Complications of Endovascular Septal Fenestration in the Management of Patients With Aortic Dissection


Introduction

Endovascular fenestration is used to manage complicated aortic dissection in a manner analogous to open surgical septectomy. The intent to create a large communication between the aortic true and false lumina providing free interluminal flow and equalization of pressure differentials. The technique depends on the clinical situation. The two most commonly reported include endovascular balloon septectomy and longitudinal guidewire-mediated septectomy.

Balloon fenestration of the dissection septum is most frequently performed in acute dissection complicated by branch vessel ischemia. The purpose is to create a hole or tear within the septum separating the true and false lumina. This produces a more balanced admixture of blood flow in the aortic lumina and functionally reduces or relieves malperfusion of tissue beds supplied by branch arteries originating from a previously compromised aortic lumen.

Guidewire-mediated longitudinal septal fenestration is typically used in cases of chronic dissection associated with false lumen aneurysm formation within the thoracic and/or abdominal aorta. In the setting of chronic dissection, branch vessel malperfusion is rarely critical, and the role of fenestration therefore has another focus. In selected patients at high risk of open aneurysm repair, endograft placement may offer an alternative therapy. However, the presence of the dissection prevents the graft from obtaining an adequate seal and graft expansion. Consequently, a Type I endoleak commonly occurs.

The intent of a longitudinal fenestration is to divide the septum and to create a uniluminal segment including an appropriate transaortic diameter neck suitable for endograft anchoring around the entire outer circumference of the aorta across both lumina. Now, with the endograft channeling all the blood flow, the aneurysm sac is isolated, thus mitigating the risk of progressive aneurysm enlargement.

Fenestration and Acute Aortic Dissection

Branch vessel malperfusion, caused by acute aortic dissection, is a potentially life-threatening condition if untreated. Mechanisms of branch vessel obstruction secondary to aortic dissection are classified as static, dynamic, or a combination of both. Static involvement is caused by direct extension of the dissection process and the aortic septum into a branch artery resulting in mechanical obstruction. If associated with evidence of critical ischemia, static branch vessel compromise is typically treated by placement of stents within the true lumen of the affected branch.

Dynamic obstruction is caused by prolapse of the dissection septum over branch vessel origins. In cases of acute dissection complicated by dynamic branch vessel malperfusion, compromised flow to critical abdominal and/or leg arteries is frequently a result of false lumen compression of the aortic true lumen (true lumen collapse) that supplies these ischemic branches. When aortic true lumen obliteration exists, there is typically an imbalance in flow and pressure within the two aortic lumina. Often there is a very large primary intimal entry tear, and the resultant false lumen in-flow is frequently greater than its outflow capacity. Consequently, the aortic false lumen diastolic blood pressure is commonly greater than that in the aortic true lumen. In this clinical situation, placement of an aortic stent graft in the true lumen over the primary entry tear results in a dramatic decrease in false lumen in-flow and an almost instantaneous relief of aortic true lumen compromise and the ischemia involving branch arteries originating from it. This is the standard current therapy for so-called “dynamic branch vessel involvement.” However, in cases with unfavorable or unsuitable anatomy for endograft placement or when the appropriate device is unavailable, endovascular septal fenestration is an option. The procedure is performed within the infrarenal aorta where a balloon is inflated across the septum to create a hole or tear. In the setting of acute dissection, this tear is predictably a linear transverse rent in the lamella oriented perpendicular to the longitudinal course of the aorta. The immediate result is a decrease in the resistance to false lumen outflow, increasing flow from the false lumen. This effectively decompresses the aortic false lumen and relieves the upstream compromise affecting branch vessels originating from the true lumen.

The technique is dependent on successfully transgressing the septum—usually from the diminutive, narrowed aortic true lumen to the much larger, dominant false lumen—using a 21-gauge needle directed through a curved, relatively rigid cannula or guide catheter oriented perpendicular to the lamella. Correlation between live fluoroscopy and preprocedural computed tomography (CT) imaging helps to orient the guiding cannula so that it is pointed in the direction of the mid septum. Real-time intravascular ultrasound imaging is invaluable in confirming direction of the needle puncture. Once the needle is advanced 4 mm to 6 mm to cross the septum, a 0.014′′ or 0.018′′ guidewire is advanced until it is well proximal to the level of septal transgression. A 4-French or 5-French catheter is advanced over the needle and guidewire. After their removal, an injection of contrast media is used to confirm successful crossing. A 0.035′′ guidewire is then introduced and the catheter and guiding cannula are removed.

A series of sequentially larger diameter angioplasty balloons are then inflated across the septum. After reaching a diameter of 20–24 mm, aortography is performed to confirm the adequacy of the new communication and the flow to previously compromised branch vessels originating from the aortic true lumen. In most cases, balloon septectomy to the range of diameters previously detailed is sufficient to relieve critical compromise of aortic true lumen branches. This may be difficult to determine definitively intraprocedurally and may require close monitoring of symptoms, blood chemistry studies, and peripheral hemodynamics as appropriate in the immediate postprocedural period before a final determination of whether the fenestration was successful in reversing branch ischemia.

The salutary effect in terms of true lumen enlargement on CT imaging following balloon fenestration is never as dramatic anatomically as that observed following aortic stent graft placement of the primary entry tear, but physiologically, an improvement in true lumen flow is usually evident when the aortic fenestration is performed distal to the involved branches as opposed to more proximally in the distal thoracic segment. A balloon fenestration proximal to the involved abdominal branches should be avoided because it acts as a secondary entry tear and may exaggerate the imbalance in flow between the lumina and do little to alleviate aortic true lumen obliteration in the abdomen.

If the clinical outcome is deemed inadequate, supplemental revision may be undertaken. This may involve placement of a large self-expanding noncovered metallic stent across the fenestration, such as a baffle, guiding flow proximal in the aortic false lumen to distally in the true lumen via the existing fenestration. A large 20–24 mm diameter Wallstent (Boston Scientific Inc., Watertown, Massachusetts) that is between 40 mm and 80 mm long is frequently selected to serve as a frame to buttress open the fenestration and improve the desired hemodynamic effect.

Alternatively, the balloon fenestration may be extended or a new communication created longitudinally using a guidewire-mediated septectomy. This procedure is more commonly used in chronic dissections to create a segmental uniluminal channel. This technique is described later. Both methods are usually successful in reversing symptoms in the majority of acute dissection patients unresponsive to balloon septectomy alone.

In a study by Park et al., 16 patients received aortic fenestration and/or branch stenting as treatment; 30-day mortality was 8.3% and branch vessel malperfusion improved in 90%, although there was also expansion of the outer aortic diameter at 1-year follow-up.

In a study by Midulla et al., 35 patients with aortic dissections were treated with endovascular fenestration. All were technically successful, with 26 patients requiring additional stenting; 30-day mortality was 34%, 8 of 23 survivors suffered from ischemic complications, and all patients had a patent false lumen.

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