Aortic Mechanical Properties Research Articles

Aortic root stiffness and mechanical properties of healthy adults

BackgroundArterial stiffness, often expressed in terms of pulse wave velocity (PWV), is an important risk factor for cardiovascular disease. PWV can be determined locally and non-invasively, by means of ultrasound.AimTo assess PWV, local compliance (Cs), distensibility (Ds) and Young’s modulus of the aortic root using non-invasive ultrasound measurements.Methods10 healthy volunteers aged 21–39, 1 male, were scanned using ultrasound (GE, Vivid E95) with a phased array transducer 1.5–4.5MHz. DICOM images were recorded from the parasternal long axis: M-mode for diameter measurements, and apical 5- chamber view for blood Doppler velocity, sequentially. Each measurement was repeated 3 times for 20s. Velocity and diameter waveforms were extracted offline in Matlab based on grey-scale thresholding. PWV was determined using the ln(D) U- loop method [1]. Wall thickness was extracted from the B-mode images used to measure the diameter. Distensibility and compliance were calculated as Ds = 1/ (ρ·PWV2), Cs = dA/dP = DsA, where ρ = 1050kg/m3 blood density, A is the cross- sectional area, and Young’s modulus was calculated as previously described [2] using the Bramwell-Hill and Moens-Kortweg equations.).ResultsAcross all patients mean PWV was 3 ± 0.8m/s, mean distensibility was 1.3·10-4 ± 0.61 · 10−4Pa−1, and mean compliance was 0.6 ± 0.31m2Pa−1. The average wall thickness was 0.4 ± 0.06cm while Young’s modulus was 63.6 ± 40.4kPa. These results are comparable to corresponding values reported in the literature using other techniques.ConclusionsAortic root PWV, distensibility, compliance and Young’s modulus can be determined using ultrasound measurements of diameter and velocity. Further studies are required to investigate the potential clinical utility of aortic root parameters.

Mitochondria-targeted antioxidant therapy with MitoQ ameliorates aortic stiffening in old mice.

Aortic stiffening is a major independent risk factor for cardiovascular diseases, cognitive dysfunction, and other chronic disorders of aging. Mitochondria-derived reactive oxygen species are a key source of arterial oxidative stress, which may contribute to arterial stiffening by promoting adverse structural changes—including collagen overabundance and elastin degradation—and enhancing inflammation, but the potential for mitochondria-targeted therapeutic strategies to ameliorate aortic stiffening with primary aging is unknown. We assessed aortic stiffness [pulse-wave velocity (aPWV)], ex vivo aortic intrinsic mechanical properties [elastic modulus (EM) of collagen and elastin regions], and aortic protein expression in young (~6 mo) and old (~27 mo) male C57BL/6 mice consuming normal drinking water (YC and OC) or water containing mitochondria-targeted antioxidant MitoQ (250 µM; YMQ and OMQ) for 4 wk. Both baseline and postintervention aPWV values were higher in OC vs. YC (post: 482 ± 21 vs. 420 ± 5 cm/s, P < 0.05). MitoQ had no effect in young mice but decreased aPWV in old mice (OMQ, 426 ± 20, P < 0.05 vs. OC). MitoQ did not affect age-associated increases in aortic collagen-region EM, collagen expression, or proinflammatory cytokine expression, but partially attenuated age-associated decreases in elastin region EM and elastin expression. Our results demonstrate that MitoQ reverses in vivo aortic stiffness in old mice and suggest that mitochondria-targeted antioxidants may represent a novel, promising therapeutic strategy for decreasing aortic stiffness with primary aging and, possibly, age-related clinical disorders in humans. The destiffening effects of MitoQ treatment may be at least partially mediated by attenuation/reversal of age-related aortic elastin degradation.NEW & NOTEWORTHY We show that 4 wk of treatment with the mitochondria-specific antioxidant MitoQ in mice completely reverses the age-associated elevation in aortic stiffness, assessed as aortic pulse-wave velocity. The destiffening effects of MitoQ treatment may be at least partially mediated by attenuation of age-related aortic elastin degradation. Our results suggest that mitochondria-targeted therapeutic strategies may hold promise for decreasing arterial stiffening with aging in humans, possibly decreasing the risk of many chronic age-related clinical disorders.

