In Vivo Human Brachial Artery Elastic Mechanics

Bank, Alan J.; Kaiser, Daniel R.; Rajala, Scott; Cheng, Anthony

doi:10.1161/01.cir.100.1.41

Cited by 146 publications

(126 citation statements)

References 37 publications

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“…Young's modulus is given directly for pressures ranging from 20 to 40 mmHg in Bergel's thesis 23 ( Figure 14, p. 123) and averages 2 x 10 6 dynes/cm 2 . Bank 20 , using ultrasound measurements in living human subjects found values of E ranging from 0.5 to 5 x 10 6 dynes/cm 2 and averaging about 2 x 10 6 dynes/cm 2 in the pressure range of 0 to 40 mmHg. In aggregate these data suggest a working value for E near 1.4 x 10 6 dynes/cm 2 for the low transmural pressures operative during cuff deflation.…”

Section: Numerical Values Of Model Parametersmentioning

confidence: 97%

“…Bank 20 , for example, found for human brachial arteries in vivo that Young's modulus at normal arterial pressures is about four times greater than that at lower pressures of cuff deflation (0 to 40 mmHg). Similarly, Holzapfel and Ogden 18 showed theoretically that Young's modulus at normal arterial pressure is about four times greater than Young's modulus in the range of 0 to 40 mmHg.…”

Section: Numerical Values Of Model Parametersmentioning

confidence: 99%

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The origin of Korotkoff sounds and the accuracy of auscultatory blood pressure measurements

Babbs

2015

Journal of the American Society of Hypertension

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This study explores the hypothesis that the sharper, high frequency Korotkoff sounds come from resonant motion of the arterial wall, which begins after the artery transitions from a buckled state to an expanding state. The motion of one mass, two nonlinear springs, and one damper, driven by transmural pressure under the cuff, are used to model and compute the Korotkoff sounds according to principles of classical Newtonian physics. The natural resonance of this springmass-damper system provides a concise, yet rigorous, explanation for the origin of Korotkoff sounds. Fundamentally, wall stretching in expansion requires more force than wall bending in buckling. At cuff pressures between systolic and diastolic arterial pressure, audible vibrations (> 40 Hz) occur during early expansion of the artery wall beyond its zero pressure radius after the outward moving mass of tissue experiences sudden deceleration, caused by the discontinuity in stiffness between bucked and expanded states. The idealized spring-mass-damper model faithfully reproduces the time domain waveforms of actual Korotkoff sounds in humans. Appearance of arterial sounds occurs at or just above the level of systolic pressure. Disappearance of arterial sounds occurs at or just above the level of diastolic pressure. Muffling of the sounds is explained by increased resistance of the artery to collapse, caused by downstream venous engorgement. A simple analytical model can define the physical origin of Korotkoff sounds, suggesting improved mechanical or electronic filters for their selective detection, and confirming the disappearance of the Korotkoff sounds as the optimal diastolic endpoint.

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Section: Numerical Values Of Model Parametersmentioning

confidence: 97%

Section: Numerical Values Of Model Parametersmentioning

confidence: 99%

The origin of Korotkoff sounds and the accuracy of auscultatory blood pressure measurements

Babbs

2015

Journal of the American Society of Hypertension

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“…With increasing distending pressure, there is recruitment of collagen fibres leading to greater stiffness. Increases in heart rate can also change arterial characteristics and must be considered in these measurements as well (18,19).…”

Section: Arterial Stiffnessmentioning

confidence: 99%

“…Many of the agents tested also lower blood pressure, and this effect must be differentiated from any effects on structural remodelling or improvement in endothelial function that would favourably affect arterial stiffness. Agents that decrease arterial stiffness include nitroglycerin (18,20), angiotensinconverting enzyme inhibitors and angiotensin receptor blockers (43), and calcium channel blockers (44). The data for beta-blockers are not nearly as clear.…”

Section: Relationship Of Arterial Stiffness To Risk Factors and Theirmentioning

confidence: 99%

Arterial stiffness or endothelial dysfunction as a surrogate marker of vascular risk

