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(Radiology. 2000;214:99-106.)
© RSNA, 2000


Experimental Studies

True-Lumen Collapse in Aortic Dissection 1

Part II. Evaluation of Treatment Methods in Phantoms with Pulsatile Flow

Jin Wook Chung, MD 2, Christopher Elkins, PhD, Toyohiko Sakai, MD, Noriyuki Kato, MD, Thomas Vestring, MD, Charles P. Semba, MD, Suzanne M. Slonim, MD and Michael D. Dake, MD

1 From the Division of Cardiovascular-Interventional Radiology, Stanford University Medical Center, Stanford Vascular Center, H-3647, 300 Pasteur Dr, Stanford, CA 94304-5105. Received November 30, 1998; revision requested January 21, 1999; revision received March 19; accepted May 6. Address reprint requests to M.D.D. (e-mail: mddake@leland.stanford.edu).


    Abstract
 TOP
 Abstract
 Introduction
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
PURPOSE: To discover and evaluate the effective treatment methods to prevent or relieve true-lumen collapse in models of aortic dissection.

MATERIALS AND METHODS: Two phantoms were built to simulate type B aortic dissection. After true-lumen collapse was induced, experiments were conducted to evaluate the effectiveness of clinically relevant variables in relieving the collapse. Variables included entry-tear size, branch-vessel flow distribution, distal reentry communication between the true and false limbs, aortic fenestrations, and pump output. To test the effect of closing the entry tear, a stent-graft was deployed over the entry tear under physiologic conditions in a mock-flow loop. The difference in the effect of each variable on the prevention and relief of true-lumen collapse was also investigated.

RESULTS: It was more difficult to relieve true-lumen collapse than it was to prevent it. Placement of a stent-graft over the entry tear was the most effective method of relieving true-lumen collapse. Less-effective procedures included opening a false-lumen outflow branch and opening the distal reentry branch. Opening the fenestration-branch loops, meant to simulate the creation of artificial fenestrations in the intimal flap, did not relieve true-lumen collapse.

CONCLUSION: The definitive treatment for true-lumen collapse in aortic dissection is direct repair of the entry tear to decrease false-lumen inflow. Otherwise, increasing the false-lumen outflow and/or creating distal fenestrations between the true and false lumina distal to the level of the compromised aortic branch are less-effective alternatives.

Index terms: Aorta, dissection, 942.4124, 943.743, 981.743 • Aorta, flow dynamics • Aorta, grafts and prostheses, 942.1268 • Aorta, stenosis or obstruction, 943.743, 981.743 • Phantoms, 942.412, 943.743, 981.743


    Introduction
 TOP
 Abstract
 Introduction
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
True-lumen collapse in aortic dissection causes serious ischemia in multiple organs due to its effect on the mesenteric, renal, and lower extremity vasculatures (1). A high mortality rate occurs in patients with these conditions whether they undergo surgery or not (24). Recently, percutaneous endovascular treatment with balloon fenestration and stent placement was introduced to relieve true-lumen collapse and showed promising results (1,5,6). However, to our knowledge, no clinical or experimental study has been conducted to investigate the causes of true-lumen collapse in aortic dissection and the possible treatment methods to relieve true-lumen collapse or to determine the most effective methods. We conducted an experimental study to answer these questions by using two pulsatile phantoms. In part I of this experiment, we investigated and identified several causative factors that induced true-lumen collapse in aortic dissection.

The purpose of this study, part II of the experiment, was to find effective treatment methods to prevent or relieve true-lumen collapse in aortic dissection by using the same phantoms.


    MATERIALS AND METHODS
 TOP
 Abstract
 Introduction
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
Two dissection models were built as described in "True-Lumen Collapse in Aortic Dissection: Part I. Evaluation of Causative Factors in Phantoms with Pulsatile Flow" in this issue. One model was compliant and opaque, and the other was rigid and transparent. Each of these models simulated type B aortic dissection and had an arch with a branch vessel, a dissected aortic body, three true-lumen abdominal branch vessels, two false-lumen abdominal branch vessels, and a bifurcation with flow to the left limb from the false lumen and flow to the right limb from the true lumen. A reentry branch was added to allow communication between the lumina distal to the bifurcation.