Non-invasive aortic systolic pressure and pulse wave velocity estimation in a primary care setting: An in silico study

Everyday clinical cardiovascular evaluation is still largely based on brachial systolic and diastolic pressures. However, several clinical studies have demonstrated the higher diagnostic capacities of the aortic pressure, as well as the need to assess the aortic mechanical properties (e.g., by measuring the aortic pulse wave velocity). In order to fill this gap, we propose to exploit a set of easy-to-obtain physical characteristics to estimate the aortic pressure and pulse wave velocity. To this aim, a large population of virtual subjects is created by a validated mathematical model of the cardiovascular system. Quadratic regressive models are then fitted and statistically selected in order to obtain reliable estimations of the aortic pressure and pulse wave velocity starting from the knowledge of the subject age, height, weight, brachial pressure, photoplethysmographic measures and either electrocardiogram or phonocardiogram. The results are very encouraging and foster clinical studies aiming to apply a similar technique to a real population.

Inhibition of SRF/myocardin reduces aortic stiffness by targeting vascular smooth muscle cell stiffening in hypertension.

AimsIncreased aortic stiffness is a fundamental manifestation of hypertension. However, the molecular mechanisms involved remain largely unknown. We tested the hypothesis that abnormal intrinsic vascular smooth muscle cell (VSMC) mechanical properties in large arteries, but not in distal arteries, contribute to the pathogenesis of aortic stiffening in hypertension, mediated by the serum response factor (SRF)/myocardin signalling pathway.Methods and resultsFour month old male spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats were studied. Using atomic force microscopy, significant VSMC stiffening was observed in the large conducting aorta compared with the distal arteries in SHR (P < 0.001), however, this regional variation was not observed in WKY rats (P > 0.4). The increase of VSMC stiffness was accompanied by a parallel increase in the expression of SRF by 9.8-fold and of myocardin by 10.5-fold in thoracic aortic VSMCs from SHR vs. WKY rats, resulting in a significant increase of downstream stiffness-associated genes (all, P < 0.01 vs. WKY). Inhibition of SRF/myocardin expression selectively attenuated aortic VSMC stiffening, and normalized downstream targets in VSMCs isolated from SHR but not from WKY rats. In vivo, 2 weeks of treatment with SRF/myocardin inhibitor delivered by subcutaneous osmotic minipump significantly reduced aortic stiffness and then blood pressure in SHR but not in WKY rats, although concomitant changes in aortic wall remodelling were not detected during this time frame.ConclusionsSRF/myocardin pathway acts as a pivotal mediator of aortic VSMC mechanical properties and plays a central role in the pathological aortic stiffening in hypertension. Attenuation of aortic VSMC stiffening by pharmacological inhibition of SRF/myocardin signalling presents a novel therapeutic strategy for the treatment of hypertension by targeting the cellular contributors to aortic stiffness.

Biomechanics of Failed Pulmonary Autografts Compared to Native Aortic Roots

Progressive autograft dilatation after a Ross operation suggests that remodeling does not effectively reproduce native aortic root biomechanics. In the first of this two-part series, we compared mechanical properties of explanted autografts to pulmonary roots at pulmonary pressures. The goal of this study was to compare mechanical properties of explanted autografts to native aortic roots at systemic pressures. Autograft specimens were obtained from patients undergoing reoperation after Ross operation. Forcomparison, native aortic roots were obtained from unused donor hearts. Biaxial stretch testing was performed to determine tissue mechanical properties. Tissue stiffness was determined at patient-specific physiologic stresses corresponding to systemic pressures (80 and 120 mm Hg) and hypertensive state (200 mm Hg). Nonlinear stress-strain curves were present for both failed autografts and native aortic roots. Explanted autografts were significantly more compliant than native aortic roots at 80 mm Hg (1.53 ± 0.68 versus 2.99 ± 1.34 MPa; p= 0.011), 120 mm Hg (2.54 ± 1.18 versus 4.93 ± 2.21 MPa; p= 0.013), and 200 mm Hg (4.79 ± 2.30 versus 9.21 ± 4.16 MPa; p= 0.015). Autograft tissue stiffness at 80, 120, and 200 mm Hg was not correlated with age at the time of Ross operation (p= 0.666, p=0.639, and p= 0.616, respectively) or time in the systemic circulation (p= 0.635, p= 0.637, and p= 0.647, respectively). Failed pulmonary autografts retained a nonlinear response to mechanical loading typical of healthy arterial tissue. Despite similar wall thickness between autografts and aorta, autograft stiffness in this patient population was significantly reduced compared with native aortic roots. We demonstrated that biomechanical remodeling was inadequate in these specimens to achieve native aortic mechanical properties, which may have resulted in progressive autograft root dilatation.

