Segmental aortic wall stiffness from intravascular ultrasound at normal and subnormal aortic pressure in pigs

Segmental aortic wall stiffness was calculated from intravascular ultrasound images and intravascular pressures in six pigs at normal and subnormal aortic pressures (21 sequences of pressures and areas before and after boli of intravenous nitroglycerin). The wall stiffness was expressed as the pressure–strain elastic modulus (E_p). The E_p was calculated from the formula: E_p=ΔPRΔR^-1 (P, pressure; R, radius) in two different ways. First from maximal and minimal values of pressure and area. Second as the slope of linear regression line of ΔPR as a function of ΔR from 29 simultaneous recorded pressures and images. The average E_p value for all sequences in the different segments was 0.58 ± 0.55 10⁵ Pa (Method 1) and 0.50 ± 0.40 10⁵ Pa (Method 2). E_p increased with the distance from the heart at normal aortic pressures. At subnormal aortic pressures after intravenous nitroglycerin this relationship was not so evident. At subnormal aortic pressures the calculated E_p values were significantly reduced in the lower half of the abdominal aorta. The phase lag, i. e. hysteresis, between pressure and diameter was demonstrated. Our study shows the applicability of intravascular ultrasound as a tool to evaluate arterial wall stiffness.     

A computational model to predict aortic wall stresses in patients with systolic arterial hypertension

Computational cardiovascular mechanics has allowed scientists to create complex 3D models for the simulation of cardiovascular problems. Mechanical stress plays a crucial role in the function of the cardiovascular system; stress analysis is a useful tool for the understanding of vascular pathophysiology. By using the spiral CT imaging and computational structural analysis, we present a noninvasive method of wall stress analysis in the normal aorta. The aortic segment was extended from the origin of the inferior mesenteric artery to the aortic bifurcation. The length of this segment was 12 cm, while the maximum transverse diameter was 2.075+/-0.129 cm. A 3D aortic model was constructed based on the CT scan images. The aorta was assumed to have a uniform wall thickness of 1.5mm. The generated unstructured grid, which was used for the structural analysis, consisted of 14,440 hexahedral elements. The wall material was assumed to be hyperelastic, homogeneous, isotropic and nearly incompressible (Poisson ratio=0.45). According to experimental studies, the Young modulus of aortic wall was set equal to 4.66 MPa. The shear stress induced by the blood flow was neglected. A finite-element static structural analysis was performed. Three different cases were examined applying constant intraluminal systolic blood pressures of 120, 180 and 240 mmHg, respectively. The von Mises stress distribution and the displacements of the aortic wall were calculated. Peak wall stress for the normal load case of 120 mmHg was 22.5 N/cm2, while the max displacement was 0.44 mm. The case with the intraluminal pressure of 180 mmHg resulted into peak wall stress of 32 N/cm2 with max displacement 0.59 mm, while for 240 mmHg was 40.6N/cm2, max displacement 0.72 mm. The rise in blood pressure caused all stresses to increase. The pattern of stress distribution and the orientation of the stress were similar for all test cases. A quantitative evaluation of the aortic wall stresses under systolic hypertension is presented. The calculated values of peak wall stress are far lower to those of failure strength of healthy aortic wall specimens estimated by ex vivo mechanical testing (121.0 N/cm2). Our values are consistent with prior stress values predicted by experimental studies. The described methodology offers a significant advancement in incorporating biomechanical principles in the clinical assessment of hypertensive patients with normal or aneurysmatic aortas and can be applied in a patient-specific basis in both conditions in order to detect the vulnerable high stressed regions and the resultant risk of aortic dissection or rupture. We hypothesize that this could assist in deciding the timing of surgical intervention, especially in high-risk patients with abdominal aortic aneurysms.     

Mechanisms for activation of aortic baroreceptor C-fibres in rabbits and rats.

