Anti-apoA-1 auto-antibodies increase mouse atherosclerotic plaque vulnerability, myocardial necrosis and mortality triggering TLR2 and TLR4.

Auto-antibodies to apolipoprotein A-1 (anti-apoA-1 IgG) were shown to promote inflammation and atherogenesis, possibly through innate immune receptors signalling. Here, we aimed at investigating the role of Toll-like receptors (TLR) 2 and 4 on anti-apoA-1 IgG-induced atherosclerotic plaque vulnerability, myocardial necrosis and mortality in mice. Adult male apolipoprotein E knockout (ApoE)-/- (n=72), TLR2-/-ApoE-/- (n=36) and TLR4-/-Apo-/- (n=28) mice were intravenously injected with 50 µg/mouse of endotoxin-free polyclonal anti-apoA-1 IgG or control isotype IgG (CTL IgG) every two weeks for 16 weeks. Atherosclerotic plaque size and vulnerability were assessed by histology. Myocardial ischaemia and necrosis, respectively, were determined by electrocardiographic (ECG) changes assessed by telemetry and serum troponin I (cTnI) measurements. Impact on survival was assessed by Kaplan-Meier analyses. In ApoE-/- mice, anti-apoA-1 IgG passive immunisation enhanced histological features of atherosclerotic plaque vulnerability (increase in neutrophil and MMP-9 and reduction in collagen content), induced a substantial cTnI elevation (p=0.001), and increased mortality rate by 23 % (LogRank, p=0.04) when compared to CTL IgG. On a subgroup of ApoE-/- mice equipped with telemetry (n=4), a significant ST-segment depression was noted in anti-apoA-1 IgG-treated mice when compared to CTL IgG recipients (p< 0.001), and an acute ST-segment elevation myocardial infarction preceding mouse death was observed in one case. The deleterious effects of anti-apoA-1 IgG on atherosclerotic plaque vulnerability, myocardial necrosis and death were partially reversed in TLR2-/-ApoE-/- and TLR4-/-ApoE-/- backgrounds. In conclusion, anti-apoA-1 auto-antibodies seem to be active mediators of atherosclerotic plaque vulnerability, myocardial necrosis, and mortality in mice through TLR2- and TLR4-mediated pathways.

Brachial artery waveforms for automatic blood pressure measurement.

Theoretically the auscultatory method using Korotkoff sounds is more related to the maximum artery closure status, while the oscillometric method is more related to the overall artery closure status under the cuff. Therefore, the latter is less accurate than the former. This work introduces a new method, which is more accurate than the oscillometric method and suitable for automatic devices. To monitor the maximum artery closure status, a piezoelectric film sensor is attached to the skin just above the brachial artery and under the central section of the cuff where maximum cuff pressure is transferred to the arm. Using the waveform features obtained by this sensor, measurement errors of 0.7±2.5 and 1.27±4.53 mmHg were obtained for the systolic and diastolic pressure, respectively. These reflect small deviations from auscultatory clinical data.

Active axial stress in mouse aorta.

The study verifies the development of active axial stress in the wall of mouse aorta over a range of physiological loads when the smooth muscle cells are stimulated to contract. The results obtained show that the active axial stress is virtually independent of the magnitude of pressure, but depends predominately on the longitudinal stretch ratio. The dependence is non-monotonic and is similar to the active stress-stretch dependence in the circumferential direction reported in the literature. The expression for the active axial stress fitted to the experimental data shows that the maximum active stress is developed at longitudinal stretch ratio 1.81, and 1.56 is the longitudinal stretch ratio below which the stimulation does not generate active stress. The study shows that the magnitude of active axial stress is smaller than the active circumferential stress. There is need for more experimental investigations on the active response of different types of arteries from different species and pathological conditions. The results of these studies can promote building of refined constrictive models in vascular rheology.

A method for the quantification of the pressure dependent 3D collagen configuration in the arterial adventitia.

