and false-lumen flow) was identified in all cases. To design each stent-graft, MRI scans and angiograms were evaluated for morphometric measurements before stent implantation. Follow-up MRI was performed according to an identical protocol for all the patients to document complete closure of the interluminal communication or false-lumen thrombosis or leakage.

Implantation technique

Stent-graft placement was performed in the cardiac catheterization laboratory with the patients under general anesthesia and receiving ventila- tion. Patients were prepared to undergo surgery in case the procedure failed. The procedure was begun by injecting 5000 U of heparin and intro- ducing a 6-French pigtail catheter (Cordis, Ham- burg, Germany) into the left subclavian artery for precise guidance near the subclavian artery and for intraprocedural aortography. In all the patients, the femoral or distal iliac artery was surgically ex- posed, and a 0.89-mm (0.035-in) guidewire was inserted. When the position of the wire in the true lumen of the aorta had been confirmed by fluor- oscopy and ultrasonography, the sheath with the stent, a pusher, and a deflated large-bore latex balloon (the Talent prosthesis) was introduced. The compressed stent was advanced to the site of the interluminal communication, under guidance by simultaneous transesophageal color Doppler imaging.

Before the stent-graft was unloaded, systolic blood pressure was titrated to 50 mmHg with


J CARD SURG 2002;17:135-142

sodium nitroprusside; as soon as the position was found, the stent-graft was launched and struts expanded by balloon molding (by inflation of the balloon a t 2 to 3 atm); when the stent-struts were fully extended and there was no flow into the false lumen, the infusion of sodium nitroprusside was discontinued. Care was taken to com- pletely seal the entry with Dacron and to protect the left subclavian artery with the bare-spring end of the stent-graft. Both the sheath and the guidewire were then removed, and the incision was closed. No additional heparin or antiplatelet medication was administered after completion of the procedure.

RESULTS

In a recent publication both safety and efficacy of elective transluminal endovascular stent-graft insertion in 12 consecutive patients with descending (type B) aortic dissection were compared to results of surgery in 12 matched contr01s.l~ In all 24 patients, aortic dissection was diagnosed by MRA. In each group, the dissection involved the aortic arch in three patients and the descending thoracic aorta in all 12 patients. With the patient under general anesthesia, either surgical resection was undertaken or a custom-designed endovascular stent-graft was placed by unilateral arte- riotomy. Our findings suggest that nonsurgical reconstruction may constitute a viable therapeutic option for patients with descending dissection of the thoracic aorta and one or more indications for surgical repair, such as an aortic diameter greater than 5.5 cm, a patent false lumen with potential for expansion, or recurrent pain.15-18322 In contrast to thoracic surgery for type B dissection, trans- femoral stent-grafting was not associated with early or longer-term mortality or with serious morbidity. Our preliminary analysis even suggests that substantial cost savings could result from the reduced need for intensive care and the shorter hospital stay.

Whereas emergency surgical repair is lifesav- ing in ascending (type A) aortic d i s s e c t i ~ n , ~ ~ - ~ ~ both emergency surgery and deferred surgery for descending (type B) dissection are associated with a 6 to 67% mortality rate and offer no substantial advantage over medical therapy.19e21824t25 Also, paraplegia (or paresis) occurs in 7 to 36% of patients who undergo surgery, depending on the extent of aortic resection and the duration of

cros~-clamping.~9,2~.2~,2~ Even with intraoperative atriodistal bypass, reattachment of all the critical intercostal arteries, and induction of mild hypo- thermia, early surgical mortality is 7.1 YO in patients with chronic type B dissection and 8.7% in those with acute type B d i s s e ~ t i o n . ~ ~ - ~ l Similarly, surgery-related paraplegia or paresis occurs in 2.9% of patients with chronic type B dissection and in 19% of those with acute cases; again advanced age, excessive cross-clamping time, and inappropriate reattachment of the great anterior radiculomedullary artery are predictors of adverse out comes .31-36

Although spinal cord dysfunction was expected to develop in approximately 8% of our patients with ~tent-grafts,3~ no neurologic complications were encountered, in contrast to the outcome in patients treated surgically. Preservation of the in- tegrity of the aorta, rather than resection of the dis- sected segment, may be important to protect the spinal arteries. The use of short stent-grafts, from 80 to 150 mm in length, and deployment far from vertebrae T8 to L2, further minimize the risk of paraplegia, as compared with the risk with surgical grafts, which were 220 2 74 mm in length (p < 0.001). Most important, the stent-graft procedure took only 1.6 & 0.4 hours, as compared with 8.0 ? 2.0 hours for surgery (p < 0.001 1; it circumvented the need for circulatory arrest and cross-clamping of the aorta, and the associated ischemia and po- te n t ia l re perf us ion in j u ry.25~263 35.37