In an earlier study, we examined the pressure-response characteristics of rat aortic baroreceptors with C-fibre (non-medullated) afferents. Compared with aortic baroreceptor fibres with A-fibre (medullated) afferents, the C-fibres were activated at higher pressures and discharged more irregularly when stimulated with a steady level of pressure. Here we examine the relationship between discharge and the aortic diameter in these two types of afferents in rats and rabbits. An in vitro aortic arch/aortic nerve preparation was used to record single-fibre activity simultaneously with aortic arch pressure and diameter. Diameter was measured using a highly sensitive non-contact photoelectric device. Baroreceptor discharge was characterized by stimulating the nerve endings with either slow pressure ramps from subthreshold to 200-250 mmHg, at a rate of rise of 2 mmHg s-1, or pressure steps from subthreshold to suprathreshold levels, at amplitudes of 110-180 mmHg. In response to these inputs, C-fibres in rabbits (conduction velocities= 0.8-2.2 m s-1) behaved much like those in rats. The C-fibres had significantly higher pressure thresholds (95 +/- 3 mmHg vs. 53 +/- 2 mmHg; mean +/- SEM), lower threshold frequencies (2.4 +/- 0.5 vs. 27.7 +/- 1.8 spikes s-1), lower maximum discharge frequencies (22.7 +/- 2.3 vs. 65 +/- 5.8 spikes s-1) and more irregular discharge in response to a pressure step when compared with A-fibres (conduction velocities of 8-16 m s-1). When plotted against diameter, C-fibre ramp-evoked discharge increased gradually at first, and then rose steeply at increasingly higher ramp pressures where aortic diameter became relatively constant. In contrast, A-fibre discharge was linearly related to diameter over a wide range of pressure. These results suggest two interpretations: (1) The relation between stretch and C-fibre discharge is highly non-linear, with a marked increase in sensitivity at large diameters. (2) C-fibres are stimulated by changes in intramural stress rather than stretch.     

Mechanical properties of abdominal aortic aneurysm wall

There is a need to understand why and where the abdominal aortic aneurysm may rupture. Our goal therefore is to investigate whether the mechanical properties are different in different regions of the aneurysm. Aorta samples from five freshly excised whole aneurysms, > or = 5 cm in diameter, from five patients, average age 71 +/- 10 years, were subjected to uniaxial testing. We report the wall thickness, yield stress and strain, and parameters that describe nonlinear stress-strain curves for the anterior, lateral and posterior regions of the aneurysm. The posterior region was thicker than the anterior region (2.73 +/- 0.46 mm versus 2.09 +/- 0.51 mm). The stress-strain curves were described by sigma = a epsilon(b), where sigma is true stress and epsilon is engineering strain. In the circumferential direction, the wall stiffness increased from posterior to anterior to lateral. In the longitudinal direction, the lateral and anterior regions showed greater wall stiffness than the posterior region. The wall stiffness was greater in the circumferential than longitudinal direction. The anterior region was the weakest, especially in the longitudinal direction (yield stress sigmaY = 0.38 +/- 0.18 N mm(-2)). For a less complex model the aneurysmal wall could be considered orthotropic with sigma = 12.89epsilon(2.92) and 4.95epsilon(2.84) in the circumferential and longitudinal directions. For the isotropic model, sigma =7.89epsilon(2.88). In conclusion, different regions of the aneurysm have different yield stress, yield strains, and other mechanical properties, and this must be considered in understanding where the rupture might occur.     

