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  Vol. 122 No. 3, March 1987 TABLE OF CONTENTS
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  PAPERS READ BEFORE THE 10TH ANNUAL SURGICAL SYMPOSIUM OF THE ASSOCIATION OF VETERANS ADMINISTRATION SURGEONS, WASHINGTON, DC, MAY 8-10, 1986
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Influence of Vein-Patch Angioplasty on Carotid Endarterectomy Healing

Gary W. Stewart, MD; Dennis F. Bandyk, MD; Hermann W. Kaebnick, MD; James D. Storey, MD; Jonathan B. Towne, MD

Arch Surg. 1987;122(3):364-371.


Abstract

• We studied the influence of venous patching on the patency, endothelial regeneration, and wall healing of endarterectomized carotid arteries in a canine model. Thirteen dogs underwent bilateral common carotid endarterectomies (intimectomy and partial media excision). In each dog, one artery was closed by continuous suture and the contralateral artery was closed by external jugular vein-patch angioplasty; arteries were excised at two postoperative intervals (two to three and four to five weeks) for light, scanning, and transmission electron microscopy. The patency of arteries closed primarily (9/13 [69%]) was not significantly different compared with arteries closed with venous patches (12/13[92%]). By scanning electron microscopy, regeneration of the endothelial monolayer occurred by migration from the endarterectomy end points and suture lines. Despite survival of the vein-patch endothelium, the rate and pattern of reendothelialization was not altered by venous patching. In both patched and unpatched vessels, endothelial regeneration was incomplete at two to three weeks and completed by four to five weeks. The histologic characteristics of the endarterectomized arterial wall after operation were also not influenced by the closure technique. In contrast with the healing artery wall, vein-patch walls did not develop a thickened intima. Although venous patching does not influence early patency, endothelial regeneration, or wall healing after endarterectomy, vein-patch angioplasty does increase vessel diameter and prevents the development of circumferential intimal thickening, attributes that are beneficial in minimizing restenosis.

(Arch Surg 1987;122:364-371)



Author Affiliations

From the Department of Surgery, Medical College of Wisconsin, Milwaukee (Drs Stewart, Bandyk, and Towne); and the Surgical Service (Drs Bandyk, Kaebnick, and Towne) and Department of Pathology (Dr Storey), Veterans Administration Medical Center, Milwaukee.


Footnotes

Accepted for publication Sept 19, 1986.

Read before the Tenth Annual Surgical Symposium of the Veterans Administration Surgeons, Washington, DC, May 9, 1986.

Reprint requests to Department of Surgery, Medical College of Wisconsin, 8700 W Wisconsin Ave, Milwaukee, WI 53226 (Dr Bandyk).



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