Collagen plays an important role in the response of the arterial wall to mechanical loading and presumably has a load-bearing function preventing overdistension. Collagen configuration is important for understanding this role, in particular in mathematical models of arterial wall mechanics. In this study a new method is presented to image and quantify this configuration. Collagen in the arterial adventitia is stained with CNA35, and imaged in situ at high resolution with confocal microscopy at luminal pressures from 0 to 140mm Hg. The images are processed with a new automatic approach, utilizing techniques intended for MRI-DTI data. Collagen configuration is quantified through three parameters: the waviness, the transmural angle and the helical angle. The method is demonstrated for the case of carotid arteries of the white New Zealand rabbit. The waviness indicated a gradual straightening between 40 and 80mm Hg. The transmural angle was about zero indicating that the fibers stayed within an axial-circumferential plane at all pressures. The helical angle was characterized by a symmetrical distribution around the axial direction, indicating a double symmetrical helix. The method is the first to combine high resolution imaging with a new automatic image processing approach to quantify the 3D configuration of collagen in the adventitia as a function of pressure.

Experimental investigation of collagen waviness and orientation in the arterial adventitia using confocal laser scanning microscopy.

Mechanical properties of the adventitia are largely determined by the organization of collagen fibers. Measurements on the waviness and orientation of collagen, particularly at the zero-stress state, are necessary to relate the structural organization of collagen to the mechanical response of the adventitia. Using the fluorescence collagen marker CNA38-OG488 and confocal laser scanning microscopy, we imaged collagen fibers in the adventitia of rabbit common carotid arteries ex vivo. The arteries were cut open along their longitudinal axes to get the zero-stress state. We used semi-manual and automatic techniques to measure parameters related to the waviness and orientation of fibers. Our results showed that the straightness parameter (defined as the ratio between the distances of endpoints of a fiber to its length) was distributed with a beta distribution (mean value 0.72, variance 0.028) and did not depend on the mean angle orientation of fibers. Local angular density distributions revealed four axially symmetric families of fibers with mean directions of 0°, 90°, 43° and -43°, with respect to the axial direction of the artery, and corresponding circular standard deviations of 40°, 47°, 37° and 37°. The distribution of local orientations was shifted to the circumferential direction when measured in arteries at the zero-load state (intact), as compared to arteries at the zero-stress state (cut-open). Information on collagen fiber waviness and orientation, such as obtained in this study, could be used to develop structural models of the adventitia, providing better means for analyzing and understanding the mechanical properties of vascular wall.

Impact of aortic grafts on arterial pressure: a computational fluid dynamics study.

OBJECTIVE: Vascular prostheses currently used in vascular surgery do not have the same mechanical properties as human arteries. This computational study analyses the mechanisms by which grafts, placed in the ascending aorta (proximal) and descending aorta (distal), affect arterial blood pressure. METHODS: A one-dimensional cardiovascular model was developed and adapted to include the graft geometry with in vitro measured mechanical properties. Pressure at the aortic root and haemodynamic parameters were computed and compared for a control, proximal and distal graft case. RESULTS: In comparison to the control case, the proximal graft increased characteristic impedance by 58% versus only 1% change for the distal graft. The proximal and distal graft increased pulse pressure by 21% and 10%, respectively. CONCLUSIONS: The mechanisms underlying pulse pressure increase are different for proximal and distal grafts. For the proximal graft, the primary reason for pulse pressure rise is augmentation of the forward wave, resulting from characteristic impedance increase. For the distal graft, the pulse pressure rise is associated with augmented wave reflections resulting from compliance mismatch. Overall, the proximal aortic graft resulted in greater haemodynamic alterations than the distal graft. Thus, it is likely that patients who receive ascending aorta grafts are more prone to systolic hypertension and therefore deserve closer blood pressure monitoring.

Role of elastin anisotropy in structural strain energy functions of arterial tissue.