Identification of Arterial Wall Dynamics in Conscious Dogs

Viscoelastic properties determine the dynamic behaviour of the arterial wall under pulsatile pressure and flow, suggesting time- or frequency-dependent responses to changes in wall stress and strain. The objectives of the present study were: (i) to develop a simplified model to derive simultaneously the elastic, viscous and inertial wall moduli; (ii) to assess Young's modulus as a function of frequency, in conscious, chronically instrumented dogs. Parametric discrete time models were used to characterise the dynamics of the arterial system based on thoracic aortic pressure (microtransducer) and diameter (sonomicrometry) measurements in control steady state and during activation of smooth muscle with the alpha-adrenoceptor agonist phenylephrine (5 microg kg(-1) min(-1), I.V.), in eight conscious dogs. The linear autoregressive model and a physically motivated non-linear model were fitted to the input-output (stress-strain) relationship. The aortic buffering function (complex Young's modulus) was obtained in vivo from the identified linear model. Elastic, viscous and inertial moduli were significantly increased from control state ((44.5 +/- 7.7) x 10(4) Pa; (12.3 +/- 4.7) x 10(4) Pa s; (0.048 +/- 0.028) x 10(4) Pa s(2) ) to active state ((85.3 +/- 29.5) x 10(4) Pa, P < 0.001; (22.4 +/- 8.3) x 10(4) Pa s, P < 0.05; (0.148 +/- 0.060) x 10(4) Pa s(2), P < 0.05). These moduli, obtained using the linear model, did not present significant differences compared with those derived using the non-linear model. In control conditions, the magnitude of the normalised complex Young's modulus was found to be similar to that reported in previous animal studies ranging from 1 to 10 Hz. During vascular smooth muscle activation, this modulus was found to be increased with regard to control conditions (P < 0.01) in the frequency range used in this study. The frequency-dependent Young's modulus of the aortic wall was obtained for the first time in conscious, unsedated dogs. The parametric modelling approach allows us to verify that vascular smooth muscle activation increases the elastic, viscous and inertial moduli with the advantage of being able to track their time evolution. Furthermore, under activation, the aortic wall remains stiff in the physiological frequency range, suggesting the impairment of the arterial buffering function. Experimental Physiology (2001) 86.4, 519-528.     

Diastolic myocardial stiffness in gradually developing left ventricular hypertrophy in dog

The effects of gradually developing left ventricular pressure overload on diastolic myocardial stiffness were studied in a chronic moderate hypertrophy model. A snug aortic band was placed beneath the left coronary artery in six puppies 4.5 wk of age, and hemodynamic studies were performed 33.5 wk later. In all six dogs, moderate pressure gradients (10-58 mmHg) developed across the constriction, and angiographic area of the aortic constriction was significantly smaller than for a control group, 4.9 +/- 0.5 vs. 8.4 +/- 0.8 mm2/kg, (mean +/- SE, P less than 0.05). Increases occurred in left ventricular (LV) wall thickness (1.08 +/- 0.07 vs. 0.83 +/- 0.04 cm, P less than 0.05), LV wall mass (5.2 +/- 0.3 vs. 4.1 +/- 0.2 g/kg, P less than 0.05), and wall thickness-to-radius ratio (0.67 +/- 0.04 vs. 0.50 +/- 0.03, P less than 0.01), whereas no differences were noted in LV end-diastolic pressure (11 +/- 1 vs. 9 +/- 1 mmHg), LV end-diastolic volume (LVEDV, 2.06 +/- 0.22 vs. 2.35 +/- 0.15 ml/kg) or ejection fraction (71 +/- 4 vs. 71 +/- 3%). The values of LV wall mass, LVEDV, and aortic constriction are normalized to body weight. Diastolic LV myocardial stiffness was examined in terms of the elastic stiffness-stress relations. There were small and insignificant differences in end-diastolic stress (17.3 +/- 1.5 vs. 20.4 +/- 3.8 g/cm2), myocardial stiffness constant (Km, 13.7 +/- 5.6 vs. 11.2 +/- 3.3), and end-diastolic elastic stiffness (221 +/- 67 vs. 221 +/- 79 g/cm2) between hypertrophied and control hearts. No significant differences in the elastic stiffness of hypertrophied and normal muscle were observed over the common stress range of 5-25 g/cm2. We conclude that moderate left ventricular hypertrophy in chronic, gradually developing pressure overload is an adaptation process associated with normal myocardial stiffness.     

