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Myocardial perfusion is performed by the left and the right coronary arteries, which deliver blood to the left and right ventricles, respectively. The impairment of arterial flow supply to the cardiac muscle by disease denotes a phenomenon known as ischaemia. Previous studies have demonstrated the ability of fractal dimension (FD) value of a physiological parameter in differentiating healthy/pathological behaviours. The aim of this study consisted in quantifying the loss of ventricular thickness fractal complexity in order to determine if FD is an intrinsic marker of acute coronary ischaemia. Five mongrel dogs weighing 18.8-26.5 kg (24.4 ± 3.3, mean ± SD) were submitted to this studio. A left ventricular pressure transducer and a fluid-filled catheter for later calibration of the pressure transducer were introduced through a stab wound near the apex. Two pairs of ultrasonic microcrystals (5 MHz) for continuous wall thickness measurements were implanted at the anterior and posterior walls of the left ventricle following a previously described technique. During coronary occlusion, the ischemic wall started to thin at the very onset of relaxation (showing abnormal motility), while the normoperfused wall displayed postejective thickening. Concomitantly, posterior ventricular wall thickness and anterior wall ventricular thickness showed a significant decrease in its FD value (P <0.05). In conclusion, loss of time series fractal complexity (waveform fine structure diminution or 'unwrinkling') constitutes a marker of the presence of an ischemic process. As a result, a single scalar value is sufficient to characterize the entire behaviour of the time series. This value manifested a similar trend compared to the most well-known clinical indices of myocardial ischaemia.

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UNLABELLED: Flow-mediated dilatation (FMD) is the most accepted technique for the evaluation of endothelial function. However, it has been show a great inter-subject variability limiting its clinical use. Carotid-radial pulse wave velocity (PWVcr) was proposed as an alternative tool for the evaluation of endothelial function. At the present, there is no doubt that PWVcr reduces its values in response to reactive hyperemia test (RHT) in healthy subjects. AIMS: a) to determine simultaneously the temporal profile of FMD, PWVcr and shear rate in response to RHT and b) to describe and analyze how subjects "FMD responders" or "non-responders" behave regards to PWVcr changes. METHODS: 34 Healthy young subjects were included. The PWVcr (strain gauge mechanotransducers), brachial diameter (B-Mode ultrasound and blood flow velocity (Doppler ultrasound) were measured before (baseline) the cuff was inflated and after its deflation (5 minutes). 10(th) percentiles FMD and PWVcr changes in the population were used for the definition of the subjects ("responders and non-responders"). RESULTS: Changes in PWVcr, brachial arterial diameter and shear rate were evidenced after the cuff release (p<0.05). There were differences in the PWV and FMD temporal profiles. Within "FMD responders" there were "PWV responders and non-responders". CONCLUSION: Assessing RHT-related changes in PWVcr in the context of a FMD evaluation, could be useful as a discriminator of intrinsic wall alterations giving additional information of vascular dynamics.

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Atherosclerotic plaques form at specific sites of the arterial tree, an observation that has led to the "geometric risk factor" hypothesis for atherogenesis. It is accepted that the location of atherosclerotic plaques is correlated with sites subjected to low abnormal values of wall shear stress (WSS), which is in turn determined by the specific geometry of the arterial segment. In particular, the left coronary artery (LCA) is one of the most important sites of plaque formation and its progression may lead to stroke. However, little is known about hemodynamics and WSS distributions in the LCA. The purpose of this work is to set up a method to evaluate flow patterns and WSS distributions in the human LCA based on real patient-specific geometries reconstructed from medical images.

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The early detection of biomechanical modifications in the arterial wall could be used as a predictor factor for various diseases, for example hypertension or atherosclerosis. In this work a transient elastography technique is used for the in vitro evaluation of the arterial wall elasticity. The obtained Young modulus is compared with the one obtained by a more classical approach: pressure-diameter relationships. As a sample an arterial phantom made of PolyVinyl Alcohol (PVA) gel was used. Diameter variation due to pressure variation inside the phantom was recorded by means of ultrasound. Through both techniques similar Young modulus estimations are obtained showing in this way the feasibility of applying transient elastography for the arterial wall elasticity assessment.

