Chronic Dissection Etiology is an Independent Risk Factor for Mortality after Intact Open Type I-III Thoracoabdominal Aortic Aneurysm Repair
CHRISTOPHER A. LATZ, M.D., M.P.H., Laura Boitano, M.D., M.P.H., Linda J. Wang, M.D., M.B.A, Charles DeCarlo, M.D., Anna A. Pendleton, M.D., Samuel Schwartz, M.D., Jahan Mohebali, M.D., M.P.H., Mark Conrad, M.D., MMSc..
MASSACHUSETTS GENERAL HOSPITAL, BOSTON, MA, USA.
Objectives: Many open thoracoabdominal aortic aneurysm (TAAA) repairs are performed for aneurysmal degeneration of tissue secondary to chronic aortic dissection (AD). The goal of this study was to determine if AD pathology leads to worse outcomes after TAAA repair. Methods: All open type I-III TAAA repairs performed from 1987-2015 were evaluated using a single institutional database. Primary endpoints were in-hospital death, major adverse events (MAE) and long-term survival. All repairs performed for rupture were excluded. Univariate analysis was conducted using the Fisher’s exact test for categorical variables and the Wilcoxon rank-sum test for continuous variables. Logistic multivariable regression was used for the in-hospital endpoints and survival analyses were performed with Cox Proportional Hazards modelling and Kaplan-Meier techniques. Results: Four hundred fifty-six patients had an intact open type I-III TAAA repair during the study period. 93 (20.4%) were performed on patients with AD. Those with AD were more likely to be younger (59 versus 72 years, p<0.001), have an extent 2 lesion (30.1% versus 16.3%, p<0.001), have Marfan’s syndrome (17.2% versus 0.6%, p<0.001), and were less likely to have coronary artery disease (CAD) [26.9% versus 24.7%, p=0.006] and chronic obstructive pulmonary disease (COPD) [11.8% versus 26.7%, p=0.002]. 11.8% of patients with AD died perioperatively as compared to 5.5% of those with degenerative etiology (p=0.038). 57.0% of AD patients suffered a MAE compared to 42.4% of those without AD (p=0.014). Multivariable analysis revealed AD to be an independent predictor of perioperative death (AOR: 2.9, 95% CI:1.2-7.4, p=0.020) with adjustment for age and Crawford extent. AD was also found to be independently predictive of any major adverse event (MAE) [AOR: 2.3, 95% CI: 1.3-4.0, p=0.005]. Other predictors of MAE were higher admission creatinine, history of COPD, and history of CAD. There was a survival advantage in the dissection cohort in the unadjusted (log-rank p=0.0002) but not the adjusted analysis (AD HR: 0.77, 95% CI: 0.52-1.1, p=0.2). Conclusions: Performing an open repair of type I-III TAAA for AD leads to increased perioperative mortality and morbidity. These results should be considered during all treatment phases following aortic dissection.
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