Developmental Changes in Aortic Mechanical Properties in Normal Fetuses and Fetuses with Cardiovascular Disease

We hypothesized that fetal aortic mechanical properties assessed by aortic diameter (AoD) and flow show maturational changes during the gestational period, and that these properties are different in fetuses with congenital heart diseases and fetuses with normal development. Phasic changes in ascending AoD along with Doppler flow profile were measured in 84 consecutive normal fetuses (gestational age, 18-36weeks) and in 30 consecutive fetuses with cardiovascular diseases (gestational age, 22-39weeks). AoD and cardiac output significantly increased with gestational age. Fetal aortic compliance (AC), assessed as (maximum AoD - minimum AoD)/stroke volume, significantly decreased with gestational age in normal fetuses, indicating maturational changes in aortic wall properties. Importantly, fetuses with Marfan syndrome and tetralogy of Fallot that exhibit "aortopathy" showed significantly lower AC than normal fetuses of the same gestational age, suggesting intrinsic abnormalities in aortic wall properties in these diseases. Fetuses with trisomy 18 and Noonan syndrome also had AC values below the normal ranges. Measurements of phasic changes in fetal AoD and flow measurements can provide useful information about aortic mechanical properties and may help clarify abnormal arterial hemodynamics in pathologic conditions.

Abstract 10009: Aortic Hemodynamic and Mechanical Properties are Concomitantly Reduced in Pulmonary Arterial Hypertension

Introduction: Although pulmonary arterial hypertension (PAH) has significant impact on flow and tissue remodeling in the pulmonary vasculature, previous studies indicate that PAH is also associated with increased stiffness and endothelial dysfunction in the systemic circulation. Alterations in vascular properties of the systemic circulation may have hemodynamic relevance for left ventricular adaptation to PAH. Reduced wall shear stress (WSS) and vascular elastic markers are known manifestations of vascular disease and may provide insight into the vascular behavior of the systemic circulation in PAH. Hypothesis: We hypothesized that WSS and mechanical elasticity are altered in the thoracic aorta in PAH, and that these measures correlate with pulmonary hemodynamics. Methods: As part of a prospective study, 18 patients with PAH and 5 age-matched controls underwent the same day right heart catheterization (RHC) and 4 dimensional flow cardiac magnetic resonance (4D CMR) for computation of WSS in four aortic regions (endovascular landing zones 1 to 4). The aortic capacitance was calculated as the ratio of stroke volume (SV) and pulse pressure (PP). The elastic modulus was defined as the inverse aortic strain divided by PP. The difference in median values was assessed via Wilcoxon ranked sum method and Spearman rho was used for linear regression analysis. Results: The WSS (N/m2) was significantly reduced in all four aortic zones (zone 1: 0.540 vs. 0.800, p = 0.0325; zone 2: 0.424 vs. 0.615, p = 0.0402; zone 3: 0.419 vs. 0.625, p = 0.0250; zone 4: 0.513 vs. 0.794, p = 0.0046). While aortic capacitance (mL/mmHg) was significantly reduced in the PAH subjects (1.82 vs. 5.97, p = 0.008), the elastic modulus (mmHg) was higher (3.52 vs. 8.25, p = &lt; 0.001). The most significant correlation was between the WSS in zone 4 and pulmonary vascular resistance (rho = -0.70, p = 0.006) and mean pulmonary artery pressure (rho = -0.62, p = 0.002). Conclusions: PAH is associated with reduced WSS in the thoracic aorta, suggesting reduced systemic flow conduction in PAH. WSS and mechanical vascular markers may aid in the understanding of the impact of PAH on systemic hemodynamics and tissue mechanics.

