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Journal ArticleDOI

Blood flow in arteries

01 Jan 1997-Annual Review of Fluid Mechanics (Annual Reviews 4139 El Camino Way, P.O. Box 10139, Palo Alto, CA 94303-0139, USA)-Vol. 29, Iss: 29, pp 399-434
TL;DR: The study of arterial blood flow will lead to the prediction of individual hemodynamic flows in any patient, the development of diagnostic tools to quantify disease, and the design of devices that mimic or alter blood flow.
Abstract: Blood flow in arteries is dominated by unsteady flow phenomena. The cardiovascular system is an internal flow loop with multiple branches in which a complex liquid circulates. A nondimensional frequency parameter, the Womersley number, governs the relationship between the unsteady and viscous forces. Normal arterial flow is laminar with secondary flows generated at curves and branches. The arteries are living organs that can adapt to and change with the varying hemodynamic conditions. In certain circumstances, unusual hemodynamic conditions create an abnormal biological response. Velocity profile skewing can create pockets in which the direction of the wall shear stress oscillates. Atherosclerotic disease tends to be localized in these sites and results in a narrowing of the artery lumen—a stenosis. The stenosis can cause turbulence and reduce flow by means of viscous head losses and flow choking. Very high shear stresses near the throat of the stenosis can activate platelets and thereby induce thrombosis, which can totally block blood flow to the heart or brain. Detection and quantification of stenosis serve as the basis for surgical intervention. In the future, the study of arterial blood flow will lead to the prediction of individual hemodynamic flows in any patient, the development of diagnostic tools to quantify disease, and the design of devices that mimic or alter blood flow. This field is rich with challenging problems in fluid mechanics involving three-dimensional, pulsatile flows at the edge of turbulence.
Citations
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Journal ArticleDOI
TL;DR: The molecular, cellular, and vascular processes supporting the role of low ESS in the natural history of coronary atherosclerosis and vascular remodeling are explored and likely mechanisms concerning the different natural history trajectories of individual coronary lesions are indicated.

1,350 citations

Journal ArticleDOI
TL;DR: Low-WSS segments in patients with coronary artery disease develop greater plaque and necrotic core progression and constrictive remodeling, and high-W SS segments develop greater nec rotic core and calcium progression, regression of fibrous and fibrofatty tissue, and excessive expansive remodelling, suggestive of transformation to a more vulnerable phenotype.
Abstract: BackgroundExperimental studies suggest that low wall shear stress (WSS) promotes plaque development and high WSS is associated with plaque destabilization. We hypothesized that low-WSS segments in patients with coronary artery disease develop plaque progression and high-WSS segments develop necrotic core progression with fibrous tissue regression. Methods and ResultsTwenty patients with coronary artery disease underwent baseline and 6-month radiofrequency intravascular ultrasound (virtual histology intravascular ultrasound) and computational fluid dynamics modeling for WSS calculation. For each virtual histology intravascular ultrasound segment (n=2249), changes in plaque area, virtual histology intravascular ultrasound–derived plaque composition, and remodeling were compared in low-, intermediate-, and high-WSS categories. Compared with intermediate-WSS segments, low-WSS segments developed progression of plaque area (P=0.027) and necrotic core (P<0.001), whereas high-WSS segments had progression of necro...