The vascular wall exhibits nonlinear anisotropic mechanical properties. The identification of a strain energy function (SEF) is the preferred method to describe its complex nonlinear elastic properties. Earlier constituent-based SEF models, where elastin is modeled as an isotropic material, failed in describing accurately the tissue response to inflation-extension loading. We hypothesized that these shortcomings are partly due to unaccounted anisotropic properties of elastin. We performed inflation-extension tests on common carotid of rabbits before and after enzymatic degradation of elastin and applied constituent-based SEFs, with both an isotropic and an anisotropic elastin part, on the experimental data. We used transmission electron microscopy (TEM) and serial block-face scanning electron microscopy (SBFSEM) to provide direct structural evidence of the assumed anisotropy. In intact arteries, the SEF including anisotropic elastin with one family of fibers in the circumferential direction fitted better the inflation-extension data than the isotropic SEF. This was supported by TEM and SBFSEM imaging, which showed interlamellar elastin fibers in the circumferential direction. In elastin-degraded arteries, both SEFs succeeded equally well in predicting anisotropic wall behavior. In elastase-treated arteries fitted with the anisotropic SEF for elastin, collagen engaged later than in intact arteries. We conclude that constituent-based models with an anisotropic elastin part characterize more accurately the mechanical properties of the arterial wall when compared to models with simply an isotropic elastin. Microstructural imaging based on electron microscopy techniques provided evidence for elastin anisotropy. Finally, the model suggests a later and less abrupt collagen engagement after elastase treatment.

Intracranial stents being modeled as a porous medium: flow simulation in stented cerebral aneurysms.

Intracranial aneurysms may be treated by flow diverters, alternatively to stents and coils combination. Numerical simulation allows the assessment of the complex nature of aneurismal flow. Endovascular devices present a rather dense and fine strut network, increasing the complexity of the meshing. We propose an alternative strategy, which is based on the modeling of the device as a porous medium. Two patient-specific aneurysm data sets were reconstructed using conventional clinical setups. The aneurysms selection was done so that intra-aneurismal flow was shear driven in one and inertia driven in the other. Stents and their porous medium analog were positioned at the aneurysm neck. Physiological flow and standard boundary conditions were applied. The comparison between both approaches was done by analyzing the velocity, vorticity, and shear rate magnitudes inside the aneurysm as well as the wall shear stress (WSS) at the aneurysm surface. Simulations without device were also computed. The average flow reduction reaches 76 and 41% for the shear and inertia driven flow models, respectively. When comparing the two approaches, results show a remarkable similarity in the flow patterns and magnitude. WSS, iso-velocity surfaces and velocity on a trans-sectional plane are in fairly good agreement. The root mean squared error on the investigated parameters reaches 20% for aneurysm velocity, 30.6% for aneurysm shear rate, and 47.4% for aneurysm vorticity. It reaches 20.6% for WSS computed on the aneurysm surface. The advantages of this approach reside in its facility to implement and in the gain in computational time. Results predicted by the porous medium approach compare well with the real stent geometry model and allow predicting the main effects of the device on intra-aneurismal flow, facilitating thus the analysis.

Numerical validation of a new method to assess aortic pulse wave velocity from a single recording of a brachial artery waveform with an occluding cuff.

