Transient stenotic-like occlusions as a possible mechanism for renovascular hypertension due to aneurysm

Heflin, Linden A.; Street, Carrie B.; Papavassiliou, Dimitrios V.; Kem, David C.; Wu, Dee H.; O'Rear, Edgar A.

doi:10.1016/j.jash.2009.02.004

« Previous Next »Journal of the American Society of Hypertension
Volume 3, Issue 3 , Pages 192-200, May 2009

Transient stenotic-like occlusions as a possible mechanism for renovascular hypertension due to aneurysm

Linden A. Heflin
- University of Oklahoma Bioengineering Center
- Department of Chemical, Biological and Materials Engineering, University of Oklahoma; Norman, Oklahoma, USA
Carrie B. Street
- Department of Chemical, Biological and Materials Engineering, University of Oklahoma; Norman, Oklahoma, USA
Dimitrios V. Papavassiliou, PhD
- Department of Chemical, Biological and Materials Engineering, University of Oklahoma; Norman, Oklahoma, USA
David C. Kem, MD
- Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA
Dee H. Wu, PhD
- Radiological Sciences, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA
Edgar A. O'Rear, PhD
- University of Oklahoma Bioengineering Center
- Department of Chemical, Biological and Materials Engineering, University of Oklahoma; Norman, Oklahoma, USA
- Corresponding author: Edgar A. O'Rear, PhD, Francis W. Winn Professor, School of Chemical, Biological and Materials Engineering, University of Oklahoma, T-335 Sarkeys Energy Center, 100 East Boyd Street, Norman, Oklahoma 73019. Tel: 405-325-4379; fax: 405-325-5813.

Received 1 December 2008; accepted 13 February 2009. published online 13 April 2009.

Abstract

The pathophysiologic basis of hypertension secondary to a renal artery aneurysm has not been established. Changes in renal artery geometry and resultant hemodynamic alterations activate the renin-angiotensin-aldosterone system and lead to hypertension. Hemodynamic pressure losses created by blood flowing through an abnormally structured renal artery with an aneurysm predictably would provoke a similar circumstance. The present study provides a hemodynamic rationale for this hypothesis. Using computational fluid dynamics, we have modeled renal flow for selected aneurysmal geometries. These studies reveal that pressure loss across the renal artery does not change (∼0.9 mm Hg) significantly when a nondeformable aneurysm is interposed on the system. The calculations, however, demonstrate that the pressure on the aneurysm walls supports the presence of forces deforming and thereby obstructing the renal artery. A deformed wall was assumed and various degrees of occlusion were modeled. A partial occlusion of 60% resulted in a renal artery pressure loss of ∼10 mm Hg. These simulations, when applied to aneurysms at various locations on the renal artery and with various degrees of occlusion, consistently resulted in pathologically relevant pressure losses. These findings lead to a new hypothesis of how aneurysms are associated with renovascular hypertension.

Keywords: Hemodynamics, computational fluid dynamics, renin-dependent hypertension, renal artery