DOI: 10.1148/rg.25si055513
RadioGraphics 2005;25:S229-S244
© RSNA, 2005
Endovascular Stent-Graft Treatment of Thoracic Aortic Disease1
Gonzalo Garzón, MD, PhD,
María Fernández-Velilla, MD,
Milagros Martí, MD,
Ignacio Acitores, MD,
Fernando Ybáñez, MD and
Luis Riera, MD
1 From the Departments of Radiology (G.G., M.F.V., M.M., I.A., F.Y.) and Vascular Surgery (L.R.), Hospital Universitario La Paz, Paseo de la Castellana 261, 28046 Madrid, Spain. Recipient of a Certificate of Merit award for an education exhibit at the 2004 RSNA Annual Meeting. Received February 28, 2005; revision requested March 30 and received May 16; accepted May 23. The authors discuss an investigational or unlabeled use of a commercial product, device, or pharmaceutical that has not been approved for such purpose by the FDA. All authors have no financial relationships to disclose.
Address correspondence to G.G. (e-mail: gmoll{at}eresmas.com).
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Abstract
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Aneurysmal diseases of the thoracic aorta are life-threatening conditions. In such cases, stent-graft treatment has been proposed as an alternative to surgery. The morbidity and mortality associated with endovascular repair are significantly lower than those associated with open surgery. In the largest surgical series, the mortality ranged from 5% to 20%. In studies of endovascular repair, the 30-day mortality was 0%–20% and the periprocedural stroke rate was 0%–7%. Often, open surgery is prohibited in patients with these high-risk lesions; thus, in many cases endovascular treatment is the only alternative. Thoracic aortic diseases that can be treated with endovascular stent-graft placement include aneurysms, dissection, traumatic rupture, traumatic pseudoaneurysms, intramural hematoma, penetrating atherosclerotic ulcers, and aortic rupture. Thorough preprocedure imaging is essential for selecting patients, choosing the stent-graft devices, and planning the intervention. Prerequisites for endovascular stent-graft placement are an adequate neck for graft attachment and adequate vascular access. When the ascending aorta or aortic arch is involved, surgical and endovascular procedures can be combined and performed simultaneously, allowing treatment of a wider range of cases. An experienced interdisciplinary team is needed to manage such cases.
© RSNA, 2005
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LEARNING OBJECTIVES
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After reading this article and taking the test, the reader will be able to:
- List the various types of diseases that can affect the thoracic aorta.
- Discuss the role of interventional radiologists in management of thoracic aortic diseases.
- Describe the endovascular procedures available for optimal treatment of thoracic aortic diseases.
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Introduction
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Diseases of the thoracic aorta represent life-threatening conditions. Until recently, the only effective treatment for these diseases was surgical graft replacement, involving operations that have rather high morbidity and at times are technically complex (1–3). Despite significant improvement in anesthetic techniques, surgical techniques, and perioperative care, transthoracic aortic surgery carries substantial risks of serious complications and mortality (5%–15% in elective cases and up to 50% in emergency situations) (2–6).
Recently, several reports have demonstrated the safety and efficacy of endovascular stent-graft placement for thoracic aortic disease. These reports have proposed endovascular stent-graft placement as an alternative treatment that can be associated with reduced morbidity and mortality (Table) (2,4,5,27). Also, surgical and endovascular procedures can be combined and performed simultaneously, allowing treatment of a wider range of patients. Thorough preprocedure imaging is essential to select patients for endovascular treatment, to choose the stent-graft devices, and to plan the intervention. An experienced and skillful team is needed to manage these situations. They can be successfully managed by an interdisciplinary team of radiologists and vascular and cardiac surgeons.
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Aneurysmal Diseases of the Thoracic Aorta: Mortality with Open Surgery versus 30-day Mortality with Endovascular Stent-Graft Placement
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In this article, we review the procedure details of endovascular treatment of thoracic aortic diseases, including preprocedure imaging, the stent-graft systems, the endovascular procedure, and follow-up. We discuss and illustrate the imaging findings and treatment options in aortic aneurysms, aortic dissection, traumatic aortic rupture, traumatic aortic pseudoaneurysms, intramural hematoma, penetrating atherosclerotic ulcers, and aortic rupture.
The U.S. Food and Drug Administration has not approved stent-grafts for use in the thoracic aorta at the present time, although thoracic stent-grafts are commercially available worldwide.
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Procedure Details
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Preprocedure Imaging
Computed tomographic (CT) angiography is necessary for exact preprocedure work-up and measurements. At our institution, the standardized protocol consists of an unenhanced CT study and a contrast-enhanced CT study from the thoracic inlet to the femoral artery bifurcation. In some patients in whom the CT examination is not conclusive or further information is needed to plan the endovascular procedure, digital angiography is performed. A graduated 5-F pigtail catheter with radiopaque 1-cm increments is used. An angiogram of the thoracoabdominal aorta and pelvis is obtained to assess the aortic lesion and the vascular access. We wish to highlight the importance of transesophageal echocardiography. Transesophageal echocardiography is very useful for exact visualization of the origin of the aortic lesion, especially in cases of aortic dissection, and allows evaluation of the flow in both the true and false lumina. Because of its ability to provide functional information and its multiplanar capability, magnetic resonance imaging is performed in some cases of aortic dissection.
These techniques permit us to determine the following information: (a) the location of the aortic lesion and its exact anatomy and morphology; (b) the presence of mural thrombus or calcifications; (c) the exact intraluminal measurements of the diameters of the aortic lesion and the aortic segments proximal and distal to it; (d) the relationships of the aneurysm neck with adjacent aortic branch vessels, mainly the left subclavian artery (LSA) and celiac trunk; and (e) the anatomy of the abdominal aorta and the size and tortuosity of femoral and iliac vessels.
Stent-Graft Systems
The dimensions of the stent-graft used are determined on the basis of contrast-enhanced CT images and angiographic images. Stent-grafts are selected according to the aortic diameter and length of the lesion. For optimal fixation, all stent-grafts are oversized in diameter compared with the diameter of the proximal and distal necks of the lesion, by 15%–20% in cases of atherosclerotic aneurysms and by 10%–15% in all other cases.
Two different self-expanding endovascular stent-graft devices have been used in our institution:
- From April 1997 to June 1998, endovascular stent-grafts were individually custom-made for each patient. A stainless steel endoskeleton covered with polytetrafluoroethylene was used.
- From June 1998, available commercially manufactured stent-graft systems of standard measurements were used. The prosthesis consisted of a self-expanding circumferential nitinol stent covered with low-profile polyester.
Prerequisites for Endo-vascular Stent-Graft Placement
When an endovascular stent-graft is considered for a patient with thoracic aortic disease, the following criteria must be considered.
Adequate Neck for Graft Attachment.—
To ensure an adequate neck for safe proximal and distal graft attachment, certain requirements must be met: (a) a minimum length of 15 mm from the aortic lesion, or from the entry site in dissections, to the LSA and to the celiac trunk; (b) maximum aortic landing zone diameter of 40 mm; and (c) absence of circumferential thrombus or atheroma within the landing zone.