The aortic mechanical properties in patients with the essential hypertension environmentally exposed to cigaret smoke

Context: The impairment of the aortic mechanical features constitutes the independent predictor of all-cause and cardiovascular mortality and morbidity.Objective: The purpose of the present research has been the determination of the influence of the environmental exposure to cigaret smoke on the aortic mechanical properties, namely, the stiffness and elasticity of aorta, in patients with essential hypertension.Materials and methods: The research has covered 128 people with essential hypertension: 64 nonsmokers, declaring the environmental exposure to cigaret smoke (group A) and 64 nonsmokers declaring the lack of environmental exposure to cigaret smoke selected on the case to case basis (group B). Aortic mechanical properties have been evaluated on the basis of the parameters: aortic stiffness index (AoSI), aortic strain (AoS) and aortic distensibility (AoD).Results: In group A, the average values of AoSI were significantly higher, and the average values of AoS and AoD significantly lower than in group B. It has been documented that the older age and environmental exposure to cigaret smoke form independent risk factors of increasing the aortic stiffness expressed by higher values of AoSI, whereas the older age, higher pulse pressure (PP) values and environmental exposure to cigaret smoke – independent risk factors of aortic elasticity reduction expressed for the age and “passive smoking” by lower values of AoS and AoD and for PP – lower values of AoD.Conclusion: In patients with essential hypertension, the environmental exposure to cigaret smoke seems to result in impairment of the aortic mechanical properties.

Abstract 467: Differences In Susceptibility to Abdominal Aortic Aneurysms Between 129/SvEv and C57Bl/6 Mice

Objective: Abundant evidence has demonstrated the profound influence of genetic background on cardiovascular phenotypes. Previous work in the mouse has shown that genetic background-related variations in murine models of Marfan syndrome affect thoracic aortic aneurysm formation, rupture, and lifespan of mice. Marfan syndrome mice in the C57Bl/6 genetic background are less susceptible to aneurysm formation compared to 129/SvEv mice. In this study, we hypothesize that the susceptibility to the development of abdominal aortic aneurysm (AAA) will be similarly increased in 129/SvEv mice compared to C57Bl/6 mice. Approach and Results: Mice of either C57Bl/6 or 129/SvEv background underwent AAA induction by periaortic application of CaCl2. Aortic diameters were measured at 6 weeks post induction. Aneurysm size was significantly larger in 129/SvEv mice than in C57Bl/6 mice. Histological studies showed more severe elastic lamella disruption and fragmentation in 129/SvEv mice than in C57Bl/6 mice. Macrophage infiltration was more prominent in the aortas of 129/SvEv mice than of C57Bl/6 mice. The elastic modulus was found to be higher in the aortas of the 129/SvEv mice compared to the C57Bl/6 mice. MMP-2 and MMP-9 levels, examined by gelatin zymography,were higher in the aortas of 129/SvEv mice compared to the C57Bl/6 mice. Conclusions: These data demonstrate that 129/SvEv mice are more susceptible to AAA compared to C57Bl/6 mice. The difference in the susceptibility to AAA is at least partially due to the difference in aortic elastic lamellae mechanical properties and MMP-2 and -9 expression between the two strains of mice.

