Correspondence *Department of Medical Imaging, St Vincent's Hospital Melbourne, 41 Victoria Parade, Fitzroy, Victoria 3065, Australia

Email mossoppj@svhm.org.au

The case

A 40-year-old male with a background history of poorly controlled hypertension presented to his local hospital with sudden onset chest and back pain. Two years previously he had been diagnosed with an uncomplicated acute type B aortic dissection. He was managed conservatively, with antihypertensive therapy using candesartan (an angiotensin II receptor antagonist) and atenolol (a -blocker), in conjunction with 6-monthly surveillance CT scanning. This demonstrated progressive dilatation of the proximal descending thoracic aorta from 4.5 to 5.5 cm in diameter during the initial 18 months of follow-up. Six months later, the patient deteriorated clinically, with the recurrence of severe back and chest pain, suggestive of redissection. He was therefore referred to a teaching hospital for further evaluation and management.

On presentation the patient was hypertensive (260/130 mmHg), anuric and experiencing significant chest pain. Lower limb perfusion was compromised, with weak pedal pulses. Laboratory evaluation confirmed acute renal impairment, with a serum creatinine level of 0.26. A prominent aortic knuckle and a moderate left-sided pleural effusion were detected on chest radiography.

Multislice CT imaging using the SOMATOM Sensation Cardiac 16 scanner (Siemens, Erlangen, Germany) confirmed marked aneurysmal change, with a maximal proximal descending thoracic aortic diameter of 6.5 cm (Figure 1A). In addition, dynamic obstruction of the infrarenal aortic true lumen was evident, with hypoperfusion of the renal arteries and downstream aorta (Figure 1B).

Figure 1 Multislice CT performed upon transfer of the patient to a teaching institution, 2 years after the initial diagnosis of aortic dissection.

(A) Progressive dilatation of the descending thoracic aorta was evident, with a maximal transverse diameter of 6.5 cm. (B) Abdominal CT demonstrated narrowing of the aortic true lumen, with renal malperfusion.

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Emergent surgical reconstruction of the aorta was considered; however, this was felt to carry an unacceptably high risk of mortality, given the patient's unstable condition with organ malperfusion. Endovascular aortic reconstruction was, therefore, decided upon, with a view to endograft placement over the primary entry tear aimed at preventing rupture, expansion of the true lumen and reperfusion of the renal and infrarenal aortic segments.

Angiographic evaluation revealed a high-flow primary entry tear just distal to the left subclavian artery, with severely compromised abdominal aortic and renal artery perfusion (Figure 2A and B).

Figure 2 Angiographic evaluation of the patient before and after endograft implantation.

(A) A high-flow primary entry tear was identified, just distal to the origin of the left subclavian artery. (B) Dynamic and static obstruction of abdominal aortic and renal flow, with near-static renal perfusion.

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The first stage of endovascular repair involved implantation of a 34 mm diameter, Zenith® TX2™ THORACIC TAA Endovascular Graft (Cook Inc., Bloomington, IN), under transesophageal echocardiography and angiographic guidance. This covered the origin of the subclavian artery and the primary entry tear, thereby eliminating inflow into the proximal thoracic false lumen. As part of the same procedure, stenting of the statically obstructed left renal artery ostium was performed to enable re-establishment of left renal artery inflow. The patient made satisfactory recovery after the procedure, both in terms of dramatically reduced levels of pain and successful reperfusion of the lower limbs. Urine output was re-established and renal function normalized after 4 days.

Follow-up CT scan at 1 week showed thrombosis of the upper thoracic false lumen, but persistent false lumen perfusion distally with reduced true lumen caliber. To address this, bare Z-stents (Figure 3) were inserted into the aortic true lumen to promote true lumen remodeling and distal flow. Follow-up CT examination at 1 month demonstrated thrombosis of the thoracic aortic false lumen; however, the abdominal aortic false lumen remained patent because of persistent re-entry tears in the infrarenal aorta and the left common iliac. Obliteration of these re-entry tears by covered stent-graft implantation and coil embolization induced thrombosis of the abdominal false lumen.

Figure 3 Aortic model showing Zenith® TX2™ THORACIC TAA Endovascular Graft within the proximal descending aorta, in combination with the bare Z-stent system within the distal thoracic aorta.

 

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One year later, the patient remained well and asymptomatic. Total false lumen thrombosis was maintained, and significant remodeling of the aortic true lumen had occurred (Figure 4). The patient remains under close follow-up CT surveillance and is receiving aggressive antihypertensive therapy.

Figure 4 Three-dimensional CT scan, performed 1 year after staged endovascular repair, demonstrating remodeling of the thoracoabdominal aorta and its branch vessels.

 

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Discussion of diagnosis

Aortic dissection is a catastrophic condition, with an annual incidence of 10–20 per million.^{1, 2} Without appropriate treatment, it has a mortality rate of up to 72 percent at 48 hours.^{3, 4} Etiological factors include chronic hypertension, trauma and aortic wall degeneration secondary to hereditary connective tissue disease, intramural hematoma and penetrating ulcers.⁵

Diagnosis of acute type B dissection is frequently dependent on a high index of clinical suspicion, because findings on baseline investigations, including electrocardiogram and chest radiography, are usually nonspecific.¹ The first-line imaging methods for aortic dissection are transesophageal echocardiography⁶ and multislice CT, dependent upon availability. Both these modalities provide a high diagnostic sensitivity and specificity.¹ Multislice CT allows multiplanar, three-dimensional assessment of the aortic dissection flap, false lumen flow, site of primary and secondary entry tears, and the extent of visceral and cerebral malperfusion.¹