Recently a new method has been proposed as a tool to measure arterial pulse wave velocity (PWV), a measure of the stiffness of the large arteries and an emerging parameter used as indicator of clinical cardiovascular risk. The method is based on measurement of brachial blood pressure during supra-systolic pressure inflation of a simple brachial cuff [the device is known as the Arteriograph (Tensiomed, Budapest, Hungary)]. This occlusion yields pronounced first and secondary peaks in the pressure waveform, the latter ascribed to a reflection from the aortic bifurcation, and PWV is calculated as the ratio of twice the jugulum-symphysis distance and the time difference between the two peaks. To test the validity of this working principle, we used a numerical model of the arterial tree to simulate pressures and flows in the normal configuration, and in a configuration with an occluded brachial artery. A pronounced secondary peak was indeed found in the brachial pressure signal of the occluded model, but its timing was only related to brachial stiffness and not to aortic stiffness. We also compared PWV's calculated with three different methods: PWVATG (approximately Arteriograph principle), PWVcar-fem (approximately carotid-femoral PWV, the current clinical gold standard method), and PWVtheor (approximately Bramwell-Hill equation). Both PWVATG (R2=0.94) and PWVcar-fem (R2=0.95) correlated well with PWVtheor, but their numerical values were lower (by 2.17+/-0.42 and 1.08+/-0.70 m/s for PWVATG and PWVcar-fem, respectively). In conclusion, our simulations question the working principle of the Arteriograph. Our data indicate that the method picks up wave reflection phenomena confined to the brachial artery, and derived values of PWV rather reflect the stiffness of the brachial arteries.

RC time constant of single lung equals that of both lungs together: a study in chronic thromboembolic pulmonary hypertension.

The product of resistance, R, and compliance, C (RC time), of the entire pulmonary circulation is constant. It is unknown if this constancy holds for individual lungs. We determined R and C in individual lungs in chronic thromboembolic pulmonary hypertension (CTEPH) patients where resistances differ between both lungs. Also, the contribution of the proximal pulmonary arteries (PA) to total lung compliance was assessed. Patients (n=23) were referred for the evaluation of CTEPH. Pressure was measured by right heart catheterization and flows in the main, left, and right PA by magnetic resonance imaging. Total, left, and right lung resistances were calculated as mean pressure divided by mean flow. Total, left, and right lung compliances were assessed by the pulse pressure method. Proximal compliances were derived from cross-sectional area change DeltaA and systolic-diastolic pressure difference DeltaP (DeltaA/DeltaP) in main, left, and right PA, multiplied by vessel length. The lung with the lowest blood flow was defined "low flow" (LF), the contralateral lung "high flow" (HF). Total resistance was 0.57+/-0.28 mmHg.s(-1).ml(-1), and resistances of LF and HF lungs were 1.57+/-0.2 vs. 1.00+/-0.1 mmHg.s(-1).ml(-1), respectively, P<0.0001. Total compliance was 1.22+/-1.1 ml/mmHg, and compliances of LF and HF lung were 0.47+/-0.11 and 0.62+/-0.12 ml/mmHg, respectively, P=0.01. Total RC time was 0.49+/-0.2 s, and RC times for the LF and HF lung were 0.45+/-0.2 and 0.45+/-0.1 s, respectively, not different. Proximal arterial compliance, given by the sum of main, right, and left PA compliances, was only 19% of total lung compliance. The RC time of a single lung equals that of both lungs together, and pulmonary arterial compliance comes largely from the distal vasculature.

Arterial biomechanics after destruction of cytoskeleton by Cytochalasin D.

Vascular smooth muscle is a major structural element of the arterial wall. We examined the effects of cytoskeleton destruction, after administration of Cytochalasin D, on the biomechanical properties of porcine common carotids. Compared to untreated, maximally dilated controls, Cytochalasin D-treated arteries have shown a marked increase in compliance in the elastin-dominated pressure range. After weakening the VSM stress-bearing cytoskeleton by Cytochalasin D the artery would expand, reaching a new equilibrium state. This study brings further evidence that VSM is under tension, even when it is under zero load and at maximal vasodilation. This residual tension was released upon partial destruction of the cytoskeleton with Cytochalasin D. From a biomechanical standpoint, this means that the zero stress states of the in-series and parallel elastic components are substantially different.

Methodologies to assess blood flow in cerebral aneurysms: current state of research and perspectives.

