Post-stenotic Dilatations Research Articles

The Effects of Post-Stenotic Dilatations on the Flow of Couple Stress Fluid through Stenosed Arteries

The flow of incompressible couple stress fluid in a circular tube with stenosis and dilatations has been investigated. The stenosis was assumed to be axially symmetric and mild. The flow equations have been linearized and the expressions for the resistance to the flow, velocity, pressure drop, wall shear stress have been derived. The effects of various parameters on these flow variables have been investigated. It is found that the resistance to the flow and pressure drop increase with height of the stenosis and decrease with post stenotic dilatation. Pressure drop decreases with couple stress fluid parameter for both stenosis and post stenotic dilatation. Further, the wall shear stress increases with height of the stenosis and couple stress parameter but decreases with post stenotic dilatation and couple stress fluid parameter.

Blood flow in stenosed arteries using two way, fluid-structural interaction

Blood flow in a stenosed artery was simulated using the two way, fluid-structural interactions in ANSYS---a commercial finite element and finite volume software widely used in industry. Several stenosis models were investigated using a pulsatile flow condition. In these models the form of the stenosis geometry was either axisymmetric or axis-asymmetric. The blood was modelled both as a non-Newtonian, power law fluid, and as the Casson model. The artery tissue was assumed to be a linear elastic material for the axis-symmetric stenosis model and nonlinear material for the axis-asymmetric stenosis models. A fibrous cap and lipid pool were also added into the stenosis geometry of the axis-asymmetric models to account for complexities of the physiology. The effect of the stenosis severity on arteries was investigated by examining the blood flow velocity, pressure and wall shear stress at multiple locations. References K. C. Ang and J. N. Mazumdar, Mathematical modelling of three-dimensional flow through an asymmetric arterial stenosis, Mathematical and Computer Modelling, 25, No 1, 19--29, 1997, doi:10.1016/S0895-7177(96)00182-3. W. Y. Chan, Y. Ding, J. Y. Tu, Modeling of non-Newtonian blood flow through a stenosed artery incorporating fluid-structure interaction, ANZIAM Journal, 47, 507--523, 2007, http://anziamj.austms.org.au/ojs/index.php/ANZIAMJ/article/view/1059. Santabrata Chakravarty and Prashanta Kumar Mandal, Two-Dimensional blood flow through tapered arteries under stenotic conditions, Non-Linear Mechanics, 35, 779--793, August, 2006, doi:10.1016/S0020-7462(99)00059-1. Samuel A. Kock and Jens V. Nygaard. Nikolaj Eldrup,Ernst-Torben Frund and Anette Klaeke, William P.Pausk. Erling Falk and W.Yong Kim, Mechanical Stresses in carotid plaques using MRI-based fluid-structure interaction models, Journal of Biomechanics, 41, 1651--1658, March, 2008, doi:10.1016/j.jbiomech.2008.03.019. K. W. Lee and X. Y. Xu, Modelling of flow and wall behaviour in a mildly stenosed tube, Medical Engineering and Physics, 24, 575--586, May, 2002, doi:10.1016/S1350-4533(02)00048-6. M. X. Li and J. J. Beech-Brandt and L. R. John and P. R. Hoskins and W. J. Easson, Numerical analysis pulsatile blood flow and vessel wall mechanics in different degrees of stenoses, Journal of Biomechanics, 40, 3715--3724, June, 2007, doi:10.1016/j.jbiomech.2007.06.023. B. Pincombe and J. Mazumdar, The effects of post-stenotic dilatations on the flow of a blood analogue through stenosed coronary arteries, Mathematical and Computer Modelling, 25, No 6, 57--70, 1997, doi:10.1016/S0895-7177(97)00039-3. J. Poiseuille, Observations of blood flow, Ann. Sci. Naturelles Srie 5, 2, 1836. S. U. Siddiqui and N. K. Verma and Shailesh Mishra and R. S. Gupta, Mathematical modelling of pulsatile flow of Cassons fluid in arterial stenosis, Applied Mathematics and Computation, 2007, doi:10.1016/j.amc.2007.05.070. S. U. Siddiqui and Shailesh Mishra, A study of modified Casson's fluid in modelled normal and stenotic capillary-tissue diffusion phenomena, Applied Mathematics and Computation, 189, 1048--1057, 2007, doi:10.1016/j.amc.2006.11.151. Dalin Tang and Chun Yang and David N. Ku, A 3D thin-wall model with fluid-structure interactions for blood flow in carotid arteries with symmetric and asymmetric stenoses, Computers and Structures, 72, 357--377, 1999, doi:10.1016/S0045-7949(99)00019-X. Dalin Tang and Chun Yang and Yan Huang and David N. Ku, Wall stress and strain analysis using a three-dimensional thick-wall model with fluid-structure interactions for blood flow in carotid arteries with stenoses, Computers and Structures, 72, 341--356, May, 1999, doi:10.1016/S0045-7949(99)00009-7. Dalin Tang, Chun Yang, Jie Zheng, Pamela K. Woodard, Gregorio A. Sicard, Jeffrey E. Saffiz, Shunichi Kobayashi, Thomas K. Pilgram, and Chun Yuan, 3D computational mechanical analysis for human Atherosclerotic plaques using MRI-based models with fluid-structure interactions, MICCAI, 328--336, 2004. Dalin Tang and Chun Yang and Jie Zheng and Pamela K.Woodard and Gregorio A.Sicard and Jefferey E. Saffitz and Chun Yuan, 3D mri-based multicomponent fsi models for artherosclerotic plaques, Biomedical Engineering, 32, 947--960, July, 2004.

