Interact CardioVasc Thorac Surg 2009;8:287-289. doi:10.1510/icvts.2008.185009
© 2009 European Association of Cardio-Thoracic Surgery
Case report - Vascular thoracic |
Unusual aortic stent complication after endovascular repair of the descending thoracic aorta in type B dissection in a patient with giant-cell arteritis
Paolo Porcua,
Olivier Chavanona,*,
Frederic Thonyb and
Dominique Blina
a Department of Cardiac Surgery, Grenoble University Hospital, CHU La Tronche, Grenoble 38043, France
b Department of Radiology, Grenoble University Hospital, Grenoble, France
Received 4 June 2008;
received in revised form 8 August 2008;
accepted 11 August 2008
*Corresponding author. Tel.: +33 4 76 76 54 62; fax: +33 4 76 76 52 64.
E-mail address: OChavanon{at}chu-grenoble.fr (O. Chavanon).
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Abstract
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The advent of endovascular prostheses to treat descending thoracic aortic lesions offers an alternative approach in patients who are poor candidates for surgery. We present a case of a type B descending thoracic aortic dissection with rapid aneurysmal evolution in a woman with a giant-cell arteritis, treated by endovascular repair: 26 months after, we observed the anterior dislocation of the distal segment of the stent. The dislocation required a second treatment in order to avoid the aortic wall rupture and to restore the axis of the prosthesis. This report emphasizes the difficulty of the endovascular repair in the giant-cell arteritis, because of the vascular fragility confirmed by the rapid aneurysmal evolution after the type B dissection and the appearance of the stenting complication.
Key Words: Endovascular repair; Giant-cell arteritis; Stent dislocation
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1. Introduction
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The advent of endovascular prostheses to treat descending thoracic aortic lesions offers an alternative approach in patients who are poor candidates for surgery. In a case of a type B descending thoracic aortic dissection with rapid aneurysmal evolution in a woman with a giant-cell arteritis, treated by endovascular repair: 26 months after, we observed the anterior dislocation of the distal segment of the stent.
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2. Case report
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In October 2002, a 73-year-old woman was referred for a clinical suspicion of type B aortic dissection. Cardiovascular risk factors included smoking, arterial hypertension and giant-cell arteritis (GCA) diagnosed with temporal artery biopsy and treated by prednisone (12.5 mg/day). The CT-scan confirmed the type B aortic dissection (Fig. 1a,b). After eight months follow-up (June 2003) the CT-scan control showed the aneurysmal evolution of the dissected descending thoracic aorta, a diameter of the aorta increase of 7 mm (47 mm vs. 39 mm) with the entry-hole between the 9th and 10th dorsal vertebrae. The diameter of isthmic aorta was 30 mm, the diameter of celiac aorta was 29 mm. An endovascular occlusion of the entry-hole was performed using a covered stent introduced through the right arterial femoral approach (Talent Medtronic stent 32x115 mm) with distal oversizing <5 mm. A type I endo-leak and an intimal rupture of the superior pole occurring during the first stent deployment, required a second covered stent (Talent Medtronic 34x120 mm). The second covered stent was overlapping by 5 cm with the first covered stent. The control CT-scan showed a good result and the postoperative course was uneventful. The steroid treatment was increased to 27 mg/day for a week; the CRP was 15 from the hospital resignation. The following CT-scan controls performed at 1, 6, 12, 18 months confirmed good and stable results (Fig. 1c,d). However, at 26 months follow-up (September 2005) the CT-scan and angiographic control showed an anterior dislocation of the inferior pole of the stent-graft (Fig. 2a,b). Two months later an endovascular treatment was decided in order to avoid the aortic wall rupture and to restore the axis of the prosthesis. A covered stent was deployed between the celiac trunks overlapping the distal 5 cm of the prosthesis (Talent Medtronic 34x120 mm). The treatment allowed the correction of the stent dislocation even if a baffle aspect of the aortic trunk persisted (Fig. 2c,d). After 28 months follow-up the patient is doing well and is clinically asymptomatic. The metothrexate (10 mg/week) replaced the prednisone. The CRP was <15. The CT-scan control is unchanged.
