Aortic Wall Mechanics Research Articles

Quantification of the heterogeneous effect of static and dynamic perivascular structures on patient-specific local aortic wall mechanics using inverse finite element modeling and DENSE MRI

Recent studies have highlighted the relevance of perivascular interactions on aortic wall mechanics. Most of the approaches assume static perivascular structures; however, the beating heart dynamically displaces the neighboring aorta. We develop a model to account for the effect of periaortic interactions due to static and dynamic structures by prescribing a moving elastic foundation boundary condition (EFBC) embedded into an inverse finite element algorithm using in vivo displacements from 2D displacement encoding with stimulated echoes (DENSE) MRI as target data. We applied this method at three different locations of interest, the distal aortic arch (DAA), descending thoracic aorta (DTA), and infrarenal abdominal aorta (IAA) for a total of 27 cases in healthy humans. The model reproduces the target diastole-to-systole deformation and bulk displacement of the aortic wall with median displacement errors below 0.5mm. The EFBC showed good agreement with the location of anatomical features and was consistent among individuals of similar characteristics. Results show that an energy source acting on the adventitia is required to reproduce the displacements measured at the vicinity of the heart, but not at the abdomen. The average adventitial load as a percentage of the luminal pulse-pressure was found to increase with age and to decrease along the descending aorta, from 61% at the DAA to 37% at the DTA, and 30% at the IAA. This approach offers a patient-specific method to estimate in vivo adventitial loads and aortic wall stiffness, which can bring a better understanding of normal and pathological in vivo aortic function.

Numerical analysis of stenoses severity and aortic wall mechanics in patients with supravalvular aortic stenosis

Supravalvular aortic stenosis (SVAS) is an aortic malformation characterized by a narrowing of the ascending aorta, resulting in abnormal hemodynamics and pressure drop across the stenosed region. It has been observed that the pressure drops measured from Doppler ultrasound exams often tend to be higher than those obtained from invasive cardiac catheterization. These misleadingly elevated pressure measurements may drive the decision to refer patients for surgical treatment prematurely.Considering this strong clinical association, the purpose of this work is to develop a computational modeling approach using a two-way coupled fluid-structure interaction methodology to determine an accurate prediction of trans-stenotic pressure drop and to further highlight the discrepancy between the SVAS assessment methods. Blood is modeled using Navier-Stokes equations while the aortic wall is simulated by a composite poroelastic structure to represent the three main layers of the arterial wall. The relationship between aortic wall elasticity and the blood flow conditions is examined in varying levels of stenosis, ranging from mild to severe degrees of vessel diameter narrowing.A substantial overestimation of the traditional Doppler pressure drop measurement is observed, especially for severe stenosis levels. The simulation results indicate that elasticity of the aortic wall has a relatively little effect on trans-stenotic pressure drop for the range of mild to moderate SVAS cases, but predicted to have a profound effect for severe SVAS cases. Moreover, significant sensitivity to the pressure drop across the SVAS region from stenosis severity is observed.

The Potential for Quantifying Regional Distributions of Radial and Shear Strain in the Thoracic and Abdominal Aortic Wall Using Spiral Cine DENSE Magnetic Resonance Imaging.

Aortic displacement encoding with stimulated echoes (DENSE) magnetic resonance imaging (MRI) was recently developed to assess heterogeneities in aortic wall circumferential strain (CS). However, previous studies neglected potential radial and shear strain (RSS) distributions. Herein, we present an improved aortic DENSE MRI postprocessing method to assess the feasibility of quantifying all components of the two-dimensional (2D) strain tensor. 32 previously acquired 2D DENSE scans from three distinct aortic locations were re-analyzed. Contrasting previous studies, displacements of the inner and outer aortic wall layers were processed separately to preserve RSS. Differences in regional strain between the new and old postprocessing methods were evaluated, along with interobserver, intraobserver, and interscan repeatability for all strain components. The new postprocessing method revealed an overall mean absolute difference in regional CS of 0.01 ± 0.01 compared to the prior method, with minimal impact on CS repeatability. Mean absolute magnitudes of regional RSS increased significantly compared to changes in CS (radial 0.04 ± 0.05, p < 0.001; shear 0.04 ± 0.04, p = 0.02). Most repeatability metrics for RSS were significantly worse than for CS. The unique distributions of RSS for each axial location associated well with local periaortic structures and mean aortic displacement. The new postprocessing method captures heterogeneous distributions of nonzero RSS which may provide new information for improving clinical diagnostics and computational modeling of heterogeneous aortic wall mechanics. However, future studies are required to improve the repeatability of RSS and assess the influence of partial volume effects.