In the rigid, transparent model, four fenestration-branch loops between the true and false lumina were incorporated to simulate natural or artificial balloon fenestrations. Two fenestration loops were proximal to the abdominal branch vessels, and the remaining two fenestration loops were distal to them. These models were placed in a pulsatile mock-flow loop, with water as the working fluid.

In part I, we observed the morphology of the true lumen and the presence or absence of branch-flow compromise in the two phantoms for a large number of pump settings and model configurations. True-lumen collapse was defined as true-lumen obliteration with the associated compromise of flow in a true-lumen branch. The investigated variables were pump parameters (rate and output), patterns of branch-vessel flow distribution (Fig 1), peripheral resistance of the branch vessels, entry-tear size, compliance of the phantom, and communication between the lumina through fenestration-branch loops and the distal reentry branch. As in part I, J.W.C. recorded the observations of the model.



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Figure 1. Diagram shows the patterns of flow distribution in the branch vessels. Solid lines indicate patent vessels, and dotted lines indicate closed vessels. Case 1 has equal flow distribution, with an equal number of branch vessels from the true and false lumina. Case 2 has increased true-lumen outflow and decreased false-lumen outflow by one branch each. Cases 3 and 4 have decreased false-lumen outflow due to the closing of an abdominal branch and limb, respectively. In case 5, the false lumen is a blind sac without any outflow.

 
By using the results from part I, the model parameters were set to induce true-lumen collapse and to establish baseline conditions in the model. After inducing true-lumen collapse, we tested the effectiveness of clinically relevant variables in relieving the collapse. These variables included the pattern of branch-vessel flow distribution, flow in the fenestration and distal reentry branches, flow in the arch vessel, pump output, and entry-tear size. To investigate the effect of the branch-vessel flow distribution, the false-lumen outflow was increased by opening a closed false-lumen branch vessel. The effects of flow through the arch vessel, the fenestration branches, and the distal reentry branch were investigated by opening the respective stopcock valves.

In part I, high-output states were defined as those that occurred with low settings for diastolic pressure since the low settings caused greater filling of the pump sac and resulted in higher output with each pump cycle. Low-output states resulted from high settings for diastolic pressure. Occasionally, in cases with high- and low-output collapse, there was no true-lumen collapse with the midrange diastolic-pressure settings. If there was a range of pump output in which true-lumen collapse could not be induced, attempts were made to relieve the collapse associated with high and low pump output by adjusting the pump output to the level of the "safe" midrange window.

Finally, we tested the effect of closing the entry tear by placing a stent-graft over the primary entry tear. For this purpose, a 7-cm–long, 30-mm–diameter stent-graft (Prograft Medical, Palo Alto, Calif) was introduced into the model at a point just proximal to the transparent 90° bend. Purse-string sutures were sewn into each end of the stent-graft, and the sutures were brought out of the model through the arch branch vessel and true limb by using Y-arm adapters. By pulling on each of the sutures, the stent-graft could be collapsed enough to place it over the primary entry tear (Fig 2). Releasing the sutures allowed the stent-graft to expand and cover the entry tear, occluding the flow into the false lumen (Fig 3).



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Figure 2. Photograph shows a 7-cm-long, 30-mm-diameter stent-graft. Purse-string sutures (arrows) placed around each end were inserted into the arch after disconnecting the arch joints. The left suture exited the model at the proximal part through the arch branch. The right suture extended distally through the true lumen and exited the model through a Y-arm adapter in the true limb. The stent-graft was collapsed at both ends by pulling the ends of the sutures.

 


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Figure 3. Photograph shows the placement of the stent-graft during pump operation just before the sutures were released. The proximal end (arrow) of the stent-graft is still collapsed.

 
We also investigated the differences between the effects of each variable on the prevention and relief of true-lumen collapse. To do this, we observed the baseline true-lumen status at settings that prevented true-lumen collapse. Next, model parameters were changed to induce true-lumen collapse. Finally, the preventative conditions were restored to determine if the true-lumen collapse was relieved.


