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Endoleaks, which occur when there is a continued flow of blood into the aneurysm sac following endovascular repair of a thoracic aneurysm (TEVAR), can create pressurization of the sac and a continued risk for rupture. 

In a study of 69 TEVAR patients by vascular and cardiothoracic surgeons, as well as intervention radiologists from the University of Pennsylvania in Philadelphia, the incidence and determinants of endoleaks, their impact on aneurysm sac regression and outcomes of secondary intervention in patients was evaluated. The results were published in the September issue of the Journal of Vascular Surgery. 

Twenty patients developed endoleaks and had an increased number of stents, longer aortic stent grafts, larger sac diameters and more extensive, larger aneurysms. Primary author Shane S. Parmer, MD, Attending in Vascular Surgery, Camden-Clark Memorial Hospital, Parkersburg, W.Va., said several factors predict endoleak formation including male gender, larger aneurysm size, length of aorta treated by stent grafts and number of stents used during initial repair.

“Commonly endoleaks result from flow either around the graft pieces (type I and III) or are due to alternative blood flow pathways directly into the sac (type II),” said Dr. Parmer. “Classically type II endoleaks have been observed; aggressive treatment of types I and III have been recommended.”

Each patient underwent CT angiography at regular intervals which were analyzed and measured by a lab for consistency. At the mean follow-up of 17.3 months, eight patients were type I, seven were type II, four were type III, and had more than one type of endoleak.

Successful endovascular treatment of the type I endoleaks (which are shown on CT as contiguous with the proximal or distal attachment site with early filling of the sac) resulted in sac regression. During follow-up, while the maximum aneurysm diameter with type I endoleaks initially increased, it decreased significantly following treatment. 

None of the type II endoleaks, where the endoleak sac could not be seen communicating with the distal or proximal attachment site or where there was a delayed enhancement of the sac, were treated by secondary intervention. These endoleaks increased (between -4.4 to +17 mm) despite spontaneous thrombosis having occurred in 29 percent of the patients. Patients with type III endoleaks, which are associated with functional separation of two stent graft sections, had endovascular repair and a decrease in mean maximal aneurysm diameter. There were no open conversions performed for any endoleak treatment. 

“Managing type II endoleaks through observation should be questioned,” added Dr. Parmer. “In our study mere observation was associated with continued sac expansion. Further evaluation of type II endoleaks are needed to see if repair is possible and cross-sectional imaging to monitor the durability of repairs should be considered. Actually, all patients who have TEVAR should be followed closely and consistently to identify endoleaks so that treatment, when indicated, can be offered to allow for optimal outcomes for them.”

“In addition, our data suggests that patients requiring extensive aortic coverage with multiple stents are at an increased risk for endoleak and may not do as well in the long term,” said Dr. Parmer. “Using longer devices instead of multiple short devices may provide superior results and decrease the incidence of postoperative endoleak.”