If the lesion is too close to the LSA, its origin could be intentionally covered in order to increase the proximal landing zone for the stent-graft (6,27,28). In these cases, patency of both vertebral arteries must be documented before the procedure. In our experience, revascularization was not considered to be primarily necessary and none of our patients developed vertebrobasilar or left arm ischemia. If vertebrobasilar or arm ischemia occurs, secondary revascularization with a carotidosubclavian shunt or transposition can be performed. If the lesion is too close to the origin of the celiac axis, it could be intentionally covered and an aortoceliac bypass could be performed. If the pathologic condition affects the aortic arch and the descending aorta, a combined surgical and endovascular technique is then used.
Adequate Vascular Access.—
Requirements for adequate vascular access are as follows: (a) distal vascular access of a sufficient size and (b) limited tortuosity of the iliac vessels and abdominal and thoracic aorta. Vascular access is preferably gained through surgical exposure of the right common femoral artery. If the femoral arteries are too small or diseased, the common iliac artery or abdominal aorta via a retroperitoneal approach can be used to obtain vascular access (20,29). We attach a 10-mm-diameter Dacron graft to the iliac artery or infrarenal aorta to facilitate introduction of the devices. Whenever those vascular accesses are considered inappropriate, anterograde access through the ascending aorta by direct exposure via median sternotomy can be achieved. A Dacron graft is attached to the anterior aortic wall after minimal surgical aortotomy.
Endovascular Procedure
The endovascular procedure is explained to all patients, and written informed consent is obtained in all cases. All procedures are performed by a team of interventional radiologists and vascular and cardiac surgeons in the operating room with the patient under general anesthesia. The patient is prepared for possible conversion to a surgical emergency intervention, if necessary. In addition to angiography, transesophageal echocardiography is also available to provide useful information for exact positioning of the stent-graft and detection of complications.
Initial Preparation.—
An angiography catheter is inserted through the right brachial artery, and intermittent contrast material injections are made before and during stent-graft deployment (Fig 1). When the lesion is too close to the LSA, an additional catheter is advanced in the ascending aorta via a percutaneous left brachial approach and is used as an adequate landmark for the LSA origin for delivery.
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Figure 1a. Endovascular procedure. (a) Image from digital subtraction angiography (DSA) shows a saccular aneurysm of the descending thoracic aorta. (b) DSA image shows the delivery system positioned at the desired location. The outer sheath is withdrawn for deployment of the stent-graft. (c) DSA image obtained after deployment shows correct positioning of the stent-graft in the descending aorta. (d) Postprocedure DSA image shows complete exclusion of the aneurysmal sac.
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Figure 1b. Endovascular procedure. (a) Image from digital subtraction angiography (DSA) shows a saccular aneurysm of the descending thoracic aorta. (b) DSA image shows the delivery system positioned at the desired location. The outer sheath is withdrawn for deployment of the stent-graft. (c) DSA image obtained after deployment shows correct positioning of the stent-graft in the descending aorta. (d) Postprocedure DSA image shows complete exclusion of the aneurysmal sac.
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Figure 1c. Endovascular procedure. (a) Image from digital subtraction angiography (DSA) shows a saccular aneurysm of the descending thoracic aorta. (b) DSA image shows the delivery system positioned at the desired location. The outer sheath is withdrawn for deployment of the stent-graft. (c) DSA image obtained after deployment shows correct positioning of the stent-graft in the descending aorta. (d) Postprocedure DSA image shows complete exclusion of the aneurysmal sac.
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Figure 1d. Endovascular procedure. (a) Image from digital subtraction angiography (DSA) shows a saccular aneurysm of the descending thoracic aorta. (b) DSA image shows the delivery system positioned at the desired location. The outer sheath is withdrawn for deployment of the stent-graft. (c) DSA image obtained after deployment shows correct positioning of the stent-graft in the descending aorta. (d) Postprocedure DSA image shows complete exclusion of the aneurysmal sac.
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Delivery of the Stent-Graft.—
A hydrophilic guidewire is placed in the aortic arch under fluoroscopic guidance via the elected vascular access. It is then exchanged for a stiff guidewire. After intravenous administration of 5000 IU of heparin sodium, the delivery system is passed over the stiff guidewire and positioned at the proximal end of the aortic abnormality. The exact placement site is selected on the basis of angiographic and transesophageal echocardiography information, considering aortic wall status and diameter at the neck sites. Transesophageal echocardiography is especially useful in cases of aortic dissection, allowing accurate detection of the entry tear and documenting exclusion of the false lumen.
Deployment of the Stent-Graft.—
Once the desired location is reached, the outer sheath is withdrawn to completely deploy the stent-graft. During release of the device, the systolic arterial blood pressure is lowered to 70 mm Hg. If needed, a balloon catheter can then be inflated to achieve full expansion and to anchor the stent to the aortic wall. Additional segments may be deployed distally as necessary to ensure disease exclusion. Completion angiography is performed to confirm proper stent-graft placement and complete disease exclusion and to verify the presence of correct perfusion through the graft without perigraft leakage. After removal of the delivery system, the vascular access is closed by standard surgical closure techniques. No further anticoagulation is administered.
Follow-up
Our follow-up protocol consists of CT performed before discharge, at 6 and 12 months postoperatively, and annually thereafter or whenever complications are suspected. Angiography is performed in cases of suspected complications.
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Aortic Aneurysm
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Aneurysm of the aorta is defined as a permanent localized dilatation of the aorta, involving all three wall layers, that is at least 50% greater than normal (1,30). The incidence of thoracic aortic aneurysms is approximately 6 per 100,000 persons per year (7). The afflicted population is usually elderly and predominantly male. Frequent comorbidities include hypertension, coronary artery disease, obstructive pulmonary disease, and congestive heart failure (8,31). Most aneurysms of the thoracic aorta are atherosclerotic in origin. Other causes are infection (mycotic aneurysms) and cystic medial necrosis (annuloaortic ectasia) (8,30). Atherosclerotic aortic aneurysms commonly appear as fusiform dilatation of the aorta, commonly affecting the descending aorta. Because atherosclerosis affects long segments of the aorta circumferentially, these aneurysms tend to be fusiform rather than saccular.
Thoracic aortic aneurysms have been associated with growth rates ranging from 0.07 cm/y to as rapid as 0.42 cm/y (1,32). The risk of rupture rises with increasing aneurysm size (30). Aneurysm repair is considered when symptoms (chest discomfort, signs of compression on surrounding organs) are present or when the maximum diameter of the sac exceeds 5–6 cm (1,8,27). Surgical repair with a prosthesis graft is the traditional therapy and is associated with perioperative mortality of 5%–20% and substantial morbidity (7–9). Continued refinement of the endovascular approaches has decreased the need for open surgical repair. Published studies have reported 30-day mortality rates that range from 0% to 20% and periprocedural stroke rates of 0%–7% (2,8–13).