Aortic biomechanics in hypertrophic cardiomyopathy

Background: Ventricular-vascular coupling is an important phenomenon in many cardiovascular diseases. The association between aortic mechanical dysfunction and left ventricular (LV) dysfunction is well characterized in many disease entities, but no data are available on how these changes are related in hypertrophic cardiomyopathy (HCM). Aim of the work: This study examined whether HCM alone is associated with an impaired aortic mechanical function in patients without cardiovascular risk factors and the relation of these changes, if any, to LV deformation and cardiac phenotype. Methods: 141 patients with HCM were recruited and compared to 66 age- and sex-matched healthy subjects as control group. Pulse pressure, aortic strain, stiffness and distensibility were calculated from the aortic diameters measured by M-mode echocardiography and blood pressure obtained by sphygmomanometer. Aortic wall systolic and diastolic velocities were measured using pulsed wave Doppler tissue imaging (DTI). Cardiac assessment included geometric parameters and myocardial deformation (strain and strain rate) and mechanical dyssynchrony. Results: The pulsatile change in the aortic diameter, distensibility and aortic wall systolic velocity (AWS') were significantly decreased and aortic stiffness index was increased in HCM compared to control (P < .001) In HCM AWS' was inversely correlated to age(r = − .32, P < .0001), MWT (r = − .22, P < .008), LVMI (r = − .20, P < .02), E/Ea (r = − .16, P < .03) LVOT gradient (r = − 19, P < .02) and severity of mitral regurg (r = − .18, P < .03) but not to the concealed LV deformation abnormalities or mechanical dyssynchrony. On multivariate analysis, the key determinant of aortic stiffness was LV mass index and LVOT obstruction while the role LV dysfunction in aortic stiffness is not evident in this population. Conclusion: HCM is associated with abnormal aortic mechanical properties. The severity of cardiac phenotype, not LV deformation, is interrelated to aortic stiffness in patients with HCM. The increased aortic stiffness seems to be promising module that can be added as clinical risk parameter in HCM.

Arterial Stiffness Alterations and Inflammatory Response Following Endovascular Aortic Repair

Endovascular abdominal aortic aneurysm repair (EVAR) and thoracic aortic aneurysm repair (TEVAR) have been widely incorporated into clinical practice. However, changes in arterial stiffness and post-implantation syndrome after aortic endografting remain important issues under investigation. The aneurysm sac wall motion after successful EVAR and TEVAR reflects complex interactions between all the components of the excluded aneurysm, including true compliance of the aneurysm wall itself, intra-aneurysm sac pressure, remodeling of the thrombus, and mechanical characteristics of the endograft. Experimental and clinical studies have shown that aortic endografting results in increased arterial stiffness in animal models. It can be assumed that the alterations of aortic mechanical properties can have a direct impact on heart output. The long-term impact of these mechanical changes on cardiovascular outcomes and the potential effects of different endografts on hemodynamics are important issues under investigation. Post-implantation syndrome (PIS) is a systemic inflammatory response frequently observed after endovascular treatment of aortic pathologies. The main features of PIS include fever, leukocytosis, elevated C-reactive protein levels, and coagulation disturbances. Endograft design appears to influence this inflammatory response following aortic endografting; woven polyester endografts have been shown to be associated with greater inflammatory response compared to PTFE stent grafts. The purpose of this paper is to review the literature to elucidate arterial stiffness alterations and inflammatory response after EVAR and TEVAR and the impact of endograft design on aortic stiffness and the post-inflammatory response.

Contribution of collagen fiber undulation to regional biomechanical properties along porcine thoracic aorta.

As major extracellular matrix components, elastin, and collagen play crucial roles in regulating the mechanical properties of the aortic wall and, thus, the normal cardiovascular function. The mechanical properties of aorta, known to vary with age and multitude of diseases as well as the proximity to the heart, have been attributed to the variations in the content and architecture of wall constituents. This study is focused on the role of layer-specific collagen undulation in the variation of mechanical properties along the porcine descending thoracic aorta. Planar biaxial tensile tests are performed to characterize the hyperelastic anisotropic mechanical behavior of tissues dissected from four locations along the thoracic aorta. Multiphoton microscopy is used to image the associated regional microstructure. Exponential-based and recruitment-based constitutive models are used to account for the observed mechanical behavior while considering the aortic wall as a composite of two layers with independent properties. An elevated stiffness is observed in distal regions compared to proximal regions of thoracic aorta, consistent with sharper and earlier collagen recruitment estimated for medial and adventitial layers in the models. Multiphoton images further support our prediction that higher stiffness in distal regions is associated with less undulation in collagen fibers. Recruitment-based models further reveal that regardless of the location, collagen in the media is recruited from the onset of stretching, whereas adventitial collagen starts to engage with a delay. A parameter sensitivity analysis is performed to discriminate between the models in terms of the confidence in the estimated model parameters.

