Influence of type II endoleak volume on aneurysm wall pressure and distribution in an experimental model

Carlos H. Timaran, Takao Ohki, Frank J. Veith, Evan C. Lipsitz, Nicholas J. Gargiulo, Soo J. Rhee, Mahmood B. Malas, William D. Suggs, John P. Pacanowski

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Abstract

Objective(s): We have previously shown that type II endoleak size is a predictor of aneurysm growth after aortic endografting. To better understand this observation, we investigated the influence of endoleak size on pressure transmitted to the aneurysm wall and its distribution within the aneurysm sac. Methods: In an ex vivo model, an artificial aneurysm sac was incorporated within a mock circulation comprised of rubber tubing and a pulsatile pump. Three strain-gauge pressure transducers were placed in the aneurysm wall at different locations, including the site of maximum aneurysm diameter. The aneurysm was filled with either human aneurysm thrombus or dough that mimicked thrombus and simulated type II endoleaks of varying volumes (1 to 10 mL) were created. Aneurysm wall pressure (AWP) measurements were recorded at mean arterial pressures (MAPs) of 60, 80, and 100 mm Hg. Correlation coefficients (r) and analysis of variance were used to assess the relationship between endoleak volume and AWP. Results: Increasing endoleak volume '3 cm3 resulted in proportionally increased AWP at all levels of MAP and at all sites, with highest pressures recorded at the site of the maximum aneurysm diameter (r = 0.83 when MAP = 100 mm Hg; r = 0.85 when MAP = 80 mm Hg; r = 0.88 when MAP = 60 mm Hg; P < .001). AWP plateaued when the endoleak volume was >3 cm 3. Pressure distribution within the sac was not uniform. Although the difference was within ±10%, statistically significant higher AWPs were observed at the site of maximum aneurysm diameter (P <.001). AWP also correlated with MAP. Conclusions: Increasing type II endoleak volume results in proportionally higher AWP, which is greatest at the site of maximum aneurysm diameter. This study confirms the clinical observation that type II endoleak volume and MAP may be important predictors of aneurysm expansion. Clinical Relevance: Our experimental model of a type II endoleak revealed that endoleak size is a significant factor that influences the magnitude of pressure transmission into the aneurysm wall. Increasing volume of the endoleak nidus was associated with proportionally higher aneurysm sac pressures. This mechanism may, in fact, account for the increased risk of aneurysm expansion observed in our clinical experience, thereby suggesting the need for more aggressive surveillance and possibly earlier intervention for patients with larger endoleaks.

Original languageEnglish (US)
Pages (from-to)657-663
Number of pages7
JournalJournal of Vascular Surgery
Volume41
Issue number4
DOIs
StatePublished - Apr 2005

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Endoleak
Aneurysm
Theoretical Models
Pressure
Arterial Pressure
Thrombosis
Pressure Transducers

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Surgery

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Influence of type II endoleak volume on aneurysm wall pressure and distribution in an experimental model. / Timaran, Carlos H.; Ohki, Takao; Veith, Frank J.; Lipsitz, Evan C.; Gargiulo, Nicholas J.; Rhee, Soo J.; Malas, Mahmood B.; Suggs, William D.; Pacanowski, John P.

In: Journal of Vascular Surgery, Vol. 41, No. 4, 04.2005, p. 657-663.

