Computational Fluid Dynamics Simulations of Hemodynamics in Plaque Erosion

We investigated whether local hemodynamics were associated with sites of plaque erosion and hypothesized that patients with plaque erosion have locally elevated WSS magnitude in regions where erosion has occurred. We generated 3D, patient-specific models of coronary arteries from biplane angiographic images in 3 human patients with plaque erosion diagnosed by optical coherence tomography. Using computational fluid dynamics, we simulated pulsatile blood flow and calculated both wall shear stress (WSS) and oscillatory shear index (OSI). We also investigated anatomic features of plaque erosion sites by examining branching and local curvature in X-ray angiograms of barium-perfused autopsy hearts. Neither high nor low magnitudes of mean WSS were associated with sites of plaque erosion. OSI and local curvature were also not associated with erosion. Anatomically, 8 of 13 hearts had a nearby bifurcation upstream of the site of plaque erosion. This study provides preliminary evidence that neither hemodynamics nor anatomy are predictors of plaque erosion, based upon a very unique dataset. Our sample sizes are small, but this dataset suggests that high magnitudes of WSS, one potential mechanism for inducing plaque erosion, are not necessary for erosion to occur.

[1]  W. Coulter.  Effect of Inlet Velocity Profiles on Patient-Specific Computational Fluid Dynamics Simulations of the Carotid Bifurcation , 2013 .

[2]  R D Kamm,et al.  Effects of fibrous cap thickness on peak circumferential stress in model atherosclerotic vessels. , 1992, Circulation research.

[3]  M. Kimura,et al.  Association of coronary plaque composition and arterial remodelling: a optical coherence tomography study. , 2012, Atherosclerosis.

[4]  D. L. Fry.  Acute Vascular Endothelial Changes Associated with Increased Blood Velocity Gradients , 1968, Circulation research.

[5]  E. Edelman,et al.  Prediction of the Localization of High-Risk Coronary Atherosclerotic Plaques on the Basis of Low Endothelial Shear Stress: An Intravascular Ultrasound and Histopathology Natural History Study , 2008, Circulation.

[6]  D. Giddens,et al.  Localization of culprit lesions in coronary arteries of patients with ST-segment elevation myocardial infarctions: relation to bifurcations and curvatures. , 2011, American heart journal.

[7]  J. Abe,et al.  Stress and vascular responses: atheroprotective effect of laminar fluid shear stress in endothelial cells: possible role of mitogen-activated protein kinases. , 2003, Journal of pharmacological sciences.

[8]  D. Ku,et al.  Rapid Platelet Accumulation Leading to Thrombotic Occlusion , 2011, Annals of Biomedical Engineering.

[9]  R. Virmani,et al.  Coronary plaque erosion without rupture into a lipid core. A frequent cause of coronary thrombosis in sudden coronary death. , 1996, Circulation.

[10]  D. Ku,et al.  Pulsatile Flow and Atherosclerosis in the Human Carotid Bifurcation: Positive Correlation between Plaque Location and Low and Oscillating Shear Stress , 1985, Arteriosclerosis.

[11]  David L. Hayes,et al.  Mayo Clinic Practice of Cardiology , 1996 .

[12]  B. Gersh.  Relationship of Thrombus Healing to Underlying Plaque Morphology in Sudden Coronary Death , 2011 .

[13]  Takahiro Okumura,et al.  OCT assessment of thin-cap fibroatheroma distribution in native coronary arteries. , 2010, JACC. Cardiovascular imaging.

[14]  V. Fuster,et al.  OCT-based diagnosis and management of STEMI associated with intact fibrous cap. , 2013, JACC. Cardiovascular imaging.

[15]  Hans-Christian Hege,et al.  Coronary Artery WSS Profiling Using a Geometry Reconstruction Based on Biplane Angiography , 2009, Annals of Biomedical Engineering.

[16]  A. Becker,et al.  Site of intimal rupture or erosion of thrombosed coronary atherosclerotic plaques is characterized by an inflammatory process irrespective of the dominant plaque morphology. , 1994, Circulation.

[17]  P. Eshtehardi,et al.  Intravascular Imaging Tools in the Cardiac Catheterization Laboratory: Comprehensive Assessment of Anatomy and Physiology , 2011, Journal of cardiovascular translational research.

[18]  C L Feldman,et al.  Intravascular hemodynamic factors responsible for progression of coronary atherosclerosis and development of vulnerable plaque. , 2000, Current opinion in cardiology.

[19]  C. R. Ethier,et al.  A numerical study of blood flow patterns in anatomically realistic and simplified end-to-side anastomoses. , 1999, Journal of biomechanical engineering.

[20]  Jouke Dijkstra,et al.  In vivo validation of CAAS QCA‐3D coronary reconstruction using fusion of angiography and intravascular ultrasound (ANGUS) , 2009, Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions.

[21]  Klaus Affeld,et al.  In-vivo coronary flow profiling based on biplane angiograms: influence of geometric simplifications on the three-dimensional reconstruction and wall shear stress calculation , 2006, Biomedical engineering online.

[22]  R. Virmani,et al.  Pathology of the Vulnerable Plaque , 2006 .

[23]  M. Gotsman,et al.  Endothelial Cell Damage and Thrombus Formation After Partial Arterial Constriction: Relevance to the Role of Coronary Artery Spasm in the Pathogenesis of Myocardial Infarction , 1981, Circulation.

