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a Department of Biomedical Sciences, Texas Tech University Health Sciences Center, Paul L. Foster School of Medicine, 5001 El Paso Dr, El Paso, TX 79905
b Department of Cardiothoracic and Vascular Surgery, University of Texas Medical School, 6400 Fannin St, Houston, TX 77030
(Email: charles.miller{at}ttuhsc.edu; anthony.l.estrera{at}uth.tmc.edu; hazim.j.safi{at}uth.tmc.edu).
We read with great interest the article by Fattouch and colleagues [1] on the long-term fate of the descending aorta after repair of acute type A dissection. This report shows that the natural history of the descending aorta after repaired acute type A dissection is similar to that seen in acute type B dissection, and confirms previous reports from the type B acute dissection literature that 3-year mortality in patients with a patent distal aortic lumen is in the range of 10% to 20% [2, 3]. The authors do not describe partial luminal thrombosis, which has been described in other research as a particularly grave sign [2]. This is a question of considerable importance and its omission from this report is regrettable. Their finding that full thrombosis leads to better long-term prognosis is consistent with Akutsu and colleagues [3], but conflicts with Tsai and colleagues [2], who found complete thrombosis to have a worse outcome than complete patency.
The major contribution of this report is the precision of the estimates, due both to the relatively generous sample size and the frequency and completeness of follow-up. The rate at which these aortas expand in close follow-up, nearly 3 mm/yr, is sobering and has implications for timing and mode of treatment. This contribution adds to our conviction that regular follow-up and aggressive lifelong control of hypertension are essential best practices.
As intervention strategies continue to develop, studies of the effects of intervention aimed at thrombosing the false lumen are on the horizon. Reports are beginning to appear to the effect that endovascular approaches for distal aortic dissection can facilitate thrombosis of the false lumen [4]. In this context, it is of considerable importance to resolve the question of whether a thrombosed false lumen is better or worse than a patent one. Furthermore, whether accomplishing thrombosis by intra-aortic radial force from a stent can decrease enlargement and death over time is far from certain. This question is ideally suited to a randomized trial of stenting versus watchful waiting or open surgery with close follow-up.
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