Left subclavian artery revascularization in zone 2 thoracic endovascular aortic repair is associated with lower stroke risk across all aortic diseases

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The best management strategy for the left subclavian artery (LSA) in pathologic processes of the aorta requiring zone 2 thoracic endovascular aortic repair (TEVAR) remains controversial. We compared LSA coverage with or without revascularization as well as the different means of LSA revascularization.


A retrospective chart review was conducted of patients with any aortic diseases who underwent zone 2 TEVAR deployment from 2007 to 2014. Primary end points included 30-day stroke and 30-day spinal cord injury (SCI). Secondary end points were 30-day procedure-related reintervention, freedom from aorta-related reintervention, aorta-related mortality, and all-cause mortality.


We identified 96 patients with zone 2 TEVAR who met our inclusion criteria. The mean age of the patients was 62 years, with 61.5% male. Diseases included acute aortic dissections (n = 25), chronic aortic dissection with aneurysmal degeneration (n = 22), primary aortic aneurysms (n = 21), penetrating aortic ulcers/intramural hematomas (n = 17), and traumatic aortic injuries (n = 11). Strategies for the LSA included coverage with revascularization (n = 54) or without revascularization (n = 42). Methods of LSA revascularization included laser fenestration with stenting (n = 33) and surgical revascularization: transposition (n = 10) or bypass (n = 11). Of the 54 patients with LSA revascularization, 44 (81.5%) underwent LSA intervention at the time of TEVAR and 10 (18.5%) at a mean time of 33 days before TEVAR (range, 4-63 days). For the entire cohort, the overall incidence of 30-day stroke was 7.3%; of 30-day SCI, 2.1%; and of procedure-related reintervention, 5.2%. At a mean follow-up of 24 months (range, 1-79 months), aorta-related reintervention was 15.6%, aorta-related mortality was 12.5%, and all-cause mortality was 29.2%. The 30-day stroke rate was highest for LSA coverage without revascularization (6/42 [14.3%]) compared with any form of LSA revascularization (1/54 [1.9%]; P = .020), with no difference between LSA interventions done synchronously with TEVAR (1/44 [2.3%]) vs metachronously with TEVAR (0/10 [0%]; P = .63). There was no significant difference in 30-day SCI in LSA coverage without revascularization (2/42 [4.8%]) vs with revascularization (0/54 [0%]; P = .11). There was no difference in aorta-related reintervention, aorta-related mortality, or all-cause mortality in coverage without revascularization (5/42 [11.9%], 6/42 [14.3%], and 14/42 [33.3%]) vs with revascularization (10/54 [18.5%; P = .376], 6/54 [11.1%; P = .641], and 14/54 [25.9%; P = .43], respectively). After univariate and multivariable analysis, we identified LSA coverage without revascularization as associated with a higher rate of 30-day stroke (hazard ratio, 17.2; 95% confidence interval, 1.3-220.4; P = .029).


Our study suggests that coverage of the LSA without revascularization increases the risk of stroke and possibly SCI.

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