Summary
Operated acute DeBakey type I aortic dissection has to be considered as a chronic aortic disease with the potential of late distal dilatation with aneurysm formation and need for reoperation. Several intraoperative strategies have been devised to prevent late complications. However, the increased operative risk associated with a more aggressive initial approach in an emergent setting has to be balanced against the relatively low incidence of late reoperations. Further studies will have to identify preoperative risk factors for late distal aortic complications more precisely in order to select patients who might benefit the most from these newer surgical strategies.
Résumé
Le traitement chirurgical des dissections aortique de type I de DeBakey reste palliatif. L’aorte distale reste le plus souvent disséquée en postopératoire et peut évoluer ultérieurement vers une dilatation anévrismale et nécessiter une ré-intervention. Différentes stratégies chirurgicales ont été développées afin de limiter l’incidence de ces complications tardives. Toutefois, le risque opératoire plus élevé d’une intervention chirurgicale initiale plus agressive doit être pesé par rapport à l’incidence relativement faible des ré-interventions tardives. L’identification de facteurs de risques préopératoires prédictifs de complications aortiques tardives devrait permettre de mieux sélectionner les patients pour ces nouvelles techniques.
Background
Surgery has drastically improved the outcome of acute DeBakey type I aortic dissection. Immediate surgical intervention aims to prevent ascending aortic rupture, redirect blood flow into the true vessel lumen, and correct aortic valve insufficiency. However, surgical treatment remains essentially palliative, as most operative survivors have a residual dissected aorta, often with a patent false lumen. This exposes patients to distal aortic dilatation and subsequent aneurysm formation, with its inherent risks of aortic rupture or reoperation.
The precise natural history of operated acute DeBakey type I aortic dissection remains largely unknown. The objective of the present review is to summarize existing evidence regarding the fate of the distal aorta after surgical repair of acute DeBakey type I aortic dissection. Surgical strategies aimed at preventing distal aortic complications are also reviewed.
Natural history of distal aorta after operated type A aortic dissection
The fate of the distal aorta after surgical repair of acute type A aortic dissection has been addressed using three interrelated endpoints: (1) the persistent patency of the distal false lumen; (2) distal aortic dilatation with aneurysm formation; and (3) actual reoperations on the distal aorta or its branches.
Distal false lumen patency
The main objective of the distal surgical repair is obliteration of the false lumen in order to redirect blood flow into the true lumen. However, distal repair fails to achieve this objective in the majority of cases. Indeed, the incidence of partial or complete distal false lumen patency is reported to lie between 31% and 89% .
Persistent postoperative perfusion of the distal false lumen can be related to: (1) the presence of unresected or secondary entry sites in the distal aorta; (2) aortic clamp trauma that may injure the friable dissected aorta and create a new intimal tear immediately distal to the surgical repair; or (3) a leak at the level distal aortic anastomosis ( Fig. 1 ). Sakaguchi et al. have shown that preoperative hypertension (requiring aggressive use of antihypertensive drugs) and preoperative size of the descending thoracic aorta ≥ 35 mm were significant and independent risk factors of postoperative false lumen patency . Very recently, Zhao et al. have shown that complete distal false lumen thrombosis 1 year after operation was significantly lower in patients who required postoperative anticoagulation than in those who did not (87% vs 98%, p = 0.005) . Thus, in patients in whom the native aortic valve cannot be preserved, the choice of the heart valve substitute should be made with caution, and the long-term risk of distal aortic complications should be balanced against the risk of bioprosthetic structural deterioration.
The clinical consequences of distal false lumen patency remain controversial. Several studies have evaluated the association of distal false lumen patency with distal aortic dilatation or growth rates, and long-term clinical outcomes.
Aortic dilatation
Postoperative distal false lumen patency is an independent predictor for distal aortic dilatation. Moreover, a large area of the patent false lumen (> 70% of the total area of the transsectional diameter of the aorta) is a strong predictor for secondary dilatation of the diseased downstream aorta .
Aortic growth rate
Several studies have shown that distal aortic growth rate is greater in patients with patent than with thrombosed distal false lumen . For example, Fattouche et al. found yearly aortic growth rates of 2.8 ± 0.4 mm and 1.1 ± 0.2 mm in patients with patent and occluded false lumen, respectively ( p = 0.001) . Similarly, distal anastomotic leak after ascending aortic replacement for acute type A aortic dissection contributes to greater distal aortic growth rates .
Clinical outcomes (reoperation, rupture, death)
Myrmel et al. applied criteria of evidence-based medicine on all clinical series published between 1980 and 2003, but could not find a consistent relationship between persistence of a patent distal false lumen and increased risk of reoperation, aortic rupture or death . Similarly, more recent studies have failed to show significant differences in freedom from distal aortic reoperation or survival between patients with and without a patent false lumen . In contrast, the recently published experience of the Palermo group showed significantly lower freedom from reoperation and survival rates in patients with patent false lumen .
Partial thrombosis
Some of this discrepancy might be related to the fact that most studies do not differentiate between completely patent, partially thrombosed and completely thrombosed false aortic lumen ( Fig. 2 ). Partial thrombosis can be defined as the concurrent presence of both flow and thrombus in the false lumen . Fattori et al. have shown that partial thrombosis of the false lumen is protective against dilatation as suggested by an aortic growth rate of 0.34 cm/year in patients with partial thrombosis of the false lumen versus an increase of 0.56 cm/year in patients without thrombus in the false lumen . Furthermore, the number of late postoperative events was lower in patients with partial thrombosis compared to patients with no thrombosis. In contrast, Tsai et al. have shown that partial thrombosis of the false lumen is a particularly grave sign in patients with acute DeBakey type III aortic dissection . Similar findings have very recently been reported by Song et al., who show that partial thrombosis of the false lumen after repair of acute DeBakey type I aortic dissection, compared with complete patency or complete thrombosis, is a significant and independent predictor of aortic enlargement, aorta-related reoperations and poor long-term survival . However, the mechanisms by which partial thrombosis of the false lumen compromises long-term outcome remain speculative. In patients with a completely patent false lumen, the latter may be perfused by an entry tear and decompressed through another re-entry tear. In case of partial thrombosis, however, the thrombus may occlude the re-entry tear, thus impeding outflow. This may result in increased false lumen pressure and wall tension, favouring subsequent dilatation. Alternatively, aortic wall hypoxia at the level of the thrombus might lead to increased local inflammation and neovascularization, resulting in local aortic wall weakening.
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