Research output: Contribution to journalArticle

Timaran, CH, Ohki, T, Veith, FJ, Lipsitz, EC, Gargiulo, NJ, Rhee, SJ, Malas, MB, Suggs, WD & Pacanowski, JP 2005, 'Influence of type II endoleak volume on aneurysm wall pressure and distribution in an experimental model', Journal of Vascular Surgery, vol. 41, no. 4, pp. 657-663. https://doi.org/10.1016/j.jvs.2004.12.047
Timaran, Carlos H. ; Ohki, Takao ; Veith, Frank J. ; Lipsitz, Evan C. ; Gargiulo, Nicholas J. ; Rhee, Soo J. ; Malas, Mahmood B. ; Suggs, William D. ; Pacanowski, John P. / Influence of type II endoleak volume on aneurysm wall pressure and distribution in an experimental model. In: Journal of Vascular Surgery. 2005 ; Vol. 41, No. 4. pp. 657-663.
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abstract = "Objective(s): We have previously shown that type II endoleak size is a predictor of aneurysm growth after aortic endografting. To better understand this observation, we investigated the influence of endoleak size on pressure transmitted to the aneurysm wall and its distribution within the aneurysm sac. Methods: In an ex vivo model, an artificial aneurysm sac was incorporated within a mock circulation comprised of rubber tubing and a pulsatile pump. Three strain-gauge pressure transducers were placed in the aneurysm wall at different locations, including the site of maximum aneurysm diameter. The aneurysm was filled with either human aneurysm thrombus or dough that mimicked thrombus and simulated type II endoleaks of varying volumes (1 to 10 mL) were created. Aneurysm wall pressure (AWP) measurements were recorded at mean arterial pressures (MAPs) of 60, 80, and 100 mm Hg. Correlation coefficients (r) and analysis of variance were used to assess the relationship between endoleak volume and AWP. Results: Increasing endoleak volume '3 cm3 resulted in proportionally increased AWP at all levels of MAP and at all sites, with highest pressures recorded at the site of the maximum aneurysm diameter (r = 0.83 when MAP = 100 mm Hg; r = 0.85 when MAP = 80 mm Hg; r = 0.88 when MAP = 60 mm Hg; P < .001). AWP plateaued when the endoleak volume was >3 cm 3. Pressure distribution within the sac was not uniform. Although the difference was within ±10{\%}, statistically significant higher AWPs were observed at the site of maximum aneurysm diameter (P <.001). AWP also correlated with MAP. Conclusions: Increasing type II endoleak volume results in proportionally higher AWP, which is greatest at the site of maximum aneurysm diameter. This study confirms the clinical observation that type II endoleak volume and MAP may be important predictors of aneurysm expansion. Clinical Relevance: Our experimental model of a type II endoleak revealed that endoleak size is a significant factor that influences the magnitude of pressure transmission into the aneurysm wall. Increasing volume of the endoleak nidus was associated with proportionally higher aneurysm sac pressures. This mechanism may, in fact, account for the increased risk of aneurysm expansion observed in our clinical experience, thereby suggesting the need for more aggressive surveillance and possibly earlier intervention for patients with larger endoleaks.",
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AU - Ohki, Takao

AU - Veith, Frank J.

AU - Lipsitz, Evan C.

AU - Gargiulo, Nicholas J.

AU - Rhee, Soo J.

AU - Malas, Mahmood B.

AU - Suggs, William D.

AU - Pacanowski, John P.

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N2 - Objective(s): We have previously shown that type II endoleak size is a predictor of aneurysm growth after aortic endografting. To better understand this observation, we investigated the influence of endoleak size on pressure transmitted to the aneurysm wall and its distribution within the aneurysm sac. Methods: In an ex vivo model, an artificial aneurysm sac was incorporated within a mock circulation comprised of rubber tubing and a pulsatile pump. Three strain-gauge pressure transducers were placed in the aneurysm wall at different locations, including the site of maximum aneurysm diameter. The aneurysm was filled with either human aneurysm thrombus or dough that mimicked thrombus and simulated type II endoleaks of varying volumes (1 to 10 mL) were created. Aneurysm wall pressure (AWP) measurements were recorded at mean arterial pressures (MAPs) of 60, 80, and 100 mm Hg. Correlation coefficients (r) and analysis of variance were used to assess the relationship between endoleak volume and AWP. Results: Increasing endoleak volume '3 cm3 resulted in proportionally increased AWP at all levels of MAP and at all sites, with highest pressures recorded at the site of the maximum aneurysm diameter (r = 0.83 when MAP = 100 mm Hg; r = 0.85 when MAP = 80 mm Hg; r = 0.88 when MAP = 60 mm Hg; P < .001). AWP plateaued when the endoleak volume was >3 cm 3. Pressure distribution within the sac was not uniform. Although the difference was within ±10%, statistically significant higher AWPs were observed at the site of maximum aneurysm diameter (P <.001). AWP also correlated with MAP. Conclusions: Increasing type II endoleak volume results in proportionally higher AWP, which is greatest at the site of maximum aneurysm diameter. This study confirms the clinical observation that type II endoleak volume and MAP may be important predictors of aneurysm expansion. Clinical Relevance: Our experimental model of a type II endoleak revealed that endoleak size is a significant factor that influences the magnitude of pressure transmission into the aneurysm wall. Increasing volume of the endoleak nidus was associated with proportionally higher aneurysm sac pressures. This mechanism may, in fact, account for the increased risk of aneurysm expansion observed in our clinical experience, thereby suggesting the need for more aggressive surveillance and possibly earlier intervention for patients with larger endoleaks.

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