Aneurysms affecting the ascending aorta are treated with surgical reconstruction. Aneurysms involving the descending aorta benefit from endovascular stent-graft placement as a less invasive alternative (2,7–11,16,20) (Fig 2). The treatment of aortic arch aneurysm is more complex, and surgical replacement and endovascular stent-graft repair can be combined and performed simultaneously, as a new treatment modality. Various methods have been proposed in the literature, combining endovascular stent-graft implantation with total arch reconstruction or reimplantation of the aortic arch vessels (27,33–35). In one of our patients, who had a syphilitic aneurysm involving the ascending aorta, aortic arch, and descending aorta, we performed a combined surgical-endovascular treatment (Figs 3, 4). The ascending aorta and aortic arch were replaced by an aortic graft. A patch including the origin of the aortic arch branch vessels was anastomosed to this graft, and a stent-graft was anchored to the distal end of the aortic graft to exclude the descending aortic aneurysm.
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Figure 2a. Saccular aneurysm of the descending aorta. CT scans obtained before treatment (a) and 1 year after treatment (b) show shrinkage of the excluded aneurysmal space between the preprocedure and follow-up examinations.
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Figure 2b. Saccular aneurysm of the descending aorta. CT scans obtained before treatment (a) and 1 year after treatment (b) show shrinkage of the excluded aneurysmal space between the preprocedure and follow-up examinations.
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Figure 3a. Combined surgical-endovascular treatment. (a) Drawing shows a long aneurysm involving the entire thoracic aorta. (b) The ascending aorta and aortic arch are replaced by a surgical graft. (c) The proximal end of a stent-graft is anchored to the distal end of the surgical graft. (d) The thoracic aorta is reconstructed by combining surgical and endovascular procedures.
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Figure 3b. Combined surgical-endovascular treatment. (a) Drawing shows a long aneurysm involving the entire thoracic aorta. (b) The ascending aorta and aortic arch are replaced by a surgical graft. (c) The proximal end of a stent-graft is anchored to the distal end of the surgical graft. (d) The thoracic aorta is reconstructed by combining surgical and endovascular procedures.
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Figure 3c. Combined surgical-endovascular treatment. (a) Drawing shows a long aneurysm involving the entire thoracic aorta. (b) The ascending aorta and aortic arch are replaced by a surgical graft. (c) The proximal end of a stent-graft is anchored to the distal end of the surgical graft. (d) The thoracic aorta is reconstructed by combining surgical and endovascular procedures.
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Figure 3d. Combined surgical-endovascular treatment. (a) Drawing shows a long aneurysm involving the entire thoracic aorta. (b) The ascending aorta and aortic arch are replaced by a surgical graft. (c) The proximal end of a stent-graft is anchored to the distal end of the surgical graft. (d) The thoracic aorta is reconstructed by combining surgical and endovascular procedures.
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Figure 4a. Syphilitic aneurysm of the thoracic aorta. (a) DSA image shows aneurysmal involvement of the entire thoracic aorta. (b) CT scan obtained because the patient reported acute chest pain shows thickening of the aortic wall (arrowhead), which was not present at CT performed 2 weeks earlier. (c) Postprocedure CT scan shows a stent-graft inside the dilated aorta. (d) CT scan obtained at 1-year follow-up shows shrinkage of the aneurysmal space.
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Figure 4b. Syphilitic aneurysm of the thoracic aorta. (a) DSA image shows aneurysmal involvement of the entire thoracic aorta. (b) CT scan obtained because the patient reported acute chest pain shows thickening of the aortic wall (arrowhead), which was not present at CT performed 2 weeks earlier. (c) Postprocedure CT scan shows a stent-graft inside the dilated aorta. (d) CT scan obtained at 1-year follow-up shows shrinkage of the aneurysmal space.
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Figure 4c. Syphilitic aneurysm of the thoracic aorta. (a) DSA image shows aneurysmal involvement of the entire thoracic aorta. (b) CT scan obtained because the patient reported acute chest pain shows thickening of the aortic wall (arrowhead), which was not present at CT performed 2 weeks earlier. (c) Postprocedure CT scan shows a stent-graft inside the dilated aorta. (d) CT scan obtained at 1-year follow-up shows shrinkage of the aneurysmal space.
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Figure 4d. Syphilitic aneurysm of the thoracic aorta. (a) DSA image shows aneurysmal involvement of the entire thoracic aorta. (b) CT scan obtained because the patient reported acute chest pain shows thickening of the aortic wall (arrowhead), which was not present at CT performed 2 weeks earlier. (c) Postprocedure CT scan shows a stent-graft inside the dilated aorta. (d) CT scan obtained at 1-year follow-up shows shrinkage of the aneurysmal space.
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Aortic Dissection
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Aortic dissection results from a primary tear in the aortic intima and inner layer of the aortic media that allows blood to gain access to the aortic media (36). Blood may then propagate proximally or distally within the media, creating a double-channel aorta, with an aortic dissection flap dividing the aortic lumen into true and false lumina. Reentrant tears are usually present in the intima, creating additional communication between the true and false lumina in the distal aorta (36). The most important predisposing factor is hypertension (coexistent in 70%–90%) and is more common in distal than proximal dissections. Other predisposing factors for aortic dissection are the congenital disorders of the connective tissue, in particular Marfan syndrome (14).
Dissections are categorized as acute if the patient presents within 2 weeks of onset or chronic if more than 2 weeks have elapsed (14). The Stanford classification scheme centers on whether or not the ascending aorta is involved. Stanford A dissections involve the ascending aorta, with or without descending thoracic aortic involvement. Stanford B dissections are confined to the descending thoracic aorta, beyond the origin of the LSA.
The mortality rate for untreated patients is reported to be as high as 1%–2% per hour during the first 48 hours after development of symptoms (37). If the condition is left untreated, 36%–72% of patients die within 48 hours of diagnosis and 62%–91% die within a week (38).
Specific information is necessary in aortic dissection. Preprocedure imaging techniques permit us to determine the dimensions of the false and true lumina, to locate entry and reentry sites, to document which of the major branch vessels are supplied by the false lumen and which by the true lumen, and to evaluate the diameter and extension of the dissection to the iliac and femoral arteries.
In these patients, we use tapered stent-grafts with narrower distal diameters. Stent-graft placement over the intimal entry tear restores normal blood flow in the true lumen and induces thrombosis of the false lumen (5,39). This may cause visceral ischemia if any of the major branch vessels are supplied by the false lumen. In patients in whom stent-graft placement in the thoracic true lumen does not provide adequate flow to the ischemic vascular beds, additional therapeutic procedures such as branch vessel stent placement, percutaneous balloon fenestration, or aortic stent placement can be performed (39,40).
