dc.contributor.author |
Chaniotis, AK |
en |
dc.contributor.author |
Kaiktsis, L |
en |
dc.contributor.author |
Katritsis, D |
en |
dc.contributor.author |
Efstathopoulos, E |
en |
dc.contributor.author |
Pantos, I |
en |
dc.contributor.author |
Marmarellis, V |
en |
dc.date.accessioned |
2014-03-01T01:33:02Z |
|
dc.date.available |
2014-03-01T01:33:02Z |
|
dc.date.issued |
2010 |
en |
dc.identifier.issn |
1120-1797 |
en |
dc.identifier.uri |
https://dspace.lib.ntua.gr/xmlui/handle/123456789/20287 |
|
dc.subject |
Bifurcating pipe |
en |
dc.subject |
Blood flow simulation |
en |
dc.subject |
Curved pipe |
en |
dc.subject |
Wall shear stress |
en |
dc.subject.classification |
Biophysics |
en |
dc.subject.other |
von Willebrand factor |
en |
dc.subject.other |
article |
en |
dc.subject.other |
atherosclerosis |
en |
dc.subject.other |
blood vessel wall |
en |
dc.subject.other |
cell proliferation |
en |
dc.subject.other |
coronary artery blood flow |
en |
dc.subject.other |
flow rate |
en |
dc.subject.other |
geometry |
en |
dc.subject.other |
heart cycle |
en |
dc.subject.other |
heart valve prosthesis |
en |
dc.subject.other |
internalization |
en |
dc.subject.other |
mathematical analysis |
en |
dc.subject.other |
mathematical computing |
en |
dc.subject.other |
mechanical stress |
en |
dc.subject.other |
shear stress |
en |
dc.subject.other |
simulation |
en |
dc.subject.other |
thrombocyte aggregation |
en |
dc.subject.other |
vascular disease |
en |
dc.subject.other |
Algorithms |
en |
dc.subject.other |
Blood Pressure |
en |
dc.subject.other |
Computer Simulation |
en |
dc.subject.other |
Coronary Aneurysm |
en |
dc.subject.other |
Coronary Artery Disease |
en |
dc.subject.other |
Coronary Thrombosis |
en |
dc.subject.other |
Coronary Vessels |
en |
dc.subject.other |
Humans |
en |
dc.subject.other |
Models, Cardiovascular |
en |
dc.subject.other |
Myocardial Contraction |
en |
dc.subject.other |
Periodicity |
en |
dc.subject.other |
Platelet Aggregation |
en |
dc.subject.other |
Regional Blood Flow |
en |
dc.subject.other |
Stress, Mechanical |
en |
dc.subject.other |
Time Factors |
en |
dc.subject.other |
Ventricular Function |
en |
dc.title |
Computational study of pulsatile blood flow in prototype vessel geometries of coronary segments |
en |
heal.type |
journalArticle |
en |
heal.identifier.primary |
10.1016/j.ejmp.2009.03.004 |
en |
heal.identifier.secondary |
http://dx.doi.org/10.1016/j.ejmp.2009.03.004 |
en |
heal.language |
English |
en |
heal.publicationDate |
2010 |
en |
heal.abstract |
The spatial and temporal distributions of wall shear stress (WSS) in prototype vessel geometries of coronary segments are investigated via numerical simulation, and the potential association with vascular disease and specifically atherosclerosis and plaque rupture is discussed. In particular, simulation results of WSS spatio-temporal distributions are presented for pulsatile, non-Newtonian blood flow conditions for: (a) curved pipes with different curvatures, and (b) bifurcating pipes with different branching angles and flow division. The effects of non-Newtonian flow on WSS (compared to Newtonian flow) are found to be small at Reynolds numbers representative of blood flow in coronary arteries. Specific preferential sites of average low WSS (and likely atherogenesis) were found at the outer regions of the bifurcating branches just after the bifurcation, and at the outer-entry and inner-exit flow regions of the curved vessel segment. The drop in WSS was more dramatic at the bifurcating vessel sites (less than 5% of the pre-bifurcation value). These sites were also near rapid gradients of WSS changes in space and time a fact that increases the risk of rupture of plaque likely to develop at these sites. The time variation of the WSS spatial distributions was very rapid around the start and end of the systolic phase of the cardiac cycle, when strong fluctuations of intravascular pressure were also observed. These rapid and strong changes of WSS and pressure coincide temporally with the greatest flexion and mechanical stresses induced in the vessel wall by myocardial motion (ventricular contraction). The combination of these factors may increase the risk of plaque rupture and thrombus formation at these sites. (C) 2009 Published by Elsevier Ltd on behalf of Associazione Italiana di Fisica Medica. |
en |
heal.publisher |
IST EDITORIALI POLGRAFICI INT |
en |
heal.journalName |
Physica Medica |
en |
dc.identifier.doi |
10.1016/j.ejmp.2009.03.004 |
en |
dc.identifier.isi |
ISI:000280471600004 |
en |
dc.identifier.volume |
26 |
en |
dc.identifier.issue |
3 |
en |
dc.identifier.spage |
140 |
en |
dc.identifier.epage |
156 |
en |