Maternal placental vascular compliance in rabbits

We studied compliance on the maternal side of the placenta of 20 New Zealand white rabbits, using 51Cr and 125I labels to determine erythrocyte, plasma, and whole-blood volumes per gram of placental tissue under varying maternal pressure conditions. At normal maternal arterial (Pa) and venous (Pv) pressures of 71.8 and 5.5 mmHg, placental blood volume (mean +/- SE) was 0.447 +/- 0.051 ml/g placental tissue. When venous pressure was raised (Pa = 45.5, Pv = 12.2) by occluding the inferior vena cava, blood volume increased to 0.729 +/- 0.068 ml/g, a significant 63% rise. However, when arterial pressure was lowered by occluding the aorta in two steps, dropping to Pa = 33.8, Pv = 7.0, and Pa = 13.5, Pv = 5.4, volume did not decrease significantly. We estimated intervillous space pressure (Pivs) from arterial and venous pressures assuming a ratio of venous to total resistance of 0.02. Compliance calculated from the slope of Pivs vs. volume was 0.0471 ml/mmHg per g. Maternal placental hematocrit averaged 27%, appreciably less than the circulating hematocrit of 38%. Overall, the results suggest that placental volume would be maintained during hypotension and would increase when venous pressure is elevated.     

Fluid Dynamic Analysis in a Human Left Anterior Descending Coronary Artery with Arterial Motion

A computational fluid dynamic (CFD) analysis is presented to describe local flow dynamics in both 3-D spatial and 4-D spatial and temporal domains from reconstructions of intravascular ultrasound (IVUS) and bi-plane angiographic fusion images. A left anterior descending (LAD) coronary artery segment geometry was accurately reconstructed and subsequently its motion was incorporated into the CFD model. The results indicate that the incorporation of motion had appreciable effects on blood flow patterns. The velocity profiles in the region of a stenosis and the circumferential distribution of the axial wall shear stress (WSS) patterns in the vessel are altered with the wall motion introduced in the simulation. The time-averaged axial WSS between simulations of steady flow and unsteady flow without arterial motion were comparable (–0.3 to 13.7 Pa in unsteady flow versus –0.2 to 10.1 Pa in steady flow) while the magnitudes decreased when motion was introduced (0.3–4.5 Pa). The arterial wall motion affects the time-mean WSS and the oscillatory shear index in the coronary vessel fluid dynamics and may provide more realistic predictions on the progression of atherosclerotic disease.     

Increased aortic root stiffness associated with osteogenesis imperfecta

M-mode echocardiograms obtained from 31 patients with types I and IV osteogenesis imperfecta (OI) were evaluated for increased aortic root dilatation and wall stiffness. Four patients were observed to have dilated aortic roots. The pressure-strain elastic moduli (E_p) of the majority of OI patients studied were significantly different from those of age-matched controls; the observed values of E_p were both greater and less than that of controls. At high strain in the circumferential direction, nine of 31 OI patients had aortic roots that were significantly stiffer than those of controls. Increased stiffness in the circumferential direction was associated with decreased aortic pumping efficiency. The increased stiffness observed in the circumferential direction is consistent with increased accumulation and crosslinking of collagen within the aortic wall and may reflect premature aging of OI patients.     

基于CAG三维重建与超声图像的数据融合研究

临床中,融合X射线造影图像和血管内超声图像可以辅助医生更好的对冠心病进行诊断.本研究在X射线造影系统中对导引丝和血管骨架分别三维重建的基础上,利用最佳垂平面法求得导引丝序列点的最佳切向量,首先对超声图像在导引丝上定位,然后根据造影图像与超声图像提供的导引丝和血管骨架的空间关系求得超声图像的偏心角,最后利用四元数法对超声图像在导引丝上进行准确的定向.通过临床数据进行实验表明了该方法的可行性.相对于传统的融合方法,该方法不仅实现了超声图像空间角度的确定,而且具有实现简单、计算速度快等特点.     

Nonsympathetic increased inotropic state early after aortic insufficiency

The very early left ventricular response to chronic volume overload induced by aortic insufficiency (AI) was examined in conscious dogs previously instrumented with a left ventricular micromanometer and ultrasonic crystals measuring internal diameter, segmental length, and parietal wall thickness. Acute volume loading with dextran (AVL) was compared with that 24 and 48 h after AI induced by a perforation of the aortic valve. beta-Blockade was also produced before and after AI. For a similar increase in preload in AVL and after AI, the percent change in systolic shortening of diameters and segments (% delta L) increased from 30.4 to 34.1% after AI (P less than 0.01). For matched calculated wall stress during AVL and AI, % delta L and peak velocity of shortening were significantly increased after AI, and the same results were reproduced after beta-blockade. We conclude that, at the early phase of chronic volume overload before hypertrophy appears, left ventricular hyperfunction is mainly due to a nonsympathetic increased contractility and that, in the conscious dog, the inotropic state appears to be modified by a sustained increased preload.     