With stent-graft implantation, aortic stability is induced both by thrombosis of the false lumen and by the stent-induced expansion of the true lumen and mimics the natural healing process (4,38). Incomplete closure at the entry site and nonclotting of the false lumen seem like predictors of a poor prognosis after endoluminal repair (14). However, stent-graft placement can still be advantageous because it may prevent the false lumen from enlarging over time, since systemic blood pressure is no longer transmitted from the aorta through a large primary tear in the intima (5).
Acute Type A Dissection
Patients with acute Stanford type A dissections are best treated with urgent surgical reconstruction of the ascending aorta (5,37,39,41). A new treatment modality emerges in selected patients with entry tears in the descending aorta, in whom surgical replacement of the ascending aorta and endoluminal stent-graft repair of the descending aorta entry sites are combined and performed simultaneously (15,41) (Fig 5). Early intervention may limit extension of the dissection. Regression of the false lumen over time is possible if endovascular exclusion of the entry site and decompression of the false lumen are successful. In some cases, the false lumen regresses until it is no longer apparent.
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Figure 5a. Acute Stanford type A dissection. (a) Pretreatment DSA image shows dilatation of the ascending aorta and opacification of the true (arrows) and false (*) lumina through a wide entry site. (b) Postprocedure DSA image shows the ascending aorta replaced by an aortic graft. With stent-graft deployment in the descending aorta, only the true lumen is evident. (c) CT scan obtained before treatment shows an intimal flap in the ascending and descending aorta (arrows). The false lumen is dilated; the true lumen is compressed and has a crescentic shape. Note the presence of irregular strands (cobwebs) within the false lumen (*). (d) CT scan obtained 3 months after treatment shows the ascending aorta replaced by a graft and the descending aorta replaced by a stent-graft. The false lumen has regressed until it is no longer apparent.
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Figure 5b. Acute Stanford type A dissection. (a) Pretreatment DSA image shows dilatation of the ascending aorta and opacification of the true (arrows) and false (*) lumina through a wide entry site. (b) Postprocedure DSA image shows the ascending aorta replaced by an aortic graft. With stent-graft deployment in the descending aorta, only the true lumen is evident. (c) CT scan obtained before treatment shows an intimal flap in the ascending and descending aorta (arrows). The false lumen is dilated; the true lumen is compressed and has a crescentic shape. Note the presence of irregular strands (cobwebs) within the false lumen (*). (d) CT scan obtained 3 months after treatment shows the ascending aorta replaced by a graft and the descending aorta replaced by a stent-graft. The false lumen has regressed until it is no longer apparent.
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Figure 5c. Acute Stanford type A dissection. (a) Pretreatment DSA image shows dilatation of the ascending aorta and opacification of the true (arrows) and false (*) lumina through a wide entry site. (b) Postprocedure DSA image shows the ascending aorta replaced by an aortic graft. With stent-graft deployment in the descending aorta, only the true lumen is evident. (c) CT scan obtained before treatment shows an intimal flap in the ascending and descending aorta (arrows). The false lumen is dilated; the true lumen is compressed and has a crescentic shape. Note the presence of irregular strands (cobwebs) within the false lumen (*). (d) CT scan obtained 3 months after treatment shows the ascending aorta replaced by a graft and the descending aorta replaced by a stent-graft. The false lumen has regressed until it is no longer apparent.
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Figure 5d. Acute Stanford type A dissection. (a) Pretreatment DSA image shows dilatation of the ascending aorta and opacification of the true (arrows) and false (*) lumina through a wide entry site. (b) Postprocedure DSA image shows the ascending aorta replaced by an aortic graft. With stent-graft deployment in the descending aorta, only the true lumen is evident. (c) CT scan obtained before treatment shows an intimal flap in the ascending and descending aorta (arrows). The false lumen is dilated; the true lumen is compressed and has a crescentic shape. Note the presence of irregular strands (cobwebs) within the false lumen (*). (d) CT scan obtained 3 months after treatment shows the ascending aorta replaced by a graft and the descending aorta replaced by a stent-graft. The false lumen has regressed until it is no longer apparent.
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The stent-graft deployment can represent the endovascular completion of the elephant trunk technique (42,43). Usually, the flow from the distal end of the graft mainly supplies the false lumen because it is easier to introduce the "elephant trunk" into the false lumen rather than into the true lumen, which is usually compressed. The stent-graft is inserted into the distal end of the aortic graft, and the aortic blood flow is redirected into the true lumen (Fig 6).
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Figure 6a. Stanford type A dissection treated with endovascular completion of the elephant trunk technique. (a) DSA image shows the ascending aorta and aortic arch replaced by a graft, the elephant trunk (arrowheads), which mainly supplies the false lumen (*); the true lumen is compressed (arrows). (b) Oblique sagittal reformatted CT scan shows the elephant trunk (arrowheads) connected to the false lumen (*). Note the intimal flap and compression of the true lumen (arrows) by the dilated false lumen. (c) CT scan obtained before the endovascular procedure shows the end of the elephant trunk (arrowhead) connected to the dilated false lumen in the proximal descending aorta. (d) Follow-up CT scan shows complete thrombosis of the false lumen (*).
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Figure 6b. Stanford type A dissection treated with endovascular completion of the elephant trunk technique. (a) DSA image shows the ascending aorta and aortic arch replaced by a graft, the elephant trunk (arrowheads), which mainly supplies the false lumen (*); the true lumen is compressed (arrows). (b) Oblique sagittal reformatted CT scan shows the elephant trunk (arrowheads) connected to the false lumen (*). Note the intimal flap and compression of the true lumen (arrows) by the dilated false lumen. (c) CT scan obtained before the endovascular procedure shows the end of the elephant trunk (arrowhead) connected to the dilated false lumen in the proximal descending aorta. (d) Follow-up CT scan shows complete thrombosis of the false lumen (*).
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Figure 6c. Stanford type A dissection treated with endovascular completion of the elephant trunk technique. (a) DSA image shows the ascending aorta and aortic arch replaced by a graft, the elephant trunk (arrowheads), which mainly supplies the false lumen (*); the true lumen is compressed (arrows). (b) Oblique sagittal reformatted CT scan shows the elephant trunk (arrowheads) connected to the false lumen (*). Note the intimal flap and compression of the true lumen (arrows) by the dilated false lumen. (c) CT scan obtained before the endovascular procedure shows the end of the elephant trunk (arrowhead) connected to the dilated false lumen in the proximal descending aorta. (d) Follow-up CT scan shows complete thrombosis of the false lumen (*).
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Figure 6d. Stanford type A dissection treated with endovascular completion of the elephant trunk technique. (a) DSA image shows the ascending aorta and aortic arch replaced by a graft, the elephant trunk (arrowheads), which mainly supplies the false lumen (*); the true lumen is compressed (arrows). (b) Oblique sagittal reformatted CT scan shows the elephant trunk (arrowheads) connected to the false lumen (*). Note the intimal flap and compression of the true lumen (arrows) by the dilated false lumen. (c) CT scan obtained before the endovascular procedure shows the end of the elephant trunk (arrowhead) connected to the dilated false lumen in the proximal descending aorta. (d) Follow-up CT scan shows complete thrombosis of the false lumen (*).
