Computational simulations of hemodynamic changes within thoracic, coronary, and cerebral arteries following early wall remodeling in response to distal aortic coarctation

Abstract

Mounting evidence suggests that the pulsatile character of blood pressure and flow within large arteries plays a particularly important role as a mechano-biological stimulus for wall growth and remodeling. Nevertheless, understanding better the highly coupled interactions between evolving wall geometry, structure, and properties and the hemodynamics will require significantly more experimental data. Computational fluid–solid-growth models promise to aid in the design and interpretation of such experiments and to identify candidate mechanobiological mechanisms for the observed arterial adaptations. Motivated by recent aortic coarctation models in animals, we used a computational fluid–solid interaction model to study possible local and systemic effects on the hemodynamics within the thoracic aorta and coronary, carotid, and cerebral arteries due to a distal aortic coarctation and subsequent spatial variations in wall adaptation. In particular, we studied an initial stage of acute cardiac compensation (i.e., maintenance of cardiac output) followed by early arterial wall remodeling (i.e., spatially varying wall thickening and stiffening). Results suggested, for example, that while coarctation increased both the mean and pulse pressure in the proximal vessels, the locations nearest to the coarctation experienced the greatest changes in pulse pressure. In addition, after introducing a spatially varying wall adaptation, pressure, left ventricular work, and wave speed all increased. Finally, vessel wall strain similarly experienced spatial variations consistent with the degree of vascular wall adaptation.

Differential impact of local stiffening and narrowing on hemodynamics in repaired aortic coarctation: an FSI study

“…As such, only local changes in pressure are found, related to the time delay between the backward waves. This finding is in agreement with the 1D studies performed in [5,14] and the 3D FSI study published in [8], reporting negligible clinical consequences of a local stiffening on cardiac workload and aortic pressure. In [33] an experimental porcine model was developed to investigate the effect of a noncompliant stent.…”

“…The assumption of a constant cardiac output in CoA implies an increased workload on the heart and is justified by the findings reported in [15], stating that the cardiac output and the heart rate barely change after surgically induced stenosis. We, however, believe that, due to the elevated resistance at the coarctation site an early redistribution of flow will take place, manifesting as an increased flow through the subclavian and carotid arteries and a reduction of the descending aortic flow [8].…”

“…Patients with (repaired) aortic coarctation might have intrinsic structural defects in extracellular matrix proteins due to genetic defects [42], and their aorta has been subjected to growth and remodeling [16,23] with adaptions in shape and material properties. In particular for the case of aortic coarctation, wall thickening is often observed along with a decrease in compliance of the proximal aorta due to prolonged hypertension [8,27]. As such, neither the 3D geometry, neither the assumed material constants in this paper can be considered representative for patients with (repaired) aortic coarctation.…”

“…Application of reduced order models at the distal boundaries of the fluid domain might resolve this problem [8,20]. Since the pressure drop across the CoA is proportional to the flow rate through the constriction, the flow distribution adopted in our models represents the worst case distribution, associated with the highest pressure gradients.…”

“…Although there is considerable literature on computational modeling of aortic coarctation, most studies do not account for the elasticity of the aorta and the fluid-structure interaction (FSI) [19,22,30,39,44] and/or have their focus on the hemodynamic impact of coarctation in patientspecific cases [20] or on arterial wall stress and remodeling [8]. The aim of this work is to develop a physiologically relevant 3D model of the aorta with a parametric model for the coarctation zone to predict the hemodynamic impact of (coexisting) stiffening and narrowing in CoA repair.…”