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UNLABELLED: The analysis of carotid-radial pulse wave velocity (PWVcr) changes in response to forearm transient ischemia (TI) has been proposed as an alternative approach to evaluate endothelial function. Consider flow mediated dilatation tests, PWVcr changes are characterized after 5 minutes of TI. It is unknown if lower TI times could be used and if different TI times would result in different PWVcr responses (levels and/or kinetics). OBJECTIVE: To determine PWVcr changes associated with the reactive hyperemia in response to 1, 3 or 5 minutes of forearm TI. METHODS: We measured left PWVcr change using mechano-transducers in healthy volunteers (22 ± 2 years old) before (basal) and after 1 (n=14), 3 (n=14) and 5 (n=15) minutes of TI (forearm cuff inflation), respectively. The change of level and rate in PWVcr were recorded at 15, 30, 45 and 60 seconds after cuff release. Right brachial pressure was measured. RESULTS: There were no changes in heart rate or blood pressure during the studies. Regardless of the occlusion length, TI resulted in PWVcr reduction (p < 0.05). The groups showed similar maximum PWVcr reduction. However, there were differences in the immediate PWVcr changes (-4.9 ± 0.2%; -6.8 ± 0.3% and -8.3 ± 0.5% for 1, 3 and 5 minutes of TI, respectively) (p < 0.05). Then, the immediate rate of PWVcr change differed (p < 0.05) among the different ischemia times considered. Thereafter, the differences diminished and a minute after TI the groups showed similar levels and mean rate of PWVcr reduction. CONCLUSION: Similar maximum PWVcr responses can be obtained after 1, 3, or 5 minutes of TI. Different TI times resulted in dissimilar immediate, but not later, PWVcr changes.

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Atherosclerotic plaque complication is a major cause of vascular accidents. Although a variety of factors have been proposed as key factors in these process, the mechanism that contribute to this problem remain to be characterized. Previously we demonstrated that changes in arterial wall viscous and elastic properties and/or in the filtering function (FF) could be part of the arterial wall alterations basis. If these properties are altered in arteries with atherosclerotic plaques remains to be analyzed. Our aims were 1) to analyze the arterial wall visco-elasticity and FF of carotid and femoral segments with atherosclerotic plaques, 2) to compare them with the mechanical behavior of segments without plaques (from the same artery) and of healthy arteries studied non-invasively. To this end, in each arterial segment, pressure and diameter signals were obtained, in vitro (circulation mock) and in vivo (non-invasive recordings). In atherosclerotic arteries recordings were performed on plaques and near regions without plaques. In each segment, the elasticity, the viscosity, and the wall FF were quantified. Atherosclerotic vessels, and particularly plaque regions, showed a reduced viscosity and FF. At the light of our results, hypothetical links between plaque events and changes in visco-elasticity and FF were discussed.

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In several clinical and experimental circumstances, it is widely necessary to characterize the bio-mechanical changes induced by atherosclerosis to the arterial wall. In this context, the purpose of this paper is twofold. Firstly, to propose a low cost ultrasound setup to improve artery radii determination in elasticity experiments, based on two transducers using a single channel ultrasound hardware. Secondly, to present an in vitro artificial heart system developed in our laboratory, which provides a wide range of hemodynamic parameters in arterial elasticity assessment experiments. It can be used in a liquid, stand alone mode or blowing air to a Jarvik device. This system will be integrated in future works with the proposed ultrasound setup to provide real time elasticity measurements.

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Although a variety of factors have been proposed as key factors of the atherosclerotic plaque vulnerability, the mechanisms that contribute to this problem are not yet fully characterized. In previous works we demonstrated that changes in arterial wall viscosity and elasticity and/or in the filtering function (FF) could be in the basis of arterial wall alterations. If these properties are altered in arterial wall with atherosclerotic plaques remain to be analyzed. Our aims were to analyze, the arterial wall visco-elasticity and FF of human carotid arteries with atherosclerotic plaques. To this end, instantaneous arterial diameter waveforms were obtained non-invasively (B-Mode Echography), in five sites (S1-S5) on the carotid artery. After that, diameter waveform obtained in S1 (first segment of the common carotid artery) was calibrated using pressure values, and used to quantify the pressure-diameter relationship for each segment. From pressure-diameter relationships, viscosity, elasticity and FF were quantified. Central portions of atherosclerotic plaques showed a reduced FF. At least in theoretical terms, the FF reduction could be related with the plaque vulnerability.

