scholarly journals Role of shear stress and stretch in vascular mechanobiology

2011 ◽  
Vol 8 (63) ◽  
pp. 1379-1385 ◽  
Author(s):  
Deshun Lu ◽  
Ghassan S. Kassab
Keyword(s):  
Shear Stress ◽  
Morphological Changes ◽  
Wall Stress ◽  
Internal Stresses ◽  
Mechanical Forces ◽  
Oxidative Balance ◽  
Circumferential Wall Stress ◽  
Endothelial Shear Stress ◽  
Tissue Stresses

Blood vessels are under constant mechanical loading from blood pressure and flow which cause internal stresses (endothelial shear stress and circumferential wall stress, respectively). The mechanical forces not only cause morphological changes of endothelium and blood vessel wall, but also trigger biochemical and biological events. There is considerable evidence that physiologic stresses and strains (stretch) exert vasoprotective roles via nitric oxide and provide a homeostatic oxidative balance. A perturbation of tissue stresses and strains can disturb biochemical homeostasis and lead to vascular remodelling and possible dysfunction (e.g. altered vasorelaxation, tone, stiffness, etc.). These distinct biological endpoints are caused by some common biochemical pathways. The focus of this brief review is to point out some possible commonalities in the molecular pathways in response to endothelial shear stress and circumferential wall stretch.

scholarly journals Biomechanical Forces and Atherosclerosis: From Mechanism to Diagnosis and Treatment

2020 ◽  
Vol 16 (3) ◽  
pp. 187-197
Author(s):  
Vadim V. Genkel ◽  
Alla S. Kuznetcova ◽  
Igor I. Shaposhnik
Keyword(s):  
Shear Stress ◽  
Clinical Practice ◽  
Wall Shear Stress ◽  
Atherosclerotic Plaque ◽  
Wall Stress ◽  
Therapeutic Approaches ◽  
Circumferential Wall Stress ◽  
Biomechanical Forces ◽  
Biomechanical Factors

: The article provides an overview of current views on the role of biomechanical forces in the pathogenesis of atherosclerosis. The importance of biomechanical forces in maintaining vascular homeostasis is considered. We provide descriptions of mechanosensing and mechanotransduction. The roles of wall shear stress and circumferential wall stress in the initiation, progression and destabilization of atherosclerotic plaque are described. The data on the possibilities of assessing biomechanical factors in clinical practice and the clinical significance of this approach are presented. The article concludes with a discussion on current therapeutic approaches based on the modulation of biomechanical forces.

scholarly journals Role of Endothelial Shear Stress in the Natural History of Coronary Atherosclerosis and Vascular Remodeling

2007 ◽  
Vol 49 (25) ◽  
pp. 2379-2393 ◽  
Author(s):  
Yiannis S. Chatzizisis ◽  
Ahmet Umit Coskun ◽  
Michael Jonas ◽  
Elazer R. Edelman ◽  
Charles L. Feldman ◽  
...  
Keyword(s):  
Shear Stress ◽  
Natural History ◽  
Vascular Remodeling ◽  
Coronary Atherosclerosis ◽  
History Of ◽  
Endothelial Shear Stress

Abstract 12063: High-risk Plaque Co-localizes With Low Endothelial Shear Stress and Expansive Remodeling in Human Coronary Arteries: A 3D Optical Coherence Tomography Study

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Yiannis S Chatzizisis ◽  
Konstantinos Toutouzas ◽  
Andreas A Giannopoulos ◽  
Maria Riga ◽  
Antonios P Antoniadis ◽  
...  
Keyword(s):  
Optical Coherence Tomography ◽  
Shear Stress ◽  
High Risk ◽  
Coronary Arteries ◽  
Vascular Remodeling ◽  
Pool Size ◽  
Optical Coherence ◽  
Fibrous Cap ◽  
Endothelial Shear Stress

