Carotid circumferential wall stress homeostasis in early remodeling: Theoretical approach and clinical application

2012 ◽  
Vol 40 (8) ◽  
pp. 486-494 ◽  
Author(s):  
Plamen Bokov ◽  
Gilles Chironi ◽  
Ludmila Orobinskaia ◽  
Patrice Flaud ◽  
Alain Simon
Keyword(s):  
Clinical Application ◽  
Theoretical Approach ◽  
Wall Stress ◽  
Circumferential Wall Stress

scholarly journals Associations of markers of arterial stiffness and remodeling with new-onset type 2 diabetes mellitus

2021 ◽  
Vol 28 (Supplement_1) ◽  
Author(s):  
F Ahmadizar ◽  
K Wang ◽  
F Mattace Raso ◽  
MA Ikram ◽  
M Kavousi
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Blood Glucose ◽  
Arterial Stiffness ◽  
Wall Stress ◽  
Lipid Lowering ◽  
Circumferential Wall Stress ◽  
Increased Risk

Abstract Funding Acknowledgements Type of funding sources: None. Background. Arterial stiffness/remodeling results in impaired blood flow and, eventually, decreased glucose disposal in peripheral tissues and increased blood glucose. Besides, increased arterial stiffness/remodeling may lead to hypertension, as a potential reciprocal risk factor for type 2 diabetes mellitus (T2D). We, therefore, hypothesized that increased arterial stiffness/remodeling is associated with an increased risk of T2D. Purpose. To study the associations between arterial stiffness/remodeling and incident T2D. Methods. We used the prospective population-based Rotterdam Study. Common carotid arterial properties were ultrasonically determined in plaque-free areas. Aortic stiffness was estimated by carotid-femoral pulse wave velocity (cf_PWV), carotid stiffness was estimated by the carotid distensibility coefficient (carDC). Arterial remodeling was estimated by carotid artery lumen diameter (carDi), carotid intima-media thickness (cIMT), mean circumferential wall stress (CWSmean), and pulsatile circumferential wall stress (CWSpuls). Cox proportional hazard regression analysis was used to estimate the associations between arterial stiffness/remodeling and the risk of incident T2D, adjusted for age, sex, cohort, mean arterial pressure (MAP), antihypertensive medications, heart rate, non- high-density lipoprotein (HDL)-cholesterol, lipid-lowering medications, and smoking. We included interaction terms in the fully adjusted models to study whether any significant associations were modified by sex, age, blood glucose, or MAP. Spearman correlation analyses were applied to examine the correlations between measurements of arterial stiffness/remodeling and glycemic traits. Results. We included 3,055 individuals free of T2D at baseline (mean (SD) age, 67.2 (7.9) years). During a median follow-up of 14.0 years, 395 (12.9%) T2D occurred. After adjustments, higher cf_PWV (hazard ratio (HR),1.18; 95%CI:1.04-1.35), carDi (1.17; 1.04-1.32), cIMT (1.15; 1.01-1.32), and CWSpuls (1.28; 1.12-1.47) were associated with increased risk of incident T2D. After further adjustment for the baseline glucose, the associations attenuated but remained statistically significant. Sex, age, blood glucose, or MAP did not modify the associations between measurements of arterial stiffness/remodeling, and incident T2D. Among the population with prediabetes at baseline (n = 513) compared to the general population, larger cIMT was associated with a greater increase in the risk of T2D. Most measurements of arterial stiffness/remodeling significantly but weakly correlated with baseline glycemic traits, particularly with blood glucose.  Conclusions. Our study suggests that greater arterial stiffness/remodeling is independently associated with an increased risk of T2D development. Blood glucose and hypertension do not seem to play significant roles in these associations. Further studies should disentangle the underlying mechanism that links arterial stiffness/remodeling and T2D.

Evaluation of Analytic Estimates of Ventricular Wall Stress Using the Finite Element Method

2008 ◽  
Author(s):  
Christopher M. Ingrassia ◽  
Shantanu Y. Jani ◽  
Kevin D. Costa
Keyword(s):  
Finite Element ◽  
Circumferential Stress ◽  
Wall Stress ◽  
Cardiac Mechanics ◽  
Ventricular Wall ◽  
The Finite Element Method ◽  
Regional Wall ◽  
Circumferential Wall Stress ◽  
Theoretical Assumptions ◽  
Accurate Quantification

The importance of ventricular wall stress to cardiac function has been well-documented [1, 2], although accurate quantification remains a challenge. In this study, three popular analytic formulas for estimating circumferential wall stress were comprehensively evaluated to identify the conditions for which their use may be appropriate. In particular, the equations of Laplace [3], Mirsky [4], and Janz [5] are commonly used in the fields of cardiology and echocardiography; despite the inaccuracy of key theoretical assumptions, they have been attractive for their simplicity. For validation, we employed specialized finite element methods, developed specifically for cardiac mechanics applications [6], to compute regional wall stress in a series of model chambers having systematically varying geometric and material complexity. We limited our analysis to circumferential stress for consistency with the theoretical equations, and because of its relevance to cardiac mechanics.