Modelling of blood flow resistance for an atherosclerotic artery with multiple stenoses and poststenotic dilatations

Modelling of blood flow resistance for an atherosclerotic artery with multiple stenoses and poststenotic dilatations

In-vivo flow simulation in coronary arteries based on computed tomography datasets: feasibility and initial results

The purpose of this paper was to non-invasively assess hemodynamic parameters such as mass flow, wall shear stress (WSS), and wall pressure with computational fluid dynamics (CFD) in coronary arteries using patient-specific data from computed tomography (CT) angiography. Five patients (two without atherosclerosis, three with atherosclerosis) underwent retrospectively electrocardiogram (ECG) gated 16-detector row CT using ECG-pulsing and geometric models of coronary arteries were reconstructed for CFD analysis. Blood flow was considered laminar, incompressible, Newtonian, and pulsatile. The mass flow, WSS, and wall pressure were quantified and flow patterns were visualized. The wall pressure continuously decreased towards distal segments and showed pressure drops in stenotic segments. In coronary segments without atherosclerotic wall changes, WSS remained low, even during phases of high flow velocity, whereas in atherosclerotic vessels, the WSS was elevated already at low flow velocities. Stenoses and post-stenotic dilatations led to flow acceleration and rapid deceleration, respectively, including a distortion of flow. Areas of high WSS and high flow velocities were found adjacent to plaques, with values correlating with the degree of stenosis. CFD provided detailed mass flow measurements. CFD analysis is feasible in normal and atherosclerotic coronary arteries and provides the rationale for further investigation of the links between hemodynamic parameters and the significance of coronary stenoses.

T-banding: A technique for flow reduction of a hyperfunctioning arteriovenous fistula

A common procedure for hyperfunctioning arteriovenous fistulas is banding, baring the potential for complications such as pre- and poststenotic dilatations and recurrence of high flow caused by slipping of the band itself. We describe a new technique that ensures proper fixation of the graft to prevent anastomotic aneurysms and enlarge the length of stenosis of the shunt vein in order to amplify the effect of flow reduction. This technique was used in 22 patients, with a mean flow reduction of about 50%. The procedure was effective and safe at 1 to 3 months follow-up.

The Polymorphonuclear Leukocyte and the Abdominal Aortic Aneurysm

Companion reports in this issue of Circulation under the senior authorship of G.R. Upchurch1,2 address the possible roles of polymorphonuclear (PMN) cells in the pathogenesis of the nonspecific abdominal aortic aneurysm (AAA). As the authors observe, the AAA is the 10th leading cause of death in white men ages 65 to 74, according to the 2000 National Vital Statistics report, and there were 36 000 surgical repairs. See pp 232 and 241 A study has addressed the state of National Institutes of Health (NIH) funding for research on specific diseases in relation to their burden on public health.3 The 3 leading causes of mortality (ischemic heart disease, lung cancer, and stroke; with a cumulative estimated 4877 “years of life lost”) received ≈$500 million altogether in NIH research support in the year 1990. The 3 rank-ordered leaders in receipt in NIH funding (AIDS, breast cancer, and dementia; with a cumulative estimated 1504 “years of life lost”) received ≈$21 billion dollars in NIH research support. Among the 29 diseases rank-ordered by NIH support, the AAA was not present. In the history of NIH funding for AAA research, there has been only one request for proposals. It is not immediately obvious why research on the causes and prevention of AAA has been so neglected. Perhaps the reason is the deeply embedded notion that the AAA is simply a late degenerative phase of atherosclerosis. Recent editions of major textbooks on pathology4 and medicine5 still offer the “atherosclerotic” explanation for AAA causation. A student of the editorialist has traced references for this explanation back to a treatise by Scarpa, written in Italian and translated into English in 1808. Vascular clinicians know from observation that AAA, or for that matter, lesions that begin as poststenotic dilatations (eg, an aneurysm of the subclavian …

Size reduction ascending aortoplasty: Is it dead or alive?