Background: High risk plaque accounts for the majority of acute coronary events. Low endothelial shear stress (ESS) is a key factor of the natural history of atherosclerosis. The role of ESS in high risk plaque formation is not well studied in man. Hypothesis: To explore the association of low ESS with high risk plaque and to identify the ESS milieu and vascular remodeling response in high risk vs. non high risk plaque. Methods: 35 coronary arteries from 30 patients were 3D reconstructed with fusion of coronary angiography and optical coherence tomography (Fig A-D) . ESS was calculated in the 3D reconstructed arteries using computational fluid dynamics (Fig E) and classified into low, moderate and high in 3 mm long segments. In each segment: i) fibroatheromas were classified into high risk and non high risk based on fibrous cap thickness and lipid pool size ii) vascular remodeling was classified into constrictive, compensatory and expansive. Results: Fibroatheromas in low ESS segments had significantly thinner fibrous cap compared to high ESS segments (89±84 vs.138±83 μm, p<0.05). Lipid pool size was comparable across all ESS categories. The majority of low ESS segments co-localized with high risk plaques (29 vs. 9%, p<0.05), whereas the majority of high ESS co-localized with non high risk plaques (24 vs. 9%, p<0.05, Fig F ). Compensatory and expansive remodeling was the predominant remodeling response in low ESS segments containing high risk plaques. In non-stenotic fibroatheromas (expansive or compensatory remodeling) low ESS was predominantly associated with high risk plaques (29 vs. 3%, p<0.05) whereas high ESS was associated with non high risk plaques (Fig F) . Conclusions: Novel combined anatomic and functional imaging with 3D OCT showed that low ESS and non-constrictive remodeling are associated with high risk plaque in man. Further studies are needed to assess the role of ESS and vascular remodeling in high risk plaque rupture and precipitation of clinical outcomes.

Effects of exercise on endothelium and endothelium/smooth muscle cross talk: role of exercise-induced hemodynamics

2011 ◽  
Vol 111 (1) ◽  
pp. 311-320 ◽  
Author(s):  
S. C. Newcomer ◽  
Dick H. J. Thijssen ◽  
D. J. Green
Keyword(s):  
Physical Activity ◽  
Shear Stress ◽  
Wall Stress ◽  
Beneficial Effects ◽  
Exercise Induced ◽  
Response To Exercise ◽  
And Training

Physical activity, exercise training, and fitness are associated with decreased cardiovascular risk. In the context that a risk factor “gap” exists in the explanation for the beneficial effects of exercise on cardiovascular disease, it has recently been proposed that exercise generates hemodynamic stimuli which exert direct effects on the vasculature that are antiatherogenic. In this review we briefly introduce some of the in vitro and in vivo evidence relating exercise hemodynamic modulation and vascular adaptation. In vitro data clearly demonstrate the importance of shear stress as a potential mechanism underlying vascular adaptations associated with exercise. Supporting this is in vivo human data demonstrating that exercise-mediated shear stress induces localized impacts on arterial function and diameter. Emerging evidence suggests that exercise-related changes in hemodynamic stimuli other than shear stress may also be associated with arterial remodeling. Taken together, in vitro and in vivo data strongly imply that hemodynamic influences combine to orchestrate a response to exercise and training that regulates wall stress and peripheral vascular resistance and contributes to the antiatherogenic impacts of physical activity, fitness, and training.

The Role of Shear Stress on ET-1, KLF2, and NOS-3 Expression in the Developing Cardiovascular System of Chicken Embryos in a Venous Ligation Model

Physiology ◽  
2007 ◽  
Vol 22 (6) ◽  
pp. 380-389 ◽  
Author(s):  
Bianca C. W. Groenendijk ◽  
Kim Van der Heiden ◽  
Beerend P. Hierck ◽  
Robert E. Poelmann
Keyword(s):  
Shear Stress ◽  
Heart Development ◽  
Cardiac Development ◽  
Background Information ◽  
Endothelial Shear Stress ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
Cardiovascular Anomalies ◽  
Chicken Model

In this review, the role of wall shear stress in the chicken embryonic heart is analyzed to determine its effect on cardiac development through regulating gene expression. Therefore, background information is provided for fluid dynamics, normal chicken and human heart development, cardiac malformations, cardiac and vitelline blood flow, and a chicken model to induce cardiovascular anomalies. A set of endothelial shear stress-responsive genes coding for endothelin-1 (ET-1), lung Krüppel-like factor (LKLF/KLF2), and endothelial nitric oxide synthase (eNOS/NOS-3) are active in development and are specifically addressed.

Abstract 15794: Role of Endothelial Shear Stress and Endothelial Shear Stress Gradient in Plaques Associated With Acute Erosion vs. Stable Control Plaques

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Diaa A Hakim ◽  
Zhongyue Pu ◽  
Ahmet U Coskun ◽  
Natalia Pinilla-Echeverri ◽  
Olli A Kajander ◽  
...  
Keyword(s):  
Shear Stress ◽  
Stress Gradient ◽  
Coronary Event ◽  
Plaque Disruption ◽  
Plaque Erosion ◽  
Luminal Area ◽  
History Of ◽  
Endothelial Shear Stress ◽  
And Control