Effects of acute changes in load and inotropic state on the exponential rate of fiber shortening and other indices of myocardial contractility in the anesthetized intact dog

1987 ◽  
Vol 65 (1) ◽  
pp. 46-53 ◽  
Author(s):  
José Suarez de Lezo ◽  
Pierre Casey ◽  
Anita Casey ◽  
José Luis Carrasco ◽  
José M. Arizon ◽  
...  
Keyword(s):  
Myocardial Contractility ◽  
Wall Stress ◽  
Left Ventricular ◽  
Systemic Resistance ◽  
Exponential Rate ◽  
Ventricular Contractility ◽  
Left Ventricular Contractility ◽  
Inotropic State ◽  
Circumferential Wall Stress ◽  
Inotropic Intervention

The effects of an acute increase in preload, afterload, and inotropic state on several indices of left ventricular contractility were studied in 20 anesthetized intact dogs. The behaviour of the exponential rate of fiber shortening (ERFS), a newly described index, which is based on the instantaneous fiber length – time relationship through ejection, was compared with other classical ejection and isovolumic indices of left ventricular contractility. Acute volume overload by dextran 40 infusion produced a significant increase in preload as reflected by a 103% (p < 0.01) increase in left ventricular end-diastolic pressure and a 121% (p < 0.001) increase in end-diastolic circumferential wall stress. There was also a smaller but significant increase (p < 0.05) of heart rate (30%) and of peak systolic circumferential wall stress (24%). None of the left ventricular contractility indices showed any significant change. Acute pressure overload, produced mechanically by an aortic balloon, increased the afterload significantly as reflected by a 33% (p < 0.05) rise of end-systolic circumferential wall stress and a 43% (p < 0.001) increase in systemic resistance. Stroke volume decreased significantly by 23% (p < 0.05). All ejection indices, including ERFS, were significantly diminished by 30 – 37%; all isovolumic indices showed no significant changes. Positive inotropic intervention was induced by dopamine infusion, which caused a significant 28% (p < 0.05) increase in cardiac output. End-diastolic and end-systolic circumferential wall stress were significantly diminished. All indices of left ventricular contractility increased significantly and ERFS showed the quantitatively greatest change. This study suggests that ERFS is an ejection index of myocardial contractility, which is quite sensitive to inotropic intervention, independent of preload but sensitive to afterload.

TGF-β- and CTGF-mediated fibroblast recruitment influences early outward vein graft remodeling

2007 ◽  
Vol 293 (1) ◽  
pp. H482-H488 ◽  
Author(s):  
Zhihua Jiang ◽  
Peng Yu ◽  
Ming Tao ◽  
Chessy Fernandez ◽  
Cristos Ifantides ◽  
...  
Keyword(s):  
Growth Factor ◽  
Vein Graft ◽  
Transforming Growth Factor ◽  
Mechanical Load ◽  
Wall Stress ◽  
Transforming Growth Factor Β ◽  
Tissue Growth ◽  
Vein Grafts ◽  
Circumferential Wall Stress ◽  
The Impact

Luminal shearing forces have been shown to impact both geometric remodeling and the development of intimal hyperplasia. Less well studied is the influence of intramural wall stresses on vessel growth and adaptation. Using a vein graft-fistula configuration to isolate the impact of circumferential wall stress, we identify the reorganization of adventitial myofibroblasts as the dominant histological event that limits early outward remodeling of vein grafts in response to elevated wall stress. We hypothesize that increased production of transforming growth factor-β (TGF-β) and connective tissue growth factor (CTGF) induces recruitment of myofibroblasts, promotes adventitial reorganization, and limits early outward remodeling in response to increased intramural wall stress. Vein grafts with a distal arteriovenous fistula in the neck of rabbits were constructed, resulting in a fourfold differential in circumferential wall stress. Using this model, we demonstrate 1) elevated wall stress augments the production of TGF-β and CTGF, 2) increased TGF-β expression and CTGF expression are correlated with the enhanced differentiation from fibroblasts to myofibroblasts, as evidenced by the significant increase in the α-actin-positive cells in adventitia, and 3) the levels of TGF-β, CTGF, and α-actin are inversely correlated with the magnitude of outward remodeling of the graft wall. Increased wall stress after vein graft implantation appears to induce a TGF-β- and CTGF-mediated recruitment of adventitial fibroblasts and a conversion to a myofibroblast phenotype. Although important in the maintenance of wall stability in the face of an increased mechanical load, this adventitial adaptation limits early outward remodeling of the vein conduit and may prove deleterious in maintaining long-term vein graft patency.

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.

Microfibrillar Elastic Polymer Wrapping of Rat Vena Cava for the Study of Engineered Arterial Vein Grafts

2010 ◽  
Author(s):  
Qiang Wang ◽  
Wei He ◽  
Yi Hong ◽  
William R. Wagner ◽  
David A. Vorp
Keyword(s):  
Saphenous Vein Graft ◽  
Vena Cava ◽  
Wall Stress ◽  
Cellular Injury ◽  
Vein Grafts ◽  
Ample Opportunity ◽  
Circumferential Wall Stress ◽  
Rat Vena Cava ◽  
Elastic Polymer ◽  
Polymer Wrapping

The autologous saphenous vein graft remains the graft of choice for 95% of surgeons performing coronary artery or peripheral bypass procedures. Within the first 5 years after implantation, 20%–40% of arterial vein grafts (AVG) fail due to intimal hyperplasia (IH)1. This adverse pathological response by AVGs may be in part due to their abrupt exposure to the significantly elevated circumferential wall stress associated with the arterial system2. We believe that if an AVG is given an ample opportunity to adapt and remodel to the stresses of the arterial environment, cellular injury may be reduced, thus limiting the initiating mechanisms of IH.

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.

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