title: In vitro analysis of type II endoleaks and aneurysm sac pressurization on longitudinal stent-graft displacement.
abstract: OBJECTIVE
  To evaluate the effects of type II endoleaks and sac pressurization on stent-graft displacement following endovascular aneurysm repair (EVAR).
  
  
  METHODS
  Experimental silicone infrarenal aneurysm (6-cm) models were "treated" with a Talent stent-graft deployed with 20-mm proximal and distal landing zones. Inflow and outflow vessels were created as part of the silicone model to control flow into the aneurysm sac. All aneurysm models were uniform, with a diameter neck of 31 mm, a neck length of 20 mm, and iliac artery diameters of 16 mm. The aortic model was secured in a water bath to a pulsatile pump under physiological conditions; the output phase ratio (%systole/%diastole) was set at 65/35 with a pump rate of 80 beats per minute. Commercially available bifurcated stent-grafts were then displaced in vitro utilizing a linear motion apparatus attached to a force gauge. The mean arterial pressure (MAP) and pulse pressure (PP) at the aortic inflow were 60.1 ± 3.1 and 38.3 ± 7.8 mmHg, respectively. Peak force to cause initial stent-graft migration with and without a type II endoleak was recorded and compared.
  
  
  RESULTS
  In aneurysm sacs with no endoleak, the MAP and sac PP were 32 ± 6.4 and 6 ± 1.3 mmHg, respectively (p<0.01). In aneurysm sacs with a type II endoleak, the MAP and sac PP were 54.1 ± 9.7 and 16.1 ± 4.1 mmHg, respectively (p<0.02). Peak force to initiate migration was 16.0 ± 1.41 N (range 15-18) with no endoleak vs. 23.2 ± 2.2 N (range 20-25) in those with a type IIa endoleak and 23.5 ± 2.5 N (range 20-26) in those with a type IIb endoleak (p<0.001).
  
  
  CONCLUSIONS
  Type II endoleaks are associated with a significantly increased sac pressure. Increased sac pressurization from type II endoleaks results in a significantly greater force to displace a stent-graft longitudinally. Type II endoleaks may therefore inhibit migration and offer a benefit following EVAR; however, clinical correlation of these results is required.
authors.affiliation: Department of Vascular and Endovascular Surgery, University of Texas-Southwestern, Dallas, Texas 75390-9157, USA.
authors.forename: Martyn
authors.initials: M
authors.lastname: Knowles
authors.forename: Tiago
authors.initials: T
authors.lastname: Pellisar
authors.forename: Erin H
authors.initials: EH
authors.lastname: Murphy
authors.forename: Gregory A
authors.initials: GA
authors.lastname: Stanley
authors.forename: Abraham F
authors.initials: AF
authors.lastname: Hashmi
authors.forename: M Zachary
authors.initials: MZ
authors.lastname: Arko
authors.forename: Frank R
authors.initials: FR
authors.lastname: Arko
mesh_terms: D001012:Aorta, Abdominal / Q000503:physiopathology / Q000601:surgery*; D017544:Aortic Aneurysm, Abdominal / Q000503:physiopathology / Q000601:surgery*; D001696:Biomechanical Phenomena; D001794:Blood Pressure; D001807:Blood Vessel Prosthesis; D019917:Blood Vessel Prosthesis Implantation / Q000009:adverse effects* / Q000295:instrumentation; D057867:Endoleak / Q000209:etiology* / Q000503:physiopathology; D057510:Endovascular Procedures / Q000009:adverse effects* / Q000295:instrumentation; D005548:Foreign-Body Migration / Q000209:etiology* / Q000503:physiopathology; D006801:Humans; D008422:Materials Testing; D008953:Models, Anatomic; D011474:Prosthesis Design; D011673:Pulsatile Flow; D012828:Silicones; D015607:Stents; D013314:Stress, Mechanical
chemical_list: D012828:Silicones