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Type B Dissection
The preferred treatment for most patients with Stanford type B dissection is medical therapy (5,37,41). Specific cases that are complicated by progression of dissection, impending rupture, refractory hypertension, localized false aneurysm, unremitting chest pain, or end-organ ischemia are typically treated with emergency surgery (5,27,39). However, both surgical and medical management have disappointing results. The current mortality rate among patients who receive medical therapy remains about 20%. The mortality rate for surgically repaired cases is currently about 35% and over 50% for surgical patients presenting with end-organ ischemia (4,5,9).
Over the past years, endoluminal stent-graft placement has emerged as a less invasive alternative with low periprocedural mortality and morbidity, especially in elderly patients with serious coexisting illnesses. Most series document 30-day mortality rates less than 10%, typically occurring only in patients with acute presentation and organ ischemia. These patients are already the highest-risk candidates for any form of surgical intervention (4,9,14,15). In acute dissection, the covering of the intimal entry tear may lead to complete regression of the false lumen until it is no longer apparent and no additional therapeutic procedures may be necessary (Fig 7). In chronic dissections, as the false lumen may be partially thrombosed and the intima is more rigid, exclusion of flow into the false lumen causes thrombosis and partial shrinkage of the false lumen (Fig 8).
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Figure 7a. Acute Stanford type B dissection. (a) DSA image shows a Stanford type B dissection with the false lumen (*) compressing the true lumen (arrows). (b) DSA image shows that the celiac trunk (C) and right renal artery (RRA) are supplied by the true lumen. Note the presence of a reentry tear (arrow) in the abdominal aorta. The left renal artery (LRA) is supplied by the false lumen. (c) Pretreatment CT scan shows that the dissection extends from the origin of the descending aorta, distal to the LSA origin. * = false lumen. (d) Pretreatment CT scan shows that the true lumen is compressed and gives rise to the superior mesenteric artery. * = false lumen. (e) CT scan obtained at 6-month follow-up shows complete regression of the dissection after exclusion of the entry site. (f ) CT scan obtained at 6-month follow-up shows repressurization of the true lumen and shrinkage of the thrombosed false lumen (*).
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Figure 7b. Acute Stanford type B dissection. (a) DSA image shows a Stanford type B dissection with the false lumen (*) compressing the true lumen (arrows). (b) DSA image shows that the celiac trunk (C) and right renal artery (RRA) are supplied by the true lumen. Note the presence of a reentry tear (arrow) in the abdominal aorta. The left renal artery (LRA) is supplied by the false lumen. (c) Pretreatment CT scan shows that the dissection extends from the origin of the descending aorta, distal to the LSA origin. * = false lumen. (d) Pretreatment CT scan shows that the true lumen is compressed and gives rise to the superior mesenteric artery. * = false lumen. (e) CT scan obtained at 6-month follow-up shows complete regression of the dissection after exclusion of the entry site. (f ) CT scan obtained at 6-month follow-up shows repressurization of the true lumen and shrinkage of the thrombosed false lumen (*).
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Figure 7c. Acute Stanford type B dissection. (a) DSA image shows a Stanford type B dissection with the false lumen (*) compressing the true lumen (arrows). (b) DSA image shows that the celiac trunk (C) and right renal artery (RRA) are supplied by the true lumen. Note the presence of a reentry tear (arrow) in the abdominal aorta. The left renal artery (LRA) is supplied by the false lumen. (c) Pretreatment CT scan shows that the dissection extends from the origin of the descending aorta, distal to the LSA origin. * = false lumen. (d) Pretreatment CT scan shows that the true lumen is compressed and gives rise to the superior mesenteric artery. * = false lumen. (e) CT scan obtained at 6-month follow-up shows complete regression of the dissection after exclusion of the entry site. (f ) CT scan obtained at 6-month follow-up shows repressurization of the true lumen and shrinkage of the thrombosed false lumen (*).
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Figure 7d. Acute Stanford type B dissection. (a) DSA image shows a Stanford type B dissection with the false lumen (*) compressing the true lumen (arrows). (b) DSA image shows that the celiac trunk (C) and right renal artery (RRA) are supplied by the true lumen. Note the presence of a reentry tear (arrow) in the abdominal aorta. The left renal artery (LRA) is supplied by the false lumen. (c) Pretreatment CT scan shows that the dissection extends from the origin of the descending aorta, distal to the LSA origin. * = false lumen. (d) Pretreatment CT scan shows that the true lumen is compressed and gives rise to the superior mesenteric artery. * = false lumen. (e) CT scan obtained at 6-month follow-up shows complete regression of the dissection after exclusion of the entry site. (f ) CT scan obtained at 6-month follow-up shows repressurization of the true lumen and shrinkage of the thrombosed false lumen (*).
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Figure 7e. Acute Stanford type B dissection. (a) DSA image shows a Stanford type B dissection with the false lumen (*) compressing the true lumen (arrows). (b) DSA image shows that the celiac trunk (C) and right renal artery (RRA) are supplied by the true lumen. Note the presence of a reentry tear (arrow) in the abdominal aorta. The left renal artery (LRA) is supplied by the false lumen. (c) Pretreatment CT scan shows that the dissection extends from the origin of the descending aorta, distal to the LSA origin. * = false lumen. (d) Pretreatment CT scan shows that the true lumen is compressed and gives rise to the superior mesenteric artery. * = false lumen. (e) CT scan obtained at 6-month follow-up shows complete regression of the dissection after exclusion of the entry site. (f ) CT scan obtained at 6-month follow-up shows repressurization of the true lumen and shrinkage of the thrombosed false lumen (*).
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Figure 7f. Acute Stanford type B dissection. (a) DSA image shows a Stanford type B dissection with the false lumen (*) compressing the true lumen (arrows). (b) DSA image shows that the celiac trunk (C) and right renal artery (RRA) are supplied by the true lumen. Note the presence of a reentry tear (arrow) in the abdominal aorta. The left renal artery (LRA) is supplied by the false lumen. (c) Pretreatment CT scan shows that the dissection extends from the origin of the descending aorta, distal to the LSA origin. * = false lumen. (d) Pretreatment CT scan shows that the true lumen is compressed and gives rise to the superior mesenteric artery. * = false lumen. (e) CT scan obtained at 6-month follow-up shows complete regression of the dissection after exclusion of the entry site. (f ) CT scan obtained at 6-month follow-up shows repressurization of the true lumen and shrinkage of the thrombosed false lumen (*).
