BACKGROUND: The purpose of this study was to evaluate clinical, anatomic, and procedural characteristics of patients who developed retrograde type A dissection (RTAD) after thoracic endovascular aortic repair (TEVAR) for type B aortic dissection (TBAD). METHODS: Between January 2012 and January 2017, there were 186 patients who underwent TEVAR for TBAD at a multidisciplinary aortic center. Patients who developed RTAD after TEVAR (n = 15) were compared with those who did not (no-RTAD group, n = 171). Primary outcomes were survival and need for reintervention. RESULTS: The incidence of RTAD in our sample was 8% (n = 15). Kaplan-Meier estimates found that no-RTAD patients had better survival (P = .04). Survival rates at 30 days, 1 year, and 3 years were 93%, 60%, and 60% for RTAD patients and 94%, 87%, and 80% for no-RTAD patients. One RTAD was diagnosed intraoperatively, 5 were diagnosed within 30 days of the index procedure, 6 were diagnosed within 1 year, and 3 were diagnosed after 1 year. Reintervention for RTAD was undertaken in 10 of 15 patients, with a 50% survival rate after reintervention. Partial or complete false lumen thrombosis was more frequently present in RTAD patients (P = .03). RTAD patients more frequently presented with renal ischemia (P = .04). Most RTAD patients (93%, RTAD patients; 64%, no-RTAD patients; P = .02) had a proximal landing zone in zone 0, 1, or 2. Aortic diameter was more frequently ≥40 mm in the RTAD group (47%, RTAD patients; 21%, no-RTAD patients; P = .05). Patients with RTAD had stent grafts placed in the renovisceral arteries for complicated dissections, and this approached significance (P = .05). Three RTAD patients had a type II arch (20%) compared with 53 no-RTAD patients (31%; P = .6), but a comparison of type II arch with type I or type III found no statistical significance (P = .6). No correlations were found between ratio of descending to ascending diameters, average aortic sizing, graft size, or bare-metal struts at proximal attachment zone and development of RTAD. We found no statistically significant differences in demographics, genetic disease, comorbidities, or previous repairs. CONCLUSIONS: The development of RTAD after TEVAR for TBAD does not appear to be correlated with any easily identifiable demographic feature but appears to be correlated with proximal landing zones in zone 1 and 2 and an ascending diameter >4 cm. Furthermore, the presence of partial or complete false lumen thrombosis as well as more complicated presentation with renal ischemia was significantly more frequent in patients with RTAD. TBAD patients should be observed long term, as type A dissections in our patients occurred even after 1 year.
BACKGROUND: The purpose of this study was to evaluate clinical, anatomic, and procedural characteristics of patients who developed retrograde type A dissection (RTAD) after thoracic endovascular aortic repair (TEVAR) for type B aortic dissection (TBAD). METHODS: Between January 2012 and January 2017, there were 186 patients who underwent TEVAR for TBAD at a multidisciplinary aortic center. Patients who developed RTAD after TEVAR (n = 15) were compared with those who did not (no-RTAD group, n = 171). Primary outcomes were survival and need for reintervention. RESULTS: The incidence of RTAD in our sample was 8% (n = 15). Kaplan-Meier estimates found that no-RTAD patients had better survival (P = .04). Survival rates at 30 days, 1 year, and 3 years were 93%, 60%, and 60% for RTAD patients and 94%, 87%, and 80% for no-RTAD patients. One RTAD was diagnosed intraoperatively, 5 were diagnosed within 30 days of the index procedure, 6 were diagnosed within 1 year, and 3 were diagnosed after 1 year. Reintervention for RTAD was undertaken in 10 of 15 patients, with a 50% survival rate after reintervention. Partial or complete false lumen thrombosis was more frequently present in RTAD patients (P = .03). RTAD patients more frequently presented with renal ischemia (P = .04). Most RTAD patients (93%, RTAD patients; 64%, no-RTAD patients; P = .02) had a proximal landing zone in zone 0, 1, or 2. Aortic diameter was more frequently ≥40 mm in the RTAD group (47%, RTAD patients; 21%, no-RTAD patients; P = .05). Patients with RTAD had stent grafts placed in the renovisceral arteries for complicated dissections, and this approached significance (P = .05). Three RTAD patients had a type II arch (20%) compared with 53 no-RTAD patients (31%; P = .6), but a comparison of type II arch with type I or type III found no statistical significance (P = .6). No correlations were found between ratio of descending to ascending diameters, average aortic sizing, graft size, or bare-metal struts at proximal attachment zone and development of RTAD. We found no statistically significant differences in demographics, genetic disease, comorbidities, or previous repairs. CONCLUSIONS: The development of RTAD after TEVAR for TBAD does not appear to be correlated with any easily identifiable demographic feature but appears to be correlated with proximal landing zones in zone 1 and 2 and an ascending diameter >4 cm. Furthermore, the presence of partial or complete false lumen thrombosis as well as more complicated presentation with renal ischemia was significantly more frequent in patients with RTAD. TBADpatients should be observed long term, as type A dissections in our patients occurred even after 1 year.