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Experimental and Imaging Techniques for Examining Fibrin Clot Structures in Normal and Diseased States

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Dynamics of pathologic clot formation: a mathematical model.

Evgeny A Shavlyugin¹, Leonid G Hanin, Mikhail A Khanin

¹Mathematical Modeling Laboratory, Center for Theoretical Problems of Physicochemical Pharmacology, Russian Academy of Sciences, Kosygina Street 4, Moscow 119991, Russia.

Journal of Theoretical Biology

|August 27, 2013

Summary

Pathologic clot formation, primarily driven by the intrinsic coagulation pathway and Hageman factor activation, is modeled mathematically. Inhibiting activated Factor XII and Factor XI may prevent pathological clots.

Keywords:

Intrinsic coagulation pathway Mathematical modelling Pathologic clot formation Therapeutic time window Thrombolysis

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Area of Science:

Biochemistry
Hematology
Mathematical Biology

Background:

Hageman factor (Factor XII) auto-activation initiates the intrinsic coagulation pathway.
Platelets play a crucial role in activating the intrinsic pathway during clot formation.
Pathologic clot formation is a complex process involving multiple biochemical reactions.

Purpose of the Study:

To elucidate the mechanism of pathologic clot formation.
To investigate the dynamics of clot formation focusing on the intrinsic pathway.
To develop a mathematical model for understanding pathological thrombosis.

Main Methods:

Mathematical modeling of blood coagulation cascade dynamics.
Incorporation of activated platelet effects on intrinsic pathway activation.
Estimation of kinetic constants for biochemical reactions initiating pathologic clot formation.

Main Results:

The intrinsic pathway, triggered by Hageman factor, is a predominant mechanism in pathologic clot formation.
Activated platelets significantly influence the kinetics of the intrinsic pathway.
The rate of pathologic clot formation may be considerably slower than hemostatic clot formation.

Conclusions:

Mathematical modeling provides insights into pathologic clot formation mechanisms.
Simultaneous inhibition of activated Factor XII and Factor XI is a potential prophylactic strategy.
Understanding the dynamics of clot formation can lead to novel therapeutic approaches.