The conundrum of arterial stiffness, elevated blood pressure, and aging.

Isolated systolic hypertension is a major health burden that is expanding with the aging of our population. There is evidence that central arterial stiffness contributes to the rise in systolic blood pressure (SBP); at the same time, central arterial stiffening is accelerated in patients with increased SBP. This bidirectional relationship created a controversy in the field on whether arterial stiffness leads to hypertension or vice versa. Given the profound interdependency of arterial stiffness and blood pressure, this question seems intrinsically challenging, or probably naïve. The aorta's function of dampening the pulsatile flow generated by the left ventricle is optimal within a physiological range of distending pressure that secures the required distal flow, keeps the aorta in an optimal mechanical conformation, and minimizes cardiac work. This homeostasis is disturbed by age-associated, minute alterations in aortic hemodynamic and mechanical properties that induce short- and long-term alterations in each other. Hence, it is impossible to detect an "initial insult" at an epidemiological level. Earlier manifestations of these alterations are observed in young adulthood with a sharp decline in aortic strain and distensibility accompanied by an increase in diastolic blood pressure. Subsequently, aortic mechanical reserve is exhausted, and aortic remodeling with wall stiffening and dilatation ensue. These two phenomena affect pulse pressure in opposite directions and different magnitudes. With early remodeling, there is an increase in pulse pressure, due to the dominance of arterial wall stiffness, which in turn accelerates aortic wall stiffness and dilation. With advanced remodeling, which appears to be greater in men, the effect of diameter becomes more pronounced and partially offsets the effect of wall stiffness leading to plateauing in pulse pressure in men and slower increase in pulse pressure (PP) than that of wall stiffness in women. The complex nature of the hemodynamic changes with aging makes the "one-size-fits-all" approach suboptimal and urges for therapies that address the vascular profile that underlies a given blood pressure, rather than the blood pressure values themselves.

Software and hardware systems for abdominal aortic aneurysm mechanical properties investigation

The main goal of this paper is to describe two different systems that were developed for the purpose of abdominal aortic aneurysm mechanical properties investigation and to present the results of the measurements. The first system is based on the “Bubble Inflated” method and it increases the pressure of physiological saline which affects blood vessel tissue and causes mechanical deformation. The system provides recording the data about the current value of the pressure in the physiological saline by using the appropriate pressure sensor. The second system makes stretches of the vessel tissue in uni-axial direction and save the data about the force and the elongation. Both of these systems use cameras for assessment of the deformation. Obtained results from both systems are used for numerical simulation of computer model for abdominal aortic aneurysm. It gives a new avenue for application of software and hardware systems for determination of vascular tissue properties in the clinical practice.

Altered dependence of aortic pulse wave velocity on transmural pressure in hypertension revealing structural change in the aortic wall.

Aortic pulse wave velocity (aPWV), a major prognostic indicator of cardiovascular events, may be augmented in hypertension as a result of the aorta being stretched by a higher distending blood pressure or by a structural change. We used a novel technique to modulate intrathoracic pressure and thus aortic transmural pressure (TMP) to examine the variation of intrathoracic aPWV with TMP in hypertensive (n=20; mean±SD age, 52.1±15.3 years; blood pressure, 159.6±21.2/92.0±15.9 mm Hg) and normotensive (n=20; age, 55.5±11.1 years; blood pressure, 124.5±11.9/72.6±9.1 mm Hg) subjects. aPWV was measured using dual Doppler probes to insonate the right brachiocephalic artery and aorta at the level of the diaphragm. Resting aPWV was greater in hypertensive compared with normotensive subjects (897±50 cm/s versus 784±43 cm/s; P<0.05). aPWV was equal in hypertensive and normotensive subjects when measured at a TMP of 96 mm Hg. However, dependence of aPWV on TMP in normotensive subjects was greater than that in hypertensive subjects (9.6±1.6 versus 3.8±0.7 cm/s per mm Hg increase in TMP, respectively, means±SEM; P<0.01). This experimental behavior was best explained by a theoretical model incorporating strain-induced recruitment of stiffer fibers in normotensive subjects and fully recruited stiffer fibers in hypertensive subjects. These results explain previous contradictory findings with respect to isobaric aPWV in hypertensive compared with normotensive subjects. They suggest that hypertension is associated with a profound change in aortic wall mechanical properties possibly because of destruction of elastin leading to less strain-induced stiffening and predisposition to aortic dissection.

