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In this study, coupled hemodynamic–acoustic simulations are employed to study the generation and propagation of murmurs associated with aortic stenoses where the aorta with a stenosed aortic valve is modeled as a curved pipe with a constriction near the inlet. The hemodynamics of the poststenotic flow is investigated in detail in our previous numerical study (Zhu et al., 2018, “Computational Modelling and Analysis of Haemodynamics in a Simple Model of Aortic Stenosis,” J. Fluid Mech., 851, pp. 23–49). The temporal history of the pressure on the aortic lumen is recorded during the hemodynamic study and used as the murmur source in the acoustic simulations. The thorax is modeled as an elliptic cylinder and the thoracic tissue is assumed to be homogeneous, linear and viscoelastic. A previously developed high-order numerical method that is capable of dealing with immersed bodies is applied in the acoustic simulations. To mimic the clinical practice of auscultation, the sound signals from the epidermal surface are collected. The simulations show that the source of the aortic stenosis murmur is located at the proximal end of the aortic arch and that the sound intensity pattern on the epidermal surface can predict the source location of the murmurs reasonably well. Spectral analysis of the murmur reveals the disconnect between the break frequency obtained from the flow and from the murmur signal. Finally, it is also demonstrated that the source locations can also be predicted by solving an inverse problem using the free-space Green's function. The implications of these results for cardiac auscultation are discussed. [ABSTRACT FROM AUTHOR]

A computational framework consisting of a one-way coupled hemodynamic-acoustic method and a wave-decomposition based postprocessing approach is developed to investigate the biomechanics of arterial bruits. This framework is then applied for studying the effect of the shear wave on the generation and propagation of bruits from a modeled stenosed artery. The blood flow in the artery is solved by an immersed boundary method (IBM) based incompressible flow solver. The sound generation and propagation in the blood volume are modeled by the linearized perturbed compressible equations, while the sound propagation through the surrounding tissue is modeled by the linear elastic wave equation. A decomposition method is employed to separate the acoustic signal into a compression!longitudinal component (curl free) and a shear!transverse component (divergence free), and the sound signals from cases with and without the shear modulus are monitored on the epidermal surface and are analyzed to reveal the influence of the shear wave. The results show that the compression wave dominates the detected sound signal in the immediate vicinity of the stenosis, whereas the shear wave has more influence on surface signals further downstream of the stenosis. The implications of these results on cardiac auscultation are discussed. [ABSTRACT FROM AUTHOR]

In this study, a novel reduced degree-of-freedom (rDOF) aortic valve model is employed to investigate the fluid-structure interaction (FSI) and hemodynamics associated with aortic stenosis. The dynamics of the valve leaflets are determined by an ordinary differential equation with two parameters and this rDOF model is shown to reproduce key features of more complex valve models. The hemodynamics associated with aortic stenosis is studied for three cases: a healthy case and two stenosed cases. The focus of the study is to correlate the hemodynamic features with the source generation mechanism of systolic murmurs associated with aortic stenosis. In the healthy case, extremely weak flow fluctuations are observed. However, in the stenosed cases, simulations show significant turbulent fluctuations in the ascending aorta, which are responsible for the generation of strong wall pressure fluctuations after the aortic root mostly during the deceleration phase of the systole. The intensity of the murmur generation increases with the severity of the stenosis, and the source locations for the two diseased cases studied here lie around 1.0 inlet duct diameters (Do) downstream of the ascending aorta. [ABSTRACT FROM AUTHOR]