The interdependent hemodynamic influence between abdominal aortic aneurysm and renal artery stenosis

Abstract

Cardiovascular diseases remain a leading cause of morbidity and mortality worldwide with abdominal aortic aneurysm (AAA) and renal artery stenosis (RAS) standing out as significant contributors to the vascular pathology spectrum. While these conditions have traditionally been approached as distinct entities, emerging evidence suggests a compelling interdependent relationship between AAA and RAS, challenging the conventional siloed understanding. The confluence of AAA and RAS represents a complex interplay within the cardiovascular system, one that is often overlooked in clinical practice and research. Here, we reveal a bidirectional consequential impact between these two diseases. The location of the AAA sac was investigated for its specific influence on the risk of RAS development. Although studies have shown a higher coincidence between the suprarenal AAA and RAS, our findings demonstrated that the presence of a suprarenal AAA correlated with the lowest risk of RAS development among the three investigated AAA locations. Notably, we also highlighted that the pre-existence of stenosis in the renal artery poses an elevated risk for the formation of suprarenal AAA, assessed by an increased wall shear stress gradient on the aortic wall. Our findings prompt a paradigm shift in the understanding and treatment of AAA and RAS in clinical practice.

Fig. 1

Geometry of the simulated models and the corresponding boundary conditions. (a) Symmetric models of infrarenal, juxtarenal and suprarenal AAA were used for the simulations. A healthy abdominal aorta model was designed as a control for the comparative study. (b) Infrarenal AAA model with dimensions used for construction and applied boundary conditions indicated by green and yellow labels. Velocity Boundary condition was established with a velocity inlet (yellow) and 3-element Windkessel outlets (green). (c) The inlet boundary condition was characterised by a velocity waveform mimicking the pulsatile flow nature in the abdominal aorta. (d) Close-up view of the renal artery in the stenosis model with dimensions used for model construction.

Fig. 2

Assessment of backflow in AAA models. (a) Velocity flow profiles of the healthy and three AAA models across 3 timepoints (0.20 s, 0.48 s and 0.70 s). (b) Percentage backflow area (BFA) on the cranial side of the renal artery. (c) Percentage backflow area (BFA) on the caudal side of the renal artery.

Fig. 3

Quantification of stenosis risk in different AAA models based on OSI and RRT. (a) Surface plots of the renal artery for all AAA models illustrating regions of high OSI and RRT. Insets provide closer examination of the cranial and caudal parts of the renal artery. (b) Circumferential averaged OSI with normalised area of renal artery having OSI > 0.35 across all models. (c) Circumferential averaged RRT with normalised area of renal artery having RRT > 8 Pa⁻¹ across all models.

Fig. 4

Comparing regions of renal helical flow between AAA models across 3 different timepoints. (a) Cross-sectional view of velocity streamlines showing regions of high helicity. (b) Peripheral view of the renal artery showing the propagation of vorticity downstream of the vessel branch.

Fig. 5

Evaluation of TAWSS and TAWSSG on the aortic wall in both healthy and renal artery stenosis model. (a) TAWSSG comparison between healthy and stenosis model. (b) TAWSS comparison between healthy and stenosis model.