In the light of our initial promissing results, w e have expanded the use of nonsurgical stent-graft placement for a series of 120 patients with type B dissection with suitable anatomical characteris- tics (an accessible proximal entry, at least one femoral artery without dissection, and no substantial tortuosity). Moreover, 4 patients with IMH and paraaortic leakage of blood, and 15 patients with a penetrating aortic ulcer have recieved an endovascular stent-graft (Table 1)

Tables 2 and 3 summarize the results of medical, surgical and endoluminal treatment of type B dissections as reported from recent l i terat~re. '~,~" 41 In the light of disappointing prognostic figures with surgery, the endoluminal procedures seem promising even in a meta-analytic approach.

CONCLUSIONS

Although conceptually promising, the management of AAS by stent-graft placement requires

J CARD SURG 2002: 17: 135-1 42

INCE AND NIENABER INTERVENTIONAL THERAPY IN AAS

139

TABLE 1 Stent-graft Placement in Type B Dissection, Aortic Intramural

Hematoma (IMH), and Penetrating Atherosclerotic Aortic Ulcer Entity (AAS) Success (YO) 30 Day Mortality 1 Year Mortality

Type B dissection (n = 120) 98 2 (1.7%) 2 (1 .7%) IMH (n = 4) 100 0 0 penetrating aortic ulcer (n = 15) 100 0 0

TABLE 3 Type B Dissection: Surgical Results versus

Endovascular R e ~ u l t s ~ ~ , ~ ~ , ~ ~ , ~ ~ TABLE 2

Type B Dissection: Survival of Nonoperated Versus Operated Patients39

Emergency Elective Endovascular Survival Nonoperated (YO) Operated (%) Events Surgery Surgery Stent-grafts

1 year 73-92 47 Mortality % 10-45 14-6 16 3 years 63 40 Paraplegia % 20 10 0 5 years 58-89 28 Resp. Insuff. % 6-3 1 15-40 5 10 years 25-76 Stroke YO 7 2 -

Figure 1. MRA of type B dissection showing the communication between true and false lumen (a). MRA of type 5 dissection after stent-graft placement with complete reconstruction and remodeling of the aorta (bl.


J CARD SURG 2002;17:135-142

Figure 2. MRA ofa patient with an aortic intramural hematoma before la) and afterpercutaneous stenting with complete reconstruction and aortic remodeling Ib). Note that the preinterventional extraaortic leakage of blood is com- pletely abolished.

Figure 3. MRA of a patient with a penetrating atherosclerotic aortic ulcer before (a) and after percutaneous stenting with complete reconstruction of the aortic continuity. The aneurysmal sac has been fully excluded (bl.

J CARD SURG 2002;17:135-142

INCE AND NIENABER 141 INTERVENTIONAL THERAPY IN AAS

the support of long-term follow-up data. On the other hand, over several years of follow-up after stent-graft placement for the treatment of both thoracic and abdominal aneurysms, late adverse effects were infrequent, justifying the use of stent-grafts in patients too sick or multimorbid for classic s ~ r g e r y . ~ ~ - ~ ~ Moreover, the custom design of each stent-graft currently limits the concept to patients undergoing elective procedures or requires a large stock and selection of stent-grafts to treat acutely ill patients. Finally, sophisticated imaging techniques, such as MRA, intraprocedural transesophageal echocardiography, and digital angiography, appear to be necessary to ensure optimal results. Stent-graft placement may be a promising nonsurgical strategy for the treatment of AAS in form of type B dissection, aortic intramural hematoma, and penetrating atherosclerotic aortic ulcer. Whereas dissection may develop rupture and expansion, IMH and PAU eventually predispose to full-fledged dissection. (Figs. 1, 2, and 3).

The initiation of the natural healing process (false lumen thrombosis) by sealing of the proximal entry, induces both consolidation of the false lumen and remodeling of the aortic wall. In a variety of cases of type B dissection and even in presence of distal malperfusion syndrome, interventional stent-graft placement may be offered to selected patients in lieu of surgical repair. With further refinement of the technique, more patients with severe coexisting conditions and high surgical risk may be considered for the procedure. Although the initial results of stent-graft treatment of acute aortic syndrome are promising, the concept of nonsurgical reconstruction in all entities of AAS should be subjected to ran- domized long-term evaluation.