Objective Reduction ascending aortoplasty is a controversial procedure. Some believe that it can be appropriately applied when the anatomic features are favorable. Others suggest that it should be restricted to those patients who are at unacceptably high risk for more radical procedures, and there are also those who believe that reduction ascending aortoplasty should not be applied at all. The purpose of the article is to draw conclusions on the applicability of reduction ascending aortoplasty in modern cardiovascular surgery. Methods The issue was examined in the mirror of the authors' own experiences, by review and scrutiny of the literature available on the subject, and by conducting an extensive survey of the profession. Results We found that given proper indications (ie, poststenotic dilatations of <6 cm in diameter, absence of cystic medial necrosis, and a technique that decreases aortic diameter to <3.5 cm), nonreinforced reduction ascending aortoplasty performed concomitantly with aortic valve replacement appears to be a simple and safe procedure, with low morbidity and mortality and rare late complications. External reinforcement might extend the scope of indication for reduction ascending aortoplasty to ascending aortic aneurysms associated with aortic regurgitation and to those with primary structural aortic wall disease with comparable results. Experience also has shown that late complications might be further reduced by means of proper proximal anchoring and extending the wrap past the origin of the innominate artery. Conclusions We conclude that reduction ascending aortoplasty is certainly alive. Although it does not appear to be an extremely popular operation, about half of the surgeons who responded believe it to be justified. Regardless of which modality is used, lifetime monitoring of ascending aortic size is essential and so advised. Because of recent sporadic reports of “under-the-wrap” aortic wall atrophy and rupture, the issue of reinforcement of reduction ascending aortoplasty requires continued re-evaluation.

The effects of post-stenotic dilatations on the flow of a blood analogue through stenosed coronary arteries

Previous work on the resistance to flow ratio and wall shear ratio of non-Newtonian blood flow through arteries containing aneurisms and stenoses has considered only Power Law and Casson models of fluid behaviour. Here a Bingham fluid is used to model blood. Flow through both constrictions and dilatations is considered. The effects of both a single diseased portion and pairs of abnormal wall segments in close proximity to each other are investigated. Comparison is made with earlier studies. Particular attention is paid to the effects of a post-stenotic dilatation as the ameorlation of the increase in resistance to flow ratio caused by such a situation is clinically relevant.

Geometric characterization of stenosed human carotid arteries.

The geometry of stenosed carotid bifurcations was analyzed to determine average representations for several stenosis grades. Film angiograms of 62 patients with internal carotid artery stenoses were digitized. Residual lumen boundaries were manually outlined. The outlines were processed with a computer to extract geometric measurements. The measurements were grouped according to stenosis grade and used to create average representations. Accuracy and precision of the outlining technique were +/- 0.020 common carotid diameters (CCD) and +/- 0.025 CCD, respectively. Maximum narrowing of the internal carotid artery occurred at 0.3 CCD +/- 1.5 (mean +/- standard deviation) distal to the flow divider. The region of significant narrowing extended axially 1.2 CCD +/- 1.0. Poststenotic dilatations were observed, with enlargement of 1.3 +/- 0.7 times the normal diameter of the distal internal carotid artery. A tendency toward smaller bifurcation angles with increasing stenosis severity was observed. Three-dimensional geometric models could be created for carotid bifurcations that were disease free (normal) and of arbitrary stenosis grade.

Changes in the vessel wall in the region of the carotid syphon (author's transl

The present paper reviews changes in the vessel wall in the carotid syphon, including variations in calibre, stenoses, post-stenotic dilatation and aneurysms. Particular attention is paid to a supraclinoid circular stenosis, which corresponds in its localisation to the emergence of the internal carotid artery from the dura. Reference is made to new anatomical findings in this region. The haemodynamic basis of poststenotic dilatations and the development of acquired aneurysms as a result of this mechanism are discussed. Examples of post-stenotic aneurysms are demonstrated.

CONGENITAL STENOSIS OF THE PULMONARY ARTERY BRANCHES.

Eighteen cases of stenosis of the branches of the pulmonary artery, seen at the Mayo Clinic, have been reviewed and subdivided into two main types: Type I, stenosis of the main branches of the pulmonary artery, 11 cases, and type II, stenosis of multiple peripheral branches of the pulmonary arteries, seven cases. Of special interest were two cases in which thrombosis occurred as a complication and one case in which surgical relief of multiple areas of stenosis in the peripheral branches of the pulmonary arteries was accomplished. Unexplained pulmonary hypertension necessitates further investigation, which includes cardiac catheterization for measurement of intracardiac pressure and frequently selective angiocardiography. Main branch or peripheral pulmonary artery stenosis should be suspected when a continuous murmur is heard or when poststenotic dilatations of the pulmonary artery branches or areas of decreased pulmonary vasculature can be perceived in the roentgenogram. Angiocardiography is the only technic that permits detailed anatomic evaluation of the entire pulmonary vasculature, especially in the cases associated with severe infundibular or valvular pulmonic stenosis. Stenosis of the branches of the pulmonary artery must be taken into account, when surgical repair of associated cardiovascular defects is considered. These lesions also might complicate anastomotic procedures involving the pulmonary artery in cyanotic patients.

Changes of the Digital Arteries in Rheumatoid Arthritis: A Study with the Aid of Post Mortem Brachial Arteriography

SummaryTen cases of rheumatoid arthritis and twenty control cases were investigated with the aid of post-mortem brachial arteriography. Fine-grain X-ray film was used so as to render it possible to magnify the images by eight diameters. The alterations characteristic of rheumatoid arthritis were: local obliterations and post-stenotic dilatations of the digital arteries, as well as hypervascularization and dilatations of the arterial lumens in the vicinity of usurations of bone.