Flow patterns and preferred sites of intimal thickening in diameter-mismatched vein graft interpositions.

BACKGROUND It is suspected that blood flow and flow-induced shear stress play an important role in the pathogenesis and localization of intimal hyperplasia in anastomosed vessels. However, experimental data that demonstrate the correlation between the flow and the sites of intimal thickening obtained in the same vessel are scarce. For this reason, we have studied the relationship between the flow and precise locations of wall thickening specific to the particular vessel by performing diameter-mismatched vein graft interpositions. This method created more flow disturbances than those found in our previous study, which was carried out by dividing an artery and simply suturing its ends back to their original positions. METHODS In the current study, grafting procedures consisting of 26 saphenous vein interpositions and 10 jugular vein interpositions were carried out on the femoral arteries of 22 adult mongrel dogs. The vessels were harvested at 3 months after operation, perfusion-fixed, and rendered transparent. The precise location and the size of intimal thickening and characteristics of the flow, such as flow patterns, distributions of fluid velocity, and wall shear stress, were studied in detail by means of flow visualization and cinemicrographic techniques. RESULTS It was found that the diameters of interposed saphenous vein grafts, which were about one-half the diameter of host arteries, increased drastically and became almost the same as those of the host arteries. Intimal thickening was found distal to the distal anastomotic junction in smaller diameter saphenous vein-interposed vessels and distal to the proximal anastomotic junction in larger diameter jugular vein-interposed vessels. In both cases, flow was disturbed with the formation of a slow recirculation flow due to a sudden enlargement of vessel diameter caused by a mismatch of vessel diameters at the anastomotic junction and at the location where the wall shear stress was low. CONCLUSIONS The results suggest that the key hemodynamic factors involved in the localization of intimal thickening are the low velocity of flowing blood and the resultant low shear stress acting on the vessel wall.

[1]  M. Bourassa,et al.  Comparison of late changes in internal mammary artery and saphenous vein grafts in two consecutive series of patients 10 years after operation. , 1984, Circulation.

[2]  T. Karino,et al.  Flow-dependent concentration polarization of plasma proteins at the luminal surface of a cultured endothelial cell monolayer. , 1999, Biorheology.

[3]  V. Sottiurai,et al.  Distal anastomotic intimal hyperplasia: histopathologic character and biogenesis. , 1989, Annals of vascular surgery.

[4]  T. Karino,et al.  Flow patterns and preferred sites of intimal thickening in end-to-end anastomosed vessels. , 1995, Surgery.

[5]  H. Goldsmith,et al.  Particle flow behavior in models of branching vessels. II. Effects of branching angle and diameter ratio on flow patterns. , 1985, Biorheology.

[6]  S. Wada,et al.  Theoretical study of the effect of local flow disturbances on the concentration of low-density lipoproteins at the luminal surface of end-to-end anastomosed vessels , 2002, Medical and Biological Engineering and Computing.

[7]  G. Johnson,et al.  The internal mammary artery graft. Its longevity after coronary bypass. , 1981, JAMA.

[8]  S Glagov,et al.  Hemodynamic patterns in two models of end-to-side vascular graft anastomoses: effects of pulsatility, flow division, Reynolds number, and hood length. , 1993, Journal of biomechanical engineering.

[9]  M. Motomiya,et al.  Flow Patterns in the Human Carotid Artery Bifurcation , 1984, Stroke.

[10]  T. Karino.  Microscopic structure of disturbed flows in the arterial and venous systems, and its implication in the localization of vascular diseases. , 1986, International angiology : a journal of the International Union of Angiology.

[11]  F. Loop,et al.  Long-term (5 to 12 years) serial studies of internal mammary artery and saphenous vein coronary bypass grafts. , 1985, The Journal of thoracic and cardiovascular surgery.

[12]  V. Sottiurai,et al.  Intimal hyperplasia and neointima: An ultrastructural analysis of thrombosed grafts in humans. , 1983, Surgery.

[13]  S. Wada,et al.  Prediction of LDL concentration at the luminal surface of a vascular endothelium. , 2002, Biorheology.

[14]  M. Motomiya,et al.  Flow visualization in isolated transparent natural blood vessels. , 1983, Biorheology.

[15]  T. Karino,et al.  Flow patterns and spatial distribution of atherosclerotic lesions in human coronary arteries. , 1990, Circulation research.

[16]  H. Handa,et al.  The role of hemodynamic factors in arterial wall thickening in the rat. , 1978, Atherosclerosis.

[17]  W. C. Sheldon,et al.  Influence of the internal-mammary-artery graft on 10-year survival and other cardiac events. , 1986, The New England journal of medicine.

[18]  W. Quist,et al.  A Mechanism of Failure in Dacron(r) Arterial Grafts , 1983 .

[19]  C. Zarins,et al.  Carotid Bifurcation Atherosclerosis: Quantitative Correlation of Plaque Localization with Flow Velocity Profiles and Wall Shear Stress , 1983, Circulation research.

[20]  S. Wada,et al.  Theoretical study on flow-dependent concentration polarization of low density lipoproteins at the luminal surface of a straight artery. , 1999, Biorheology.

[21]  A. Gown,et al.  Mechanisms of arterial graft failure. 1. Role of cellular proliferation in early healing of PTFE prostheses. , 1985, The American journal of pathology.

[22]  R. Frye,et al.  Pathologic changes in aortocoronary saphenous vein grafts. , 1974, The American journal of cardiology.

[23]  G. Clagett.  Mechanisms of arterial graft failure: Clowes AW, Gown AM, Hanson SR, et al. Am J Clin Pathol 1985;118:43–54 , 1986 .

[24]  S. Wacholder,et al.  The relation of risk factors to the development of atherosclerosis in saphenous-vein bypass grafts and the progression of disease in the native circulation. A study 10 years after aortocoronary bypass surgery. , 1984, The New England journal of medicine.

[25]  S. Wada,et al.  Theoretical Prediction of Low-Density Lipoproteins Concentration at the Luminal Surface of an Artery with a Multiple Bend , 2002, Annals of Biomedical Engineering.