28 3.3 Causative Factors in True-Lumen Collapse

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Contents

3.1 Introduction and Background . . . . 27 3.2 Experiments on the Hemodynamics

of True-Lumen Collapse . . . . 28 3.3 Causative Factors in True-Lumen Collapse . . . . 29 3.4 Effective Treatment for True-Lumen Collapse . . . . 30 3.5 Conclusions . . . . 31

3.1 Introduction and Background

Aortic dissection is the most frequent nontraumatic ca- tastrophe that affects the aorta, with an annual inci- dence exceeding that of spontaneous rupture of aortic aneurysms [1]. Aortic dissection occurs with a fre- quency of 10±20 cases per million population per year.

Approximately 30% (85 of 272 [2], 106 of 325 [3]) of patients with aortic dissection have one or more ischemic complications of the peripheral vasculature, including stroke, paraplegia, loss of peripheral pulses, and compromised renal or mesenteric perfusion. The surgical mortality rates for patients with acute aortic dissection complicated by compromise of a peripheral arterial branch exceed 50% [3]; visceral and renal ischemia are important independent predictors of death as a result of surgery [2].

In the past, the direct propagation of a dissection flap into an aortic branch with the resultant compromise or obstruction of the true lumen was considered to be the basic mechanism for ischemic complications in the peripheral vasculature. This understanding was based on observations of cross-clamped or decom- pressed aortas without flow and on findings at ne- cropsy.

Recently, collapse or obliteration of the true lumen was proposed as another important mechanism for compromise of the aortic branch in aortic dissection [4, 5]. This is based on antemortem cross-sectional imaging studies, including those performed with intravascu-

lar ultrasonography, that facilitate an appreciation of the effects of flow on the anatomic relationships between the flap, aortic lumina, and branch vessels [4, 5].

In this setting, the plane of the dissection flap spares the branch vessel. Instead, the flap is positioned in a curtainlike fashion across the origin of the vessel, which causes dynamic obstruction of the branch artery [5].

According to the report by Williams et al. [6], dynamic obstruction due to true-lumen collapse was the cause of the infradiaphragmatic organ or limb ischemia in 20 of 24 patients. Among the 20 patients, 14 had ischemia in multiple organs that involved the mesenteric, renal, and lower-limb circulations. 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, there have been few clinical and experimental studies 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.

Patients with chronic dissection often develop late complications mainly related to the patency of the false lumen [7]. In these cases, there is progressive dilatation of the false lumen that can lead to eventual rupture. An acute aortic diameter of greater than 4 cm in type B dissections has been found to be an indicator of possible future rupture [8, 9]. While some studies suggest medically treating dissections with maximum diameters less than 5 cm[10], others support surgery or placement of stent-grafts when the false lumen is greater than 4 cm[8], 5 cm[11], or 6 cm[12] in order to avoid certain rupture in the future. Obviously, there is considerable uncertainty about the critical diameter of the false lumen and how to treat false lumen aneurysms.

While formation and development of dissections are not well understood, it is generally accepted that hemodynamics plays a major role in the initiation, acute propagation, and chronic development of dissections. In all three of these stages, hemodynamic effects couple with mechanical and biological processes in the arterial walls. It may be some time before the initiation and propagation mechanics of dissection will be understood

Hemodynamics of Aortic Dissection

Chris Elkins and Michael D. Dake

3

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as they involve hemodynamic forces interacting with the aortic wall in both its healthy and its diseased state.

There are many studies of the hemodynamic effects in aneurysmal growth. In most cases, aortic dilatation evolves slowly over several years (1 mm per year [10]) and can be treated medically. Relatively less effort is being spent on understanding the problemof branch vessel ischemia and, in particular, the special case of true-lumen collapse. Yet, this problem is of critical im- portance in both acute and chronic dissection and is highly related to hemodynamics.

3.2 Experiments on the Hemodynamics of True-Lumen Collapse

An in vitro study at Stanford created two aortic dissection phantoms to investigate the causative factors for true-lumen collapse and to develop effective treatments [13, 14]. One phantomwas compliant and opaque (Fig. 3.1), and the other was rigid and transparent

(Fig. 3.2). The rigid, transparent phantomwas created to allow visual observation of the true lumen along the length of the aorta. Each phantomhad the following physical features to model a Stanford type B aortic dissection: an aortic arch, true and false lumens with abdominal branch vessels, and a distal bifurcation. These phantoms were placed in a pulsatile mock-flow loop, with water as the working fluid. The effects of anatomic factors (entry-tear size, branch-vessel flow distribution, fenestrations, distal reentry communication) and physiologic factors (peripheral resistance in the branch vessels, pump output and rate, vascular compliance) on true-lumen collapse were investigated. The morphology of the true lumen was observed. Branch pressures and flow rates were measured.