594 citations

Journal ArticleDOI
25 Jun 2009-Nature
TL;DR: A critical role for biomechanical forces in haematopoietic development is revealed in mouse embryos using mouse embryonic stem cells differentiated in vitro and that abrogation of nitric oxide, a mediator of shear-stress-induced signalling, compromises haem atopOietic potential in vivo and in vivo is revealed.
Abstract: Biomechanical forces are emerging as critical regulators of embryogenesis, particularly in the developing cardiovascular system. After initiation of the heartbeat in vertebrates, cells lining the ventral aspect of the dorsal aorta, the placental vessels, and the umbilical and vitelline arteries initiate expression of the transcription factor Runx1 (refs 3-5), a master regulator of haematopoiesis, and give rise to haematopoietic cells. It remains unknown whether the biomechanical forces imposed on the vascular wall at this developmental stage act as a determinant of haematopoietic potential. Here, using mouse embryonic stem cells differentiated in vitro, we show that fluid shear stress increases the expression of Runx1 in CD41(+)c-Kit(+) haematopoietic progenitor cells, concomitantly augmenting their haematopoietic colony-forming potential. Moreover, we find that shear stress increases haematopoietic colony-forming potential and expression of haematopoietic markers in the para-aortic splanchnopleura/aorta-gonads-mesonephros of mouse embryos and that abrogation of nitric oxide, a mediator of shear-stress-induced signalling, compromises haematopoietic potential in vitro and in vivo. Collectively, these data reveal a critical role for biomechanical forces in haematopoietic development.

465 citations

Journal ArticleDOI
TL;DR: A review of the modeling studies and experiments on steady and unsteady, two-and three-dimensional flows in arteries, and in arterial geometries most relevant in the context of atherosclerosis can be found in this article.
Abstract: ▪ Abstract The relationship between flow in the arteries, particularly the wall shear stresses, and the sites where atherosclerosis develops has motivated much of the research on arterial flow in recent decades. It is now well accepted that it is sites where shear stresses are low, or change rapidly in time or space, that are most vulnerable. These conditions are likely to prevail at places where the vessel is curved; bifurcates; has a junction, a side branch, or other sudden change in flow geometry; and when the flow is unsteady. These flows, often but not always involving flow separation or secondary motions, are also the most difficult ones in fluid mechanics to analyze or compute. In this article we review the modeling studies and experiments on steady and unsteady, two-and three-dimensional flows in arteries, and in arterial geometries most relevant in the context of atherosclerosis. These include studies of normal vessels—to identify, on the basis of the fluid mechanics, lesion foci—and stenotic ves...

460 citations

Journal ArticleDOI
TL;DR: In this article, the authors review recent advances in understanding the fundamental mechanics of flexible-tube flows and discuss physiological applications spanning the cardiovascular system, respiratory system, and elsewhere in the body (involving active peristaltic transport driven by fluid structure/muscle interactions).
Abstract: ▪ AbstractAlmost all vessels carrying fluids within the body are flexible, and interactions between an internal flow and wall deformation often underlie a vessel's biological function or dysfunction. Such interactions can involve a rich range of fluid-mechanical phenomena, including nonlinear pressure-drop/flow-rate relations, self-excited oscillations of single-phase flow at high Reynolds number and capillary-elastic instabilities of two-phase flow at low Reynolds number. We review recent advances in understanding the fundamental mechanics of flexible-tube flows, and discuss physiological applications spanning the cardiovascular system (involving wave propagation and flow-induced instabilities of blood vessels), the respiratory system (involving phonation, the closure and reopening of liquid-lined airways, and Marangoni flows on flexible surfaces), and elsewhere in the body (involving active peristaltic transport driven by fluid-structure/muscle interactions).

423 citations

References
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Journal ArticleDOI
TL;DR: Carotid endarterectomy is highly beneficial to patients with recent hemispheric and retinal transient ischemic attacks or nondisabling strokes and ipsilateral high-grade stenosis of the internal carotid artery.
Abstract: Background Without strong evidence of benefit, the use of carotid endarterectomy for prophylaxis against stroke rose dramatically until the mid-1980s, then declined. Our investigation sought to determine whether carotid endarterectomy reduces the risk of stroke among patients with a recent adverse cerebrovascular event and ipsilateral carotid stenosis. Methods We conducted a randomized trial at 50 clinical centers throughout the United States and Canada, in patients in two predetermined strata based on the severity of carotid stenosis--30 to 69 percent and 70 to 99 percent. We report here the results in the 659 patients in the latter stratum, who had had a hemispheric or retinal transient ischemic attack or a nondisabling stroke within the 120 days before entry and had stenosis of 70 to 99 percent in the symptomatic carotid artery. All patients received optimal medical care, including antiplatelet therapy. Those assigned to surgical treatment underwent carotid endarterectomy performed by neurosurgeons or vascular surgeons. All patients were examined by neurologists 1, 3, 6, 9, and 12 months after entry and then every 4 months. End points were assessed by blinded, independent case review. No patient was lost to follow-up. Results Life-table estimates of the cumulative risk of any ipsilateral stroke at two years were 26 percent in the 331 medical patients and 9 percent in the 328 surgical patients--an absolute risk reduction (+/- SE) 17 +/- 3.5 percent (P less than 0.001). For a major or fatal ipsilateral stroke, the corresponding estimates were 13.1 percent and 2.5 percent--an absolute risk reduction of 10.6 +/- 2.6 percent (P less than 0.001). Carotid endarterectomy was still found to be beneficial when all strokes and deaths were included in the analysis (P less than 0.001). Conclusions Carotid endarterectomy is highly beneficial to patients with recent hemispheric and retinal transient ischemic attacks or nondisabling strokes and ipsilateral high-grade stenosis (70 to 99 percent) of the internal carotid artery.

