No abstract

Surgical ventricular restoration (SVR) is designed to normalize distorted ventricular shape and size in patients with left ventricular (LV) dysfunction and akinetic and dyskinetic segments. This study is aimed to quantify the characteristics of LV as a pump for a case before and after SVR, which is followed by coronary artery bypass grafting (CABG). We hypothesize that SVR+CABG improves heart flow. A patient with heart failure had magnetic resonance (MR) scans before and 4 months after SVR. LV endocardial geometries were semi-automated segmented and reconstructed using our customized algorithm. The arbitrary Lagrangian-Eulerian formulation of Navier-Stokes equations was solved to derive the flow patterns and calculate pressure differences in LV. After SVR, LV ejection fraction increased from 34% to 48% in patient but was still lower than normal (70%). Second, LV vortices were stronger than pre-surgery but still weaker than normal. The maximum pressure differences between ventricular base and apex increased from 180 to 400 Pa during diastole, from 252 to 560 Pa during systole, respectively. As anticipated, SVR reduced LV volumes and augmented LV ejection fraction. Three-dimensional CFD/MRI modeling suggests that improved diastolic and systolic ventricular function after SVR is associated with changes in intraventricular blood flow.

Tortuous aneurysmal arteries are often associated with a higher risk of rupture but the mechanism remains unclear. The goal of this study was to analyze the buckling and post-buckling behaviors of aneurysmal arteries under pulsatile flow. To accomplish this goal, we analyzed the buckling behavior of model carotid and abdominal aorta with aneurysms by utilizing fluid-structure interaction (FSI) method with realistic waveforms boundary conditions. FSI simulations were done under steady-state and pulsatile flow for normal (1.5) and reduced (1.3) axial stretch ratios to investigate the influence of aneurysm, pulsatile lumen pressure and axial tension on stability. Our results indicated that aneurysmal artery buckled at the critical buckling pressure and its deflection nonlinearly increased with increasing lumen pressure. Buckling elevates the peak stress (up to 118%). The maximum aneurysm wall stress at pulsatile FSI flow was (29%) higher than under static pressure at the peak lumen pressure of 130 mmHg. Buckling results show an increase in lumen shear stress at the inner side of the maximum deflection. Vortex flow was dramatically enlarged with increasing lumen pressure and artery diameter. Aneurysmal arteries are more susceptible than normal arteries to mechanical instability which causes high stresses in the aneurysm wall that could lead to aneurysm rupture.

The heart is an organ which pumps blood around the body by contraction of muscular wall. There is a coupled system in the heart containing the motion of wall and the motion of blood fluid; both motions must be computed simultaneously, which make biological computational fluid dynamics (CFD) difficult. The wall of the heart is not rigid and hence proper boundary conditions are essential for CFD modelling. Fluid-wall interaction is very important for real CFD modelling. There are many assumptions for CFD simulation of the heart that make it far from a real model. A realistic fluid-structure interaction modelling the structure by the finite element method and the fluid flow by CFD use more realistic coupling algorithms. This type of method is very powerful to solve the complex properties of the cardiac structure and the sensitive interaction of fluid and structure. The final goal of heart modelling is to simulate the total heart function by integrating cardiac anatomy, electrical activation, mechanics, metabolism and fluid mechanics together, as in the computational framework.

Tortuous carotid arteries are often seen in aged populations and are associated with atherosclerosis, but the underlying mechanisms to explain this preference are unclear. Artery buckling has been suggested as one potential mechanism for the development of tortuous arteries. The objective of this study, accordingly, was to determine the effect of buckling on cell proliferation and associated NF-κB activation in arteries. We developed a technique to generate buckling in porcine carotid arteries using long artery segments in organ culture without changing the pressure, flow rate, and axial stretch ratio. Using this technique, we examined the effect of buckling on arterial wall remodeling in 4-day organ culture under normal and hypertensive pressures. Cell proliferation, NF-κB p65, IκB-α, ERK1/2, and caspase-3 were detected using immunohistochemistry staining and immunoblot analysis. Our results showed that cell proliferation was elevated 5.8-fold in the buckling group under hypertensive pressure (n = 7, P < 0.01) with higher levels of NF-κB nuclear translocation and IκB-α degradation (P < 0.05 for both). Greater numbers of proliferating cells were observed on the inner curve side of the buckled arteries compared with the outer curve side (P < 0.01). NF-κB colocalized with proliferative nuclei. Computational simulations using a fluid-structure interaction model showed reduced wall stress on the inner side of buckled arteries and elevated wall stress on the outer side. We conclude that arterial buckling promotes site-specific wall remodeling with increased cell proliferation and NF-κB activation. These findings shed light on the biomechanical and molecular mechanisms of the pathogenesis of atherosclerosis in tortuous arteries.