Long-Term Outcome of Aortic Dissection With Patent False Lumen: Predictive Role of Entry Tear Size and Location

Abstract

Conclusion: A patent false lumen after aortic dissection has a high risk of complications. Marfan syndrome, aortic diameter, and a large entry tear located in the proximal part of the dissection identify high-risk subgroups of patients who may benefit from earlier and more aggressive therapy. Summary: Persistence of a patent false lumen in the descending aorta after type A or type B aortic dissection is associated with poor prognosis (Bernard Y et al, Am J Cardiol 2001;87:1378-82). The expectation was that thoracic endovascular aortic repair for early management of aortic dissection, by occluding the intimal tear and promoting false lumen thrombosis, would result in better outcomes for the aortic dissection patient. To date however, no study has demonstrated that elective endovascular treatment in the early course of aortic dissection reduces mortality. In fact, the INSTEAD trial failed to show a benefit in 2-year survival and adverse event rates after early treatment of type B aortic dissection (Nienaber AN et al, Circulation 2009;120:2519-28). The “logic” of treating aortic dissection in the subacute phase with endografts, coupled with the results of the INSTEAD trial, has led investigators to try to identify clinical and imaging predictors of prognosis and therefore, by inference, which patients may benefit from early intervention after thoracic aortic dissection. The authors sought to define such clinical and imaging variables in the subacute phase of aortic dissection. They analyzed 184 consecutive patients: 108 surgically treated type A and 76 medically treated type B dissections who were discharged after acute aortic dissection with a patent false lumen. Before discharge, transesophageal echocardiograms were preformed. Computed tomography angiography was performed at 3 months and yearly thereafter. Median follow-up was 6.42 years (quartile 1 to 3: 3.31 to 10.49). During follow-up, 49 patients died (22 type A, 27 type B), of which 31 deaths were sudden deaths. Late surgical or endovascular treatment was indicated in 10 type A and 25 type B patients. Survival free from sudden death and surgical/endovascular treatment was 0.90, 0.81, and 0.46 (95% confidence interval, 0.36-0.55) at 3, 5, and 10 years, respectively. Multivariate analysis identified maximum baseline descending aortic diameter (hazard ratio [HR], 1.32 [1.10-1.59]; P = .003), proximal location (HR, 1.84 [1.06-3.19]; P = .03), and entry tear size (HR, 1.13 [1.08-1.2]; P < .001) as predictors of dissection-related adverse events. Mortality was predicated by maximum descending aortic diameter (HR, 1.36 [1.08-1.70]; P = .008), entry tear size (HR, 1.1 [1.04-1.16]; P = .001), and Marfan syndrome (HR, 3.66 [1.65-8.13]; P = .001). Comment: This study focuses on clinical and imaging predictors potentially identified early on after type A or type B dissection that may affect late mortality or need for further intervention. Given the results of the INSTEAD trial and the known adverse affects of a patent false lumen after aortic dissection, studies such as this focusing on variables that can be identified after dissection as possible indicators for early endovascular therapy are clearly needed. Although patients with Marfan syndrome are not thought to be optimal candidates for endovascular treatments, non-Marfan patients with large proximal aortic tears and large aortas would seem to be two subgroups that would benefit from further study for “prophylactic” endovascular thoracic aortic repair after acute thoracic aortic resection.