The impact of the aortic cusps fusion pattern and valve disease severity on the aortic wall mechanics in patients with bicuspid aortic valve

The ascending aorta dilatation in the bicuspid aortic valve (BAV) patients is often attributed to congenital abnormalities of the aortic wall, but it may be related to hemodynamic disturbances in the course of BAV disease. At present, ascending aortic diameter is used as almost sole but weak predictor of aortic dissection and rupture in BAV. We examined the association between aortic wall mechanics and severity of aortic valve disease including different cusps fusion patterns using conventional echocardiography and tissue Doppler imaging (TDI). We prospectively studied 106 BAV patients: 72 with right-left (R-L) coronary cusp fusion were matched 1:1 to 34 patients with right-noncoronary (R-N) cusp fusion obtaining 34 pairs of patients. Peak systolic radial velocity and acceleration of the ascending aortic wall, measured by TDI, were used as an index of hemodynamic stress imposed on the aorta. Paired analysis showed higher aortic wall radial velocity (4.71 ± 1.61 cm/s vs. 3.33 ± 1.44 cm/s, p = 0.001) and acceleration (1.08 ± 0.46 m/s2 vs. 0.80 ± 0.34 m/s2, p = 0.015) in-R-L compared to R-N fusion. Pearson correlation showed association of ascending tubular aortic diameter with age (r = 0.258, p = 0.012), weight (r = 0.323, p = 0.001), peak aortic valve gradient (r = 0.386, p = 0.0001), aortic root diameter (r = 0.439, p < 0.0001), and R-N fusion pattern (r = 0.209, p = 0.043). Aortic root diameter was related to male gender (r = 0.296, p = 0.003), weight (r = 0.381, p = 0.0001), ascending aortic diameter (r = 0.439, p < 0.0001), and severity of aortic regurgitation (r = 0.337, p = 0.0009). Regional differences in aortic wall motion between different BAV cusp fusion patterns and association of aortic diameters with the severity of aortic valve disease, both suggest a deleterious hemodynamic impact of cusp fusion patterns and aortic valve dysfunction on ascending aortic wall. Assessment of aortic hemodynamic by TDI is feasible and could be potentially used to improve prediction of acute aortic complications, thus helping to establish optimal timing of aortic surgery in BAV patients.

Computational evaluation of an extra-aortic elastic-wrap applied to simulated aging anisotropic human aorta models

Structural changes occurring to the aortic wall can result in vascular stiffening. This is represented by a loss of vascular compliance during pulsatile flow, resulting in increased systolic and pulse blood pressure, particularly in populations aged 50 and over. Aortic stiffness is thought to be permanent and an active de-stiffening strategy is yet to be developed. Extra aortic elastic wrapping has been proposed as a surgical technique to boost aortic distensibility and treat hypertension in the elderly. Previously, in-vivo and in-vitro testing have suggested a pulse-pressure reduction potential of elastic wrapping in the stiffened aortas. Herein, we explore the feasibility of elastic aortic wrapping to improve simulated aortic compliance across the age span. Detailed computational studies of the anisotropic aortic wall mechanics, using data from human subjects, were performed, evaluating key performance properties for the interaction between the aortic wall and elastic aortic wrap procedure. Main determinants of the procedure’s efficiency are identified using a pre-defined aortic stiffness and wrap elasticity. Finite element analysis predicts that segmental aortic distensibility can be increased if elastic wrapping is applied to a simulated stiff aorta. Elastic aortic wrapping is calculated to have little impact on the compliance of an initially distensible aorta.