With intracranial aneurysms disease bringing a weakened arterial wall segment to initiate, grow and potentially rupture an aneurysm, current understanding of vessel wall biology perceives the disease to follow the path of a dynamic evolution and increasingly recognizes blood flow as being one of the main stakeholders driving the process. Although currently mostly morphological information is used to decide on whether or not to treat a yet unruptured aneurysm, among other factors, knowledge of blood flow parameters may provide an advanced understanding of the mechanisms leading to further aneurismal growth and potential rupture. Flow patterns, velocities, pressure and their derived quantifications, such as shear and vorticity, are today accessible by direct measurements or can be calculated through computation. This paper reviews and puts into perspective current experimental methodologies and numerical approaches available for such purposes. In our view, the combination of current medical imaging standards, numerical simulation methods and endovascular treatment methods allow for thinking that flow conditions govern more than any other factor fate and treatment in cerebral aneurysms. Approaching aneurysms from this perspective improves understanding, and while requiring a personalized aneurysm management by flow assessment and flow correction, if indicated.

An assessment of ductus venosus tapering and wave transmission from the fetal heart.

Pressure and flow pulsations in the fetal heart propagate through the precordial vein and the ductus venosus (DV) but are normally not transmitted into the umbilical vein (UV). Pulsations in the umbilical vein do occur, however, in early pregnancy and in pathological conditions. Such transmission into the umbilical vein is not well understood. In particular, the effect of the impedance changes in the DV due to its tapered geometry is not known. This paper presents a mathematical model that we developed to study the transmission of pulsations, originating in the fetal heart, through the DV to the umbilical vein. In our model, the tapered geometry of the DV was found to be of minor importance and the only effective reflection site in the DV appears to be at the DV inlet. Differences between the DV inlet and outlet flow were also found to be minor for medium to large umbilical vein-DV diameter ratios. Finally, the results of a previously proposed lumped model were found to agree well with the present model of the DV-umbilical vein bifurcation.

Three- and four-element Windkessel models: assessment of their fitting performance in a large cohort of healthy middle-aged individuals.

Lumped-parameter models are used to estimate the global arterial properties by fitting the model to measured (aortic) pressure and flow. Different model configurations coexist, and it is still an open question as to which model optimally reflects the arterial tree and leads to correct estimates of arterial properties. An assessment was made of the performance of (a) the three-element Windkessel model (WK3) consisting of vascular resistance R, total arterial compliance C, and characteristic impedance Zc; (b) a four-element model with an inertance element L placed in parallel with Zc (WK4-p); and (c) a four-element model with L placed in series with Zc (WK4-s). Models were fitted to data measured non-invasively in 2404 healthy subjects, aged between 35 and 55 years. It was found that model performance segregated into two groups. In a group containing 20 per cent of the dataset (characterized by low blood pressure and wave reflection) the WK4-p model outperformed the other models, with model behaviour as envisioned by its promoters. In these cases, the WK3 and WK4-s models led to increased overestimation of total arterial compliance and underestimation of characteristic impedance. However, in about 80 per cent of the cases, the WK4-p model showed a behaviour that was very similar to that of the WK3 and WK4-s models. Here, the WK4-s model yielded the best quality of fit, although model parameters reached physically impossible values for L in about 12 per cent of all cases. The debate about which lumped-parameter model is the better approximation of the arterial tree is therefore still not fully resolved.

Oscillatory shear stress and reduced compliance impair vascular functions.

Shear stress has been shown to influence endothelial cell gene expression and morphology. In particular, low and bi-directional shear stress, mimicking conditions at plaque-prone areas, down-regulates the expression of several atheroprotective genes, and up-regulates that of other genes considered as pro-inflammatory. Another mechanical situation thought to have a negative influence on vascular functions is arterial stiffness. Loss of arterial compliance occurs during ageing, in diabetic as well as in hypertensive patients. In this work we investigated the effects of these two particular hemodynamic environments (bi-directional shear stress and reduced compliance), using a recently developed perfusion system allowing to expose native arteries in vitro to complex hemodynamic environments. We were able to show that both plaque-prone shear stress and reduced compliance trigger endothelial dysfunction, but via different mechanisms. Only reduced compliance affected vascular contractility, inducing a dedifferentiation of smooth muscle cells and a consequent loss of norepinephrine sensitivity.

