ABSTRACT
Since first introduced, the endovascular repair of infrarenal aortic aneurysms has been gaining increased acceptance as favorable early-outcome reports increase in numbers and feasibility reports proliferate, expanding the anatomical indications for this approach (7,16,19–21,24,40). Despite the strong enthusiasm for this new method, the consistent findings of high postprocedure endoleak rates (up to 21%) appears to represent a real and poorly understood problem (3–6,9,11,13,14,17,25,29,33–37,39). Data presented from the EVT (Endovascular Technologies) and Medtronic trails at an FDA panel indicated up to 48% endoleak rates on early CT scan follow-up. While great concern has been expressed over persistent anchoring site (type I) endoleaks (particularly proximal endoleaks), little is known about the significance of type II endoleaks (related to the inferior mesenteric artery, 222lumbars, and other collateral vessels) (1). Data from the EUROSTAR registry on 1554 patients from 1994 to 1999 documented a 16% rate of endoleaks detected at the completion of the procedure and a 9% rate of endoleaks one month after the procedure. A significant percentage of endoleaks (related to anchoring sites or collateral vessels) appear to spontaneously disappear after variable periods of follow-up, whereas new endoleaks, not previously observed, may appear on a delayed fashion (3,8,18). Therefore, the time interval that defines a persistent endoleak that triggers concern varies widely among investigating centers. Even after the endoleak thromboses and is no longer detectable on computed tomography (CT) scan, it is unknown whether this occurrence eliminates transmitted pressure through the unexcluded thrombus to the aneurysm sac. If there remains transmitted systemic pressure to unexcluded aneurismal aorta, one might anticipate that, analogous to an unrepaired thrombosed aneurysm, the risk of rupture would remain. Some patients with persistent endoleaks have been reported to experience progressive aneurysm dilatation and fatal rupture (38). Even more perplexing are the reported cases where an endoleak is not detectable by conventional radiographic imaging techniques, but the aneurysm sac continues to expand and/or the patient incurs aneurysm rupture (12). Thrombus within the aneurysm sac may transmit both mean and pulse pressure to the wall of the aneurysm, and therefore thrombus alone may not be protective against aneurysm expansion and rupture. For example, aortic aneurysms thrombosed by ligating the iliac arteries may still go on to rupture. Schurink et al. (25–30) measured the pressure within the aneurysmal thrombus, at its thickest point, in nine patients undergoing open repair of infrarenal aortic aneurysms. They noted that both mean and pulse pressures within the thrombus were similar to systemic pressure measurements. However, in a pig experimental model where 16 saccular aneurysms were connected to the aorta by branches of varying lengths and diameters (simulating different size collateral-endoleaks), the thrombosed or partially thrombosed aneurysm sacs were not systemically pressurized. In this experimental mode, an open branch “endoleak” of any size was capable of producing pulsatile systemic pressure within the aneurysm sac, independent of the size of the “endoleak.” Pulsatile systemic pressure within these experimental aneurysms sacs were successfully obliterated be either spontaneous thromboses of the “endoleak” or Gelfoam or Histoacryl glue induced thromboses the “endoleak” but not the sac. However, the mean aneurysm pressure after thrombosis was significantly increased as the diameter of the thrombosed “endoleak” was increased, again suggesting that thrombus can transmit pressure if the diameter of the conduit (collateral branch) is sufficiently wide. If the “endoleak” remained open, the sac 223remained pressurized, regardless of whether or not the aneurysm sac was thrombosed.
