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Ann Thorac Surg 1995;59:501
© 1995 The Society of Thoracic Surgeons
Department of Cardiothoracic and Vascular Surgery The Sanger Clinic, PA 1001 Blythe Blvd Suite 300, PO Box 32861 Charlotte, NC 28203
Most aneurysms are caused by abnormally high wall stress, and most aneurysms rupture because of abnormally high wall stress—a force that acts on the aortic wall and is directly proportional with the aortic diameter and inversely with wall thickness and strength. The conventional way to bring wall stress down to normal, and thus prevent rupture, is to replace the aneurysmatic aortic segment with a synthetic vascular prosthesis of appropriate diameter and strength. Although in the majority of patients this indeed remains the method of choice, in some special situations where the anatomy is favorable, such as is the case in ``pear'' or ``teardrop''-shaped aneurysms of the ascending aorta, aortoplasty, a less radical procedure, may suffice. Such an approach has been applied by my colleagues and me for the past two decades for the treatment of some ascending aortic aneurysms and more recently by Williams for the management of chronic descending aortic dissections.
In this article, Barnett and associates also make a strong case in favor of aortoplasty. There are, however, several points with which I disagree with them, both in technique and in indication. They use external wall reinforcement only selectively, and in about half of their patients aortic remodeling was applied alone. This approach, although it effectively addresses one of the principal components of increased wall stress, ie, the aortic diameter, leaves the second equally important contributor, wall thickness and strength, unattended. In other words, aortoplasty eliminates the aneurysm, but it does not prevent recurrence! If the patient otherwise would live long enough, the same factor that caused the aorta to dilate in the first place, the weakness of the aortic wall, would lead to aneurysm formation again.
Recognizing the above, I recommend that aortic remodeling always should be combined with wall reinforcement using an externally applied, well-tailored Dacron vascular prosthesis. My colleagues and I have shown this combined procedure to have a long and a respectable follow-up with results comparable with or better than those of radical aortic root replacement. Exceptions to this recommendation may be moderate-sized poststenotic aneurysms in which the cause of the dilatation, ie, stenosis, has been surgically corrected.
Aortoplasty alone as applied by Barnett and associates may suffice in patients with advanced age whose lifetime is too short for their aneurysm to recur or in remodeling those with poststenotic ascending aortic dilatations that most probably would not rupture anyhow. It seems, however, to be highly inadequate for younger patients including those with Marfan's syndrome—a group Barnett and associates wisely avoided in their series of unprotected aortoplasties.
By the way, I do not believe that Marfan's disease represents a contraindication to aortic remodeling, but remodeling should be combined with external wall reinforcement (I do not like to use the word ``wrapping'' because it is reminiscent of the cellophane ``wrap'' of the 1950s). As a matter of fact, I regard ascending aortic dilatations of medium to severe size in a patient with Marfan's syndrome as an ideal indication for aortic remodeling, especially if the procedure requires a valve replacement, because of annular dilatation.
Similarly, I do not hesitate to perform aortic remodeling if the sinuses of Valsalva are dilated as well, but only if there is a need for aortic valve replacement, and thus the aortic annulus is stabilized by the insertion of a prosthetic valve. In such cases the aortoplasty is carried deep into the noncoronary sinus and the externally applied Dacron tube is anchored to the valve prosthesis using sutures carried through the aortic wall.
In conclusion, in my view, about a third of the patients with ascending aortic aneurysms, including those with Marfan's traits, could be safely and effectively treated with aortic remodeling instead of graft replacement, especially if they require aortic valve replacement as well. The normal aortic geometry, thus restored, should be further secured by the external application of a well-fitted Dacron vascular graft anchored proximally to either the commissures or, if a prosthetic valve was implanted, to the prosthetic valve itself.
Related Article
Ann. Thorac. Surg. 1995 59: 497-501.
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