    RESULTS
 TOP
 Abstract
 Introduction
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
Tables 1 and 2 summarize the baseline true-lumen status according to the pattern of branch-vessel flow distribution, the diastolic pressure of the pump (pump output), and the patency of the distal reentry communication and arch vessels. (Abbreviations used in the tables appear in the Key Box.) In the baseline status of case 5, there was a safe window for pump output without true-lumen collapse. Patent false-lumen exit branches (case 3 in Table 1 and cases 2–4 in Table 2) effectively prevented true-lumen collapse (compression) in high-output states but not in low-output states. (True-lumen collapse in high-output cases can also be thought of as true-lumen compression since the flow into the false lumen squeezes or compresses the true lumen, making it smaller.) In Tables 1 and 2, cases with patent distal reentry communication and arch vessels showed only small differences, compared with the baseline cases.


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TABLE 1. Baseline Status of the True-Lumen Branches
 

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TABLE 2. Baseline Status of the True-Lumen Branches
 

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Key Box for Abbreviations Used in Tables
 
Tables 3 and 4 summarize the results after we attempted to relieve true-lumen collapse by changing the model parameters from those in the baseline in case 5 (Tables 1 and 2). Included are the results from changing the branch-vessel flow distribution, opening the distal reentry branch, opening the arch vessel, and adjusting the pump output to the level of the safe window. The creation of false-lumen exit branches was effective at relieving medium-output (Table 3) and high-output (Table 4) true-lumen compression. Opening the distal reentry branch alone had little effect on the true-lumen collapse, but it greatly enhanced the effectiveness of opening the false-lumen branches. Opening the arch vessel showed little additional benefit.


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TABLE 3. Relief of True-Lumen Collapse or Compression in Case 5
 

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TABLE 4. Relief of True-Lumen Collapse or Compression in Case 5
 
Adjusting the pump output—lowering the pump output in cases of high-output compression and increasing the pump output in cases of low-output collapse—did not have any effect on true-lumen collapse. However, when adjusting the pump output was combined with opening the arch vessel, the flow through the first true-lumen abdominal branch improved (Table 3). When it was combined with opening the distal reentry communication, the flow through all three true-lumen abdominal branches was recovered, although the true lumen appeared compressed (Table 3). The combination of adjusting the pump output and opening the second false-lumen abdominal branch resulted in the complete recovery of the collapsed true lumen in both the high- and low-output conditions (Table 3). In the cases with lower peripheral resistance in the true-lumen branches, true-lumen collapse was more difficult to relieve. For instance, complete recovery at all pump settings was achieved only by combining pump adjustment with the opening of the false-lumen and distal reentry branches (Table 4).

Overall, it was more difficult to relieve true-lumen collapse than it was to prevent it. For example, in case 4 in Table 1, high-output true-lumen compression developed when the diastolic pressure of the pump was less than 15 mm Hg. However, when we opened the second false-lumen abdominal branch (which created a branch-vessel flow distribution identical to that of case 4) after complete obliteration of the true lumen, complete recovery of the true lumen could be achieved only in the range of the diastolic-pressure settings from 45 to 55 mm Hg (Table 3).

Tables 5 and 6 summarize the effects of preexistent fenestrations in the aorta and flow in the distal reentry branch. With the small 10-mm entry tear (Table 5), fenestration-branch loops in the aorta were slightly effective at preventing true-lumen collapse in the low-output states. Opening all four fenestration branches prevented compromise of the true-lumen abdominal branches in the cases with diastolic-pressure settings for low-output. In contrast, the presence of a distal reentry communication between the true and false limbs prevented true-lumen collapse not only in the low-output states but also in the high-output states. With a large 30-mm entry tear in case 5 (Table 6), neither aortic fenestrations nor distal reentry communication effectively prevented true-lumen collapse. In case 4 with the large entry tear, distal reentry communication prevented true-lumen collapse better than did aortic fenestration (Table 6).


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TABLE 5. Effect of Preexistent Fenestrations in the Aorta and Distal Reentry Communication
 

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TABLE 6. Effect of Preexistent Fenestrations in the Aorta and Distal Reentry Communication
 
Creating an aortic fenestration was ineffective at relieving true-lumen collapse, whereas opening the distal reentry branch was successful (Table 7). By comparing the results in Tables 5 and 7, aortic fenestration was better suited for the prevention of true-lumen collapse than for its relief.