Introduction: The role of endothelial shear stress (ESS) in the natural history of plaque growth and TCFA formation/destabilization has been studied, but the role in plaque erosion is unknown. High ESS gradient (ESSG) has been hypothesized to promote plaque erosion, but no studies have included matched “control” stable plaques with the same minimal luminal area (MLA) and reference luminal area (RLA) but no adverse coronary event. Hypothesis: To compare ESS and ESSG between coronary plaques that developed erosion and similar morphology plaques that remain stable. Methods: We studied a subset of patients from both TOTAL and COMPLETE trials who underwent angiography and OCT evaluation: 27 patients (27 arteries: 18 LAD, 3 LCX, 6 RCA). Plaques were divided into Plaque Erosion (n=16) from TOTAL study with OCT features of plaque erosion and Control (n=11) plaques (non-culprit lesions from COMPLETE) with matched MLA and RLA and no OCT evidence of plaque disruption. Orthogonal angiographic views were used to generate a 3-D arterial reconstruction, and angio centerline was merged with OCT centerline. Local ESS distribution was assessed by computational flow dynamics and reported in consecutive 3-mm segments. Results: Table 1 shows differences in ESS between Plaque Erosion and Control Plaques Conclusions: In coronary plaques with similar severe obstruction (MLA) and reference area (RLA), plaque erosion is associated with higher coronary flow, max ESS, and ESSG in any direction, in the proximal-to-distal direction, and in the circumferential direction compared to plaques that remain stable. Future studies will determine which "feature (s)" of high ESS or ESSG are independently associated with erosion.

Vulnerable Anatomy; The Role of Coronary Anatomy and Endothelial Shear Stress in the Progression and Vulnerability of Coronary Artery Lesions: Is Anatomy Destiny?

2010 ◽  
pp. 495-506 ◽  
Author(s):  
Charles L. Feldman ◽  
Yiannis S. Chatzizisis ◽  
Ahmet U. Coskun ◽  
Konstantinos C. Koskinas ◽  
Morteza Naghavi ◽  
...  
Keyword(s):  
Shear Stress ◽  
Coronary Artery ◽  
Coronary Artery Lesions ◽  
Coronary Anatomy ◽  
Endothelial Shear Stress

Control of Circumferential Wall Stress and Luminal Shear Stress Within Intact Vascular Segments Perfused Ex Vivo

2008 ◽  
Vol 130 (5) ◽  
Author(s):  
Mohammed S. El-Kurdi ◽  
Jeffrey S. Vipperman ◽  
David A. Vorp
Keyword(s):  
Shear Stress ◽  
Cardiac Cycle ◽  
Ex Vivo ◽  
Wall Stress ◽  
Pid Controllers ◽  
Wave Form ◽  
Outer Diameter ◽  
Blood Gas ◽  
Circumferential Wall Stress ◽  
Temperature Levels

Proportional, integral, and derivative (PID) controllers have proven to be robust in controlling many applications, and remain the most widely used control system architecture. The purpose of this work was to use this architecture for designing and tuning two PID controllers. The first was used to control the physiologic arterial circumferential wall stress (CWS) and the second to control the physiologic arterial shear stress (SS) imposed on intact vascular segments that were implanted into an ex vivo vascular perfusion system (EVPS). In order to most accurately control the stresses imposed onto vascular segments perfused ex vivo, analytical models were derived to calculate the CWS and SS. The mid-vein-wall CWS was calculated using the classical Lamé solution for thick-walled cylinders in combination with the intraluminal pressure and outer diameter measurements. Similarly, the SS was calculated using the Hagen–Poiseuille equation in combination with the flow rate and outer diameter measurements. Performance of each controller was assessed by calculating the root mean square of the error (RMSE) between the desired and measured process variables. The performance experiments were repeated ten times (N=10) and an average RMSE was reported for each controller. RMSE standard deviations were calculated to demonstrate the reproducibility of the results. Sterile methods were utilized for making blood gas and temperature measurements in order to maintain physiologic levels within the EVPS. Physiologic blood gases (pH, pO2, and pCO2) and temperature within the EVPS were very stable and controlled manually. Blood gas and temperature levels were recorded hourly for several (N=9)24h perfusion experiments. RMSE values for CWS control (0.427±0.027KPa) indicated that the system was able to generate a physiologic CWS wave form within 0.5% error of the peak desired CWS over each cardiac cycle. RMSE values for SS control (0.005±0.0007dynes∕cm2) indicated that the system was able to generate a physiologic SS wave form within 0.3% error of the peak desired SS over each cardiac cycle. Physiologic pH, pO2, pCO2, and temperature levels were precisely maintained within the EVPS. The built-in capabilities and overall performance of the EVPS described in this study provide us with a novel tool for measuring molecular responses of intact vascular segments exposed to precisely simulated arterial biomechanical conditions.

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