Abstract 493: Ultrasound-Based Image Registration Algorithm for Measuring Regional Wall Strain Changes Leading to Abdominal Aortic Aneurysm Rupture

OBJECTIVES: Size-based assessments of AAA do not accurately identify rupture risk. AAA rupture potential is related to wall failure which is dependent on material properties and compliance. Our hypothesis is that transcutaneous ultrasound (US) regional strain measurements can be used to quantify changes in aortic wall mechanical properties indicative of an increase in rupture risk. METHODS: A patient-specific AAA cryogel phantom was fabricated and mechanical compliance and tested on an in vitro hemodynamic simulator. A Sonix-Touch system imaged the phantom through the maximum axial diameter under physiologic, pulsatile conditions with increasing mean arterial pressure (MAP) of 95, 120, 140, 160, and 180 until rupture (200mmHg). An US image registration algorithm was used to measure the circumferential wall strain from systole to diastole. RESULTS: The spatial mean of the circumferential wall strain (%) in the known location of rupture (solid box) decreased from 2.7, 2.0, 2.4, 1.7, 1.6, and 1.2 for MAP of 95, 120, 141, 160, 180 and 200 mm Hg (rupture) respectively. For comparison the mean strain levels in the adjacent wall of the aneurysm (dashed) were 3.4, 3.4, 3.0, 3.2, 2.1 and 1.8 for the same MAP. The mean diameter of the AAA increased from 5.48cm, 5.83cm, 6.13cm, 6.34cm, 6.54cm, and 6.69cm (rupture) over the range of MAP. CONCLUSIONS: At the location of eventual rupture, the mean regional strain decreased as the diameter of the phantom enlarged and progressed to rupture relative to other regions of the wall. This suggests the possibility of applying regional AAA wall strain as a more accurate method of predicting AAA rupture risk.

Acute effects of ultrafiltration on aortic mechanical properties determined by measurement of pulse wave velocity and pulse propagation time in hemodialysis patients.

Objective:The effects of acute hemodialysis session on pulse wave velocity are conflicting. The aim of the current study was to assess the acute effects of ultrafiltration on the aortic mechanical properties using carotid-femoral (aortic) pulse wave velocity and pulse propagation time.Methods:A total of 26 (12 women, 14 men) consecutive patients on maintenance hemodialysis (mean dialysis duration: 40.7±25.6 (4-70) months) and 29 healthy subjects (13 women, 16 men) were included in this study. Baseline blood pressure, carotid-femoral (aortic) pulse wave velocity, and pulse propagation time were measured using a Complior Colson device (Createch Industrie, France) before and immediately after the end of the dialysis session.Results:While systolic blood pressure, diastolic blood pressure, mean blood pressure, pulse pressure, and pulse wave velocity were significantly higher in patients on hemodialysis than in healthy subjects, pulse propagation time was significantly higher in healthy subjects. Although body weight, systolic blood pressure, diastolic blood pressure, mean blood pressure, pulse pressure, and pulse wave velocity were significantly decreased, heart rate and pulse propagation time were significantly increased after ultrafiltration. There was a significant positive correlation between pulse wave velocity and age, body height, waist circumference, systolic blood pressure, diastolic blood pressure, mean blood pressure, pulse pressure, and heart rate.Conclusion:Although hemodialysis treatment may chronically worsen aortic mechanical properties, ultrafiltration during hemodialysis may significantly improve aortic pulse wave velocity, which is inversely related to aortic distensibility and pulse propagation time.

