I am thinking how thrombus (veins, arteries and heart) can move.

Secondary mechanisms come to my mind only:

  • some enzyme which lyses it, probably adhesion mechanism.
  • Blood circulation (flow rate) is one secondary measure, I think.

I am not sure if there exist any primary mechanisms:

  • In veins, there are valves which probably can help thrombus go forward by pushing.
  • Veins can also dilate so dilation of vessel can help.

Arteries do net dilate their diameter. So aim would be there to maximise laminar flow, and decrease turbulence.

So probably the question is related somehow to the laminar flow which could help thrombus to move.

How can thrombus move in veins, arteries and heart?

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    $\begingroup$ Have you found the answer of this one? Is this the thing :ncbi.nlm.nih.gov/pmc/articles/PMC3681659 $\endgroup$ Aug 7, 2014 at 20:57
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    $\begingroup$ @DevashishDas I considered your pointed paper. I added my considerations about it. I think the paper makes big simplifications about the processes in movement of thrombus. $\endgroup$ Aug 8, 2014 at 9:33

1 Answer 1


This answer aims to list existing models and do meta-analysis about them. This answer is a draft.

There are many models made based on the thrombus movement. One of them is proposed by DevashishDas' answer but it seems to focus only on the first stage of hemostasis:

The model assumes thrombin is generated on the surface of activated platelets in the thrombus core and is transported through the fibrin network that surrounds the core both by advective flow of fluid permeating through the fibrin network and by diffusion through the fibrin gel.

and particularly the model keeps these values constant and simplifies

To calibrate the model, we experimentally determined fibrin clot permeability and thrombin diffusion rates through a fibrin network.

which I think should be dynamic (not constant) because of the three endothelium main factors listed below. Endothelium is a dynamic structure controlling the fibrin clot.

Thrombus Hemodynamics Model

which is about the first stage of hemostasis because of its simplification about fibrin clot permeability and thrombin diffusion rates.


There are three stages of hemostasis altogether which work parallel together:

  • primary (formation of the platelet plug)
  • secondary (formation of fibrin through the coagulation cascade)
  • tertiary hemostasis (formation of plasmin for breakdown of the clot)

Primary hemostasis is the formation of the primary platelet plug. It involves

  • platelets
  • blood vessel wall
  • von Willebrand factor

Normal endothelium prevents hemostasis. Injury of endothelium

  • involves vasoconstriction (local)
  • enhances adherence of platelets to exposed platelet subendothelial surfaces and activation of coagulation process

The formation of primary platelet plug involves

  • Platelet adhesion,
  • Platelet activation, and
  • Platelet aggregation.

Main steps in blood coagulation:

  • Formation of prothrombin activator complex (thrombokinase)
  • Conversion of plasma protein prothrombin into thrombin
  • Conversion of dissolved plasma fibrinogen into fibrin (makes filamen- tous skeleton of fibrin clot)

Clot retraction

  • The platelets in the clot contain contractile proteins.
  • They bring the edges of the wound together, which also reduces the chance of further bleeding - not vasoconstriction here!
  • The contraction process also supports the wound healing process as it brings the ends of the wound together.

Clot retraction is the process of getting clot towards fibrinolysis process. Fibrinolysis is the process where a fibrin clot (product of coagulation) is broken down. Its main enzyme plasmin cuts the fibrin mesh at various places, leading to the production of circulating fragments that are cleared by other proteases or by the kidney and liver. Clot retraction and fibrinolysis are necessary to remove clot so wound healing can proceed.

Myogenic and metabolic autoregulation by endothelium

Myogenic control involves the localized response of vascular smooth muscle to passive stretch - reflex contraction when stretched to decrease flow, reflex relax- ation when stretch is reduced to vasodilate and increase flow. This maintains a relatively constant flow locally when pressure fluctuates.

Myogenic and metabolic Autoregulation is the automatic adjustment (local) of blood flow to each tissue in proportion to its needs (oxygen, nutrients, ...), and is controlled intrinsically by modifying the diameter of local arterioles. It involves localised response of vascular smooth muscle to passive stretch - reflex contraction when stretched to decrease flow, reflex relaxation when stretch is reduced to vasodilate and increase flow. This maintains a relatively constant flow locally when pressure fluctuates.

There are three types of substances secreted by the endothelium (1):

  1. NO
  2. Endothelium hyperpolarising factors
  3. Endothelins.

where I think the modelling should focus on these three factors.


  1. My discussion with a researcher in this field 7/2014
  2. My notes in three Physiology courses during years 2011-2014
  3. Costanzo, Physiology, book
  4. Guyton, Physiology, book

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