Invited commentary

Abdominal aortic aneurysm diameter is the primary factor that has been used to direct aneurysm therapy. Aortic morphologic characteristics have failed to have a demonstrable impact on clinical decision-making for several reasons. Foremost, the morphologic assessments must be readily available to clinicians, inexpensive, and easy to measure and have clinically defined thresholds that direct care. However, defining aneurysm morphologic features does have additional value beyond directing therapy. Clinicians, researchers, and engineers alike are constantly exploring the boundary conditions on which to base new medical treatments; these morphologic features can help direct new therapies. Advent and adoption of endovascular aneurysm repair have limited the opportunity to examine aortic wall tissue. In the current manuscript, Barrett et al monopolize the opportunity to subject harvested aortic aneurysm wall to mechanical stretch forces that parallel physiologic conditions. It is intuitive that degraded aortic wall will demonstrate varying degrees of stiffness and response to stress. However, it is uncertain which morphologic features affect those features. The authors reinforce the assumption that the aortic wall is subjected to extreme asymmetry when uniform stress is applied. Regions of high stiffness, marked by calcium deposition, are surrounded by vulnerable regions of low stiffness. The regions surrounding calcium are subjected to greater degrees of deformation, which translates to increased strains; in some regions surrounding calcium, the wall demonstrated two to four times the strain compared with reference regions. In addition, the authors demonstrated that stiff intraluminal thrombus also alters surrounding aortic wall mechanical properties similar to that of calcium. Regions of high strain also correlated with wall thinning and stretching visualized on electron microscopy. Interestingly, aortic diameter did not correlate with changes in aortic wall mechanics. Routine clinical imaging readily detects calcium burden within the aortic wall, and each patient demonstrates varying degrees of calcium within the aneurysm. The localized variation in aortic wall mechanics may provide additional information to identify patients at risk for rupture. In the future, this information may be used to adjust surveillance or to offer therapy, but for now, it will provide another boundary condition to better explain aneurysm wall mechanics and resultant aneurysm behavior. The opinions or views expressed in this commentary are those of the authors and do not necessarily reflect the opinions or recommendations of the Journal of Vascular Surgery or the Society for Vascular Surgery. On the influence of wall calcification and intraluminal thrombus on prediction of abdominal aortic aneurysm ruptureJournal of Vascular SurgeryVol. 67Issue 4PreviewParameters other than maximum diameter that predict rupture of abdominal aortic aneurysms (AAAs) may be helpful for risk-benefit analysis in individual patients. The aim of this study was to characterize the biomechanical-structural characteristics associated with AAA walls to better identify the related mechanistic variables required for an accurate prediction of rupture risk. Full-Text PDF Open Archive

Massive aggrecan and versican accumulation in thoracic aortic aneurysm and dissection.

Proteoglycan accumulation is a hallmark of medial degeneration in thoracic aortic aneurysm and dissection (TAAD). Here, we defined the aortic proteoglycanome using mass spectrometry, and based on the findings, investigated the large aggregating proteoglycans aggrecan and versican in human ascending TAAD and a mouse model of severe Marfan syndrome. The aortic proteoglycanome comprises 20 proteoglycans including aggrecan and versican. Antibodies against these proteoglycans intensely stained medial degeneration lesions in TAAD, contrasting with modest intralamellar staining in controls. Aggrecan, but not versican, was increased in longitudinal analysis of Fbn1mgR/mgR aortas. TAAD and Fbn1mgR/mgR aortas had increased aggrecan and versican mRNAs, and reduced expression of a key proteoglycanase gene, ADAMTS5, was seen in TAAD. Fbn1mgR/mgR mice with ascending aortic dissection and/or rupture had dramatically increased aggrecan staining compared with mice without these complications. Thus, aggrecan and versican accumulation in ascending TAAD occurs via increased synthesis and/or reduced proteolytic turnover, and correlates with aortic dissection/rupture in Fbn1mgR/mgR mice. Tissue swelling imposed by aggrecan and versican is proposed to be profoundly deleterious to aortic wall mechanics and smooth muscle cell homeostasis, predisposing to type-A dissections. These proteoglycans provide potential biomarkers for refined risk stratification and timing of elective aortic aneurysm repair.