1.

2.

3.

4.

REFERENCES

Vilacosta I, San Roman JA, Aragoncillo P, et al: Penetrating atherosclerotic aortic ulcer: Documen- tation by transesophageal echocardiography. J Am Coll Cardiol 1998;32:83-89. Nienaber CA, Von Kodolitsch Y: Therapeutic management of patients with Marfan’s Syndrome. Car- diol Rev 1999;7:332-341. Coady MA, Rizzo JA, Hammond GL, et al: Pene- trating ulcer of the thoracic aorta: What is it? How do we recognize it? How do we manage it? J Vasc Surg 1998;27:1006-I 01 6. Vilacosta I , an Roman JA, Ferreiros J, et al: Natural history and serial morphology of aortic intramural

hematoma: A novel variant of aortic dissection. Am Heart J 1997;134:495-507.

5. Nienaber CA, Von Kodolitsch Y: Metaanalyse zur

6

7

8

9.

10.

11.

12.

13.

14.

15.

16.

17.

18.

Prognose der thorakalen Aortendissektion: Letali- tat im Wandel der letzten vier Jahrzehnte. Herz 1992;17:398-416. Kodolitsch Y, Schwartz AG, Nienaber CA: Clinical prediction of acute aortic dissection. Arch Intern Med 2000;160:2977-2982. Hagan PG, Nienaber CA, lsselbacher EM, et al: The International Registry of Acute Aortic Dissection (IRAD): New insights into an old disease. JAMA

Mohr-Kahaly S, Erbel R, Kearney P, et al: Aortic intramural hemorrhage visualized by transesophageal echocardiography: Findings and prognostic implications. J Am Coll Cardiol 1994;23:658-664. Nienaber CA, Von Kodolitsch Y, Petersen B, et al: Intramural hemorrhage of the thoracic aorta: Diag- nostic and therapeutic implications. Circulation 1995;

Vilacosta I, Martin de Dios R, GonzBlez Pinto A: Aor- tic intramural hematoma during coronary angio- plasty: Insights into the pathogenesis of intramedial hemorrhage. J Am SOC Echocardiogr 2000;13:403- 406. Ohmi M, Tabayashi K, Moizumi Y, et al: Extremely rapid regression of aortic intramural hematoma. J Thorac Cardiovasc Surg 1999;58:1855-I 856. Nienaber CA, Spielmann RP, Von Kodolitsch Y, et al: Diagnosis of thoracic aortic dissection: Mag- netic resonance imaging versus transesophageal echocardiography. Circulation 1 992;85:434-447. Nienaber CA, Von Kodolitsch Y, Brockhoff CJ, et al: Comparison of conventional and transesophageal echocardiography with magnetic resonance imaging for anatomical mapping of thoracic aortic dissection: A dual noninvasive imaging study with anatomical and/or angiographic validation. Int J Card Imaging 1994;lO:l-14. Nienaber CA, Fattori R, Lund G. et at: Nonsurgical reconstruction of thoracic aortic dissection by stent- graft placement. N Engl J Med 1999;340:1539- 1545. Dinis da Gama A: The surgical management of aortic dissection: From uniformity to diversity, a con- tinuous challenge. J Cardiovasc Surg (Torino) 1991;

Svensson LG: Natural history of aneurysms of the descending and thoracoabdominal aorta. J Card Surg 1997;12:279-284. Kato M, Bai HZ, Sat0 K, et al: Determining surgical indications for acute type B dissection based on enlargement of aortic diameter during the chronic phase. Circulation 1995;92:Suppl 11:ll-107-11-112. Glower DD, Fann JI, Speier RH, et al: Comparison of medical and surgical therapy for uncomplicated

2000;283:897-903.

9211465-1472.

32:141-153.


J CARD SURG 2002:17:135-142

descending aortic dissection. Circulation 1990;82:

19. Miller DC: The continuing dilemma concerning medical versus surgical management of patients with acute type B dissections. Semin Thorac Car- diovasc Surg 1993;5:33-46.

20. Masuda Y, Yamada Z, Morooka N, et al: Prognosis of patients with medically treated aortic dissections. Circulation 1991;84:Suppl 111:111-7-111-13.

21. Svensson LG, Crawford ES, Hess KR, et al: Dissec- tion of the aorta and dissecting aortic aneurysms: Improving early and long-term surgical results. Cir- culation 1990;82:Suppl IV:IV-24-IV-38.

