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Aorta Center and Marfan and Connective Tissue Disorder Clinic, The Cleveland Clinic Foundation, Cleveland, Ohio
* Address correspondence to Dr Svensson, Aorta Center, The Cleveland Clinic Foundation, 9500 Euclid Ave, F25, Cleveland, OH 44195 (Email: svenssl{at}ccf.org).
The group from Buffalo [1] present an important series of patients in whom stents were inserted for distal aortic dissection and raise two questions: is there less pain and a survival gain for stenting aortic dissections? For acute dissections, in most centers, endovascular treatment is preferable for complications of acute aortic dissection, particularly ischemia. Hence, for acute dissection, the Society of Thoracic Surgeons and the multispecialty expert consensus and guidelines committee made this a class I (should be performed), level of evidence A, recommendation for endograft treatment (Table 12 [2]). For acute dissection with no complications, the guidelines were class II B (not recommended, may be considered) level of evidence B, although this requires further study. For subacute dissections, based on the INvestigation of STEnt grafts in patients with type B Aortic Dissection (INSTEAD) randomized trial [2], the recommendations are similar to those for acute dissection with no complications, because survival was better in the medically treated control arm in the INSTEAD trial. The guidelines also had the same recommendations (class II B, level of evidence B) for chronic aortic dissection (for symptomatic aneurysms or size > 5.5 cm).
This current article by Alves and colleagues [1] has one of the longest follow-up periods and raises further questions about how best to treat patients with chronic dissection. First, are the early results better? Postoperative pain is less and recovery is quicker. However, mortality is similar (4%) to previous series from centers with experience with chronic dissection open repairs, which reported 4% (n = 96) [3] and 6% (n = 204) [4]. Also with a direct risk adjusted comparison of all descending and thoracoabdominal aneurysms and dissections, mortality was 5% for endografting (n = 352) vs 8.3% for open repair (n = 372; p = 0.2) [5]. As the authors point out, stroke may be increased, although spinal cord injury is equivalent [5] at 5% (n = 204) [4]. Thus in suitable patients, early results are relatively equivalent with less pain, but is there a long-term survival gain?
There are two issues to consider concerning late survival and events for chronic dissection. First, is survival better? And second, whether late events, namely more late reinterventions, are a better course than the price to be paid for open surgical repair with a more definitive early curative procedure vs a more palliative endovascular one. In the article by Alves and colleagues, late 5-year survival is very good, at approximately 92% to 93%, assuming patients were adequately followed-up (Fig 2A). If hospital deaths are included, survival drops to approximately 89%, which still is very good. By comparison, open repaired chronic dissection at 3 years, including operative deaths, has an 82% survival for proximal descending repairs, 74% for total descending aortic repairs, and 65% for thoracoabdominal repairs [3]. Thus, survival may be better with stent grafting, even though late ruptures may be more frequent with endovascular repair [1, 3]. Even if survival may be better, then does reintervention matter, considering that Alves and colleagues had 37% overall late failures at 2.5 years? For chronic dissection it was 22% reintervention and total events 33%. In the series of 690 open aortic dissection repairs, including all distal repairs (descending and thoracoabdominal repairs), freedom from reoperation was 91% for 389 distal patient repairs at 5 years and 80% at 10 years [3].
Why are reinterventions more frequent? Stenting chronic aortic dissection has a number of issues that will need to be overcome to reduce late reinterventions:
For chronic aortic dissections, the reasons for type I proximal leaks are the difficulty in seating the graft at a 45- to 90-degree angle, the dissection often involves the left subclavian artery (approximately 25% in the current series were covered but only 5% needed reintervention for ischemia), the proximal true lumen may be severely narrowed, the septum is fibrotic and less expansile, covering the false lumen entry may be difficult, and more proximal seating may cover the left common carotid artery origin, or cause proximal aortic dissection (once in this series, but 2% to 3% in most series). Late rupture may occur in the aneurysmal segment (and this is usually the only reason for late reintervention, namely aneurysmal formation) because segmental intercostal lumbar arteries perfuse the false lumen or a distal septal tear perfuses the false lumen.
Secondly, whether thrombosis in the false lumen is protective or not, because the thrombus is still likely pressurized, is not known. Whether at a later date an occlusion device should be inserted in the false lumen just about the celiac axis to encourage false lumen thrombosis is not known. This should be considered for later insertion, to reduce the risk of paralysis at the initial intervention, and reduce also the risk of renal failure, in case the left kidney, the usual side, is perfused by the false lumen. Although, this may reduce the late risk of aneurysm rupture, it has never been studied.
Third, intuitively, it would seem that a circumferential open graft anastomosis would restrict distal aortic enlargement and aneurysm formation. This would not hold true if the distal anastomosis is beveled to accommodate distal descending intercostal artery reimplantation. In the series of 690 patients, a residual aneurysm had a strong influence on late survival at 5 years (95% without, 86% with), and for 389 distal repairs, a residual aneurysm was a very strong predictor of late survival (p = 0.0173); hence, partial repair of aneurysms with stent grafts that ignore distal aneurysms, for example, thoracoabdominal aneurysms or false lumen aneurysms, cannot be justified just because the stent occludes the true lumen. By implication, late distal aneurysms may also be more frequent with endovascular stenting, as occurred in this series.
In conclusion, what are the implications of this study? I believe we can say with a high level of equipoise that a prospective randomized study between open repair and endovascular grafting for symptomatic aneurysms or aortas exceeding 5.5 cm in diameter in the descending aorta is justified. The forthcoming study funded by the National Institutes of Health will answer many of the questions concerning the role and selection of patients for endovascular study.
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