Stent graft-induced new entry after endovascular repair for Stanford type B aortic dissection
Background Stent graft-induced new entry (SINE), defined as the new tear caused by the stent graft and excluding those arising from natural disease progression or iatrogenic injury from the endovascular manipulation, has been increasingly observed after thoracic endovascular aortic repair (TEVAR) fo...
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Published in | Journal of vascular surgery Vol. 52; no. 6; pp. 1450 - 1457 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
New York, NY
Mosby, Inc
01.12.2010
Elsevier |
Subjects | |
Online Access | Get full text |
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Summary: | Background Stent graft-induced new entry (SINE), defined as the new tear caused by the stent graft and excluding those arising from natural disease progression or iatrogenic injury from the endovascular manipulation, has been increasingly observed after thoracic endovascular aortic repair (TEVAR) for Stanford type B dissection in our center. SINE appears to be remarkably life threatening. We investigated the incidence, mortality, causes, and preventions of SINE after TEVAR for Stanford type B dissection. Methods Data for 22 patients with SINE were retrospectively collected and analyzed from 650 patients undergoing TEVAR for type B dissection from August 2000 to June 2008. An additional patient was referred to our center 14 months after TEVAR was performed in another hospital. The potential associations of SINE with Marfan syndrome, location of SINE and endograft placement, and the oversizing rate were analyzed by Fisher exact probability test or t test. Results We found 24 SINE tears in 23 patients, including SINE at the proximal end of the endograft in 15, at the distal end in 7, and at both ends in 1. Six patients died. SINE incidence and mortality reached 3.4% and 26.1%, respectively. Two SINE patients were diagnosed with Marfan syndrome, whereas there were only 6 Marfan patients among the 651 patients. The 16 proximal SINEs were evidenced at the greater curve of the arch and caused retrograde type A dissection. The eight distal SINEs occurred at the dissected flap, and five caused enlarging aneurysm whereas three remained stable. The endograft was placed across the distal aortic arch during the primary TEVAR in all 23 patients. The incidence of SINE was 33.33% among Marfan patients vs 3.26% among non-Marfan patients ( P = .016). There was no significant difference in mortality between proximal and distal SINE (25% vs 28.6%, P > .99), incidence of SINE between endograft placement across the arch and at the straight portion of descending thoracic aorta (23 of 613 vs 0 of 38, P = .39), and the oversizing rate between SINE and non-SINE patients (13% ± 4.5% vs 16% ± 6.5%, P = .98). Conclusions SINE appears not to be rare after TEVAR for type B dissection and is associated with substantial mortality. The stress yielded by the endograft seems to play a predominant role in its occurrence. It is important to take this stress-induced injury into account during both design and placement of the endograft. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0741-5214 1097-6809 |
DOI: | 10.1016/j.jvs.2010.05.121 |