Chronic Over-Expression of Heat Shock Protein 27 Attenuates Atherogenesis and Enhances Plaque Remodeling: A Combined Histological and Mechanical Assessment of Aortic Lesions

AimsExpression of Heat Shock Protein-27 (HSP27) is reduced in human coronary atherosclerosis. Over-expression of HSP27 is protective against the early formation of lesions in atherosclerosis-prone apoE−/− mice (apoE−/−HSP27o/e) - however, only in females. We now seek to determine if chronic HSP27 over-expression is protective in a model of advanced atherosclerosis in both male and female apoE−/− mice.Methods and ResultsAfter 12 weeks on a high fat diet, serum HSP27 levels rose more than 16-fold in male and female apoE−/−HSP27o/e mice, although females had higher levels than males. Relative to apoE−/− mice, female apoE−/−HSP27o/e mice showed reductions in aortic lesion area of 35% for en face and 30% for cross-sectional sinus tissue sections – with the same parameters reduced by 21% and 24% in male cohorts; respectively. Aortic plaques from apoE−/−HSP27o/e mice showed almost 50% reductions in the area occupied by cholesterol clefts and free cholesterol, with fewer macrophages and reduced apoptosis but greater intimal smooth muscle cell and collagen content. The analysis of the aortic mechanical properties showed increased vessel stiffness in apoE−/−HSP27o/e mice (41% in female, 34% in male) compare to apoE−/− counterparts.ConclusionsChronic over-expression of HSP27 is atheroprotective in both sexes and coincides with reductions in lesion cholesterol accumulation as well as favorable plaque remodeling. These data provide new clues as to how HSP27 may improve not only the composition of atherosclerotic lesions but potentially their stability and resilience to plaque rupture.

Development of the system for abdominal aortic aneurysm mechanical properties research using “Bubble Inflated” method

The main goal of this paper was to determine the biomechanical parameters of abdominal aortic aneurysm using the Bubble Inflated method. In other words, the main task of this paper was to develop a system which would be able to increase the pressure of physiological saline which affects blood vessel tissue and causes its deformation. This deformation is recorded using a camera and providing data at each moment about pressure values which affect tissue and were detected by using a pressure sensor.

Reduced ascending aorta distensibility relates to adverse ventricular mechanics in patients with hypoplastic left heart syndrome: Noninvasive study using wave intensity analysis

To evaluate the aortic arch elastic properties and ventriculoarterial coupling efficiency in patients with single ventricle physiology, with and without a surgically reconstructed arch. We studied 21 children with single ventricle physiology after bidirectional superior cavopulmonary surgery: 10 with hypoplastic left heart syndrome, who underwent surgical arch reconstruction, and 11 with other types of single ventricle physiology but without arch reconstruction. All children underwent pre-Fontan magnetic resonance imaging. No patient exhibited aortic recoarctation. Data on aortic wave speed, aortic distensibility and wave intensity profiles were all extracted from the magnetic resonance imaging studies using an in-house-written plug-in for the Digital Imaging and Communications in Medicine viewer OsiriX. Children with hypoplastic left heart syndrome had significantly greater wave speed (P=.002), and both stiffer (P=.004) and larger (P<.0001) ascending aortas than the patients with a nonreconstructed arch. Aortic distensibility was not influenced by ventricular stroke volume but depended on a combination of increased aortic diameter and abnormal wall mechanical properties. Those with hypoplastic left heart syndrome had a lower peak wave intensity and reduced energy carried by the forward compression and the forward expansion waves, even after correction for stroke volume, suggesting an abnormal systolic and diastolic function. Lower wave energy was associated with an increased aortic diameter. Using a novel, noninvasive technique based on image analysis, we have demonstrated that aortic arch reconstruction in children with hypoplastic left heart syndrome is associated with reduced aortic distensibility and unfavorable ventricular-vascular coupling compared with those with single ventricle physiology without aortic arch reconstruction.