DISCUSSION
Wrapping of the AA was first described by Bahnson and Nelson in 19561, who performed aortic AA reduction using a side clamp and wrapping in 2 patients. Both suddenly died 4 and 5 months after surgery. Wrapping in the early period was associated with oval excision of the AA (aortoplasty) and was only an external support and not a tool to reduce the size of the aorta11. Results of aortoplasty and wrapping were satisfying12,13, but a meta-analysis of Plonek et al14 with 722 cases concluded that isolated aortic wrapping had better results than wrapping and aortoplasty or wrapping and aortic plication. However, even if wrapping of the AA is technically simple, the report of complications intrinsic to the technique with/out aortoplasty prevented a wide application of this strategy15-21. In contrast, replacement of the AA is a well-studied procedure, reproduceable and easy to perform, with uniformly good results. Wrapping of the AA involves the use of a conventional vascular prosthesis of a preselected size, smaller than that of the AA, with the aim to avoid further dilatation of the aorta and the related complications. A problem is the formation of folds22. The size of a vascular graft is, at maximum, 36 mm. Then the reduction is at least 10 mm or more. The presence of folds, due to a severe mismatch between the graft and the size of the AA, changes the flow patterns and can lead to compression and erosion of the aortic wall. Neri et al15, in 2 patients who underwent a reoperation, found that the reinforced aorta was significantly thinner, with a sclerotic microstructure in which layers were no longer present. Also, the atrophied aortic wall showed cellular and neovascular infiltration and common in a foreign-body reaction. On the contrary, the samples retrieved from the non-reinforced aorta showed a basically normal histologic structure. At the basis of these changes there are the compromise of the vasa vasorum that nourish the middle layer of the aorta, chronic inflammatory response to the foreign material, and sustained compression of the aortic wall between the pressure of blood and of the external prosthesis. As a consequence of these changes, the aorta becomes a passive conduit with biomechanical characteristics similar to those of a synthetic vascular prosthesis. These changes seem to be less evident when the AA is reinforced with a dacron (macro-porous) mesh instead of a vascular conduit23, probably due to its greater elasticity.
An external support that reinforces the vessel without interfering with the pattern of flow is very attractive, but not free of drawbacks. The aorta is a very strong structure. Aortic rupture does not occur if the intraluminal pressure ranges from 790 to 2070 mm Hg24. Robertson and Smith, injecting water into the media of 42 fresh human aortas, found that the lowest pressure required to exceed the cohesive strength of the media was 273 mm Hg and the highest was 975 mm Hg, with a mean of 566 mm Hg25. Therefore, the aorta is highly resistant to rupture or dissection. Recently, an appealing theory on the genesis of intramural hematoma and aortic dissection was reproposed26,27. Vasa vasorum dysfunction is the link between these entities, which are seen as progression of one into the other. Rupture and bleeding of the vasa vasorum into the media are the causes of intramural hematoma. It can remain limited to the thickness of the aorta or cause an intimal tear, which is at the basis of classic aortic dissection. The vasa vasorum fill during diastole as in the coronary circulation. Thus, an increase in arterial diastolic pressure results in reduced perfusion28, which can cause vessel wall hypoxia and neoangiogenesis, with the neovessels more fragile and prone to bleed. Hypertension also can reduce blood flow by distortion or compression of the vasa, generating changes in the walls of the vasa vasorum with critical ischemia and necrosis of the media. Other factors (eg, inflammation) can induce aberrant and adverse remodelling of the aortic wall, including smooth muscle cell loss in the media and extracellular matrix degradation in the media and the adventitia. The consequence is chronic dilation of the aorta, but an acute aortic syndrome can superimpose at any moment. Increased tension or chronic inflammation due to wrapping can cause localized hematoma or necrosis, weakening the aortic wall. The benefit of reducing wall stress reducing the diameter has to be compared with the interference with the nourishment of the aortic wall.
Wrapping also modifies the biomechanical characteristics of the blood flow in the entire arterial system29. The synthetic materials used to externally reinforce the aorta are much less elastic than a healthy or diseased native aorta, which alters the pressure of the entire arterial system. This fact has been associated with a higher risk of cardiovascular events in hypertensive patients30. On the other hand, the compliance mismatch between the native and the reinforced aorta leads to hemodynamic changes that increase the circumferential wall stress in the aortic segments at the interface of supported and unsupported aorta29, shifting distally the area of greatest expansion31. This particular aspect was emphasized in a recent paper from Kim et al32, where the Authors compared the long term outcome of wrapping compared to conventional replacement of the AA in propensity matched patients. After a median follow up of 7.1 years, the proximal arch dilated in the wrapping group (0.343 mm/year), but not in the replacement group. In the wrapping group preoperative AA size was a risk factor for proximal arch dilatation, with a cut off value of 47.15 mm. Total adverse aortic event (reoperation of ascending or arch aorta, dissection or rupture, redilatation of the aortic arch) were higher in the wrapping group (24.3% vs 14.3%, p=0.010) during the follow up. Then, graft migration because of proximally or distally incomplete fixation of the prosthesis can cause proximal and distal redilatation, but proximal arch dilatation can be due to mechanisms intrinsic to the concept of wrapping even if presence of a correct surgical technique.
We decided, in presence of a moderately dilated AA, to change the strategy of wrapping. The size of the AA remained unchanged or reduced only of a few mm (fig. 1E), to avoid all the previously described possible complications, in particular folds and vasa vasorum compression. The use of FAP allowed us to follow the natural curvature of the vessel and to adapt proportionally to all the different portions of the aorta (fig. 1D). Moreover, it was observed that FAP is able to stretch in its two axes33 and that the systolic deformation of the epicardial surface is characterized by a longitudinal shortening of 10%34. This property can act as shock absorber during the changes of the intra-aortic pressure, avoiding the aorta to become a static and passive conduit.
As our target is to stabilize the ascending aorta, the aorta does not fold internally and the hemodynamic stress at the distal portion of the AA remains unchanged. The concept we applied is similar to that one reported by Robicseck et al35 who described the use of a tubular dacron prosthesis, if necessary enlarged by a dacron oval patch, to reinforce the aortic wall, procedure that the Authors called “external grafting”. The targets were patients with a moderately dilated AA, “too big to leave in and too small to take out”, as the population by us treated.
Our results have been good in all patients, without any early or late aortic complication. The AA size remained stable with time. However, the main limitation of this report is the small number of patients, only 10, even if with a reasonable follow up. Moreover, the follow up was performed with echocardiographic parameters, as many of the patients had no preoperative CT scan and an echocardiogram was easy to perform.
In conclusion, we think that wrapping of the AA (from the STJ till the beginning of the proximal arch) can have still a place when the AA is moderately dilated. The use of FAP allows to avoid further dilatation, maintaining more or less the same diameter at the moment of wrapping, without interfering with the nourishment of the aortic wall and with the hemodynamic patterns. The rationale of wrapping has to be changed, from reduction to values more or less normal (by 10 or more mm) to pure stabilization of the actual diameter to avoid any further dilatation.