Estimation of arterial compliance in aortic regurgitation: three methods evaluated in pigs

Three methods for measuring arterial compliance when aortic regurgitation is present are examined. The first two methods are based on a Windkessel model composed of two elements, compliance C and resistance R. Arterial compliance was estimated from diastolic pressure waveforms and diastolic regurgitant flow for one method, and from systolic aortic pressure waveforms and systolic flow for the other method. The third method was based on a three-element Windkessel model, composed of characteristic resistance r, compliance C and resistance R. In this method arterial compliance was calculated by adjusting the model to the modulus and phase of the first harmonic term of the aortic input impedance. The three methods were compared and validated in six anaesthetised pigs over a broad range of aortic pressures. The three methods were found to give quantitatively similar estimates of arterial compliance at mean aortic pressures above 60 mm Hg. Below 60 mm Hg, estimates of arterial compliance varied widely, probably because of poor validity of the Windkessel models in the low pressure range.     

Blood pressure regulation V: in vivo mechanical properties of precapillary vessels as affected by long-term pressure loading and unloading

Recent studies are reviewed, concerning the in vivo wall stiffness of arteries and arterioles in healthy humans, and how these properties adapt to iterative increments or sustained reductions in local intravascular pressure. A novel technique was used, by which arterial and arteriolar stiffness was determined as changes in arterial diameter and flow, respectively, during graded increments in distending pressure in the blood vessels of an arm or a leg. Pressure-induced increases in diameter and flow were smaller in the lower leg than in the arm, indicating greater stiffness in the arteries/arterioles of the leg. A 5-week period of intermittent intravascular pressure elevations in one arm reduced pressure distension and pressure-induced flow in the brachial artery by about 50 %. Conversely, prolonged reduction of arterial/arteriolar pressure in the lower body by 5 weeks of sustained horizontal bedrest, induced threefold increases of the pressure-distension and pressure-flow responses in a tibial artery. Thus, the wall stiffness of arteries and arterioles are plastic properties that readily adapt to changes in the prevailing local intravascular pressure. The discussion concerns mechanisms underlying changes in local arterial/arteriolar stiffness as well as whether stiffness is altered by changes in myogenic tone and/or wall structure. As regards implications, regulation of local arterial/arteriolar stiffness may facilitate control of arterial pressure in erect posture and conditions of exaggerated intravascular pressure gradients. That increased intravascular pressure leads to increased arteriolar wall stiffness also supports the notion that local pressure loading may constitute a prime mover in the development of vascular changes in hypertension.     

Determination of aortic compliance from magnetic resonance images using an automatic active contour model

The possibility of monitoring changes in aortic elasticity in humans has important applications for clinical trials because it estimates the efficacy of plaque-reducing therapies. The elasticity is usually quantified by compliance measurements. Therefore, the relative temporal change in the vessel cross-sectional area throughout the cardiac cycle has to be determined. In this work we determined and compared the compliance between three magnetic resonance (MR) methods (FLASH, TrueFISP and pulse-wave). Since manual outlining of the aortic wall area is a very time-consuming process and depends on an operator's variability, an algorithm for the automatic segmentation of the artery wall from MR images through the entire heart cycle is presented. The reliable detection of the artery cross-sectional area over the whole heart cycle was possible with a relative error of about 1%. Optimizing the temporal resolution to 60 ms we obtained a relative error in compliance of about 7% from TrueFISP (1.0 x 1.0 x 10 mm3, signal-to-noise ratio (SNR) > 12) and FLASH (0.7 x 0.7 x 10 mm3, SNR > 12) measurements in volunteers. Pulse-wave measurements yielded an error of more than 9%. In a study of ten volunteers, a compliance between C = 3 x 10(-5) Pa(-1) and C = 8 x 10(-5) Pa(-1) was determined, depending on age. The results of the TrueFISP and the pulse-wave measurements agreed very well with one another (confidence interval of 1 x 10(-5) Pa(-1)) while the results of the FLASH method more clearly deviated from the TrueFISP and pulse-wave (confidence interval of more than 2 x 10(-5) Pa(-1)).     