Aquaporin-1 facilitates pressure-driven water flow across the aortic endothelium.

Aquaporin-1, a ubiquitous water channel membrane protein, is a major contributor to cell membrane osmotic water permeability. Arteries are the physiological system where hydrostatic dominates osmotic pressure differences. In the present study, we show that the walls of large conduit arteries constitute the first example where hydrostatic pressure drives aquaporin-1-mediated transcellular/transendothelial flow. We studied cultured aortic endothelial cell monolayers and excised whole aortas of male Sprague-Dawley rats with intact and inhibited aquaporin-1 activity and with normal and knocked down aquaporin-1 expression. We subjected these systems to transmural hydrostatic pressure differences at zero osmotic pressure differences. Impaired aquaporin-1 endothelia consistently showed reduced engineering flow metrics (transendothelial water flux and hydraulic conductivity). In vitro experiments with tracers that only cross the endothelium paracellularly showed that changes in junctional transport cannot explain these reductions. Percent reductions in whole aortic wall hydraulic conductivity with either chemical blocking or knockdown of aquaporin-1 differed at low and high transmural pressures. This observation highlights how aquaporin-1 expression likely directly influences aortic wall mechanics by changing the critical transmural pressure at which its sparse subendothelial intima compresses. Such compression increases transwall flow resistance. Our endothelial and historic erythrocyte membrane aquaporin density estimates were consistent. In conclusion, aquaporin-1 significantly contributes to hydrostatic pressure-driven water transport across aortic endothelial monolayers, both in culture and in whole rat aortas. This transport, and parallel junctional flow, can dilute solutes that entered the wall paracellularly or through endothelial monolayer disruptions. Lower atherogenic precursor solute concentrations may slow their intimal entrainment kinetics.

Smooth Muscle-Dependent Changes in Aortic Wall Dynamics during Intra-Aortic Counterpulsation in an Animal Model of Acute Heart Failure

Intra-aortic balloon pumping (IABP) may modify arterial biomechanics; however, its effects on arterial wall properties during acute cardio-depression have not yet been fully explored. This dynamical study was designed to characterize the effects of IABP on aortic wall mechanics in an in vivo animal model of acute heart failure. Aortic pressure, diameter and blood flow were measured in six anesthetized sheep with acute cardio-depression by halothane (4%), before and during IABP (1:2). Aortic characteristic impedance and aortic wall stiffness indexes were calculated. acute experimental cardio-depression resulted in a reduction in mean aortic pressure (p<0.05) and an increase in the characteristic impedance (p<0.005), incremental elastic modulus (p<0.05), stiffness index (p<0.05) and Peterson elastic modulus (p<0.05). IABP caused an increase in the cardiac output (p<0.005) and a reduction in the systemic vascular resistances (p<0.05). In addition, the aortic impedance, incremental elastic modulus, stiffness index and Peterson modulus were significantly reduced during IABP (p<0.05). Our findings show that IABP caused changes in aortic wall impedance and intrinsic wall properties, improving the arterial functional capability and the left ventricular afterload by a reduction in both. Systemic vascular resistances and aortic stiffness were also improved by means of smooth muscle-dependent mechanisms.