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Figure 8a. Chronic Stanford type B dissection. (a) DSA image shows an entry tear (arrow) in the distal descending aorta and injected contrast material in the false lumen. The dissection extends distally into the abdominal aorta. The abdominal branch vessels are supplied by the compressed true lumen. C = celiac trunk, LRA = left renal artery, RRA = right renal artery, SMA = superior mesenteric artery. (b) DSA image obtained after stent-graft placement shows complete exclusion of the false lumen. The flow to all visceral vessels from the true lumen is maintained. (c) Pretreatment CT scan shows compression of the true lumen by the dilated false lumen (*) at the level of the entry site. (d) Pretreatment CT scan shows that the celiac trunk is supplied by the true lumen. Note the partial thrombosis of the false lumen (*). (e) CT scan obtained at 3-month follow-up shows that exclusion of the entry site has led to thrombosis of the thoracic component of the false lumen (*). (f) CT scan obtained at 3-month follow-up shows that the caliber of the abdominal aorta has been reestablished. The false lumen is completely thrombosed (*).
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Figure 8b. Chronic Stanford type B dissection. (a) DSA image shows an entry tear (arrow) in the distal descending aorta and injected contrast material in the false lumen. The dissection extends distally into the abdominal aorta. The abdominal branch vessels are supplied by the compressed true lumen. C = celiac trunk, LRA = left renal artery, RRA = right renal artery, SMA = superior mesenteric artery. (b) DSA image obtained after stent-graft placement shows complete exclusion of the false lumen. The flow to all visceral vessels from the true lumen is maintained. (c) Pretreatment CT scan shows compression of the true lumen by the dilated false lumen (*) at the level of the entry site. (d) Pretreatment CT scan shows that the celiac trunk is supplied by the true lumen. Note the partial thrombosis of the false lumen (*). (e) CT scan obtained at 3-month follow-up shows that exclusion of the entry site has led to thrombosis of the thoracic component of the false lumen (*). (f) CT scan obtained at 3-month follow-up shows that the caliber of the abdominal aorta has been reestablished. The false lumen is completely thrombosed (*).
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Figure 8c. Chronic Stanford type B dissection. (a) DSA image shows an entry tear (arrow) in the distal descending aorta and injected contrast material in the false lumen. The dissection extends distally into the abdominal aorta. The abdominal branch vessels are supplied by the compressed true lumen. C = celiac trunk, LRA = left renal artery, RRA = right renal artery, SMA = superior mesenteric artery. (b) DSA image obtained after stent-graft placement shows complete exclusion of the false lumen. The flow to all visceral vessels from the true lumen is maintained. (c) Pretreatment CT scan shows compression of the true lumen by the dilated false lumen (*) at the level of the entry site. (d) Pretreatment CT scan shows that the celiac trunk is supplied by the true lumen. Note the partial thrombosis of the false lumen (*). (e) CT scan obtained at 3-month follow-up shows that exclusion of the entry site has led to thrombosis of the thoracic component of the false lumen (*). (f) CT scan obtained at 3-month follow-up shows that the caliber of the abdominal aorta has been reestablished. The false lumen is completely thrombosed (*).
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Figure 8d. Chronic Stanford type B dissection. (a) DSA image shows an entry tear (arrow) in the distal descending aorta and injected contrast material in the false lumen. The dissection extends distally into the abdominal aorta. The abdominal branch vessels are supplied by the compressed true lumen. C = celiac trunk, LRA = left renal artery, RRA = right renal artery, SMA = superior mesenteric artery. (b) DSA image obtained after stent-graft placement shows complete exclusion of the false lumen. The flow to all visceral vessels from the true lumen is maintained. (c) Pretreatment CT scan shows compression of the true lumen by the dilated false lumen (*) at the level of the entry site. (d) Pretreatment CT scan shows that the celiac trunk is supplied by the true lumen. Note the partial thrombosis of the false lumen (*). (e) CT scan obtained at 3-month follow-up shows that exclusion of the entry site has led to thrombosis of the thoracic component of the false lumen (*). (f) CT scan obtained at 3-month follow-up shows that the caliber of the abdominal aorta has been reestablished. The false lumen is completely thrombosed (*).
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Figure 8e. Chronic Stanford type B dissection. (a) DSA image shows an entry tear (arrow) in the distal descending aorta and injected contrast material in the false lumen. The dissection extends distally into the abdominal aorta. The abdominal branch vessels are supplied by the compressed true lumen. C = celiac trunk, LRA = left renal artery, RRA = right renal artery, SMA = superior mesenteric artery. (b) DSA image obtained after stent-graft placement shows complete exclusion of the false lumen. The flow to all visceral vessels from the true lumen is maintained. (c) Pretreatment CT scan shows compression of the true lumen by the dilated false lumen (*) at the level of the entry site. (d) Pretreatment CT scan shows that the celiac trunk is supplied by the true lumen. Note the partial thrombosis of the false lumen (*). (e) CT scan obtained at 3-month follow-up shows that exclusion of the entry site has led to thrombosis of the thoracic component of the false lumen (*). (f) CT scan obtained at 3-month follow-up shows that the caliber of the abdominal aorta has been reestablished. The false lumen is completely thrombosed (*).
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Figure 8f. Chronic Stanford type B dissection. (a) DSA image shows an entry tear (arrow) in the distal descending aorta and injected contrast material in the false lumen. The dissection extends distally into the abdominal aorta. The abdominal branch vessels are supplied by the compressed true lumen. C = celiac trunk, LRA = left renal artery, RRA = right renal artery, SMA = superior mesenteric artery. (b) DSA image obtained after stent-graft placement shows complete exclusion of the false lumen. The flow to all visceral vessels from the true lumen is maintained. (c) Pretreatment CT scan shows compression of the true lumen by the dilated false lumen (*) at the level of the entry site. (d) Pretreatment CT scan shows that the celiac trunk is supplied by the true lumen. Note the partial thrombosis of the false lumen (*). (e) CT scan obtained at 3-month follow-up shows that exclusion of the entry site has led to thrombosis of the thoracic component of the false lumen (*). (f) CT scan obtained at 3-month follow-up shows that the caliber of the abdominal aorta has been reestablished. The false lumen is completely thrombosed (*).
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Traumatic Aortic Rupture
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Blunt thoracic aortic injury is a life-threatening situation that occurs as the result of severe deceleration injuries, predominantly during motor vehicle collisions (44). In more than 80% of cases, rupture is complete, through all three layers of the aorta (45). The most commonly injured site is the proximal descending aortic segment, just distal to the LSA (17,45). Of patients with this diagnosis, 57%–94% die at the scene or at an emergency room (16,17,44). For those patients who survive to the emergency room but do not undergo aortic repair, rupture occurs in 33% within 24 hours (44). These data support the standard doctrine of surgical repair performed as expeditiously as possible in order to avoid rupture.
However, the mortality and morbidity from open surgical repair are not insignificant, mainly because traumatic ruptures of the aorta are often associated with extensive accessory lesions due to the nature of the trauma (16,17,44,46). The mortality rate associated with emergent surgery is 15%–50% (16–18), while morbidity occurs in 3%–36% of cases (44). These patients are beneficiaries of a less invasive endovascular procedure (16,17) (Fig 9). The mortality rate associated with endovascular repair is 0%–20% (16–19). The ability to treat patients who are not surgical candidates with a thoracic stent-graft is a definite benefit over conventional surgical treatment.
