Low-density vulnerable thrombus/plaque volume on preoperative CT predicts spinal cord ischemia after endovascular repair for thoracic aortic aneurysm.

INTRODUCTION Similar to open surgical repair (OSR), thoracic endovascular aortic repair (TEVAR) carries a risk of spinal cord ischemia (SCI). However, the generally lower incidence of SCI after TEVAR than after OSR despite the inability to preserve the intercostal arteries indicates different pathophysiological mechanisms with the two procedures. We hypothesized that a microembolism from an aortic mural thrombus is the main cause of SCI, and this study aimed to evaluate the association between the density of a mural thrombus in the descending thoracic aorta and the development of SCI. METHODS A retrospective review of a prospectively assembled database was performed for all patients who underwent surgery at a single institution between October 2008 and December 2018. Patient demographics and procedure-related variables were collected. The volume and Hounsfield unit (HU) value of mural thrombi in the whole descending thoracic aorta were estimated by preoperative CT using a 3D workstation. Logistic regression analysis was performed to identify risk factors for SCI development. RESULTS Of the 367 patients who underwent TEVAR during the study period, 155 patients were excluded from this study because of previous arch surgery (n = 59), previous descending thoracic aortic surgery (n = 6), previous TEVAR (n = 6), unavailable optimal preoperative CT data (n = 17), double-barreled dissection (n = 40), and other reasons. The mean ± SD age of the remaining cohort (212 patients) was 75.8 ± 6.4 years, and 42 patients (19.8%) were women. Fourteen patients (6.6%) developed SCI after TEVAR. The low mean density of the mural thrombus, total thrombus volume, low-density (-100 ≤ HU <30) thrombus volume, intermediate-density (30 ≤ HU <150) thrombus volume, treatment length, urgent surgery, and baseline dialysis significantly differed between patients with and without SCI. Although subsequent multivariate analysis could not be performed due to the small number of SCI events, vulnerable low-density thrombus/plaque was a stronger predictor among aneurysm-related factors of SCI after TEVAR in the univariate analysis. Well-known risk factors, such as distal coverage between T8 and L1, left subclavian artery coverage, prior abdominal aortic surgery, and prophylactic spinal drainage, did not show significant differences. CONCLUSION This study demonstrates that among aneurysm-related factors, a lower-density mural thrombus/plaque in the descending thoracic aorta is a predictor of SCI development after TEVAR. These results suggest that microembolism is one of the important mechanisms of SCI after TEVAR, which may change the prophylactic strategy.