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Fig. 1. The CT-scan shows the aortic thoracic dissection before the endovascular repair (a, b). After 18 months follow-up of endovascular repair, the CT-scan appears stable (c, d), but a more attentive observation shows a slight change in the distal segment of the stent.
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Fig. 2. After 26 months follow-up, the CT-scan control shows an anterior subtotal dislocation of the distal segment of the stent, with a worrying appearance image remake to the CT-scan (a). The angiographic control confirmed the axis change (b). By trans femoral approach, a covered stent between the celiac trunks overlapping the distal 5 cm of the prosthesis was placed. The CT-scan (c) and the angiography (d) control show the restoration of a normal internal axis of the abdominal aorta, despite the persistence of a ‘chicane’ aspect.
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3. Discussion
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Giant-cell arteritis is an inflammatory vasculopathy in which T cells and macrophages infiltrate the wall of medium and large arteries. Formation of aortic aneurysms may result from necrosis of smooth muscle cells and fragmentation of elastic membranes [1]. The GCA primarily affects the aorta and its extracranial branches. The clinical findings in GCA are broad, but commonly include visual loss, headache, scalp tenderness, jaw claudication, cerebrovascular accidents, aortic arch syndrome, thoracic aorta aneurysm, and dissection. Glucocorticosteroids are the cornerstone of treatment GCA [2]. The incidence of GCA is about 17 cases/year per 100,000 habitants over the age of 50 years [3]. The association of GCA with aortic aneurysm and aortic dissection was explored by Evans in a population-based study comparing the incidence of aortic aneurysm and dissection in 96 patients with GCA compared with the general population [4]. The authors concluded that patients with GCA were 17.3 times more likely to develop thoracic aortic aneurysm and 2.4 times more likely to develop abdominal aortic aneurysm compared with the general population. In one study, Nuenninghoff et al. [5] showed that the thoracic aortic dissection in GCA was associated with a markedly increased mortality, and confirmed the high mortality in the group with thoracic aortic dissection. Probably the number of aneurysms or descending thoracic aorta dissection caused from the GCA is underestimated; in fact, there are cases in which the diagnosis of GCA was made after occurrence of an aneurysm or a dissection of the thoracic descending aorta [6].
In this context, literature gives many options, either surgical or endovascular and/or pharmacologic [7–10]. Penin and colleagues described two cases of type B aortic dissection treated pharmacologically by corticoid-therapy with good results to eight months follow-up [7].
Three operated cases with traditional surgery were reported, with good immediate result but unknown follow-up. An endovascular repair in a case of GCA with a 6.5-cm false aneurysm of the descending thoracic aorta complicated by focal dissection and intramural hematoma was described by Engelke et al. with a difficult management due after eight months with development of a similar 1.5-cm false aneurysm below the thoracic stent-graft, complicated by focal intramural haematoma, but the follow-up was limited to 12 months, a shorter time than in our observation, as the complication appeared 26 months after the stenting. Our case, despite these difficulties, has today a follow-up of 54 months after the initial endovascular repair and 28 months after the last endovascular repair. From the literature, the use of corticotherapy for the control of GCA is recommended [2], although, in our case, we have observed the stent dislocation despite the steroids administration. To explain this evolution, despite the corticotherapy, we found several possibilities: 1) anatomically, the celiac aorta is surrounded by soft tissue without strong supports, 2) structurally, the destruction of the middle tunic of the aorta in GCA, weakened the arterial wall which is constantly constrained by the radial force of the stent, and 3) hemodynamically, the sphygmic wave is varying from the stent to the aortic wall. We suppose that the interaction of these causes can explain why this anterior stent dislocation happened at this level, in this patient.
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References
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Abstract
1. Introduction