Intermittent short-duration exposure to low wall shear stress induces intimal thickening in arteries exposed to chronic high shear stress

Background : Intimal hyperplastic thickening (IHT) is a frequent cause of prosthetic bypass graft failure. Induction and progression of IHT is thought to involve a number of mechanisms related to variation in the flow field, injury and the prosthetic nature of the conduit. This study was designed to examine the relative contribution of wall shear stress and injury to the induction of IHT at defined regions of experimental end-to-side prosthetic anastomoses. Methods and Results: The distribution of IHT was determined at the distal end-to-side anastomosis of seven canine Iliofemoral PTFE grafts after 12 weeks of implantation. An upscaled transparent model was constructed using the in vivo anastomotic geometry, and wall shear stress was determined at 24 axial locations from laser Doppler anemometry measurements of the near wall velocity under conditions of pulsatile flow similar to that present in vivo. The distribution of IHT at the end-to-side PTFE graft was determined using computer assisted morphometry. IHT involving the native artery ranged from 0.0±0.1 mm to 0.05±0.03 mm. A greater amount of IHT was found on the graft hood (PTFE) and ranged from 0.09±0.06 to 0.24±0.06 mm. Nonlinear multivariable logistic analysis was used to model IHT as a function of the reciprocal of wall shear stress, distance from the suture line, and vascular conduit type (i.e. PTFE versus host artery). Vascular conduit type and distance from the suture line independently contributed to IHT. An inverse correlation between wall shear stress and IHT was found only for those regions located on the juxta-anastomotic PTFE graft. Conclusions: The data are consistent with a model of intimal thickening in which the intimal hyperplastic pannus migrating from the suture line was enhanced by reduced levels of wall shear stress at the PTFE graft/host artery interface. Such hemodynamic modulation of injury induced IHT was absent at the neighboring artery wall.

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Intimal Thickening Sourced From Low Wall Shear Stress in Human Left Coronary Artery Was Observed by Optical Coherence Tomography

ASME 2011 Summer Bioengineering Conference, Parts A and B ◽

10.1115/sbc2011-53017 ◽

2011 ◽

Author(s):

Jin Suo ◽

Michael McDaniel ◽

Parham Eshtehardi ◽

Saurabh S. Dhawan ◽

Lucas H. Timmins ◽

...

Keyword(s):

Optical Coherence Tomography ◽

Shear Stress ◽

Coronary Artery ◽

Wall Shear Stress ◽

Optical Coherence ◽

Intimal Thickening ◽

Cfd Models ◽

Computational Fluid Dynamics Cfd ◽

Wall Shear ◽

Artery Disease

The high resolution of optical coherence tomography (OCT) may offer improved description of luminal surfaces and intimal thickening in human coronary arteries by comparison to other imaging modalities, such as intravascular ultrasound (IVUS). We investigated the left anterior descending (LAD) coronary artery of a patient using both OCT and IVUS methods and found an asymmetrical distribution of intimal thickness (IT) around the lumen circumference in the OCT images, whereas the IVUS images showed a lumen with no asymmetry in IT. We reconstructed a 3D coronary artery model from the OCT slices that represented the morphological details of local luminal surfaces accurately and used this to simulate the pulsatile flow field in the model employing computational fluid dynamics (CFD). The pulsatile wall shear stress (WSS) distribution on the LAD surface was derived, and time-averaged WSS was computed. The data for IT and WSS distributions in the LAD segment were compared, and a linear inverse relationship between IT and WSS was found; higher WSS (> 25±5 dynes per square centimeter) favors thinner intima (< 0.12±0.05 millimeters) and lower WSS (< 12±5 dynes per square centimeter) favors thicker intima (> 0.33±0.05 millimeters). The enhanced spatial resolution of OCT offers an improved imaging technique for developing CFD models and assessing early atherosclerosis in patients with coronary artery disease.

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Arterial enlargement, tortuosity, and intimal thickening in response to sequential exposure to high and low wall shear stress

Journal of Vascular Surgery ◽

10.1016/j.jvs.2003.10.058 ◽

2004 ◽

Vol 39 (3) ◽

pp. 601-612 ◽

Cited By ~ 98

Author(s):

Eiketsu Sho ◽

Hiroshi Nanjo ◽

Mien Sho ◽

Mikio Kobayashi ◽

Masayo Komatsu ◽

...

Keyword(s):

Shear Stress ◽

Wall Shear Stress ◽

Intimal Thickening ◽

Wall Shear

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Arterial Enlargement, Tortuosity, and Intimal Thickening in Response to Sequential Exposure to High and Low Wall Shear Stress

Yearbook of Vascular Surgery ◽

10.1016/s0749-4041(08)70007-1 ◽

2006 ◽

Vol 2006 ◽

pp. 4

Author(s):

G.L. Moneta

Keyword(s):

Shear Stress ◽

Wall Shear Stress ◽

Intimal Thickening ◽

Wall Shear

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The relationship between wall shear stress distributions and intimal thickening in the human abdominal aorta

BioMedical Engineering OnLine ◽

10.1186/1475-925x-2-18 ◽

2003 ◽

Vol 2 (1) ◽

Cited By ~ 30

Author(s):

Michael Bonert ◽

Richard L Leask ◽

Jagdish Butany ◽

C Ross Ethier ◽

Jerry G Myers ◽

...