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Figure 9a. Traumatic aortic rupture after an automobile accident. (a) DSA image shows enlargement of the aortic lumen distal to the LSA origin (arrows). A traumatic aortic rupture was suspected. (b) CT scan shows enlargement of the mediastinum (M), hemothorax (HT), and irregularity of the aortic contour. (c) DSA image obtained after stent-graft deployment shows exclusion of the aortic rupture. (d) CT scan obtained at 6-month follow-up shows the stent-graft covering the origin of the descending aorta. The mediastinum is normal, and the pleural effusion has disappeared.
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Figure 9b. Traumatic aortic rupture after an automobile accident. (a) DSA image shows enlargement of the aortic lumen distal to the LSA origin (arrows). A traumatic aortic rupture was suspected. (b) CT scan shows enlargement of the mediastinum (M), hemothorax (HT), and irregularity of the aortic contour. (c) DSA image obtained after stent-graft deployment shows exclusion of the aortic rupture. (d) CT scan obtained at 6-month follow-up shows the stent-graft covering the origin of the descending aorta. The mediastinum is normal, and the pleural effusion has disappeared.
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Figure 9c. Traumatic aortic rupture after an automobile accident. (a) DSA image shows enlargement of the aortic lumen distal to the LSA origin (arrows). A traumatic aortic rupture was suspected. (b) CT scan shows enlargement of the mediastinum (M), hemothorax (HT), and irregularity of the aortic contour. (c) DSA image obtained after stent-graft deployment shows exclusion of the aortic rupture. (d) CT scan obtained at 6-month follow-up shows the stent-graft covering the origin of the descending aorta. The mediastinum is normal, and the pleural effusion has disappeared.
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Figure 9d. Traumatic aortic rupture after an automobile accident. (a) DSA image shows enlargement of the aortic lumen distal to the LSA origin (arrows). A traumatic aortic rupture was suspected. (b) CT scan shows enlargement of the mediastinum (M), hemothorax (HT), and irregularity of the aortic contour. (c) DSA image obtained after stent-graft deployment shows exclusion of the aortic rupture. (d) CT scan obtained at 6-month follow-up shows the stent-graft covering the origin of the descending aorta. The mediastinum is normal, and the pleural effusion has disappeared.
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Traumatic Aortic Pseudoaneurysm
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If the aorta is only partially transected following a blunt trauma, and if such an injury is not suspected clinically and the patient survives, a localized false aneurysm may subsequently develop over a period of months to years. Pseudoaneurysms represent saccular dilatations that do not contain aortic intima (30). They continue to communicate with the aortic lumen through the tear and tend to expand with time. The most commonly injured site is the aortic isthmus, a segment involved in more than 90% of cases, just distal to the LSA (17). Because chronic traumatic aneurysms are not uniformly stable, they are usually repaired electively. Open-chest surgery for repair of chronic traumatic aneurysm results in a mortality rate of 5%–18% and a morbidity rate of 11%–50% (17).
Endovascular treatment shows excellent mid-term results. In published series, the technical success rate was 100% and no cases of late treatment failure occurred (11,20). The traumatic aortic injury involves a limited portion of the aortic circumference, and the stent-graft is usually fixed to normal aortic walls (11). In some patients, the anatomic situation is disadvantageous for stent-graft deployment because the injured site is just distal to the LSA origin, limiting the landing zone for anchoring a stent-graft. In these cases, covering the LSA origin can increase the fixation site (Fig 10).
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Figure 10a. Posttraumatic aortic pseudoaneurysm. (a) DSA image shows a posttraumatic pseudoaneurysm located close to the LSA (arrow). (b) DSA image obtained after stent-graft deployment shows that the origin of the LSA has been covered (arrow) to extend the proximal anchoring zone. A spontaneous subclavian steal was established (arrowhead) with no signs of vertebrobasilar or left arm ischemia. (c, d) CT scans obtained before treatment (c) and 1 year after treatment (d) show a decrease in the size of the pseudoaneurysm after exclusion. Note the significant calcifications in the aneurysm wall.
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Figure 10b. Posttraumatic aortic pseudoaneurysm. (a) DSA image shows a posttraumatic pseudoaneurysm located close to the LSA (arrow). (b) DSA image obtained after stent-graft deployment shows that the origin of the LSA has been covered (arrow) to extend the proximal anchoring zone. A spontaneous subclavian steal was established (arrowhead) with no signs of vertebrobasilar or left arm ischemia. (c, d) CT scans obtained before treatment (c) and 1 year after treatment (d) show a decrease in the size of the pseudoaneurysm after exclusion. Note the significant calcifications in the aneurysm wall.
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Figure 10c. Posttraumatic aortic pseudoaneurysm. (a) DSA image shows a posttraumatic pseudoaneurysm located close to the LSA (arrow). (b) DSA image obtained after stent-graft deployment shows that the origin of the LSA has been covered (arrow) to extend the proximal anchoring zone. A spontaneous subclavian steal was established (arrowhead) with no signs of vertebrobasilar or left arm ischemia. (c, d) CT scans obtained before treatment (c) and 1 year after treatment (d) show a decrease in the size of the pseudoaneurysm after exclusion. Note the significant calcifications in the aneurysm wall.
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Figure 10d. Posttraumatic aortic pseudoaneurysm. (a) DSA image shows a posttraumatic pseudoaneurysm located close to the LSA (arrow). (b) DSA image obtained after stent-graft deployment shows that the origin of the LSA has been covered (arrow) to extend the proximal anchoring zone. A spontaneous subclavian steal was established (arrowhead) with no signs of vertebrobasilar or left arm ischemia. (c, d) CT scans obtained before treatment (c) and 1 year after treatment (d) show a decrease in the size of the pseudoaneurysm after exclusion. Note the significant calcifications in the aneurysm wall.
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Intramural Hematoma
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Intramural hematoma is characterized by hematoma formation within the medial layer of the aortic wall in the absence of an associated intimal tear (21). It is probably caused by spontaneous rupture of the aortic vasa vasorum with propagation of subintimal hemorrhage (47,48). This hemorrhage weakens the aorta and may progress to outward rupture of the aortic wall or inward disruption of the intima, the latter leading to communicating aortic dissection. Atherosclerosis and hypertension are predisposing factors, but hematoma can develop in normal vessels (23).
Mortality from intramural hematoma in the first 3 months of evolution is high (19%) (49). The mortality of intramural hematoma with involvement of the ascending aorta has been considered to be similar to that of aortic dissection; thus, early surgical graft repair is the standard treatment in these patients (21,49). Asymptomatic patients with involvement of the descending aorta can be monitored closely during medical treatment, with intervention reserved for patients who develop complications such as persistent pain, penetrating atherosclerotic ulcer, signs of impending rupture, progressive maximal aortic wall thickness and compression of the true lumen, enlarging aortic diameter, or compromise of a major arterial branch (21,47,48).
