Different Blood Flow Models in Coronary Artery Diseases: Effects on hemodynamic parameters

Author(s):  
L.T. Gaudio ◽  
M.V. Caruso ◽  
S. De Rosa ◽  
C. Indolfi ◽  
G. Fragomeni
2014 ◽  
Vol 42 (5) ◽  
pp. 1012-1023 ◽  
Author(s):  
Paris Perdikaris ◽  
George Em. Karniadakis

2014 ◽  
Vol 59 (7) ◽  
pp. 1533-1556 ◽  
Author(s):  
Michael Bindschadler ◽  
Dimple Modgil ◽  
Kelley R Branch ◽  
Patrick J La Riviere ◽  
Adam M Alessio

2021 ◽  
pp. 1-18
Author(s):  
Abdulgaphur Athani ◽  
N.N.N. Ghazali ◽  
Irfan Anjum Badruddin ◽  
Sarfaraz Kamangar ◽  
Ali E. Anqi ◽  
...  

BACKGROUND: The blood flow in the human artery has been a subject of sincere interest due to its prime importance linked with human health. The hemodynamic study has revealed an essential aspect of blood flow that eventually proved to be paramount to make a correct decision to treat patients suffering from cardiac disease. OBJECTIVE: The current study aims to elucidate the two-way fluid-structure interaction (FSI) analysis of the blood flow and the effect of stenosis on hemodynamic parameters. METHODS: A patient-specific 3D model of the left coronary artery was constructed based on computed tomography (CT) images. The blood is assumed to be incompressible, homogenous, and behaves as Non-Newtonian, while the artery is considered as a nonlinear elastic, anisotropic, and incompressible material. Pulsatile flow conditions were applied at the boundary. Two-way coupled FSI modeling approach was used between fluid and solid domain. The hemodynamic parameters such as the pressure, velocity streamline, and wall shear stress were analyzed in the fluid domain and the solid domain deformation. RESULTS: The simulated results reveal that pressure drop exists in the vicinity of stenosis and a recirculation region after the stenosis. It was noted that stenosis leads to high wall stress. The results also demonstrate an overestimation of wall shear stress and velocity in the rigid wall CFD model compared to the FSI model.


2013 ◽  
Vol 19 (4) ◽  
pp. 319-330 ◽  
Author(s):  
B. Hametner ◽  
T. Weber ◽  
C. Mayer ◽  
J. Kropf ◽  
S. Wassertheurer

2012 ◽  
Vol 45 (2) ◽  
pp. 918-923 ◽  
Author(s):  
Bernhard Hametner ◽  
Thomas Weber ◽  
Christopher Mayer ◽  
Johannes Kropf ◽  
Siegfried Wassertheurer

Author(s):  
K. S. Burrowes ◽  
A. R. Clark ◽  
A. Marcinkowski ◽  
M. L. Wilsher ◽  
D. G. Milne ◽  
...  

Pulmonary embolism (PE) is the most common cause of acute pulmonary hypertension, yet it is commonly undiagnosed, with risk of death if not recognized promptly and managed accordingly. Patients typically present with hypoxemia and hypocapnia, although the presentation varies greatly, being confounded by co-mordidities such as pre-existing cardio-respiratory disease. Previous studies have demonstrated variable patient outcomes in spite of similar extent and distribution of pulmonary vascular occlusion, but the pathophysiological determinants of outcome remain unclear. Computational models enable exact control over many of the compounding factors leading to functional outcomes and therefore provide a useful tool to understand and assess these mechanisms. We review the current state of pulmonary blood flow models. We present a pilot study within 10 patients presenting with acute PE, where patient-derived vascular occlusions are imposed onto an existing model of the pulmonary circulation enabling predictions of resultant haemodynamics after embolus occlusion. Results show that mechanical obstruction alone is not sufficient to cause pulmonary arterial hypertension, even when up to 65 per cent of lung tissue is occluded. Blood flow is found to preferentially redistribute to the gravitationally non-dependent regions. The presence of an additional downstream occlusion is found to significantly increase pressures.


2018 ◽  
Vol 15 (149) ◽  
pp. 20180546 ◽  
Author(s):  
Fredrik E. Fossan ◽  
Jorge Mariscal-Harana ◽  
Jordi Alastruey ◽  
Leif R. Hellevik

As computational models of the cardiovascular system are applied in modern personalized medicine, maximizing certainty of model input becomes crucial. A model with a high number of arterial segments results in a more realistic description of the system, but also requires a high number of parameters with associated uncertainties. In this paper, we present a method to optimize/reduce the number of arterial segments included in one-dimensional blood flow models, while preserving key features of flow and pressure waveforms. We quantify the preservation of key flow features for the optimal network with respect to the baseline networks (a 96-artery and a patient-specific coronary network) by various metrics and quantities like average relative error, pulse pressure and augmentation pressure. Furthermore, various physiological and pathological states are considered. For the aortic root and larger systemic artery pressure waveforms a network with minimal description of lower and upper limb arteries and no cerebral arteries, sufficiently captures important features such as pressure augmentation and pulse pressure. Discrepancies in carotid and middle cerebral artery flow waveforms that are introduced by describing the arterial system in a minimalistic manner are small compared with errors related to uncertainties in blood flow measurements obtained by ultrasound.


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