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The Journal of Thoracic and Cardiovascular Surgery, Vol 81, 61-68, Copyright © 1981 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association

ARTICLES

Repair of dissection of the thoracic aorta. Evaluation of false lumen utilizing computed tomography

K Turley, DJ Ullyot, JD Godwin, JM Wilson, M Lipton, E Carlsson and PA Ebert

During the period 1975 to 1980, 21 patients with thoracic aortic dissections underwent surgical treatment. The operative technique was resection and tube graft replacement of the segment of the aorta containing the entry point into the false channel. Eleven Type A and 10 Type B dissections were resected. The hospital survival rate was 95%. The single operative death occurred in a patient with an acute Type A dissection. Three patients had total resection of the dissected segment; three had clotted false lumina; five had distal anastomosis to true and false lamina; and 10 had distal anastomosis to the true lumen only, with proximal entry into the false lumen obliterated by incorporating both intimal and adventitial walls in a single suture line. The late survival rate was 95% (mean 32 months, range 8 to 63 months). No late ruptures occurred. Computed tomography (CT) with contrast enhancement was used to evaluate the aorta and any residual false lumen at follow-up. Seven of eight patients in whom obliteration was attempted and CT scans performed demonstrated persistence of false lumen perfusion; in six of the eight, preoperative angiograms were adequate for evaluation of false lumen runoff. Major vessels arose from the false lumen in all cases, except in the one patient in whom obliteration was later successful. This report demonstrates that there is persistence of false lumen perfusion in patients in whom obliteration is attempted, and the mechanism of this persistence is the presence of major vessel runoff. It suggests that the mechanism by which long-term survival is achieved is by resection of the segment of aorta containing the entry site, which is frequently the site of subsequent enlargement and rupture, rather than obliteration of the false channel.

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