Zone zero thoracic endovascular aortic repair: A proposed modification to the classification of landing zones

Objective: Endovascular stent-grafting provides an alternative treatment option for high-risk patients with ascending aortic disease. The feasibility of this approach has been demonstrated before. We assess the updated experience with ascending thoracic endovascular aortic repair and propose a modification of the landing zone classification based on the outcomes. Methods: From 2006 to 2016, 39 patients deemed very high risk for open replacement underwent endovascular repair of ascending aorta for acute type A dissection (12, 31%), intramural hematoma (2, 5%), pseudoaneurysm (22, 56%), and chronic dissection suture line entry tear (3, 8%). Ascending thoracic endovascular aortic repair was performed in 36 patients. In 3 patients with pseudoaneurysm, occluder devices were used. Computed tomography imaging analysis was performed, and the extent of aortic pathology was designated by segmental proximity to the left ventricle. Segmental anatomy of the proximal aorta was designed as zone 0A from the annulus to the distal margin of highest coronary, 0B extends from above the coronary to the distal margin of right pulmonary artery, and 0C extends from the right pulmonary artery border to the innominate artery. Multivariable time to event Cox regression analysis was performed to predict mortality, and long-term survival was estimated using the Kaplan-Meier method. Results: Operative mortality was 13%; all 5 deaths occurred after emergency ascending thoracic endovascular aortic repair for type A dissection. Other complications included stroke in 4 patients (10%), myocardial infarction in 2 patients (5%), tracheostomy in 2 patients (5%), and dialysis in 2 patients (5%). In patients with acute type A dissection, the ascending pathology extended into zone 0A in 10 (71%) and 0B in 4 (29%). Among those with pseudoaneurysm, the location of the defect was in 0B in 11 (50%), 0C in 10 (45%), and 0A in 1. Among the patients with chronic dissection, the defect was located in 0C in all 3 (100%). After multivariable adjustment, Cox regression predicted significantly higher hazard of mortality with disease involving zone 0A versus 0C (P = .020) and older age (P = .026). Kaplan-Meier estimate of survival was also significantly worse in patients with disease extension into 0A versus 0C (P = .0018). At 30 days, 1 year, and 5 years, the overall survival was 81%, 74%, and 64% and freedom from reintervention was 85%, 77%, and 68%, respectively. Conclusions: The modified zone zero classification is useful for characterizing extent of ascending aortic pathology and assessing prognosis. Location of the defect varies by pathology, and the presence of 0A disease predicts worse outcomes. Design of endovascular devices should be tailored to the aortic pathology and zone characteristics.