[24]  Takafumi Hiro,et al.  Localized elevation of shear stress is related to coronary plaque rupture: a 3-dimensional intravascular ultrasound study with in-vivo color mapping of shear stress distribution. , 2008, Journal of the American College of Cardiology.

[25]  A. Quarteroni,et al.  Multiscale models of the vascular system , 2009 .

[26]  Barbara Norton McCord.  Fatigue of atherosclerotic plaque , 1992 .

[27]  R. Virmani,et al.  The accumulation of specific types of proteoglycans in eroded plaques: a role in coronary thrombosis in the absence of rupture , 2004, Current opinion in lipidology.

[28]  Peter M. Rothwell,et al.  Site of Carotid Plaque Ulceration in Relation to Direction of Blood Flow: An Angiographic and Pathological Study , 2003, Cerebrovascular Diseases.

[29]  Charles A. Taylor,et al.  Outflow boundary conditions for three-dimensional finite element modeling of blood flow and pressure in arteries , 2006 .

[30]  Alfio Quarteroni,et al.  Multiscale modelling of the circulatory system: a preliminary analysis , 1999 .

[31]  S. Goto,et al.  Disturbed blood flow induces erosive injury to smooth muscle cell‐rich neointima and promotes thrombus formation in rabbit femoral arteries , 2010, Journal of thrombosis and haemostasis : JTH.

[32]  Felix Yang,et al.  The impact of gender on vessel size in patients with angiographically normal coronary arteries. , 2006, Journal of interventional cardiology.

[33]  Patrick W Serruys,et al.  Advanced three-dimensional quantitative coronary angiographic assessment of bifurcation lesions: methodology and phantom validation. , 2013, EuroIntervention : journal of EuroPCR in collaboration with the Working Group on Interventional Cardiology of the European Society of Cardiology.

[34]  P. Lelkes,et al.  Gene expression profiling of vascular endothelial cells exposed to fluid mechanical forces: relevance for focal susceptibility to atherosclerosis. , 2004, Endothelium : journal of endothelial cell research.

[35]  D. Ku,et al.  Pulsatile Flow in a Model Carotid Bifurcation , 1983, Arteriosclerosis.

[36]  D. Giddens,et al.  Geometric and Hemodynamic Evaluation of 3-Dimensional Reconstruction Techniques for the Assessment of Coronary Artery Wall Shear Stress in the Setting of Clinical Disease Progression , 2011 .

[37]  Michail I. Papafaklis,et al.  Natural History of Experimental Coronary Atherosclerosis and Vascular Remodeling in Relation to Endothelial Shear Stress: A Serial, In Vivo Intravascular Ultrasound Study , 2010, Circulation.

[38]  C. Ross Ethier,et al.  Effects of Cardiac Motion on Right Coronary Artery Hemodynamics , 2003, Annals of Biomedical Engineering.

[39]  P. Shah,et al.  Mechanisms of plaque vulnerability and rupture. , 2003, Journal of the American College of Cardiology.

[40]  D. Ku.  BLOOD FLOW IN ARTERIES , 1997 .

[41]  C. Yuan,et al.  Plaque Rupture in the Carotid Artery Is Localized at the High Shear Stress Region: A Case Report , 2007, Stroke.

[42]  Akiko Maehara,et al.  Consensus standards for acquisition, measurement, and reporting of intravascular optical coherence tomography studies: a report from the International Working Group for Intravascular Optical Coherence Tomography Standardization and Validation. , 2012, Journal of the American College of Cardiology.

[43]  P. Shah,et al.  Inflammation and Plaque Vulnerability , 2009, Cardiovascular Drugs and Therapy.

[44]  A. Tedgui,et al.  Current perspective on the role of apoptosis in atherothrombotic disease. , 2001, Circulation research.

[45]  David N. Ku,et al.  A Mechanistic Model of Acute Platelet Accumulation in Thrombogenic Stenoses , 2001, Annals of Biomedical Engineering.

[46]  M. Desnos,et al.  In Vivo Induction of Endothelial Apoptosis Leads to Vessel Thrombosis and Endothelial Denudation: A Clue to the Understanding of the Mechanisms of Thrombotic Plaque Erosion , 2004, Circulation.

[47]  Rolf Rannacher,et al.  ARTIFICIAL BOUNDARIES AND FLUX AND PRESSURE CONDITIONS FOR THE INCOMPRESSIBLE NAVIER–STOKES EQUATIONS , 1996 .

[48]  S. Alper,et al.  Hemodynamic shear stress and its role in atherosclerosis. , 1999, JAMA.

[49]  O. Tricot,et al.  Relation between endothelial cell apoptosis and blood flow direction in human atherosclerotic plaques. , 2000, Circulation.

[50]  M. Nelson,et al.  Gender differences in coronary artery diameter reflect changes in both endothelial Ca2+ and ecNOS activity. , 1999, The American journal of physiology.

[51]  Michael C. McDaniel,et al.  Coronary Artery Wall Shear Stress Is Associated With Progression and Transformation of Atherosclerotic Plaque and Arterial Remodeling in Patients With Coronary Artery Disease , 2011, Circulation.

[52]  J. M. Siegel,et al.  Computational Analysis of Flow in a Curved Tube Model of the Coronary Arteries: Effects of Time-varying Curvature , 1998, Annals of Biomedical Engineering.