Continuous measurement of aortic radius changein vivo with an intra-aortic ultrasonic catheter

The radii of the inner and outer walls of the aorta and the intravascular blood pressure were recorded simultaneously in the descending thoracic aorta of intact, living dogs using 7·5 MHz ultrasound. Blood pressure and the A-mode signals containing wall echoes were also recorded on videotape which was later replayed for processing. Thein vivo data were compared with data obtained on the same vessels post mortem. The change in radius due to a pressure change from 80 to 125 mmHg was calculated from thein vivo andin vitro data. After normalising the radius changes with respect to the radius at 80 mm Hg, the ratio of thein vivo andin vitro values ranged from 0·66 to 1·36 with a mean of 0·94. The changes in radius were comparable with previously reported values obtained using various techniques.     

Use of non-invasive finger blood pressure monitoring in the estimation of aortic pressure at rest and during the Mueller manoeuvre.

The aim of this investigation was to evaluate whether reliable estimates of aortic pressure can be derived using non-invasive finger blood pressure monitoring. Finger blood pressure (Ohmeda 2300 Finapres device; Finapres, Englewood, CO) was compared with simultaneous ascending aortic pressure measured with a catheter-transducer system both at rest and during acute negative intrathoracic pressure (the Mueller manoeuvre). Thirty-eight patients aged 17-73 years were studied. All were undergoing routine diagnostic or therapeutic cardiac catheterization. Beat-to-beat values of systolic, diastolic and mean non-invasive finger and invasive aortic blood pressure were measured at rest and factors which might have an influence on the difference between methods were examined. The mean finger-aortic difference was +5 +/- 14 mmHg for systolic, -2 +/- 7 mmHg for diastolic, -5 +/- 8 mmHg for mean and +6 +/- 13 mmHg for pulse pressure. In multivariate linear regression analysis, the difference in systolic pressure was related to aortic systolic pressure (standardized coefficient beta = -0.33, P = 0.01), heart rate (beta = 0.49, P < 0.000), age (beta = -0.29, P < 0.025) and height (beta = 0.40, P < 0.005). The linear regression equations to derive resting aortic pressures from the non-invasive finger pressure readings had correlation coefficients between 0.83 and 0.87 and standard errors of estimate between 6 and 14 mmHg. During the Mueller manoeuvre, Finapres reproduced average pressure changes reliably compared with intra-aortic pressure. Due to moderate inter-individual variation in the finger-aortic differences the correlation coefficients ranged from 0.83 to 0.93 and the standard errors of estimate from 3 to 6 mmHg. Non-invasive finger blood pressure monitoring could be used to estimate central aortic mean and diastolic blood pressure fairly reliably at rest, but with respect to systolic pressure the variance in finger-aortic difference was marked. The average intra-aortic pressure changes caused by the Mueller manoeuvre were reliably reproduced by the Finapres device.     

Noninvasive assessment of mechanical properties of peripheral arteries

An ultrasound examination was used to noninvasively determine the changes in mechanical properties associated with age for the common carotid, brachial, popliteal, femoral, and tibial arteries. Forty-two normal male subjects, ranging in age from 8 to 60 years of age, were examined. The subjects were placed in one of three age groups: <29 years of age, 29 to 38, and >38. Mechanical properties including percentage variation in diameter, pressure-strain, and circumferential elastic modulus were determined from changes in wall thickness and pulse pressure. Percentage variation in diameter (PVD) was seen to decrease with age for all arteries except the brachial, which remained relatively constant. Pressure-strain (Ep) and circumferential elastic moduli (Eo) were seen to increase with age in all arteries except the brachial, which remained relatively constant. Values of Ep and Eo were normalized into a stiffness index by dividing by the value found for the brachial artery. Stiffness indexes for the common carotid and femoral arteries were observed to increase more rapidly with age than the indexes obtained for the popliteal and tibial arteries. It is proposed that the stiffness index and changes in this parameter that occur with age may be useful in noninvasively assessing the progression of atherosclerosis.     

