Implications of secondary aortic intervention after thoracic endovascular aortic repair for acute and chronic type B dissection

Document Type

Journal Article

Publication Date



Journal of Vascular Surgery








Aortic dissection; Reinterventions; Secondary interventions; TEVAR; Type B aortic dissection


Background: Thoracic endovascular aortic repair (TEVAR) has become a mainstay of therapy for acute and chronic type B aortic dissection (TBAD). Dynamic aortic morphologic changes, untreated dissected aorta, and persistent false lumen perfusion have significant consequences for reintervention after TEVAR for TBAD. However, few reports contrast differences in secondary aortic intervention (SAI) after TEVAR for TBAD or describe their influence on mortality. This analysis examined incidence, timing, and types of SAI after TEVAR for acute and chronic TBAD and determined their impact on survival. Methods: All TEVAR procedures for acute and chronic TBAD (2005-2016) were retrospectively reviewed. Patients with staged (<30 days) or concomitant ascending aortic arch repair or replacement were excluded. Acuity was defined by symptom onset (0-30 days, acute; >30 days, chronic). SAI procedures were grouped into open (intended treatment zone or remote aortic site), major endovascular (TEVAR extension or endograft implanted at noncontiguous site), and minor endovascular (side branch or false lumen embolization) categories. Kaplan-Meier methodology was used to estimate freedom from SAI and survival. Cox proportional hazards were used to identify SAI predictors. Results: TEVAR for TBAD was performed in 258 patients (acute, 49% [n = 128]; chronic, 51% [n = 130]). Mean follow-up was 17 ± 22 months with an overall SAI rate of 27% (n = 70; acute, 22% [28]; chronic, 32% [42]; odds ratio, 1.7; 95% confidence interval, 0.9-2.9; P =.07]. Median time to SAI was significantly less after acute than after chronic dissection (0.7 [0-12] vs 7 [0-91] months; P <.001); however, freedom from SAI was not different (1-year: acute, 67% ± 4%, vs chronic, 68% ± 5%; 3-year: acute, 65% ± 7%, vs chronic, 52% ± 8%; P =.7). Types of SAI were similar (acute vs chronic: open, 61% vs 55% [P =.6]; major endovascular, 36% vs 38% [P =.8]; minor endovascular, 21% vs 21% [P = 1]). The open conversion rate (either partial or total endograft explantation: acute, 10% [13/128]; chronic, 15% [20/130]; P =.2) and incidence of retrograde dissection (acute, 6% [7/128]; chronic, 4% [5/130]; P =.5) were similar. There was no difference in survival for SAI patients (5-year: acute + SAI, 55% ± 9%, vs acute without SAI, 67% ± 8% [P =.3]; 5-year: chronic + SAI, 72% ± 6%, vs chronic without SAI, 72% ± 7% [P =.7]). Factors associated with SAI included younger age, acute dissection with larger maximal aortic diameter at presentation, Marfan syndrome, and use of arch vessel adjunctive procedures with the index TEVAR. Indication for the index TEVAR (aneurysm, malperfusion, rupture, and pain or hypertension) or remote preoperative history of proximal arch procedure was not predictive of SAI. Conclusions: SAI after TEVAR for TBAD is common. Acute TBAD has a higher proportion of early SAI; however, chronic TBAD appears to have ongoing risk of remediation after the first postoperative year. SAI types are similar between groups, and the occurrence of aorta-related reintervention does not affect survival. Patients' features and anatomy predict need for SAI. These data should be taken into consideration for selection of patients, device design, and surveillance strategies after TEVAR for TBAD.