7,496 citations

Journal ArticleDOI
TL;DR: These studies confirm earlier findings under steady flow conditions that plaques tend to form in areas of low, rather than high, shear stress, but indicate in addition that marked oscillations in the direction of wall shear may enhance atherogenesis.
Abstract: Fluid velocities were measured by laser Doppler velocimetry under conditions of pulsatile flow in a scale model of the human carotid bifurcation. Flow velocity and wall shear stress at five axial and four circumferential positions were compared with intimal plaque thickness at corresponding locations in carotid bifurcations obtained from cadavers. Velocities and wall shear stresses during diastole were similar to those found previously under steady flow conditions, but these quantities oscillated in both magnitude and direction during the systolic phase. At the inner wall of the internal carotid sinus, in the region of the flow divider, wall shear stress was highest (systole = 41 dynes/cm2, diastole = 10 dynes/cm2, mean = 17 dynes/cm2) and remained unidirectional during systole. Intimal thickening in this location was minimal. At the outer wall of the carotid sinus where intimal plaques were thickest, mean shear stress was low (-0.5 dynes/cm2) but the instantaneous shear stress oscillated between -7 and +4 dynes/cm2. Along the side walls of the sinus, intimal plaque thickness was greater than in the region of the flow divider and circumferential oscillations of shear stress were prominent. With all 20 axial and circumferential measurement locations considered, strong correlations were found between intimal thickness and the reciprocal of maximum shear stress (r = 0.90, p less than 0.0005) or the reciprocal of mean shear stress (r = 0.82, p less than 0.001). An index which takes into account oscillations of wall shear also correlated strongly with intimal thickness (r = 0.82, p less than 0.001). When only the inner wall and outer wall positions were taken into account, correlations of lesion thickness with the inverse of maximum wall shear and mean wall shear were 0.94 (p less than 0.001) and 0.95 (p less than 0.001), respectively, and with the oscillatory shear index, 0.93 (p less than 0.001). These studies confirm earlier findings under steady flow conditions that plaques tend to form in areas of low, rather than high, shear stress, but indicate in addition that marked oscillations in the direction of wall shear may enhance atherogenesis.

2,623 citations

Journal ArticleDOI
TL;DR: The experiments of McDonald and his co-workers have shown that in the larger arteries of the rabbit and the dog there is a reversal of the flow, and the simple mathematical treatment has strong similarities with the theory of the distribution of alternating current in a conductor of finite size.
Abstract: The experiments of McDonald and his co-workers (McDonald, 1952, 1955; Helps & McDonald, 1953) have shown that in the larger arteries of the rabbit and the dog there is a reversal of the flow. Measurements of the pressure gradient (Helps & McDonald, 1953) showed a phase-lag between pressure gradient and flow somewhat analogous with the phase-lag between voltage and current in a conductor carrying alternating current, and the simple mathematical treatment given below has strong similarities with the theory of the distribution of alternating current in a conductor of finite size.

1,675 citations

Book
01 Jun 1974

1,455 citations