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TABLE 7. Relief of True-Lumen Collapse or Compression from Opening the Fenestrations in the Aorta and Distal Reentry Communication
 
Table 8 summarizes the results of placing a stent-graft over the primary entry tear during the operation of the pump. Stent-graft placement effectively relieved true-lumen collapse, especially in the cases without communication between the true and false lumina or in the cases with communication through only the distal reentry branch. When there was no outflow from the false lumen (case 5), the presence of fenestrations in the aorta impeded the complete recovery of the true lumen. When all four fenestration-branch loops were open, it was impossible to relieve true-lumen collapse in case 5 with the high-output states.


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TABLE 8. Effect of Closing the Entry Tear with a Stent-Graft to Relieve True-Lumen Collapse
 

    DISCUSSION
 TOP
 Abstract
 Introduction
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
The optimal therapeutic approach for patients with aortic dissection complicated by branch obstruction has not been established. The primary surgical treatment is resection of the primary entry tear in the thoracic aorta with redirection of the blood flow, preferentially into the true lumen. Repair of the thoracic aorta was reported to reverse peripheral pulse deficits (lower limb ischemia) in about 90% (44 of 48) of patients (4).

Uncomplicated acute type B dissections are usually medically managed because the surgical mortality rate for patients with acute type B dissection is historically high (79) and because the long-term outcome is similar in both medically treated patients and surgically treated patients (8,10,11). If ischemia persists after repair of the thoracic aorta or if the patient is not considered a candidate for surgical repair of the entry tear in the thoracic aorta, revascularization procedures, including surgical fenestration of the aorta with or without graft placement (12) and a variety of direct or extraanatomic bypass operations, have been performed (3,13).

Deficits in the peripheral pulses are usually successfully managed with surgical repair of the thoracic aorta, surgical fenestration of the aorta, or femorofemoral bypass, without a substantial increase in surgical mortality. In cases of mesenteric or renal ischemia, the surgical mortality rate is very high (50%–80%) despite an aggressive surgical approach with repair of the thoracic aorta and direct revascularization of the obstructed vessels (3,4). Therefore, patients with mesenteric and renal ischemia are considered higher-risk candidates for surgery. Recently, endovascular treatment with balloon fenestration and stents was introduced. With this percutaneous management strategy, revascularization of the obstructed vessels is successful in more than 90% of patients; the procedure-related mortality rate is 25% or less (1,6,14).

The rational treatment for aortic-branch compromise in aortic dissection is predicated on an understanding of the mechanisms involved. Recently, two distinct mechanisms for branch ischemia were clarified. One is static obstruction due to direct propagation of the dissection into the branch vessel; the other is dynamic obstruction due to collapse of the aortic true lumen (15). Static obstruction of the branch arteries can be best managed with direct revascularization of the obstructed vessel by means of an endovascular stent or a bypass graft. For dynamic obstruction, there are many available treatment options, including surgical repair of the primary entry tear, surgical fenestration of the aorta, placement of a bypass graft to reperfuse the threatened organ or limb, and placement of endovascular stents and balloon fenestration of the dissection flap. Until now, these treatments were performed without verification of their effect in experimental studies and without a clear understanding of the hemodynamics in a double-barreled aorta.

In these experiments, with progressive augmentation of the causative factors for true-lumen collapse, compromise of aortic-branch flow initially occurred distally in the lower-limb vessels. This subsequently propagated to include the proximal abdominal vessels. According to the results of this experiment, isolated lower-limb ischemia was the mildest form of true-lumen collapse. In the most severe form of true-lumen collapse, all true-lumen branches were compromised, with negligible flow through them.

The severity of true-lumen collapse is an important determinative factor in the success of the treatment. In the marginal state of true-lumen collapse, minor natural fluctuations in contributing factors—including cardiac output, blood pressure, heart rate, and peripheral resistance in the branch vessels—can cause or relieve true-lumen collapse. In fact, deficits in peripheral pulses may wax and wane (16) and may be relieved spontaneously after the administration of antihypertensive medications or after retrograde arteriography (13,17,18). The results of our experiment (Tables 3 and 4) clearly showed that the creation of false-lumen outflow and distal reentry communication relieved true-lumen collapse in less-severe borderline cases. However, the extreme cases of true-lumen collapse were very difficult to treat and were resistant to these medical interventions.

