Static Branch Involvement

One manifestation that may arise when the advancing dissection septum intersects an aortic branch is static branch vessel involvement (Fig. 36-4). In static involvement, the aortic dissection flap extends directly into the branch for a variable distance. In contrast to the geometry described earlier, orientation of the septal trajectory is such that the branch ostium is incompletely engaged by the edge of the dissection plane. Rather than being circumferentially shorn by the septum, there is only partial circumferential involvement of the branch by the dissection. The aortic flap extends into the branch, creating a false lumen within the artery. As a result, the individual branch has both a true and false lumen like the aorta.

Figure 36-4 Magnetic resonance imaging (MRI) of static branch vessel involvement of iliac arteries.

A, Coronal image of pelvis identifies a flap extending into right common iliac artery (CIA) and down to distal external iliac artery (EIA). Flow is evident in both true and false lumens within the right iliac artery. This is an example of static involvement with direct flap extension from the aorta into a branch. At the end of the dissection within the EIA, there is a distal reentry tear. This terminal tear establishes double-barrel flow within the iliac artery, which is rarely associated with ischemic symptoms. B-C, Similar coronal views show flap extension into left iliac system, but a segmental flow void (black segment) within false lumen of left CIA. This is associated with a no-reentry situation at distal extent of false lumen. No reentry within a branch is typically associated with obstruction of true lumen by a dilated false lumen cul-de-sac. The flow void noted may represent thrombosis in a blind channel or simply no blood flow. The usual consequence of this phenomenon of no reentry is branch vessel ischemia due to a lack of false lumen perfusion and compromised true lumen branch flow.

Similar to the aorta, a branch affected by static involvement may have multiple fates. At the end of the dissection where the flap terminates in the branch, a reentry tear in the false lumen may or may not occur. If a reentry tear occurs at the end of the false lumen, branch perfusion results from blood flow in both the true and false lumens. In many such cases, dual lumen perfusion is not associated with ischemic branch vessel symptoms. If reentry does not occur in cases of static branch vessel involvement, however, the false lumen within the branch has no outflow. The absence of a distal tear to allow communication with the vascular bed beyond the dissection may impair blood flow significantly. This no reentry state within the branch’s false lumen renders perfusion limited to that contributed by the true lumen. Unfortunately, the true lumen may be compromised by the engorged false lumen. The blind pouch of the false lumen, without outflow, swells to a maximum dimension at its distal end. The pressure exerted by the false lumen severely distorts and compresses the true lumen to markedly reduce branch vessel flow. Commonly, the degree of ischemia experienced by the involved vascular bed may be significant and can lead to irreversible tissue necrosis if not relieved quickly.

In no-reentry situations, a local solution directed at improving flow within the affected artery is required because the problem is localized within the specific branch. Two options for endovascular treatment are possible. Resistance to outflow within the false lumen may be decreased by creating a distal tear or fenestration within the blind channel. This can be accomplished with the end of a guidewire or other endovascular probe placed within the false lumen through the aortic false lumen. This approach is associated with practical challenges, including the avoidance of distal extension of the dissection process, safe penetration of the false lumen wall to create an effective outflow tear, and determination of the presence of thrombus within the blind sac of stagnant false lumen blood to avoid its distal embolization.

In most cases, the preferred strategy involves increasing branch flow by decreasing the resistance to true lumen blood flow. This is performed by placing a stent in the true lumen of the branch through catheterization from the aortic true lumen. The stent is typically placed from beyond the end of the false lumen in the branch back to the aortic true lumen. A self-expanding nitinol stent is commonly employed because this distance is frequently greater than 2 cm and because there is a risk of squeezing any existing clot out of the false lumen with a balloon-expandable stent. These stents are sized to the total transarterial diameter of the branch and allowed to progressively expand on their own (post deployment) without supplemental balloon dilation. There are many successful reports of this approach in mesenteric, renal, and iliac arteries affected by no-reentry or static involvement.^8,9,18,19

Occasionally, static branch vessel involvement with reentry anatomy and double-barrel flow may require endovascular intervention. The most common indication for stent placement in this setting occurs with involvement of a renal artery (Fig. 36-5). The kidney supplied by a dissected renal artery may be affected by the physical presence of a flap within the branch. The variable flow reduction caused by the flap, and resultant disrupted pattern of true and false lumen perfusion, may contribute to an exacerbation of hypertension. In cases where high blood pressure is sustained and recalcitrant to numerous intravenous (IV) medications, endovascular intervention may be warranted to restore a single lumen without flap. The approach to treatment involves placement of a balloon-expandable renal stent within the true lumen of the renal artery through the aortic true lumen. In most cases, this type of reentry involvement does not extend into the branch as far as the no-reentry extension. Thus, stents less than 2-cm long are typically implanted. This technique is well established at most centers that manage cases of aortic dissection frequently.

Figure 36-5 Computed tomography (CT) images of true and false lumen relationships to renal arteries.

Axial (A) and coronal (B) CT images at level of left renal artery show that left renal artery is supplied by the false lumen (left aortic lumen). True lumen is located along right wall of aorta, and flap shows a characteristic natural fenestration or defect corresponding to left renal ostium. Flap around fenestration has small tail-like extensions pointing to the left that represent the initial few millimeters of left renal intimal lining that were torn away with the retracted aortic septum.

Dynamic Branch Involvement

In addition to primary branch pathology that occurs as a complication of aortic dissection, another mechanism, dynamic branch vessel involvement, may be responsible for organ ischemia. Dynamic branch involvement is a phenomenon associated with obstruction to branch vessel flow by an aortic septum that has prolapsed over the branch ostia like a curtain. In contrast to static involvement, where the aortic flap extends directly into a branch, dynamic obstruction occurs as an aortic process exclusively without an associated branch lesion. Propagation of the aortic flap may create a circumferential cleavage of the aortic wall surrounding the branch ostium (Fig. 36-6). Factors associated with this event include the flap trajectory, the resultant orientation of the septal plane proximal to the branch, and the inclusion of the ostium by the cleaved flap as it extends past. In this situation, the dissection septum surrounds the branch ostium as it tears distally. The cleavage plane extends 1 to 2 mm into the branch, and then circumferentially reenters, creating a cylindrical tear, coring out a short segment of the intimal/medial lining of the most proximal aspect of the branch. The septum retracts into the aortic lumen with a fenestration corresponding to the branch orifice. This gives the flap a stencil-like appearance when viewed en face, with the number of holes related to the number of branch vessels involved by this phenomenon. When imaged in an axial plane, the affected artery appears to originate exclusively from the aortic false lumen. Closer inspection usually allows identification of a tear in the flap at the level or adjacent to the level of the branch. The flap often displays small projections angled from the edge of the tear, giving its outline on axial imaging an appearance similar to the contour of a metal rivet, the short-legged extensions corresponding to the amputated proximal lining of the branch.

Figure 36-6 Magnetic resonance imaging (MRI) demonstrates dynamic branch vessel involvement, with aortic true lumen collapse and accompanying static no-reentry obstruction of left common iliac artery (CIA).

A-C, Axial MRI shows wafer-thin crescent-shaped true lumen collapsed against anterior aortic wall at level of visceral arteries. Aortic septum prolapses like a curtain across the origins of branches originating from true lumen, with resultant malperfusion and multiorgan ischemia. D, At the level just below aortic bifurcation, there is marked asymmetry in appearance of CIAs. Lumen of left CIA has a flow void (black circle) due to static involvement without reentry that coexists with the dynamic process observed more proximally.