Treatment and management

Conservative management in the form of analgesia and aggressive blood pressure control, to achieve a target systolic pressure of less than 110 mmHg, is the mainstay of therapy for acute type B dissection, with intervention reserved for complicated cases.⁴ This approach is based on the observation that mortality rates of less than 10% can be achieved with pharmacotherapy alone, in contrast to a 50–60% mortality rate seen with early surgical intervention for acute type B dissection.⁴ The prognosis, however, is poor for chronic type B dissection managed conservatively. Persistent false lumen perfusion can lead to progression of dissection and aneurysmal dilatation of the aorta, with complications such as rupture and organ malperfusion secondary to branch vessel compromise occurring in 30% of cases.^{7, 8, 9, 10}

In response to the high morbidity and mortality associated with surgical aortic replacement, especially in the presence of visceral ischemia, endovascular management of acute and chronic aortic dissection was pioneered in the past decade, with reported survival rates as high as 100%.^{11, 12, 13} The traditional approach to endovascular repair of type B dissection involves placement of a stent graft across the primary entry tear with the aim of depressurizing the false lumen with induction of proximal false lumen thrombosis. Because of re-entry tears or intimal fenestrations related to branch vessels, however, false lumen flow often persists in the lower thoracic and abdominal aorta, thereby preventing complete thrombosis. The repair is therefore incomplete and the dissection persists, with the potential for aneurysmal change, rupture or redissection.

To address the problem of persistent false lumen perfusion, and the complexity of dissection morphology, the novel approach of staged total aortic and branch vessel endovascular reconstruction has been adopted to enable a more holistic repair of the dissected aorta.

The first stage usually involves endograft closure of the primary entry tear and bare Z-stenting of the true lumen, thereby supporting the true lumen and stabilizing the dissection flap. The endograft length is usually 120–150 mm. The extent of bare stenting is determined following endograft placement and is based on the extent of the dissection and any distal true lumen or branch compromise. Stenting may involve the thoracic or thoracoabdominal aorta to ensure that mesenteric vessels are included. The first stage aims to prevent rupture and malperfusion, and is performed under general anesthetic with surgical femoral arteriotomy.

Follow-up surveillance with CT and ultrasonography, usually within 1 week of stage one of the procedure, assesses the extent of false lumen thrombosis and the presence of re-entry tears. Dependent on the clinical setting, secondary entry tears are sealed in a second-stage procedure using a variety of endovascular approaches, usually entailing placement of branch vessel covered stents or short segment aortic endografts. The second stage aims to achieve a more complete aortic repair and is usually performed percutaneously. Because not all patients require this approach, staging of the procedures reduces anesthetic time as well as contrast dose, allows recovery of any end-organ ischemia and allows more considered evaluation of the need for any further interventions beyond primary entry tear closure.

The Z-stent system used is a one-piece cylindrical device constructed from self-expanding stainless steel Z-stent segments sewn together with polyester sutures (TXD systems, William Cook Europe, Bjaeverskov, Denmark). The stent is used as a distal component in combination with the Zenith® TX2™ THORACIC TAA Endovascular Graft (William Cook Europe, Bjaeverskov, Denmark) and is intended to assist remodeling of the dissection by providing support to delaminated segments of the aorta (Figure 3). The stent is available in multiple lengths (70–130 mm).

Although total aortic and branch vessel reconstruction is more involved than the traditional approach, it does not appear, in our experience, to be associated with a greater incidence of procedural difficulties. Aortic Z-stenting appears to be a safe ancillary procedure, which in practice poses no risk to branches fed from the false lumen (for instance mesenteric or intercostal arteries), because flow through fenestrations in the intimal flap persists; furthermore, bare stenting reduces the length of the endografted thoracic aorta, which in turn can reduce the small risk of spinal ischemia. No evidence of Z-stent migration or stent-related intimal trauma has been encountered in our 4-year experience or in previous reports of Z-stent implantation for aortic dissection.^{14, 15} To minimize the theoretical risk of trauma, however, stents are deployed in non-curved segments of the aorta and are self-expanding; additionally, the stents are moderately oversized to provide satisfactory wall apposition.

We have performed this procedure in 25 patients presenting with complicated type B dissection. Induction of false lumen thrombosis in the thoracoabdominal aorta has been achieved in 85% of patients, with reparative aortic remodeling seen on follow-up imaging. In none of these cases has there been evidence of progressive aneurysmal dilatation or other remote-phase complication. In fact, survival at mean follow-up of 2.5 years is 100%.¹⁶

Conclusions

The classical endovascular approach to type B dissection has, therefore, demonstrated advantages over medical treatment; however, it does not address the problem of continued false lumen patency, which in turn promotes remote-phase complications such as progressive aneurismal change. To address this problem, the more holistic staged endovascular repair of both the thoracic and abdominal aorta (the STABLE procedure) can be carried out (Figure 5A–C). This approach permits remodeling to restore normal aortic morphology, and is potentially a future direction for endovascular therapy of aortic dissection.

Figure 5 STABLE (staged thoracoabdominal and branch vessel endoluminal repair) procedure for the treatment of type B aortic dissection.

(A) Native aortic dissection. (B) Post-endograft and bare Z-stent implantation within the true lumen. (C) Covered stent or bare stent reconstruction of branch vessels and re-entry tears, with false lumen thrombosis and remodeling.

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Subject areas under which this article appears: Vascular disease | Intervention