After true-lumen collapse had been 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

Fig. 3.1. Compliant model of aortic dissection. Compliant and opaque phantommodel of type B aortic dissection with entry tear, true and false lumens, branch vessels, and distal bifurcation. This phantomwas placed in a pulsatile mock-flow loop to observe and measure the effects of a variety of anatomical and physiological factors on branch-vessel flow rates

Fig. 3.2.Rigid model of aortic dissection. Rigid and transparent model of type B aortic dissection allowed visual observation of the true lumen along the length of the aorta. This allowed direct evaluation of the relative effectiveness of altering clinically relevant variables in relieving the complications of dissection with aortic true-lumen collapse

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stent-graft was deployed over the entry tear under physiologic conditions. The difference in the effect of each variable on the prevention and relief of true-lumen collapse was also investigated.

Although not specifically aimed at true lumen collapse, another study used phase contrast MRI to look at the morphology of dissections in 14 patients and to quantify blood flow in the true and false lumens in the descending aorta at the level of the diaphragm[7].

True-lumen collapse was observed in one case: a case with a blind ending false lumen, a lumen with an entry tear but no outlet.

3.3 Causative Factors in True-Lumen Collapse

Findings from the Stanford in vitro experiment demonstrated that the true lumen collapsed with an increase in the size of the entry tear, a decrease in the false-lumen outflow caused by occluding the false-lumen branch vessels, and an increase in the true-lumen outflow created by lowering the peripheral resistance in true-lumen branch vessels.

On the basis of the observations, it is important to consider how easily blood flows into a lumen (inflow capacity) relative to how easily it flows out of a lumen (outflow capacity). A critical parameter is the ratio of inflow capacity to outflow resistance for a given lumen.

In the study, it is hypothesized that the difference between these ratios for the true and false lumens gener- ates a transmural pressure gradient across the dissection flap and that this pressure gradient moves the flap.

Not only was this demonstrated in the phantom experiments, but an example of this is found in the in vivo magnetic resonance data for a dissection with a blind-ending false lumen [7]. In this case, blood flows into both lumens. It stagnates in the false lumen and accelerates through the constricted true lumen. The false lumen has a high inflow capacity but a low outflow capacity (a high ratio), while the true lumen has similar values for its inflow and outflow capacity (a lower ratio). True-lumen collapse occurs in this case because the false lumen has a higher ratio. An alternative expla- nation based on similar principles employs the Bernoul- li principle in which static pressure is traded for fluid velocity. To be strictly correct, some assumptions are required and the instantaneous flows should be compared since the flow is pulsatile, but it is obvious that the stagnated false-lumen flow will have a high pressure, while the accelerated true-lumen flow will have a low pressure. This pressure difference is large enough to move the dissection flap.

Low peripheral resistance in the true-lumen abdominal branches can contribute to true lumen collapse.

Williams et al. [15] presented data from a patient in

whomsudden restoration of true-lumen outflow resulted in a true-lumen collapse and in a profound systolic-pressure deficit. That clinical experience strongly supports the observations that an increase in the true- lumen outflow accelerates true-lumen collapse. Williams et al. [15] also suggest that if false-lumen pressure ex- ceeds true-lumen pressure, an element of true-lumen compression may be added to the intrinsic true-lumen collapse. The Stanford experiment demonstrated the presence of true-lumen compression in cases with high pump output states and confirmed a higher false-lumen pressure in these situations.

In the phantom experiments, observations were compared for steady and pulsatile flow conditions. Pulsatile flow prevented true-lumen collapse in many conditions.

It is believed that this may be related to wave propagation which is a function of phantomcompliance and geometry. There are similar waves in the pulsatile flow within the human vascular system although they are not exactly the same. In light of this, the observations made in the experiment suggest that the regulation of heart rate and systemic pressure may provide a feasible treatment for the prevention of true-lumen collapse in patients with dissection.

An evaluation of the effects of the communication channels between the true and false lumens (i.e., fenestrations and reentry tears) showed that a distal communication was better at preventing true-lumen collapse.

The beneficial effect of the fenestrations in the phantom aorta was unexpectedly limited or absent. In fact, fenestrations proximal to the abdominal branch vessels slightly aggravated the true-lumen collapse; this suggests that they may have acted as additional entry tears.

The distal reentry communication between the true and false limbs showed variable effectiveness in preventing true-lumen collapse, depending on its size.

Although the distal reentry communication in our mod- els simulated a distal reentry tear, strictly speaking, it was close to a femorofemoral bypass. Therefore, radiologic fenestrations just above the iliac bifurcation or femorofemoral bypass may mitigate the effects of true-lumen collapse.

In conclusion, true-lumen collapse in aortic dissection was demonstrated in phantoms with pulsatile flow;

it strongly depended on the difference between the ratios of the inflow capacity to the outflow capacity for the true and false lumens. Low peripheral resistance in the true-lumen branches contributed to true lumen collapse. High-output compression of the true lumen de- veloped in the conditions in which the false-lumen outflow was restricted compared with the inflow. Fenestra- tions in the dissection flap proximal to the aortic bifurcation had little effect on true-lumen collapse, whereas distal reentry communications showed a considerable effect in preventing true-lumen collapse.

Practical application: Both the rigid and the compliant phantoms simulated the gross morphology of the

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human aorta. However, there were many differences fromthe human aorta in the compliance of the vascular wall, the hemodynamic characteristics of the pulsatile flow, the viscosity of the working fluid, and the detailed anatomy of the dissection. Therefore, one should be cautious when applying the results to human aortic dissection. The purpose of the study was to give insight into the pathophysiology and treatment of true-lumen collapse in aortic dissection and to motivate further experimental and clinical studies.