Regional wall mechanics and blunt traumatic aortic rupture at the isthmus

Blunt traumatic aortic injury (BTAI) is part of a spectrum of diseases termed acute aortic syndrome that accounts for 20% of road traffic accident related deaths. The injury has a complex aetiology with a number of putative mechanisms accounting for the injury profile, characteristics of which include a transverse primary intimal tear located at the aortic isthmus. We hypothesised that an understanding of regional aortic wall mechanics would contribute to an understanding of the aetiology of BTAI. Samples of porcine aorta were prepared from ascending (A), descending (D) and peri-isthmus regions (I). A histological analysis of aortic wall architecture was performed at the site of attachment of the ligamentum arteriosum. Samples were mounted in a bubble inflation clamping rig, connected via a solenoid release valve to a compressed air reservoir. Using a pressure transducer and high-speed camera (1000fps) we collected data on wall thickness, rupture pressure and radial extension, allowing calculation of ultimate tensile stress. Histological analysis at the point of attachment of the ligamentum arteriosum to the isthmus shows some heterogeneity in cellular architecture extending deep into the tunica media. Wall thickness was significantly different between the three sampled regions (A>I>D, p<0.05). However, we found no difference in absolute rupture pressure between the three regions (kPa), (A, 300+/-28.9; I, 287+/-48.3; D, 321+/-29.6). Radial extension (cm) was significantly greater in A vs I (p<0.05), (A, 1.85+/-0.114; I, 1.66+/-0.109; D, 1.70+/-0.138). Ultimate tensile stress (kPa), (A, 3699+/-789; I, 3248+/-1430; D, 4260+/-1626) was significantly greater in D than I (p<0.05). The mechanism of blunt traumatic aortic rupture is not mechanically simple but must correspond to a complex combination of both relative motion of the structures within the thorax and local loading of the tissues, either as a result of their anatomy or due to the nature of the impact. A pressure spike alone is unlikely to be the primary cause of the peri-isthmus injury but may well be a contributory prerequisite.

Aortic Wall Mechanics in the Marfan Syndrome Assessed by Transesophageal Tissue Doppler Echocardiography

The aim of this study was to investigate the value of tissue Doppler imaging (TDI) using transesophageal echocardiography (TEE) in assessing the elastic properties of the thoracic aorta in patients with Marfan's syndrome. Aortic distensibility, stiffness index, and pulse-wave velocity were calculated using M-mode data in a TEE short-axis view in 31 patients with Marfan's syndrome and 22 normal controls. Acceleration time, maximum wall expansion velocity (Vmax), and wall strain were determined from TDI tracings. Indexes derived from TDI differed at a greater level of significance than M-mode-derived indexes in patients with dilated and normal aortas. Significant predictors of aortic dilation were systolic blood pressure, aortic stiffness index, Vmax, and strain. Decreased aortic strain and Vmax and increased stiffness index were predictive of aortic dissection (odds ratios 4.5, 3.3, and 2.2). In conclusion, the TDI assessment of aortic wall mechanics is complementary to standard M-mode measurements in discriminating normal subjects from patients with Marfan's syndrome and is accurate in predicting aortic dilation and dissection.

Wall Motion Velocities of Abdominal Aorta Measured by Tissue Doppler Imaging in Normal Children

Tissue Doppler imaging (TDI) offers a new technique for assessing aortic wall expansion/contraction velocities and may provide a noninvasive approach to aortic wall mechanics. The purpose of this study was to determine the normal values of abdominal aortic wall motion velocities and the effect of age on these velocities in normal children. We examined 103 normal children. Using TDI, maximum wall expansion velocity during systole (peak S) and maximum wall contraction velocity during diastole (peak D) were measured. M-mode diameter of the abdominal aorta and systolic, diastolic, and mean arterial pressures were measured. Aortic stiffness was measured as (I(n)[BP(syst)/BP(diast)])/(D(s)-D(d)/D(d), where I(n) is the natural log, D(s) is the maximal abdominal aortic diameter during systole, and D(d) is the abdominal aortic diameter at end-diastole. In all subjects, wall motion velocities of the abdominal aorta were recorded. The mean values for peak S and peak D were 4.23, 1.14 and 2.16, 0.45 cm/sec, respectively. Both peak S and peak D were low in infants and increased significantly with age (r = 0.63, p < 0.0001 and r = 0.36, p = 0.0002, respectively), systolic blood pressure (r = 0.42 and 0.47, respectively, p < 0.0001), and diastolic blood pressure (r = 0.24, p = 0.016 and r = 0.28, p = 0.0038, respectively). Aortic stiffness index of the abdominal aorta was constant with age and did not correlate with peak S or peak D. Abdominal aortic wall motion velocities can be easily assessed by TDI. Age-related changes in the aortic wall motion velocities are observed in normal children. This study provides baseline information for further quantitative assessment of arterial stiffness in children with congenital or acquired heart disease.