Effect of elastin degradation on carotid wall mechanics as assessed by a constituent-based biomechanical model.

Arteries display a nonlinear anisotropic behavior dictated by the elastic properties and structural arrangement of its main constituents, elastin, collagen, and vascular smooth muscle. Elastin provides for structural integrity and for the compliance of the vessel at low pressure, whereas collagen gives the tensile resistance required at high pressures. Based on the model of Zulliger et al. (Zulliger MA, Rachev A, Stergiopulos N. Am J Physiol Heart Circ Physiol 287: H1335-H1343, 2004), which considers the contributions of elastin, collagen, and vascular smooth muscle cells (VSM) in an explicit form, we assessed the effects of enzymatic degradation of elastin on biomechanical properties of rabbit carotids. Pressure-diameter curves were obtained for controls and after elastin degradation, from which elastic and structural properties were derived. Data were fitted into the model of Zulliger et al. to assess elastic constants of elastin and collagen as well as the characteristics of the collagen engagement profile. The arterial segments were also prepared for histology to visualize and quantify elastin and collagen. Elastase treatment leads to a diameter enlargement, suggesting the existence of significant compressive prestresses within the wall. The elastic modulus was more ductile in treated arteries at low circumferential stretches and significantly greater at elevated circumferential stretches. Abrupt collagen fiber recruitment in elastase-treated arteries leads to a much stiffer vessel at high extensions. This change in collagen engagement properties results from structural alterations provoked by the degradation of elastin, suggesting a clear interaction between elastin and collagen, often neglected in previous constituent-based models of the arterial wall.

Nonlinear isochrones in murine left ventricular pressure-volume loops: how well does the time-varying elastance concept hold?

The linear time-varying elastance theory is frequently used to describe the change in ventricular stiffness during the cardiac cycle. The concept assumes that all isochrones (i.e., curves that connect pressure-volume data occurring at the same time) are linear and have a common volume intercept. Of specific interest is the steepest isochrone, the end-systolic pressure-volume relationship (ESPVR), of which the slope serves as an index for cardiac contractile function. Pressure-volume measurements, achieved with a combined pressure-conductance catheter in the left ventricle of 13 open-chest anesthetized mice, showed a marked curvilinearity of the isochrones. We therefore analyzed the shape of the isochrones by using six regression algorithms (two linear, two quadratic, and two logarithmic, each with a fixed or time-varying intercept) and discussed the consequences for the elastance concept. Our main observations were 1) the volume intercept varies considerably with time; 2) isochrones are equally well described by using quadratic or logarithmic regression; 3) linear regression with a fixed intercept shows poor correlation (R(2) < 0.75) during isovolumic relaxation and early filling; and 4) logarithmic regression is superior in estimating the fixed volume intercept of the ESPVR. In conclusion, the linear time-varying elastance fails to provide a sufficiently robust model to account for changes in pressure and volume during the cardiac cycle in the mouse ventricle. A new framework accounting for the nonlinear shape of the isochrones needs to be developed.

Gelsolin superfamily proteins: key regulators of cellular functions.

Cytoskeletal rearrangement occurs in a variety of cellular processes and involves a wide spectrum of proteins. Among these, the gelsolin superfamily proteins control actin organization by severing filaments, capping filament ends and nucleating actin assembly [1]. Gelsolin is the founding member of this family, which now contains at least another six members: villin, adseverin, capG, advillin, supervillin and flightless I. In addition to their respective role in actin filament remodeling, these proteins have some specific and apparently non-overlapping particular roles in several cellular processes, including cell motility, control of apoptosis and regulation of phagocytosis (summarized in table 1). Evidence suggests that proteins belonging to the gelsolin superfamily may be involved in other processes, including gene expression regulation. This review will focus on some of the known functions of the gelsolin superfamily proteins, thus providing a basis for reflection on other possible and as yet incompletely understood roles for these proteins.

