Keywords: atherosclerosis, hemodynamic hypotheses, comparative study, hemodynamic characteristics, vision technique, computer simulation.

Atherosclerosis, which is a degenerative vascular disease, is believed to occur in the blood vessels due to deposition of cholesterol or low density lipoprotein(LDL). Atherosclerotic lumen narrowing causes reduction of blood flow due to hemodynamic features. Several hypothetical theories related to the hemodynamic effects have been reported: high shear stress theory, low shear stress theory, high shear stress gradient theory, flow separation and turbulence theory, and high pressure theory [1,2,3,4,5]. However, no one theory clearly explains the causes of atherosclerosis. The objective of the present study was to investigate the mechanism of the generation of atherosclerosis. In the study, the database of Korean carotid and coronary arteries for geometrical and hemodynamic clinical data was established. The atherosclerotic sites were predicted by the computer simulations. The results of the computer simulation were compared with the in vivo experimental results, and then the pathogenesis of atherosclerosis by using the clinical data and several hypothetical theories were investigated.

To understand the generation of atherosclerosis, an in-depth knowledge of blood flows through different human arteries is required . The basic vessel models were adopted based on the in vivo measurements using the angiography. We have tried to establish the database of the carotid and coronary arteries for Korean subjects. Duplex scan (ATL Inc.) was used to obtain the images of the flow characteristics. And the geometric dimensions of the models were taken from the measured data by the angiography. The reconstructed blood vessel models were obtained from 2-dimentional CT (Computed Tomography) images by using the vision techniques.

The computer simulation was applied to investigate the relationship between arteriosclerosis and the hypothetical theories [6].

The pressure distribution at the inlet region was higher than that at the outlet region. The pressure values were varied in the artery due to the geometric arrangements of the arterial system with respect to the curved area and bifurcated region. The results of the pressure distributions in the region of curved and bifurcated arterial segments showed a similar distribution when compared with the adjacent areas of the curved and bifurcated regions. No negative values of the transmutable pressure appeared in the regions of the vessel walls. From the above results we found it very difficult to predict the cause of atherosclerosis by the pressure related hypothesis.

The flow patterns in the complex geometrical sites such as the carotid and coronary arteries exhibit non-uniform wall shear stress. The high shear stress region was that at a flow divider of the bifurcation. At the dividers of bifurcations and branches the shear stress became much greater than 100 dyne/cm2. The intima in high shear stress regions was exposed to higher shear stress. Thus, the endothelial cells at the flow divider were damaged.

The recirculation zone is observed in the sinus of the ICA, and this zone varies during the systole/diastole phase. The wall shear stress varies from the negative value to the positive value during a cycle. It is speculated that the abrupt change of wall shear stress in the sinus may be responsible for the initial formation of atherosclerosis.

From the investigation, it was concluded carefully that the mechanism of the generation of atherosclerosis was related to the hemodynamic effects such as flow separation and oscillatory wall shear stress on the vessel walls.

Acknowledgements

This work was supported by grant No. R01-2002-000-00561-0 from the Basic Research Program of the Korea Science & Engineering Foundation.

1

Texon, M., Imparato, A.M., Helpern, M., "Role of vascular dynamics in the development of atherosclerosis", JAMA, 194,168-172., 1965. doi:10.1001/jama.194.11.1226

2

Fox J.A. and Hugh A.E., "Localization of atheroma: a theory based on boundary layer separation", Br Heart J. Vol. 28(3), 388-399, 1966. doi:10.1136/hrt.28.3.388

3

Tucker C. and Myron I. C., "NF-B: pivotal mediator or innocent bystander in atherogenesis?" J. Clin Invest. Vol. 107(3), 255-264, 2001. doi:10.1172/JCI10373

4

Fry, D.L., "Response of the Arterial Wall to Certain Physical Factors. Atherogenesis: Initiating Factors", A Ciba Foundation Symp., ASP, Amsterdam, The Neterlands., 40-83. 1972.

5

Caro, C.G., Fitz-Gerald, J.M. and Schroter, R.C., "Atheroma and Arterial Wall Shear:Observation, Correlation and Proposal of a Shear Dependent Mass Transfer Mechanism for Atherogenesis," Proc. R. Soc. B 177, 109-159, 1971. doi:10.1098/rspb.1971.0019

6

Lee, B.K., Kwon, H.M., Hong, B.K., Park, B.E., Suh, S.H., Cho, M.T., Lee, C.S., Kim, M.C., Kim, C.J, Yoo, S.S. and Kim, H.S., "Hemodynamic effects on atherosclerosis-prone coronary artery: wall shear stress/rate distribution and impedance phase angle in coronary and aortic circulation", Yonsei Med J. Vol. 42(4):375-383, 2001.

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