Anderson

2006

Canadian Journal of Cardiology

151

113

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T he understanding of the pathophysiology of atherosclerosis and its vascular complications has increased dramatically over the past decade. Numerous measurable biomarkers play a role in the atherosclerosis process, and are associated with clinically important vascular events. Not only has their evaluation advanced our knowledge of the atherosclerotic process but it has also accelerated a search for new diagnostic tools to aid in risk stratification. Putative factors include soluble biomarkers and imaging assessments of vascular structure and function. The endothelium plays a key role in vascular homeostasis through the release of a variety of paracrine factors that interact with platelets, inflammatory cells and the vessel wall. The endothelium's central location allows it to sense and respond to a variety of perturbations. Endothelial dysfunction is an early marker of disease. Risk factors can also affect mechanical properties such as arterial stiffness, which is now recognized as a major contributor to systolic hypertension in elderly people. Methods of assessing endothelial function and arterial stiffness are available for clinical research and recent evidence suggests that these measures may provide important prognostic information. ATTRIBUTES OF A SURROGATE BIOMARKEREpidemiological studies, such as Framingham, have allowed longitudinal assessment of cardiovascular events and the development of simple scoring tables for risk calculation (1,2). These factors involved include blood pressure, lipid profile, smoking status and age. More recently, many factors thought to be associated with the atherosclerotic process have been studied. Some of these have been shown to correlate with clinical outcomes and have been deemed biomarkers (3,4). However, association does not necessarily imply causation and, due to a variety of limitations, most of these markers will not be useful for the clinical evaluation of risk or drug therapy (5). To become clinically important, a biomarker must fulfill the criteria for a surrogate marker. A surrogate substitutes for clinically important end points with respect to how an individual feels, functions or survives. Classic examples include blood pressure and low density lipoprotein cholesterol. These are targets of treatment. A surrogate should meet the following criteria:• Adds independent information above currently used criteria;• Is reliably and reproducibly measured;• Accounts for a significant proportion of disease risk;• Provides good predictive value;• Is reasonably associated with the underlying pathophysiology;• If it is to be used in risk prevention, is present before the clinical appearance of the outcome; and• Is available and practical for widespread application (5-8). ADVANCES IN VASCULAR BIOLOGY

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“…In experiments, inhibition of basal NO synthesis by N-monomethyl-Larginine (L-NMMA) increased, 9,10 while NO donor nitroglycerine decreased arterial stiffness. 11 The genes coding for the AT1 receptor and eNOS have been found to be polymorphic. The relationships of their alleles to hypertension and other cardiovascular abnormalities have been investigated in several studies.…”

Section: Introductionmentioning

confidence: 99%

Synergistic effect of angiotensin II type 1 receptor and endothelial nitric oxide synthase gene polymorphisms on arterial stiffness

et al. 2007

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Angiotensin II and nitric oxide belong to important factors in the functional and structural changes of vessel wall, leading to its increased stiffness. We investigated, whether common mutations of angiotensin II type 1 receptor (AGTR 1 ) and endothelial nitric oxide synthase (eNOS) are associated with increased arterial stiffness. Two polymorphisms, A 1166 C of AGTR 1 and T 786 C of Enos, were estimated in a random, general population-based sample of 250 subjects. Arterial stiffness was measured using Sphygmocor as aortic (carotid-femoral) and peripheral (femoral-tibial) pulse wave velocities (PWV). Carriers of 3-4 mutant alleles from both polymorphisms, that is, homozygous for both mutations or homozygous for one and heterozygous for the second one, showed significantly higher peripheral PWV (17.9272.40) than those with none or only 1-2 mutant alleles (12.3770.51; Po0.003). Carriers of 3-4 mutant alleles had three times higher risk of having increased peripheral PWV (X13.63 m s À1 , that is, in the top quartile) and this association remained significant after adjustment for potential confounders. No association was found between estimated genotypes and aortic PWV. In conclusion, combination of A 1166 C of AGTR 1 and T 786 C of eNOS mutations increased stiffness of muscular-type arteries.

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In Vivo Human Brachial Artery Elastic Mechanics

Cited by 146 publications

References 37 publications

The origin of Korotkoff sounds and the accuracy of auscultatory blood pressure measurements

The origin of Korotkoff sounds and the accuracy of auscultatory blood pressure measurements

Arterial stiffness or endothelial dysfunction as a surrogate marker of vascular risk

Synergistic effect of angiotensin II type 1 receptor and endothelial nitric oxide synthase gene polymorphisms on arterial stiffness

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