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Biomechanical and functional properties of tissue engineered vascular grafts must be similar to those observed in native vessels. This supposes a complete mechanical and structural characterization of the blood vessels. To this end, static and dynamic mechanical tests performed in the sheep thoracic and abdominal aorta and the cava vein were contrasted with histological quantification of their main constituents: elastin, collagen and muscle cells. Our results demonstrate that in order to obtain adequate engineered vascular grafts, the absolute amount of collagen fibers, the collagen/elastin ratio, the amount of muscle cells and the muscle cells/elastic fibers ratio are necessary to be determined in order to ensure adequate elastic modulus capable of resisting high stretches, an adequate elastic modulus at low and normal stretch values, the correct viscous energy dissipation, and a good dissipation factor and buffering function, respectively.

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Each artery conduces blood (conduit function, CF) and smoothes out the pulsatility (buffering function, BF), while keeping its wall protected against the high oscillations of the pulse waves (damping function, xi). These functions depend on each segment viscoelasticity and capability to store and dissipate energy. When a graft/prosthesis is implanted, the physiological gradual transition in the viscoelasticity and functionality of adjacent arterial segments is disrupted. It remains to be elucidated if the cryografts would allow keeping the physiological biomechanical transition. The aim of this study was to evaluate the cryografts capability to reproduce the functional, energetic and reflection properties of patients' arteries and fresh homografts. Common carotid's pressure, diameter and wall-thickness were recorded in vivo (15 patients) and in vitro (15 cryografts and 15 fresh homografts from donors). Calculus: elastic (Epd) and viscous (Vpd) indexes, CF, BF, dissipated (WD) and stored (WPS) energy and xi. The graft-patient's artery matching was evaluated using the reflection coefficient (Gamma) and reflected power (WGamma). Cryografts did not show differences in Epd, Vpd, BF, CF, WD, WPS, and xi, in respect to fresh homografts and patients' arteries, ensuring a reduced Gamma and WGamma. Cryografts could be considered as alternatives in arterial reconstructions since they ensure the gradual transition of patients' arteries biomechanical and functional behavior.

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There is a pressing need to obtain adequate vascular substitutes for arterial by-pass or reconstruction. Since the performance of venous and commercially prosthetic grafts is not ideal and the availability of autologous arteries is limited, the use of cryopreserved arteries has emerged as a very attractive alternative. In this sense, the development of an inter-continental network for cryopreserved tissue exchange would improve international cooperation increasing the possibilities of obtaining the requested materials. In this work, the effects of an inter-continental shipment, which includes cryopreservation, on the biomechanical properties of sheep aortas were evaluated by means of the arterial complex elastic modulus. It is shown that these properties were preserved after the shipment. The actual possibilities of establishing a network for arterial exchange for the international cooperation are discussed.

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AIM: An adventitia dependent regulation of the vascular smooth muscle tone has been described. However, if the adventitia plays an active role on arterial wall biomechanical behaviour and functions remains to be established. Our aim was to characterize the influence of adventitia on arterial wall mechanical properties and the arterial conduit and buffer functions. METHODS: Ovine brachiocephalic arteries were studied in vivo (n = 8) and in vitro (with null tone) in a circulation mock (n = 8). Isobaric, isoflow and isofrequency studies were performed. In each segment, pressure and diameter waves were assessed before and after adventitia removal. From the arterial stress-strain relationship, we derived the elastic and the viscous modulus. The buffering and conduit functions were calculated using the Kelvin-Voigt's time constant and the inverse of the characteristic impedance, respectively. RESULTS: In in vivo studies arterial diameter decreased after adventitia removal (P < 0.05). Elastic and viscous modulus in in vivo studies were significantly higher in adventitia-removed arteries, compared with values in intact vessels (P < 0.05). This behaviour was not observed in in vitro experiments. An impairment of buffer and conduit functions was observed in vivo after adventitia removal (P < 0.05), while both functions remain unchanged in in vitro studies (P > 0.05). CONCLUSIONS: Arterial wall viscosity and elasticity were influenced by adventitia removal in in vivo studies, possibly by a smooth muscle-dependent mechanism, since it was not present in in vitro experiments. Adventitia would be involved in a physiological mechanism of arterial wall viscous and elastic properties regulation, that could influence arterial buffering and conduit functions.