844-5 Assessment of aortic wall mechanics in Marfan syndrome by transesophageal echocardiography and tissue Doppler imaging

844-5 Assessment of aortic wall mechanics in Marfan syndrome by transesophageal echocardiography and tissue Doppler imaging

Evaluation of aortic wall mechanics in marfan syndrome by transesophageal tissue doppler echocardiography

Evaluation of aortic wall mechanics in marfan syndrome by transesophageal tissue doppler echocardiography

Aminoguanidine and aortic wall mechanics, structure, and composition in aged rats.

With aging, the aortic wall becomes stiffer. This could be because of changes in wall stress or composition. We investigated whether a specific change in wall composition, ie, accumulation of advanced glycation end products (AGEs) on the extracellular matrix, is a major factor. We measured aortic mechanics, geometry, and composition in 3-, 10-, 15-, 20-, and 30-month-old inbred normotensive Wistar-Glaxo/Rijswick rats and in a group of 30-month-old rats treated from 20 months onward with aminoguanidine (AG, 42 mg/kg per day), an inhibitor of AGE formation. Thoracoabdominal aortic (pressure) pulse-wave velocity (PWV) increased progressively with age (44% from 3 to 30 months). This age-related increase in aortic PWV was not related to changes in wall stress. For all ages, central (and peripheral) aortic mean blood pressures were not statistically different. Dilatation occurred (18% increase in internal diameter from 3 to 30 months), but this was accompanied by outward hypertrophic remodeling, with an increase in the medial cross-sectional area of 95% and in the ratio of medial thickness to internal diameter of 29%. Wall stress decreased with age (-34%). There was an increase in the ratio of elastic modulus (calculated from the Moens-Korteweg equation) to wall stress (calculated from the Lamé equation, 117% from 3 to 30 months), suggesting that a change in the composition of the wall is responsible for the age-linked increase in wall stiffness. Dry weight decreased slightly but significantly (-14%) with age. Total protein, elastin, collagen, and nonscleroprotein protein [total-(elastin+collagen)] contents did not change with age, but calculated densities of all 4 were halved (as the medial cross-sectional area doubled). The elastin/collagen ratio was statistically similar at all ages. The only significant effect of AG treatment was a fall in PWV (-20%), leading to a fall in the elastic modulus/wall stress ratio (-27% at 10 months of AG treatment versus 30 months of no treatment). In conclusion, the age-related increase in aortic wall stiffness is prevented by 10 months of treatment with AG, which has no effect on wall stress or composition, suggesting that AG may improve aortic wall stiffness by lowering the degree of AGE-induced cross-linking of the extracellular matrix scleroproteins, such as collagen.

Aortic wall mechanics and composition in a transgenic mouse model of Marfan syndrome.

In Marfan syndrome, mutations of the fibrillin gene (FBN1) lead to aneurysm of the thoracic aorta, making the aortic wall more susceptible to dissection, but the precise sequence of events underlying aneurysm formation is unknown. We used a rodent model of Marfan syndrome, the mgR/mgR mouse (with mgR: hypomorphic FBN1 mutation), which underexpresses FBN1, to distinguish between a defect in the early formation of elastic fibers and the later disruption of elastic fibers. The content of desmosine plus isodesmosine was used as an index of early elastogenesis; disruption of elastic fibers was analyzed by histomorphometry. Because disruption of the medial elastic fibers may produce aortic stiffening, so amplifying the aneurysmal process, we measured thoracoabdominal pulse wave velocity as an indicator of aortic wall stiffness. Both mgR/mgR and wild-type (C57BL/6J-129SV) strains were normotensive, and wall stress was not significantly modified because the increase in internal diameter (0.80+/-0.06 vs 0.63+/-0.03 mm in wild type, P<0.05) was accompanied by increased medial cross-sectional area. The aortic wall stiffened (4-fold increase in the elastic modulus-to-wall stress ratio). Desmosine content was not modified (mgR/mgR 432+/-31 vs wild type 492+/-42 microg/mg wet weight, P>0.05). Elastic fibers showed severe fragmentation: the percentage of the media occupied by elastic fibers was 18+/-3% in mgR/mgR mice vs 30+/-1% in wild-type mice, with the number of elastic segments being 1.9+/-0.2 vs 1.4+/-0.1x10(-6)/mm(2) in the wild type (both P<0.05). In conclusion, underexpression of FBN1 in mice leads to severe elastic network fragmentation but no change in cross-linking, together with aortic dilatation. This result suggests that fragmentation of the medial elastic network and not a defect in early elastogenesis is 1 of the determinants of aortic dilatation in Marfan syndrome.

