Development of acquired arteriovenous fistulas in rats due to venous hypertension

Dural sinus thrombosis has been hypothesized as a possible cause of dural arteriovenous fistulas (AVF's). The pathogenesis and evolution from thrombosis to actual development of an AVF are still unknown. To study dural fistula formation, a surgically induced venous hypertension model in rats was created by producing an arteriovenous shunt between the carotid artery and the external jugular vein. The external jugular vein beyond the anastomosis was ligated 2 to 3 months after surgery and angiography was performed to identify any new acquired AVF's. Forty-six male Sprague-Dawley rats, each weighing approximately 300 gm, were used for this study. In Group I, 22 rats underwent a common carotid artery anastomosis to the external jugular vein, which is the largest draining vein from the transverse sinus via the posterior facial vein, followed by proximal external jugular vein ligation. In Group II, 13 rats underwent the same surgical procedure, followed by contralateral posterior facial vein occlusion. Group III served as the control group, in which 11 rats underwent only unilateral external jugular vein occlusion with or without contralateral posterior facial vein occlusion. The shunts in Groups I and II were ligated at 2 to 3 months following surgery, and transfemoral angiography was performed immediately before and after occlusion. New acquired AVF's had developed in three rats (13.6%) in Group I, three rats (23.1%) in Group II, and no rats (0%) in Group III. One of these newly formed fistulas was located at the dural sinus, analogous to the human dural AVF. The other five were located in the subcutaneous tissue, including the face and neck. The dural AVF in the rat was present on follow-up angiography at 1 week after the bypass occlusion. It is concluded that chronic venous hypertension of 2 to 3 months' duration, without associated venous or sinus thrombosis, can induce new AVF's affecting the dural sinuses or the subcutaneous tissue.