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Computational Investigations of the Role of Flow in Thrombosis

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Computational Investigations of the Role of Flow in Thrombosis

Aaron L. Fogelson

, Robert D. Guy

University of Utah

Departments of Mathematics and Bioengineering 155 South 1400 East, 233 JWB

Salt Lake City, UT 84112 USA e-mail: fogelson@math.utah.edu

web page:http://www.math.utah.edu/˜fogelson

ABSTRACT

Arterial blood clots (thrombi) that form as a consequence of artherosclerotic plaque rupture are com-prised largely of aggregates of platelets. These thrombi form under conditions in which the flow changes substantially both in space (initially because of the plaque, later also because of the clots) and in time (as the thrombi develop). This talk will discuss a multiscale continuum model that describes platelet thrombosis initiated by a ruptured atherosclerotic plaque in a coronary-artery-sized vessel. It includes full treatment of the fluid dynamics, and the aggregation of platelets in response to the plaque rup-ture and further chemical signals, and the feedback of the growing thrombi on the fluid motion. In the model, the growing clots influence the fluid motion by a distribution of forces that act on the fluid rather than by an explicit change in fluid domain geometry. The full model treats events on two spatial scales, the millimeter scale of the vessel and the micron scale of the platelets. An approximate closure version of the model allows elimination of the smaller scale while retaining important features, such as strain-dependent embolization, of the full model.

The thrombosis model has features in common with viscoelastic polymer flow models but poses ad-ditional computational challenges because material properties (e.g., elastic modulus) vary sharply in space and in time in a manner determined by the evolving system.

Simulations will be presented that demonstrate model behaviors including the growth of wall-adherent platelet thrombi to occlude the vessel and stop the flow, and the transient growth and subsequent em-bolization (fragmentation) of thrombi leaving behind a passivated injured surface.

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