Keyword(s):

Shear Stress ◽

Wall Shear Stress ◽

Abdominal Aorta ◽

Stress Distributions ◽

Intimal Thickening ◽

Wall Shear ◽

The Relationship ◽

Human Abdominal Aorta

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The Role of Fluid Mechanics in the Localization and Detection of Atherosclerosis

Journal of Biomechanical Engineering ◽

10.1115/1.2895545 ◽

1993 ◽

Vol 115 (4B) ◽

pp. 588-594 ◽

Cited By ~ 341

Author(s):

D. P. Giddens ◽

C. K. Zarins ◽

S. Glagov

Keyword(s):

Fluid Dynamics ◽

Shear Stress ◽

Wall Shear Stress ◽

Fluid Dynamic ◽

Atherosclerotic Plaques ◽

Intimal Thickening ◽

Intimal Thickness ◽

Wall Shear ◽

Dynamic Variables

Fluid dynamics research over the past twenty years has contributed immensely to our knowledge of atherosclerosis. The ability to detect localized atherosclerotic plaques using noninvasive ultrasonic methods was advanced significantly by investigations into the nature and occurrence of velocity disturbances created by arterial stenoses, and diagnosis of carotid bifurcation disease using a combination of ultrasonic imaging and Doppler measurement of blood velocity is now quite routine. Since atherosclerotic plaques tend to be localized at sites of branching and artery curvature and since these locations would be expected to harbor complex flow patterns, investigators postulated that fluid dynamics might play an initiating role in atherogenesis. Several fluid dynamic variables were proposed as initiating factors. Investigations were undertaken during the 1980s in which fluid dynamic model experiments with physiologic geometries and flow conditions were employed to simulate arterial flows and in which morphometric mapping of intimal thickness was performed in human arteries. Correlations between fluid dynamic variables and intimal thickness revealed that atherosclerotic plaques tended to occur at sites of low and oscillating wall shear stress; and these observations were reinforced by studies in a monkey model of atherosclerosis. Concomitantly, it was realized that arteries adapt their diameters so as to maintain wall shear stress in a narrow range of values around 15 dynes/cm2, findings which were based both on observations of normal arteries and on animal studies in which flow rates were manipulated and arterial diameter adaptation was measured. Currently, a working hypothesis for the role of fluid dynamics in atherogenesis is that intimal thickening is a normal response to low wall shear stress, and this intimal thickening can develop into an early atherosclerotic plaque under certain circumstances such as excessive low density lipoprotein concentrations in blood.

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Effect of wall shear stress on intimal thickening of arterially transplanted autogenous veins in dogs

Journal of Vascular Surgery ◽

10.1067/mva.1985.avs0020430 ◽

1985 ◽

Vol 2 (3) ◽

pp. 430-433 ◽

Cited By ~ 6

Author(s):

Kazumasa Morinaga ◽

Kenichiro Okadome ◽

Masazumi Kuroki ◽

Taizo Miyazaki ◽

Yoichi Muto ◽

...

Keyword(s):

Shear Stress ◽

Wall Shear Stress ◽

Intimal Thickening ◽

Wall Shear

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Effect of wall shear stress on intimal thickening of arterially transplanted autogenous veins in dogs

Journal of Vascular Surgery ◽

10.1016/0741-5214(85)90097-7 ◽

1985 ◽

Vol 2 (3) ◽

pp. 430-433 ◽

Cited By ~ 86

Author(s):

Kazumasa Morinaga ◽

Kenichiro Okadome ◽

Masazumi Kuroki ◽

Taizo Miyazaki ◽

Yoichi Muto ◽

...

Keyword(s):

Shear Stress ◽

Wall Shear Stress ◽

Intimal Thickening ◽

Wall Shear

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Response of Arteries to Near-Wall Fluid Dynamic Behavior

Applied Mechanics Reviews ◽

10.1115/1.3120861 ◽

1990 ◽

Vol 43 (5S) ◽

pp. S98-S102 ◽

Cited By ~ 56

Author(s):

D. P. Giddens ◽

C. K. Zarins ◽

S. Glagov

Keyword(s):

Fluid Dynamics ◽

Blood Flow ◽

Shear Stress ◽

Smooth Muscle ◽

Wall Shear Stress ◽

Fluid Dynamic ◽

Intimal Thickening ◽

Long Term Changes ◽

Wall Shear

Arteries are living tissues which react and adapt to their environment, particularly in relation to changes in the rate of blood flow required to supply peripheral tissues or organs. Medium and small size arteries increase in diameter in response to short-term demands for increased flow and decrease in diameter in the event of diminished demands. Such immediate reactions are regulated primarily by vasoactive substances acting directly on smooth muscle cells of the media or by release of smooth muscle relaxation or contraction factors elaborated by endothelial cells. Chronic or long-term changes in arterial diameter appear to be governed directly by near-wall flow phenomena, e.g. the fluid dynamic wall shear. Recent evidence suggests that the normal tendency of arteries to respond to long-term changes in the shear field can result in intimal thickening and that this response may also favor the development of atherosclerosis. Thus, there appears to be a close relationship between fluid dynamics and the structure of arteries. From the fluid dynamics viewpoint, the pulsatile, three dimensional nature of blood flow requires sophisticated experimental methods in order to provide adequate data for correlation with biological studies. Research within the past decade has led to the conclusion that arteries seek a vessel diameter-blood flow combination which results in a flow-induced mean wall shear stress of approximately 15 dynes/sq.cm. If this value is chronically exceeded, vessel enlargement develops. If normal baseline shear stress is not restored by this increase in radius, the local response may continue. Conversely, reduced wall shear tends to induce intimal thickening in order to reduce lumen radius and thus increase wall shear toward normal levels. Under certain conditions this reaction may progress to the development of atherosclerotic plaques. Despite this knowledge, key points remain to be clarified. Is it the wall shear stress or the wall shear rate which determines the reaction? The former possibility implies that a mechanical shear-related stimulus is at the heart of the biological response mechanisms while the latter suggests a mass transport-related mechanism.

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