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The Favaloro University initiated the academic path in biomedical sciences in Buenos Aires, Argentina. As a very promising area, the biomedical world offers the integration between several domains, complementing medicine with engineering topics. The profile of the graduated students proved to be very versatile, allowing their instantaneous incorporation to the competitive market in this vast field. The university strategy is to concentrate basic science in the first 3 years and add the specific biological/medical concepts in the last 2 years. The students achieve a bachelor degree that integrates their knowledge in basic sciences. Afterwards, they attend a professional 2 year cycle, choosing between biomedical, physics and medical computing branches. The results proved to be effective in terms of professional and academic quality, market insertion and even the creation of promising seeds for future enterprises.

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Systemic arteries show higher vascular disease than pulmonary ones. The aim of this study was to establish regional and functional differences in the mechanical properties of arteries in both circulations. Pressure (Konigsberg) and diameter (Sonomicrometry) were measured in seven artery segments corresponding to each sheep (N=7) using a previously developed mock circulation loop...

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The aim of this study was to compare the mechanical and intrinsic effects of an angiotensin converting enzyme inhibitor, vs a beta-blocker, on brachial arterial compliance. In a double blind study, 34 essential hypertensive patients were treated for 3 months with either ramipril 2.5-5.0 mg daily (n = 17, age 57 +/- 7 y, 11 males) or atenolol 50-100 mg daily (n = 17, age 53 +/- 8 y, 11 males). Blood pressure (BP), brachial artery diameter (D), brachial-radial pulse wave velocity (PWV) and effective compliance (Ceff), were measured before and at the end of the study. Isobaric evaluation (Ciso) was performed in the entire population studied at an average mean BP of 110 mmHg. Ramipril significantly reduced BP from 155 +/- 16/94 +/- 6 mmHg to 140 +/- 15/85 +/- 7 mmHg (p < 0.001) without affecting heart rate (HR; 74 +/- 10 vs. 75 +/- 12 bpm). In addition, it significantly improved both PWV (18%; p < 0.001) and arterial compliance (45%; p < 0.001), from which 35% was related to a pressure independent effect (p < 0.01). Atenolol also induced a reduction in both BP (159 +/- 17/96 +/- 10 to 133 +/- 13/81 +/- 8 mmHg; p < 0.001) and HR (76 +/- 10 to 57 +/- 7 bpm; p < 0.001). In a similar way, PWV (11%; p < 0.05) and Ceff (30%; p < 0.05) were significantly improved without significant change in Ciso. This suggests that blood pressure reduction was responsible for compliance improvement. In conclusion, it is suggested that atenolol induces only hemodynamic changes, mediated mainly by BP reduction. In contrast, the improved brachial buffering function observed after ramipril involves not only hemodynamic changes, but also changes mediated by other mechanisms, such as modification of wall structures.

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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.

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The aim of this study was to compare the mechanical and intrinsic effects of an angiotensin converting enzyme inhibitor, vs a beta-blocker, on brachial arterial compliance. In a double blind study, 34 essential hypertensive patients were treated for 3 months with either ramipril 2.5-5.0 mg daily (n = 17, age 57 +/- 7 y, 11 males) or atenolol 50-100 mg daily (n = 17, age 53 +/- 8 y, 11 males). Blood pressure (BP), brachial artery diameter (D), brachial-radial pulse wave velocity (PWV) and effective compliance (Ceff), were measured before and at the end of the study. Isobaric evaluation (Ciso) was performed in the entire population studied at an average mean BP of 110 mmHg. Ramipril significantly reduced BP from 155 +/- 16/94 +/- 6 mmHg to 140 +/- 15/85 +/- 7 mmHg (p < 0.001) without affecting heart rate (HR; 74 +/- 10 vs. 75 +/- 12 bpm). In addition, it significantly improved both PWV (18

; p < 0.001) and arterial compliance (45

; p < 0.001), from which 35

was related to a pressure independent effect (p < 0.01). Atenolol also induced a reduction in both BP (159 +/- 17/96 +/- 10 to 133 +/- 13/81 +/- 8 mmHg; p < 0.001) and HR (76 +/- 10 to 57 +/- 7 bpm; p < 0.001). In a similar way, PWV (11

; p < 0.05) and Ceff (30

; p < 0.05) were significantly improved without significant change in Ciso. This suggests that blood pressure reduction was responsible for compliance improvement. In conclusion, it is suggested that atenolol induces only hemodynamic changes, mediated mainly by BP reduction. In contrast, the improved brachial buffering function observed after ramipril involves not only hemodynamic changes, but also changes mediated by other mechanisms, such as modification of wall structures.

