Effect of Red Blood Cells on Platelet Activation and Thrombus Formation in Tortuous Arterioles

Chesnutt, Jennifer K.W.; Han, Hai‐Chao

doi:10.3389/fbioe.2013.00018

Cited by 16 publications

(15 citation statements)

References 75 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Aneurysm asymmetry is another factor that is related to increased rupture risk (Fillinger et al 2004; Doyle et al 2009). Buckling deformation changes the blood flow in the aneurysm, which can alter the wall shear stress and affects intra-lumen thrombus distribution (Chesnutt and Han 2011; Chesnutt and Han 2013). While some of these changes are similar to normal arteries (Han 2012), they may be severe in aneurysms.…”

Section: Discussionmentioning

confidence: 99%

Mechanical instability of normal and aneurysmal arteries

Lee¹,

Sanyal²,

Xiao³

et al. 2014

Journal of Biomechanics

Self Cite

View full text Add to dashboard Cite

Tortuous arteries associated with aneurysms have been observed in aged patients with atherosclerosis and hypertension. However, the underlying mechanism is poorly understood. The objective of this study was to determine the effect of aneurysms on arterial buckling instability and the effect of buckling on aneurysm wall stress. We investigated the mechanical buckling and post-buckling behavior of normal and aneurysmal carotid arteries and aorta’s using computational simulations and experimental measurements to elucidate the interrelationship between artery buckling and aneurysms. Buckling tests were done in porcine carotid arteries with small aneurysms created using elastase treatment. Parametric studies were done for model aneurysms with orthotropic nonlinear elastic walls using finite element simulations. Our results demonstrated that arteries buckled at a critical buckling pressure and the post-buckling deflection increased nonlinearly with increasing pressure. The presence of an aneurysm can reduce the critical buckling pressure of arteries, although the effect depends on the aneurysm’s dimensions. Buckled aneurysms demonstrated a higher peak wall stress compared to unbuckled aneurysms under the same lumen pressure. We conclude that aneurysmal arteries are vulnerable to mechanical buckling and mechanical buckling could lead to high stresses in the aneurysm wall. Buckling could be a possible mechanism for the development of tortuous aneurysmal arteries such as in the Loeys-Dietz syndrome.

show abstract

Section: Discussionmentioning

confidence: 99%

Mechanical instability of normal and aneurysmal arteries

Lee¹,

Sanyal²,

Xiao³

et al. 2014

Journal of Biomechanics

Self Cite

View full text Add to dashboard Cite

show abstract

“…However, red blood cells are known to push platelets toward vessel walls in straight vessels, and this effect greatly increases the concentration of platelets near walls [60,61]. Hence, we would expect that red blood cells would cause thrombosis to be initiated more quickly than in our simulations.…”

Section: Discussionmentioning

confidence: 74%

“…Hence, we would expect that red blood cells would cause thrombosis to be initiated more quickly than in our simulations. Additionally, after the onset of thrombosis, thrombi and occlusions might form more slowly due to collisions of red blood cells that may detach platelets from thrombi, as seen in our previous work on initial thrombus formation in tortuous microvessels [61]. As well, another computational study of thrombus formation due to an injured section of a plane wall in a simple shear low showed that although the presence of red blood cells resulted in shorter thrombi containing more platelets, the process of thrombus formation in general was not signi icantly affected by the presence of red blood cells [62].…”

Section: Discussionmentioning

confidence: 85%

Untitled

2017

J Cardiol Cardiovasc Med

View full text Add to dashboard Cite

Tortuous microvessels alter blood fl ow and stimulate thrombosis but the physical mechanisms are poorly understood. Both tortuous microvessels and abnormally large platelets are seen in diabetic patients. Thus, the objective of this study was to determine the physical effects of arteriole tortuosity and platelet size on the microscale processes of thrombotic occlusion in microvessels. A new lattice-Boltzmann method-based discrete element model was developed to simulate the fl uid fl ow fi eld with fl uid-platelet coupling, platelet interactions, thrombus formation, and thrombotic occlusion in tortuous arterioles. Our results show that vessel tortuosity creates high shear stress zones that activate platelets and stimulate thrombus formation. The growth rate depends on the level of tortuosity and the pressure and fl ow boundary conditions. Once thrombi began to form, platelet collisions with thrombi and subsequent activations were more important than tortuosity level. Thrombus growth narrowed the channel and reduced the fl ow rate. Larger platelet size leads to quicker decrease of fl ow rate due to larger thrombi that occluded the arteriole. This study elucidated the important roles that tortuosity and platelet size play in thrombus formation and occlusion in arterioles.

show abstract

“…In this section, the computational simulation conditions are described first, followed by descriptions of the employed activation models for platelets and the endothelium. Details of the discrete element method have been previously published [14-16], and a brief description is provided in the Appendix.…”

Section: Methodsmentioning

confidence: 99%

“…Our shear-induced platelet activation model, as developed and applied in [16, 30, 31], assumed that a platelet became activated if it experienced a shear stress above a critical shear stress ( T crit ). This model was in agreement with in vivo and in vitro observations of shear-induced platelet activation and aggregation that occurred within milliseconds [12, 32, 33].…”

Section: Methodsmentioning

confidence: 99%

Simulation of the microscopic process during initiation of stent thrombosis

Chesnutt

Han

2015

Computers in Biology and Medicine

Self Cite

View full text Add to dashboard Cite

Objective Coronary stenting is one of the most commonly used approaches to open coronary arteries blocked due to atherosclerosis. However, stent struts can induce stent thrombosis due to altered hemodynamics and endothelial dysfunction, and the microscopic process is poorly understood. The objective of this study was to determine the microscale processes during the initiation of stent thrombosis. Methods We utilized a discrete element computational model to simulate the transport, collision, adhesion, and activation of thousands of individual platelets and red blood cells in thrombus formation around struts and dysfunctional endothelium. Results As strut height increased, the area of endothelium activated by low shear stress increased, which increased the number of platelets in mural thrombi. These thrombi were generally outside regions of recirculation for shorter struts. For the tallest strut, wall shear stress was sufficiently low to activate the entire endothelium. With the entire endothelium activated by injury or denudation, the number of platelets in mural thrombi was largest for the shortest strut. The type of platelet activation (by high shear stress or contact with activated endothelium) did not greatly affect results. Conclusions During the initiation of stent thrombosis, platelets do not necessarily enter recirculation regions or deposit on endothelium near struts, as suggested by previous computational fluid dynamics simulations. Rather, platelets are more likely to deposit on activated endothelium outside recirculation regions and deposit directly on struts. Our study elucidated the effects of different mechanical factors on the roles of platelets and endothelium in stent thrombosis.

show abstract

Effect of Red Blood Cells on Platelet Activation and Thrombus Formation in Tortuous Arterioles

Cited by 16 publications

References 75 publications

Mechanical instability of normal and aneurysmal arteries

Mechanical instability of normal and aneurysmal arteries

Untitled

Simulation of the microscopic process during initiation of stent thrombosis

Contact Info

Product

Resources

About