22. Dinsmore RE, Willerson JT, Buckley MJ: Dissect- ing aneurysm of the aorta: Aortographic features affecting prognosis. Radiology 1972;105:567-572.

23. Rizzoli G, Mazzucco A, Fracasso A, et al: Early and late survival of repaired type A aortic dissection. Eur J Cardiothorac Surg 1990;4:575-583.

24. Fuster V, Halperin JL: Aortic dissection: A medical perspective. J Card Surg 1994;9:713-728.

25. Svensson LG, Crawford ES: Aortic dissection and aortic aneurysm surgery: Clinical observations, ex- perimental investigations, and statistical analyses. Curr Probl Surg 1992;29:913-1057.

26. Borst HG, Jurmann M, Buhner B, et al: Risk of re- placement of descending aorta with a standard- ized left bypass technique. J Thorac Cardiovasc Surg 1994107126-133.

27. Svensson LG, Crawford ES, Hess KR, et al: Vari- ables predictive of outcome in 832 patients undergoing repairs of the descending thoracic aorta. Chest 1993;104:1248-1253.

28. Hagan P, Nienaber CA, Das S, et al: Acute aortic dissection: Presentation, management and outcomes in 1996. Results from the International Reg- istry for Aortic Dissection (IRAD). (Abstrract) J Am Coll Cardiol 1998;31 :Suppl A:217A.

29. Kouchoukos NT, Daily BB, Rokkas CK, et al: Hy- pothermic bypass and circulatory arrest for operations on the descending thoracic and thoracoabdominal aorta. Ann Thorac Surg 1995;60:

30. Kouchoukos NT, Dougenis D: Surgery of the thoracic aorta. N Engl J Med 1997;336:1876-I 888.

31. Coselli JS, LeMaire SA, de Figueiredo LP, et al : Paraplegia after thoracoabdominal aortic aneurysm

SUPPI IV:IV-39-IV-46.

67-77.

repair: Is dissection a risk factor? Ann Thorac Surg

32. Schepens MAAM, Defauw JJAM, Hamerlijnck RPHM, et al: Use of left heart bypass in the surgical repair of thoracoabdominal aortic aneurysms. Ann Vasc Surg 1995;9:327-338.

33. Panneton JM, Hollier LH: Dissecting descending thoracic and thoracoabdominal aortic aneurysms. Ann Vasc Surg 1995;9:596-605.

34. Acher CW, Wynn MM, Hoch JR, et al: Combined use of cerebral spinal fluid drainage and naloxone reduces the risk of paraplegia in thoracoabdominal aneurysm repair. J Vasc Surg 1994;19:236-248.

35. Svensson LG, Hess KR, Coselli JS, et al : Influence of segmental arteries, extent, and atriofemoral bypass on postoperative paraplegia after thoracoab dominal aortic operations. J Vasc Surg 1994;20:255 262.

36. Svensson LG, Crawford ES, Hess KR, et al : Experi- ence with 1509 patients undergoing thoracoabdominal aortic operations. J Vasc Surg 1993;17:357-370.

37. Schor JS, Yerlioglu ME, Galla JD, et al: Selective management of acute type B aortic dissection: Long-term follow-up. Ann Thorac Surg 1996;61:

38. Dake MD, Kato N, Mitchell RS, et al: Endovascular stent-graft placement for the treatment of acute aortic dissection. N Engl J Med 1999; 340:1524-I 531.

39. Miller DC: The continuing dilemma concerning medical versus surgical management of patients with acute type B dissections. Semin Thorac Car- diovasc Surg 1993;5:33-46.

40. Kato M, Hirano T, Kaneko M, et al: Outcomes of stent-graft treatment of false lumen in aortic dissection. Circulation 1998;11-305-l1 312.

41. Miller DC, Mitchell RS, Dake MD: Midterm results of first generation endovascular stent-grafts for descending thoracic aortic aneurysms. In: Proceed- ings of the Sixth Aortic Surgery Symposium, New York, April 30 May 1, 1998: 34-35. Abstract.

42. Dake MD, Miller DC, Semba CP, et al: Transluminal placement of endovascular stent-grafts for the treatment of descending thoracic aortic aneursyms. N Engl J Med 1994;331 :I 729-1 734.

43. Mitchell RS, Dake MD, Semba CP, et al: Endovas- cular stent-graft repair of thoracic aortic aneurysms. J Thorac Cardiovasc Surg 1999;l l l : I 054-1 062.

1997;63:28-36.

1339-1 341.

the concept of interventional therapy in acute aortic syndrome

Documents