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A new automated computerized system (IôTEC) that assesses concomitantly the instantaneous temporal arterial diameter and intimal media thickness (IMT) obtained from B-mode ultrasound (US) images was validated by sonomicrometry in sheep, by an echo-tracking system in humans, and by a Lucite phantom in vitro. Differences between methods for diameter measurements did not vary in any systematic way, with no significant differences in the lower frequency range. Ultrasonic measurements of the true phantom gap sizes showed high correlation (r2 = 0.98,p < 0.001) with no systematic errors. Carotid and femoral arteries in humans were strongly related between IôTEC and echo-tracking device (r2 = 0.94 carotid; R2 = 0.88 femoral, p < 0.001), with a Gaussian distribution of the errors. This new method showed high intra- and interobserver repeatability of arterial diameter and IMT, allowing consistent characterization of arterial dynamics in humans.

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Increases in arterial wall viscosity and intima-media thickness (IMT) were found in hypertensive patients. Because smooth muscle cells are responsible for the viscous behavior of the arterial wall and they are involved in the process of thickening of the intima-media complex, this study evaluates the relationship between carotid thickness and wall viscosity. The simultaneous and noninvasive assessment of the intima-media complex and arterial diameter waveform was performed using high-resolution ultrasonography. This technique was contrasted against sonomicrometry in sheep, showing that the waveforms obtained by both methods were similar. The common carotid arteries of 11 normotensive subjects (NTA) and 11 patients with mild to moderate essential hypertension (HTA) were measured noninvasively by using tonometry and an automatic densitometric analysis of B-mode images to obtain IMT and instantaneous pressure and diameter loops. A viscoelastic model was used to derive the wall viscosity index (eta) using the hysteresis loop elimination criteria. In NTA, eta was 2.73+/-1.66 (mm Hg x s/mm) and IMT was 0.58+/-0.08 (mm), whereas in HTA, eta was 5.91+/-2.34 (P<.025) and IMT was 0.70+/-0.12 (P<.025), respectively. When all data of eta versus IMT of NTA and HTA were pooled in a linear regression analysis, a correlation coefficient of r=.71 (P<.05) was obtained. Partial correlation between eta and IMT holding constant pressure was r=.59 (P<.05). In conclusion, wall viscosity increase was associated with a higher IMT even maintaining blood pressure fixed, suggesting that the intima-media thickening might be related to smooth muscle alterations manifested as an increase in viscous behavior.

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The influence of the renin-angiotensin system (RAS) on the aortic wall mechanical properties under angiotensin I converting enzyme inhibition (enalaprilat, 0.3 mg/kg iv) or angiotensin II receptor (AT1) blockade (E-3174, 1 mg/kg iv) was examined in eight normotensive and eight renovascular hypertensive conscious dogs. Aortic diameter (D; sonomicrometry)-pressure (P; microtransducer) hysteresis loops during steady state and during rapid distal aortic occlusion allowed (after hysteresis elimination) calculation of the aortic wall viscosity index, the purely elastic P-D relationship, and derivation into compliance-pressure curves. At the early stage ofrenovascular hypertension when activation of RAS is more pronounced, aortic wall stiffness and wall viscosity were increased as compared with normotensive states. Blood pressure remained unchanged in normotensive animals and was reduced during hypertension after antihypertensive treatments. In hypertensive animals, enalaprilat and E-3174 decreased viscosity index and shifted the compliance-pressure curve upward with respect to pretreatment conditions. In normotensive dogs, whereas E-3174 did not change the compliance-pressure curve and viscosity index, enalaprilat increased compliance and reduced viscosity index. We concluded that in normotensive dogs converting enzyme inhibition modifies arterial viscoelastic parameters by angiotensin-independent mechanisms that contribute to the modulation of the buffering function of large arteries.

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