Comparative assessment of intimal hyperplasia development after 14 days in two different experimental settings: tissue culture versus ex vivo continuous perfusion of human saphenous vein.

BACKGROUND: Intimal hyperplasia (IH) is a vascular remodeling process which often leads to failure of arterial bypass or hemodialysis access. Experimental and clinical work have provided insight in IH development; however, further studies under precise controlled conditions are required to improve therapeutic strategies to inhibit IH development. Ex vivo perfusion of human vessel segments under standardized hemodynamic conditions may provide an adequate experimental approach for this purpose. Therefore, chronically perfused venous segments were studied and compared to traditional static culture procedures with regard to functional and histomorphologic characteristics as well as gene expression. MATERIALS AND METHODS: Static vein culture allowing high tissue viability was performed as previously described. Ex vivo vein support system (EVVSS) was performed using a vein support system consisting of an incubator with a perfusion chamber and a pump. EVVSS allows vessel perfusion under continuous flow while maintaining controlled hemodynamic conditions. Each human saphenous vein was divided in two parts, one cultured in a Pyrex dish and the other part perfused in EVVSS for 14days. Testing of vasomotion, histomorphometry, expression of CD 31, Factor VIII, MIB 1, alpha-actin, and PAI-l were determined before and after 14days of either experimental conditions. RESULTS: Human venous segments cultured under traditional or perfused conditions exhibited similar IH after 14 days as shown by histomorphometry. Smooth-muscle cell (SMC) was preserved after chronic perfusion. Although integrity of both endothelial and smooth-muscle cells appears to be maintained in both culture conditions as confirmed by CD31, factor VIII, and alpha-actin expression, a few smooth-muscle cells in the media stained positive for factor VIII. Cell-proliferation marker MIB-1 was also detected in the two settings and PAI-1 mRNA expression and activity increased significantly after 14 days of culture and perfusion. CONCLUSION: This study demonstrates the feasibility to chronically perfuse human vessels under sterile conditions with preservation of cellular integrity and vascular contractility. To gain insights into the mechanisms leading to IH, it will now be possible to study vascular remodeling not only under static conditions but also in hemodynamic environment mimicking as closely as possible the flow conditions encountered in reconstructive vascular surgery.

Hemodynamics induced after acute reduction of proximal thoracic aorta compliance.

OBJECTIVE: to investigate the affect of reduced aortic compliance on cardiovascular hemodynamics. MATERIALS AND METHOD: fourteen Yucatan miniature swine were divided into two equal groups, a Sham Operated Group and a Banding Group. A Teflon prosthesis was wrapped around the aortic arc in order to limit proximal aortic compliance (Banding Group). Data were recorded operatively (after implantation of a pressure sensor and a flow probe in the ascending aorta), after banding (only in the Banding Group) and at 2 days postoperatively. RESULTS: after banding, compliance decreased by 52 +/- 13% ((-)X +/- SEM) (p < 0.01) while systolic and pulse pressure increased by 37 +/- 8% (p < 0.05) and 87 +/- 31% (p < 0.01), respectively. Diastolic pressure, mean blood pressure, cardiac output and systemic vascular resistance did not change significantly. Aortic characteristic impedance increased nearly 2.5 times. Amplitudes of forward and reflected pressure waves (derived from the aortic pressure wave) increased by 96 +/- 41% and 174 +/- 46%, respectively (p < 0.05), while the time delay between the two decreased by 36 +/- 7% (p < 0.05). CONCLUSIONS: about half of the total arterial compliance is located in the proximal thoracic aorta. Arterial reconstruction of the proximal aorta with a non-compliant graft results in a significant decrease in systemic arterial compliance, which in turn increases systolic and pulse pressure. The development of more compliant prosthesis, which matches the host artery compliance, is expected to reduce the hemodynamic changes induced after their implantation.