Role of total arterial compliance and peripheral resistance in the determination of systolic and diastolic aortic pressure.

The goal of the study was to define the major arterial parameters that determine aortic systolic (Ps) and diastolic (Pd) pressure in the dog. Measured aortic flows were used as input to the two-element windkessel model of the arterial system, with peripheral resistance calculated as mean pressure over mean flow and total arterial compliance calculated from the decay time in diastole. The windkessel model yielded an aortic pressure wave from which we obtained the predicted systolic (Ps, wk) and diastolic (Pd, wk) pressure. These predicted pressures were compared with the measured systolic and diastolic pressures. The measurements and calculations were carried out in 7 dogs in control conditions, during aortic occlusion at four locations (the trifurcation, between trifurcation and diaphragm, the diaphragm and the proximal descending thoracic aorta) and during occlusion of both carotid arteries. Under all conditions studied the predicted systolic and diastolic pressure matched the experimental ones very well: Ps, wk = (1.000 +/- 0.0055) Ps with r = 0.958 and Pd, wk = (1.024 +/- 0.0035) Pd with r = 0.995. Linear regression for pulse pressure gave PPwk = (0.99 +/- 0.016) PP (r = 0.911). We found the accuracy of prediction equally good under control conditions and in presence of aortic or carotid artery occlusions. Multiple regression between pulse pressure and arterial resistance and total arterial compliance yielded a poor regression constant (r2 = 0.19) suggesting that the two arterial parameters alone cannot explain pulse pressure and that flow is an important determinant as well. We conclude that, for a given ejection pattern (aortic flow), two arterial parameters, total arterial resistance and total arterial compliance are sufficient to accurately describe systolic and diastolic aortic pressure.     

Glutaraldehyde-fixed kangaroo aortic wall tissue: histology,crosslink stability and calcification potential

Stentless aortic heart valve substitutes, manufactured from biological tissues, are fixed with glutaraldehyde to cross-link collagen, reduce antigenicity, and sterilize the tissue. Despite improved cross linking, reduced antigenicity, and various anticalcification measures, the aortic wall tissue present in these prostheses tends to calcify. The aim of this study was to assess the morphology, collagen cross-link stability, and calcification potential of glutaraldehyde-preserved kangaroo aortic wall tissue as opposed to porcine aortic wall tissue. Porcine and kangaroo aortic wall tissues were fixed in 0.625% buffered glutaraldehyde. Histology and cross-link stability were examined. Calcification potential was determined in the subcutaneous rat model. Kangaroo aortic wall tissue was significantly (p < 0.01) less calcified than porcine aortic wall tissue (26.67 +/- 6.53 versus 41.959 +/- 2.75 microg/mg tissue) at 8 weeks. In conclusion, the histological differences between kangaroo and porcine aortic wall tissue correlate well with the reduced calcification potential of kangaroo aortic wall tissue. The reduced calcification potential could result in improved long-term durability of stentless kangaroo heart valves as bioprostheses.     

The effect of aortic wall and aortic leaflet stiffening on coronary hemodynamic: a fluid–structure interaction study

Pathologies of the aortic valve such as aortic sclerosis are thought to impact coronary blood flow. Recent clinical investigations have observed simultaneous structural and hemodynamic variations in the aortic valve and coronary arteries due to regional pathologies of the aortic valve. The goal of the present study is to elucidate this observed and yet unexplained phenomenon, in which a local pathology in the aortic valve region could potentially lead to the initiation or progression of coronary artery disease. Results revealed a considerable impact on the coronary flow, velocity profile, and consequently shear stress due to an increase in the aortic wall or aortic leaflet stiffness and thickness which concur with clinical observations. The cutoff value of 0.75 for fractional flow reserve was reached when the values of leaflet thickness and aortic wall stiffness were approximately twice and three times their normal value, respectively. Variations observed in coronary velocity profiles as well as wall shear stress suggest a possible link for the initiation of coronary artery disease.