BACKGROUND: This was an experimental study of endovascular aortic surgery, looking at the relationship between the size of an endoleak, pressure in the aneurysm sac and the effect of thrombosis produced by coagulation. METHODS: In three pigs, 16 saccular aneurysms were connected to the aorta by various side branches with different diameters and lengths ('endoleaks'). Mean and pulse pressures were measured in the systemic circulation as well as in the aneurysm sac during the experiment. Duplex ultrasonography was used to determine whether the endoleak and the aneurysm were patent or thrombosed. Thrombosis was influenced by systemic tranexamic acid, fibrinogen in the aneurysm sac, Gelfoam in both endoleak and aneurysm sac, and by Histoacryl glue in the endoleak. RESULTS: With an open endoleak, the mean pressure in the aneurysm and the aorta was identical. Mean aneurysm pressure was lower with a thrombosed endoleak and was related to the diameter of the endoleak. Pulse pressure was recorded in the aneurysm sac when there was an open endoleak and a non-thrombosed aneurysm, and was related to the diameter of the open endoleak. Thrombosed endoleaks never produced pulse pressure in the aneurysm. If Histoacryl and Gelfoam induced thrombosis of the endoleak, the decrease in mean aneurysm pressure was identical to that resulting from the spontaneous thrombosis of endoleaks. CONCLUSION: An open endoleak results in systemic arterial pressure in the aneurysm sac. Pulse pressure is detected if the aneurysm is patent, but absent if there is complete or partial thrombosis of the aneurysm. Endoleak thrombosis, either spontaneous or by embolization, is accompanied by a decrease in mean pressure and the absence of pulse pressure in the aneurysm sac. The extent to which these experimental findings are comparable to the clinical situation represents a field of further research.
BACKGROUND: This was an experimental study of endovascular aortic surgery, looking at the relationship between the size of an endoleak, pressure in the aneurysm sac and the effect of thrombosis produced by coagulation. METHODS: In three pigs, 16 saccular aneurysms were connected to the aorta by various side branches with different diameters and lengths ('endoleaks'). Mean and pulse pressures were measured in the systemic circulation as well as in the aneurysm sac during the experiment. Duplex ultrasonography was used to determine whether the endoleak and the aneurysm were patent or thrombosed. Thrombosis was influenced by systemic tranexamic acid, fibrinogen in the aneurysm sac, Gelfoam in both endoleak and aneurysm sac, and by Histoacryl glue in the endoleak. RESULTS: With an open endoleak, the mean pressure in the aneurysm and the aorta was identical. Mean aneurysm pressure was lower with a thrombosed endoleak and was related to the diameter of the endoleak. Pulse pressure was recorded in the aneurysm sac when there was an open endoleak and a non-thrombosed aneurysm, and was related to the diameter of the open endoleak. Thrombosed endoleaks never produced pulse pressure in the aneurysm. If Histoacryl and Gelfoam induced thrombosis of the endoleak, the decrease in mean aneurysm pressure was identical to that resulting from the spontaneous thrombosis of endoleaks. CONCLUSION: An open endoleak results in systemic arterial pressure in the aneurysm sac. Pulse pressure is detected if the aneurysm is patent, but absent if there is complete or partial thrombosis of the aneurysm. Endoleak thrombosis, either spontaneous or by embolization, is accompanied by a decrease in mean pressure and the absence of pulse pressure in the aneurysm sac. The extent to which these experimental findings are comparable to the clinical situation represents a field of further research.