As our understanding of dissection grows, the fate of the false lumen through the progression of disease is becoming a more important variable that predicts outcome, writes Tara Mastracci. If stenting is performed in the acute or subacute phase, in a majority of patients, the false lumen will thrombose to the level of the stent, or beyond, promoting aortic remodelling and thus decreasing the need for further intervention. However, in that subset of patients in whom the false lumen remains perfused or pressurised, aneurysmal degeneration occurs and the risk of rupture and death remains a persistent threat.
In these situations where aneurysmal degeneration leads to aortic growth, the gold standard and traditional approach to treatment has been total aortic repair. This is a major operation that can only be sustained by a younger, healthy cohort, and still has a large risk of morbidity. In the modern era, much like for degenerative aneurysm disease, conventional open surgery has been replaced by a complex aortic repair permitting relining of the aorta through the visceral segment and down to the aortic bifurcation. The benefit of this technique is that it allows for coverage of all the entry tears into the false lumen, thus permanently diverting flow into the true lumen. Centres with some experience in this approach report good short-term results, and acknowledge the challenge of manipulating complex aortic grafts in a narrowed and constricted true lumen.
Embolisation of the false lumen is a technique developed and reported by a select few surgical groups to promote thrombosis of the false lumen, and in so doing, increase the chance of aortic remodelling without subjecting the patient to a large intervention. The techniques are variable and seem to be centre-specific, but range from the use of custom-designed plugs, to septal occluders placed in the intimal tear alone, to a glue and coil combination used to fill the false lumen. The allure of these techniques is that they seem to force thrombosis of the false lumen, which according to our understanding of the natural history of dissection, should promote remodelling and aortic regeneration.
Unfortunately there is limited evidence to support these claims. Most of the published literature consists of case reports or very small series ranging from 1–21 patients, with a maximum follow-up of 63 months, but an average follow-up of much less. And although authors report satisfactory imaging results, with a high likelihood of false lumen thrombosis, there have been deaths from aortic rupture reported, and the rate of aneurysm shrinkage is actually disappointing over the first few years. This leaves the analytical reader left wondering if the presence of thrombotic material in the false lumen promotes thrombosis but does not depressurise the sac.
In conclusion, although the concept and potential for false lumen embolisation techniques seems interesting, further research is needed to prove its role in the armamentarium of the modern vascular surgeon.
Tara Mastracci, Royal Free Hospital, London, UK