Among the investigated variables, the most effective way to relieve true-lumen collapse was to obliterate the entry tear with the placement of a stent-graft. This result reinforced the rationale and the effectiveness of the current surgical approach in clinical practice to repair the thoracic aorta and suggested that procedures with stent-grafts can be effective alternatives to surgery for the treatment of true-lumen collapse in type B dissection.

The creation of a false-lumen outflow branch effectively relieved high-output compression of the true lumen. Currently, it is commonly thought that the compromised branch should be revascularized from the true lumen. However, according to the results of this experience, revascularization of the obstructed true-lumen branch increased the true-lumen outflow and exacerbated true-lumen collapse. Williams et al (19) presented data from a patient in whom sudden restoration of true-lumen outflow resulted in true-lumen collapse and a profound systolic-pressure deficit. Therefore, in the setting of true-lumen collapse, if an aortic branch is dissected and is supplied by both the true and false lumina, revascularization of the branch from the false lumen is recommended to relieve true-lumen collapse.

Distal reentry communication between the true and false limbs also had a positive effect on true-lumen collapse. When the entry tear was closed with a stent-graft, the cases with distal reentry flow showed better results than those with fenestration-branch loops between the true and false lumina in the aorta (Table 8). The distal reentry communication used in our experiment better resembled a femorofemoral bypass graft than an actual distal reentry communication created with endovascular techniques in a clinical situation. This result suggests a femorofemoral bypass can be used to treat isolated limb ischemia, with the possible beneficial effect of relieving true-lumen collapse.

As an endovascular technique, balloon fenestration has been a first-line treatment for true-lumen collapse. Surprisingly, the results of our experiment do not support the effectiveness of the procedure. One possible explanation is that the effect of aortic fenestrations was investigated in a noncompliant, rigid phantom that was different from the human aorta. There is also the possibility that the simulated fenestration-branch loops may not have accurately represented the fenestrations in the dissection flap. We used 7.9-mm–internal diameter tubing for the fenestration-branch loops, which may have been too small. In part I of our experiment, we investigated the effect of the size of the distal reentry communication and found that a larger reentry communication more readily relieved true-lumen collapse. Despite the limitations of our models, the effect of creating an aortic fenestration is considered to be smaller than that of establishing a distal reentry communication, if they are the same size.

Clinical experience also shows that balloon fenestration alone is successful in relieving true-lumen collapse in less than 50% of the patients (1,6). At best, fenestration abolishes the pressure gradient between the true and false lumina. Because of the elastic recoil within the dissection flap, the true-lumen does not reexpand throughout its length, even after successful fenestration (1). Consequently, it is often necessary to buttress the open true lumen with intravascular stents (1,6,14).

A question that requires further study is, what determines the ideal position for balloon fenestration? Fenestration at the supraceliac aorta has been frequently performed with some success (14,20). Williams et al (1) recommend the creation of fenestrations at the level of the compromised vessel. In our experiments, it was difficult to compare the relative effectiveness of the different fenestration sites in relieving true-lumen collapse because the fenestration itself showed little salutary effect. However, when we opened the fenestration-branch loops proximal to the abdominal branch vessels after complete obliteration of the true lumen, the flow direction through the loops proceeded from the true lumen to the false lumen. This suggests that proximal fenestration loops may have acted as additional entry tears, effectively increasing the surface area of the primary intimal tear.

Although true-lumen collapse was not relieved when the fenestration loops distal to the abdominal branch vessels were opened, the flow through the loops proceeded from the false lumen to the true lumen, which indicated that the distal fenestration loops may have acted to decompress the false lumen. In addition, the distal fenestration was better at preventing true-lumen collapse. The results of these experiments also suggest that fenestration should be performed at or below the level of the compromised vessels, preferably just above the iliac bifurcation. Fenestration above the level of the celiac artery is not advisable.

