You are here

The Hemorheologic-Hemodynamic Theory of Atherosclerosis -- Viscosity and Localized Stasis (Part 2)

Viscosity and Localized Stasis

In arteries during systole, there is a gradient of blood velocity with the highest velocity in the center of the vessel and the lowest against the arterial wall [1].

Figure 1Figure 1. This diagram shows how changes in vascular geometry naturally create areas of low shear. Blood velocity is proportional to the length of the arrows. In the parent artery (bottom), the velocity profile is parabolic and symmetrical around the center. After the bifurcation, the fastest blood in each daughter vessel is nearer the inner wall, and the slowest blood against the outer wall. This is a consequence of erythrocyte momentum, which causes erythrocytes to resist changes in direction. Therefore, areas of low shear are created against the outer vessel wall. This effect is accentuated progressively by increasing blood velocity, which increases erythrocyte momentum. Thus, changes in vascular geometry create the potential for conditions permissive for development of a thrombus: stasis of blood and decreased production of antithrombotic molecules by the endothelium.

Other changes in geometry such as curves, obstructions, and dilatations also create areas of relative low and high shear.

In a vein, the velocity profile would be flatter and flow slower, i.e., the arrows would be shorter. If you recognize the diagram in Figure 1, please let me know the source so I can give credit.

In areas of vascular branching, curving and dilatation, focal blood pooling occurs in the low shear environment against the arterial wall if flow exceeds a critical value of Reynolds number. This phenomenon is seen in nature when rapidly flowing water encounters an obstruction, forming eddies and pools. Blood is a non-Newtonian fluid, meaning its viscosity progressively increases with decreasing shear. In areas of pooling, a vicious cycle can develop in which increased viscosity leads to decreased flow, further increasing viscosity and decreasing flow, leading ultimately to stasis and thrombosis in the absence of adequate fibrinolytic activity. Besides increasing viscosity, decreased blood flow promotes thrombosis by decreasing influx of fibrinolytic molecules and decreasing efflux of activated clotting factors. Platelets activated by high shear 2] in the central column of blood can be directed to the vicinity of the arterial wall by eddy currents. In these areas, decreased blood flow decreases endothelial production of molecules with antithrombotic activity such as nitric oxide and prostacyclin, further promoting thrombosis. This is akin to endothelial dysfunction which in mainstream atherogensis theory is thought to be caused by putative cytopathic effects of oxidized LDL.

Figure 2

Figure 2. This is an ultrasound image of the carotid artery and jugular vein. Arterial blood flow is pictured in orange-yellow and red, and venous blood, which is flowing in the opposite direction back to the heart, is blue. Blood velocity and direction can be estimated by looking at the color scale at the right side of the diagram. Arterial blood is rapid, while venous blood flow is slower and in the opposite direction. There is an atherosclerotic plaque or thrombus, colored gray and black, on the outer arterial wall, opposite of the jugular vein. This image demonstrates the effect of Reynolds number. As arterial blood, going from right to left, encounters the obstruction, vascular diameter decreases and blood velocity increases, changing color from red to orange-yellow. Thus, Reynolds number has increased. At the far side of the obstruction, a portion of blood actually slows and reverses direction, which can be seen as the blue area adjacent to the obstruction and outer arterial wall. Image courtesy of Bob Perret, M.D.

Figure3

Figure 3. This ultrasound shows how complex flow in an artery can be. In the artery, small areas of high velocity blood are immediately adjacent to areas of slower blood going in the opposite direction (blue). There is an obstruction against the inner wall of the carotid, adjacent to the vein. There is also an obstruction on the opposite wall as well. Image courtesy of Bob Perret, M.D.

Next Section: Arterial Stiffening (Part 3)


References:

1. Kensey KR, Cho YI. The Origin of Atherosclerosis. Volume 1: An Introduction to Hemodynamics. EPP Medica, 2001, p. 68-73.

2. Brown CH 3rd, Leverett LB, Lewis CW, Alfrey CP Jr, Hellums JD. Morphological, biochemical, and functional changes in human platelets subjected to shear stress. Journal of Laboratory and Clinical Medicine 1975;86:462-71.

ⓒ 2011 Gregory Sloop. All Rights Reserved.

 

Stay Connected