3.4 Effective Treatment for True-Lumen Collapse

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 re- ported to reverse peripheral pulse deficits (lower limb ischemia) in about 90% (44 of 48) of patients [2].

Uncomplicated acute type B dissections are usually medically managed because the surgical mortality rate for patients with acute type B dissection is historically high [16±18] and because the long-termoutcome is similar in both medically treated patients and surgically treated patients [17, 19, 20]. Where ischemia persisted after repair of the thoracic aorta or where the patient was 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 [21] and a variety of direct or extraanatomic bypass operations, have been performed [3, 22].

Deficits in the peripheral pulses are usually success- fully 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 [2, 3]. 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 [4, 6, 23].

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 [5].

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 avail- able 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. With experience from the in vitro experiments these treatments are now performed with verification of their effect in experimental studies and with a clear understanding of the hemodynamics in a double-barreled aorta.

In the 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, isolated lower-limb ischemia was the mildest formof true-lumen collapse. In the severest formof 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 factors7including cardiac output, blood pressure, heart rate, and peripheral resistance in the branch vessels7can cause or relieve true-lumen collapse. In fact, deficits in peripheral pulses may wax and wane [24] and may be relieved spontaneously after the administration of antihypertensive medications or after retrograde arteriography [22, 25, 26]. The results of the experiment clearly showed that the creation of false- lumen outflow and distal reentry communication relieved true-lumen collapse in less-severe borderline cases. How- ever, the extreme cases of true-lumen collapse were very difficult to treat and were resistant to these medical inter- ventions.

Among the variables investigated, 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 effec- tively relieved the high pressure in the false lumen compressing the true lumen. Currently, it is commonly thought that the compromised branch should be revas- cularized fromthe true lumen. However, according to the results, revascularization of the obstructed true-lumen branch increased the true-lumen outflow and exa-

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cerbated true-lumen collapse. Williams et al. [15] presented data froma patient in whomsudden 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 the 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 fenestrations between the true and false lumens in the aorta. The distal reentry communication used in the experiment better resembled a femorofemoral bypass graft than an actual distal reentry communication created with endovascular tech- niques 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 the experiment do not support the effectiveness of the procedure. One possible ex- planation is that the effect of aortic fenestrations was investigated in a noncompliant, rigid phantom that was different fromthe human aorta. There is also the possi- bility that the simulated fenestration-branch loops may not have accurately represented the fenestrations in the dissection flap. In the first part of the experiment, it was found that a larger reentry communication more readily relieved true-lumen collapse. Despite the limita- tions of the phantoms, the effect of creating an aortic fenestration is considered to be smaller than that of es- tablishing 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 [4, 6]. At best, fenestration abolishes the pressure gradient between the true and false lumens. Because of the elastic recoil within the dissection flap, the true-lumen does not reexpand throughout its length, even after successful fenestration [6]. Consequently, it is often necessary to buttress the open true lumen with intravascular stents [4, 6, 23].

A question that requires further study is, what deter- mines the ideal position for balloon fenestration? Fenes- tration at the supraceliac aorta has been frequently performed with some success [23, 27]. Williams et al. [6]

recommend the creation of fenestrations at the level of the compromised vessel. In the 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 fenestrations were established proximal to the abdominal branch vessels after com-

plete obliteration of the true lumen, the flow direction through the loops proceeded fromthe true lumen to the false lumen. This suggests that proximal fenestration loops may have acted as additional entry tears, effec- tively increasing the area of the primary entry tear.

Although true-lumen collapse was not relieved when the fenestrations were established distal to the abdominal branch vessels, the flow through the loops proceeded from the false lumen to the true lumen, which indicated that the distal fenestrations may have acted to decompress the false lumen. In addition, the distal fenestration was better at preventing true-lumen collapse.

The results of the 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 fromthis 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 fromit. 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 ob- structing dissection flap at the level of the orifices in the compromised vessels and with creation of an outflow channel fromthe false lumen by using balloon fenestrations or intravascular stents.

Practical applications: 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 false lumen compressing the true lumen variety or to the high true lumen outflow collapsing the true lumen 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.

3.5 Conclusions

Typically in untreated aortic dissection, the blood flow through the true lumen is unidirectional and bidirec- tional in the false lumen, and the false lumen flow has higher irregularity (velocity fluctuations due to vortex- like structures) [7]. True-lumen collapse in type B dissection strongly depends on the ratios of inflow capacity and outflow capacity for both lumens. A higher ratio in the false lumen is characteristic of dissections with true-lumen collapse. Both anatomic and physiologic factors can affect true-lumen collapse.

On the basis of the results of experiments and on ac- cumulated clinical experiences, it is possible to propose

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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. Iso- lated 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 extends directly 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 fromthe 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. Although not investigated here, the stent-grafting of the primary tear may have additional beneficial effects in chronic cases by preventing continued growth of the false lumen since false lumen patency seems to be linked strongly to late complications from aneurysmal growth.

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