Conventional open repair is associated with high morbidity and mortality rates, especially in this complicated setting in patients who typically are not ideal surgical candidates because of advanced age and/or coexisting medical diseases. Published 30-day mortality after open surgery is reported to range from 10% to 50% (21,22). Less invasive strategies that rely on endovascular placement of stent-grafts to cover the intramural hematoma have recently been investigated. Indeed, the endovascular approach may have considerable advantages in this disease compared with conventional surgical repair (21,24) (Fig 11). Published series report 30-day mortality rates from 0% to 16% (23,24).
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Figure 11a. Intramural hematoma. (a) DSA image shows external compression of the aortic lumen at the origin of the descending aorta (arrows). (b) CT scan obtained before treatment shows that the area of aortic wall thickening remains unenhanced after administration of contrast material. (c) DSA image obtained after stent-graft deployment to cover the extension of the intramural hematoma shows that the external compression has disappeared.
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Figure 11b. Intramural hematoma. (a) DSA image shows external compression of the aortic lumen at the origin of the descending aorta (arrows). (b) CT scan obtained before treatment shows that the area of aortic wall thickening remains unenhanced after administration of contrast material. (c) DSA image obtained after stent-graft deployment to cover the extension of the intramural hematoma shows that the external compression has disappeared.
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Figure 11c. Intramural hematoma. (a) DSA image shows external compression of the aortic lumen at the origin of the descending aorta (arrows). (b) CT scan obtained before treatment shows that the area of aortic wall thickening remains unenhanced after administration of contrast material. (c) DSA image obtained after stent-graft deployment to cover the extension of the intramural hematoma shows that the external compression has disappeared.
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Penetrating Atherosclerotic Ulcer
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Penetrating atherosclerotic ulcers of the aorta are caused by the ulceration of atheromatous plaques that disrupt the internal elastic lamina, with subsequent hematoma formation within the media of the aortic wall (25,26,50–52). Progression of the ulcerative process can lead to hematoma formation in the aortic media, aortic dissection, adventitial pseudoaneurysm formation, and transmural aortic rupture (25,50). They usually occur in elderly patients with severe atherosclerotic disease and hypertension and typically involve the descending thoracic aorta (25,26,51,52). The prevalence of acute rupture of thoracic aortic ulcers is about 21%–47% (3,23,47).
As no predictive factor for rupture is known, the current attitude is to surgically treat all ulcers of the ascending aorta (23). However, treatment of descending aortic lesions is more controversial. Asymptomatic and uncomplicated ulcers may be managed medically with close radiologic follow-up (50,53). In contrast, in symptomatic or progressing lesions, early treatment is mandatory. Perioperative mortality rates after surgical open repair of penetrating atherosclerotic ulcers range from 7.1% to 25%, and neurologic deficit is reported in up to 28.6% of cases (25).
Stent-graft repair represents a good alternative to surgery (Fig 12), especially in elderly patients, who frequently present with comorbidities (23,25,26,50). A small number of series have documented encouraging results, with greater than 90% technical success and low mortality (23,50,54). The only mid-term data, from the Stanford group, document that endovascular stent-graft repair is associated with low perioperative morbidity and mortality (19% and 12%, respectively) in selected high surgical risk, elderly patients with penetrating atherosclerotic ulcers located in the descending thoracic aorta (26). Persistent or recurrent pain, hemodynamic instability, progressively enlarging lesions, intramural hematoma expansion or dissection that occurs despite maximal medical therapy, and a rapidly expanding aortic diameter have been considered indications for intervention (23,25,26,50–52). Initial maximum ulcer diameter of 20 mm or more and initial maximum ulcer depth of 10 mm or greater have been related to a high risk of disease progression (24).
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Figure 12a. Penetrating atherosclerotic ulcer. (a) CT scan shows a contrast material–filled outpouching in the distal thoracic aorta. The outpouching is surrounded by a thrombosed pseudoaneurysm. (b) DSA image shows the contrast material–filled structure (arrow) projecting beyond the expected confines of the aortic lumen. (c) DSA image obtained after stent-graft deployment shows successful exclusion of the penetrating ulcer and the pseudoaneurysm.
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Figure 12b. Penetrating atherosclerotic ulcer. (a) CT scan shows a contrast material–filled outpouching in the distal thoracic aorta. The outpouching is surrounded by a thrombosed pseudoaneurysm. (b) DSA image shows the contrast material–filled structure (arrow) projecting beyond the expected confines of the aortic lumen. (c) DSA image obtained after stent-graft deployment shows successful exclusion of the penetrating ulcer and the pseudoaneurysm.
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Figure 12c. Penetrating atherosclerotic ulcer. (a) CT scan shows a contrast material–filled outpouching in the distal thoracic aorta. The outpouching is surrounded by a thrombosed pseudoaneurysm. (b) DSA image shows the contrast material–filled structure (arrow) projecting beyond the expected confines of the aortic lumen. (c) DSA image obtained after stent-graft deployment shows successful exclusion of the penetrating ulcer and the pseudoaneurysm.
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Aortic Rupture
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Aortic aneurysms, dissections, traumatic pseudoaneurysms, intramural hematomas, and penetrating atherosclerotic ulcers may progress to acute aortic rupture (3,16,20,26,31) (Fig 13). Standard therapy involves surgical placement of an interposition graft through a thoracotomy (19). However, many of these patients are quite elderly and have many comorbidities that make them poor surgical candidates. Stent-graft placement may be performed with less risk than emergency surgical treatment in these patients. This approach offers a less invasive therapeutic option, even in patients who would not otherwise be considered surgical candidates (3,6,11,17,19,25).
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Figure 13a. Rupture of a penetrating atherosclerotic ulcer. (a) CT scan shows a large penetrating ulcer (*) that has progressed to a transmural aortic rupture. Note the intramural hematoma (H), large hemomediastinum (M), and bilateral hemothorax (HT). (b) Follow-up DSA image shows complete exclusion of the rupture site.
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Figure 13b. Rupture of a penetrating atherosclerotic ulcer. (a) CT scan shows a large penetrating ulcer (*) that has progressed to a transmural aortic rupture. Note the intramural hematoma (H), large hemomediastinum (M), and bilateral hemothorax (HT). (b) Follow-up DSA image shows complete exclusion of the rupture site.
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Conclusions
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Endovascular techniques are emerging as an alternative approach in the treatment of thoracic aortic disease. This approach offers a less invasive therapeutic option to standard surgical techniques, even in patients who have associated diseases that make them poor surgical candidates. When the aortic arch is involved, surgical and endovascular procedures can be combined and performed simultaneously, allowing treatment of a wider range of patients.
Our experience, as well as those of others, suggests that this technique can now be considered an effective alternative to open surgery. However, long-term follow-up is necessary to assess the durability of both the device and the repair after stent-graft placement in the thoracic aorta.
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Footnotes
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Abbreviations: DSA = digital subtraction angiography, LSA = left subclavian artery
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References
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Abstract
LEARNING OBJECTIVES