In conclusion, findings from this study suggest that there are two complementary principles in the treatment of true-lumen collapse in aortic dissection: Decrease the flow into the false lumen, and increase the flow from it. Surgical repair of the thoracic aorta and coverage of the entry tear with a endovascular stent-graft fulfill the former principle. The latter principle can be achieved with balloon fenestration of the obstructing dissection flap at the level of the orifices in the compromised vessels and with creation of an outflow channel from the false lumen by using balloon fenestrations or intravascular stents.Practical applications: These in vitro experiments demonstrate that there are two kinds of true-lumen collapse in low- and high-output states, with an intermediate "safe window" of pump output between the two states that was not associated with the induction of true-lumen compromise. Once established, an adjustment of the pump output alone did not relieve true-lumen collapse. However, when it was combined with opening the distal reentry communication or with creating outflow from the false lumen, there was a remarkable improvement in the collapsed true lumen.

The successful translation of these in vitro observations to clinical application requires the definition of whether true-lumen collapse in a particular human aortic dissection belongs to the high-output compression variety or to the low-output collapse variety. Further investigations are necessary to clarify the roles of heart rate, blood pressure, and cardiac output in true-lumen collapse in aortic dissection and how manipulations of these physiologic parameters may prove to be clinically beneficial.

On the basis of the results of these experiments and on accumulated clinical experiences, it is possible to propose a new protocol for the endovascular treatment of true-lumen collapse in type B aortic dissection. Placement of a stent-graft over the primary entry tear can stand alone as a definitive treatment. If stent-graft placement is not feasible or indicated, there are other options. Isolated unilateral lower-limb ischemia purely due to true-lumen collapse may be managed with balloon fenestration alone at the level of the iliac bifurcation. If there is a severe true-lumen compression associated with compromised flow to the lower limbs and abdominal branches, it can be treated with distal balloon fenestration of the dissection flap at the level of the aortic bifurcation. If the dissection directly extends into an aortic branch, any compromise in the flow to the branch associated with the true-lumen collapse is best managed with revascularization of the branch from the false lumen by using intravascular stents. If these maneuvers fail to relieve the true-lumen collapse, a stent may be placed in the true lumen of the aorta.


    Footnotes
 
2 Current address: Department of Radiology, Seoul National University College of Medicine, Seoul, Korea. Back

See also the article by Chung et al (pp 87–98 ) in this issue.

Author contributions: Guarantor of integrity of entire study, M.D.D.; study concepts, J.W.C., C.E., T.S., M.D.D.; study design, J.W.C., C.E., T.S., N.K., M.D.D.; definition of intellectual content, J.W.C., C.E., M.D.D.; literature research, J.W.C.; experimental studies, J.W.C., C.E., T.S., N.K., T.V.; data acquisition, J.W.C., C.E., T.S., N.K., T.V.; data analysis, J.W.C., C.E., M.D.D.; manuscript preparation, J.W.C., C.E., M.D.D., C.P.S., S.M.S.; manuscript editing and review, C.E., M.D.D., C.P.S., S.M.S.


    References
 TOP
 Abstract
 Introduction
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 

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D. Bockler, H. Schumacher, M. Ganten, H. von Tengg-Kobligk, M. Schwarzbach, C. Fink, H.-U. Kauczor, H. Bardenheuer, and J.-R. Allenberg
Complications after endovascular repair of acute symptomatic and chronic expanding Stanford type B aortic dissections.
J. Thorac. Cardiovasc. Surg., August 1, 2006; 132(2): 361 - 368.e4.
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RadioGraphicsHome page
C. Sebastia, S. Quiroga, R. Boye, M. Perez-Lafuente, E. Castella, and A. Alvarez-Castells
Aortic Stenosis: Spectrum of Diseases Depicted at Multisection CT
RadioGraphics, October 1, 2003; 23(90001): S79 - 91.
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J. Thorac. Cardiovasc. Surg.Home page
N. Kato, T. Shimono, T. Hirano, T. Suzuki, M. Ishida, H. Sakuma, I. Yada, and K. Takeda
Midterm results of stent-graft repair of acute and chronic aortic dissection with descending tear: The complication-specific approach
J. Thorac. Cardiovasc. Surg., August 1, 2002; 124(2): 306 - 312.
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Am. J. Roentgenol.Home page
J. Sailer, P. Peloschek, T. Rand, M. Grabenwoger, S. Thurnher, and J. Lammer
Endovascular Treatment of Aortic Type B Dissection and Penetrating Ulcer Using Commercially Available Stent-Grafts
Am. J. Roentgenol., December 1, 2001; 177(6): 1365 - 1369.
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