Aortic wall mechanics in children utilizing a novel application of doppler tissue imaging Mark A. Fogel, Zhu Tian, Jack Rychik. The Children's Hospital of Philadelphia, Philadelphia, PA, University of Pennsylvania School of Medicine, Philadelphia, PA

Aortic wall mechanics in children utilizing a novel application of doppler tissue imaging Mark A. Fogel, Zhu Tian, Jack Rychik. The Children's Hospital of Philadelphia, Philadelphia, PA, University of Pennsylvania School of Medicine, Philadelphia, PA

Abdominal Aortic Aneurysm Wall Mechanics and their Relation to Risk of Rupture

Purpose to see whether aneurysmal aortic wall mechanics can be used as a predictor of abdominal aortic aneurysm (AAA) rupture. Method among 285 individuals, followed conservatively for AAA and monitored for aneurysm growth and wall mechanics on at least one occasion at our institution between January 1991 and January 1998, eleven subsequently ruptured. Wall mechanics were estimated as stiffness (β). This was calculated from diameter and pulsatile diameter change, determined non-invasively by an ultrasonic echo-tracking system and blood pressure obtained by the auscultatory method. The results were compared with those of 121 individuals electively operated on for AAA. Results no difference in aortic stiffness was found between those that subsequently ruptured (β=35, median) compared to those non-ruptured (β=38, median) AAAs (p=0.855). There was no difference in diameter in ruptured (58.8 mm) compared with non-ruptured (54.1 mm) AAAs (p=0.129). All ruptured AAAs showed an expansion of diameter over time. Conclusion this study shows no difference in aneurysmal aortic wall mechanics in those AAAs that subsequently ruptured compared with electively operated AAAs. The results indicate that it is not possible to use aneurysmal aortic wall stiffness as a predictor of rupture.

Influence of sympathetic stimulation on the mechanical properties of the aorta in humans

The mechanical properties of the aorta play a major role in the regulation of blood pressure and cardiac performance. The effect of sympathetic stimulation on the mechanical properties of the human abdominal aorta was studied in 19 healthy volunteers, divided into young (25 +/- 2 years) and elderly individuals (69 +/- 2 years) of both sexes. A non-invasive ultrasonic echo-tracking system for measurement of systolic/diastolic variation of aortic diameter in combination with intra-aortic pressure measurements was used to determine wall mechanics. The pressure-diameter (P-D) relationship and the distensibility indices, stiffness (beta) and pressure strain elastic modulus (Ep) of the abdominal aorta were obtained. Measurements were made at rest and during sympathetic stimulation induced by lower body negative pressure (LBNP). As a sign of sympathetic activation, the peripheral resistance increased by 74-96% (P < 0.001) during LBNP. However, the mechanical properties of the abdominal aorta remained unaltered, as estimated either from the P-D relationship or from the indices Ep and beta, both in the young (rest: Ep = 0.53 +/- 0.18, beta = 4.5 +/- 1.5; LBNP: Ep = 0.51 +/- 0.15, beta = 4.5 +/- 1.2, NS) and in the elderly (rest: Ep = 2.17 +/- 0.70, beta = 17.6 +/- 5.8; LBNP: Ep = 2.11 +/- 0.60, beta = 16.9 +/- 3.9, NS). In conclusion, this investigation shows that LBNP-induced sympathetic activation does not change aortic wall mechanics. Thus, sympathetic modulation of the aortic smooth muscle contractile activity seems to be unimportant in the blood pressure regulation.