Urinary bladder matrix scaffolds strengthen esophageal hiatus repair.

BACKGROUND: Laparoscopic repair of the hiatal hernia is associated with a recurrence rate between 12% and 42% depending on the defect size. Although the impact of hiatal reinforcement on long-term recurrence remains controversial, the main limitation of this approach has been the risk of adverse events related with the use of synthetic materials in the vicinity of the esophagus. METHODS: A total of 14 female domestic pigs underwent laparoscopic primary hiatal hernia repair of a simulated defect in the esophageal hiatus. Seven of the hiatal repairs were reinforced with an extracellular matrix (ECM) scaffold, whereas the remaining seven served as primary repair controls. Animals were survived for 8 wk. At necropsy, after gross morphologic evaluation, samples were sent for mechanical testing and histology. RESULTS: The repaired defect site reinforced with ECM scaffolds showed a robust closure of the crura in all cases with a smooth peritoneal-like structure covering the entire repair. Average load at failure of the treated group was found to be significantly stronger than that of the controls (185.8 ± 149.7 g versus 57.5 ± 57.5 g, P < 0.05). Similarly, the stiffness was significantly higher in the treated animals (57.5 ± 26.9 g/mm versus 19.1 ± 17.5 g/mm; P < 0.01). Interestingly, there was no difference in elongation at failure (7.62 ± 2.02 mm versus 7.87 ± 3.28 mm; P = 0.44). CONCLUSIONS: In our animal survival model, we have provided evidence that the addition of an ECM to augment a primary hiatal repair leads to tissue characteristics that may decrease the possibility of early failure of the repair. This may translate to decreased recurrence rates. Further study is necessary.

Vascular accesses for haemodialysis in the upper arm cause greater reduction in the carotid-brachial stiffness than those in the forearm: study of gender differences.

Purpose. To evaluate in chronically haemodialysed patients (CHPs), if: (1) the vascular access (VA) position (upper arm or forearm) is associated with differential changes in upper limb arterial stiffness; (2) differences in arterial stiffness exist between genders associated with the VA; (3) the vascular substitute (VS) of choice, in biomechanical terms, depends on the previous VA location and CHP gender. Methods. 38 CHPs (18 males; VA in upper arm: 18) were studied. Left and right carotid-brachial pulse wave velocity (PWV(c-b)) was measured. In in vitro studies, PWV was obtained in ePTFE prostheses and in several arterial and venous homografts obtained from donors. The biomechanical mismatch (BM) between CHP native vessel (NV) and VS was calculated. Results/Conclusions. PWV(c-b) in upper limbs with VA was lower than in the intact contralateral limbs (P < 0.05), and differences were higher (P < 0.05) when the VA was performed in the upper arm. Differences between PWV(c-b) in upper limbs with VA (in the upper arm) with respect to intact upper limbs were higher (P < 0.05) in males. Independently of the region in which the VA was performed, the homograft that ensured the minimal BM was the brachial artery. The BM was highly dependent on gender and the location in the upper limb in which the VA was performed.

Effects of aging on thoracic aorta size and shape: a non-contrast CT study.

Measures of atherosclerosis burden like coronary artery calcification are performed using non-contrast heart CT. However, additional information can be derived from these studies, looking beyond the coronary arteries without exposing the patients to further radiation. We present a semi-automated method to assess ascending, arch and descending aorta geometry from non-contrast CT datasets in 250 normotensive patients. We investigated the effect of aging on thoracic aorta morphometry. The algorithm identifies the aortic centerline coordinates following a toroidal path for the curvilinear portion and axial planes for descending aorta. Then it reconstructs oblique planes orthogonal to the centerline direction and a circle fitting process estimates the vessel cross-section. Finally, global thoracic aorta dimensions (diameter, volume and length) and shape (vessel curvature and tortuosity, aortic arch width and height) are calculated. From a multivariate analysis, adjusted for gender and body-size area, aortic volume and arch width were the descriptors that better represented the aortic size and shape alterations with aging. The thoracic aorta suffers an expanding and unfolding process with aging that deserves further attention to prevent aortic aneurisms.

Estimation of coronary length-volume allometric relations of human arteries in vivo using CT.

Assessing the individual geometry of the coronary arteries in a patient can help to explain diffuse artery disease. Some allometric functions, relating arterial length and volume, were verified in porcine arteries and human autopsies but not in vivo. In this work we use skeletonization methods on MSCT images to render the whole coronary tree in healthy and cardiovascular patients. Twenty patients with and without coronary artery disease were recruited. The coronary was segmented with minimum user intervention. Vessels were separated and measured. A 3D coronary map was individually calculated. The allometric length-volume function L=k(v)V(ß) was evaluated in each patient and plotted in a Log-Log scale. The coefficient k(v) ranged 1.00 ± 0.35. Slopes ranged ß = 0.69-0.88 and seemed to overlap in the scatter Log plot. The analysis of covariance verified this perception and concluded that lines were parallel. In other words, the allometric function stood for all patients. Values were not different from other studies in humans and pigs. The combination of multislice CT with morphological extraction algorithms was effective to extract allometric functions from coronary arteries in patients and can be easily applied in the clinic.

Validity of a new method to estimate mean arterial pressure at brachial level.

The value of mean arterial pressure (MBP) is of clinical importance, and is required for peripheral resistance calculation as well as for central blood pressure calibration procedures. MBP is usually estimated at the upper arm using systolic and diastolic sphygmomanometers pressure values, as 33% of pulse pressure (PP) above diastolic pressure. In a previous work, we proposed to use 38%. The aim of this study was to investigate the validity of the proposed formula to calculate MBP, when assessing subjects with a wide range of blood pressure and pulse wave velocity (PWV) levels. In 73 volunteers (56 ± 10 years, range: 27-82; pulse pressure: 59 ± 12 mmHg, range: 43-86; PWV: 10 ± 2 m/s, range: 8-17) arterial pressure waveforms were obtained at the left brachial artery by applanation tonometry. Diastolic (DBP) and systolic (SBP) brachial pressure were obtained with oscillometric device. Brachial-radial PWV was obtained at the same arm using mechano-transducers. MBP computed as 38% of PP above diastolic pressure, introduces an error of only 0.1% in brachial MBP estimation, independent of pressure and PWV levels.

Arterial wall structure and dynamics in type 2 diabetes mellitus methodological aspects and pathophysiological findings.

Type 2 Diabetes Mellitus (DM), or adult-onset diabetes, is being considered as a new pandemic. Cardiovascular disease is the major cause of morbidity and mortality in type 2 DM, due to arterial structure and functional changes. Assessment of arterial structure and biomechanics, by non-invasive methods and parameters, can be used to detect early alterations related to DM. Three markers of vascular disease may help to a better evaluation of vascular dysfunction in type 2 DM patients: carotid intimamedia thickness (IMTc), arterial stiffness, assessed by pulse wave velocity (PWV), and endothelial function, evaluated through the brachial artery flow-mediated dilation (FMD). Among these parameters, IMTc is considered a marker of structural vessel wall properties, and arterial stiffness reflects functional wall properties. Endothelial function represents the arterial way to actively regulate its diameter (smooth muscle-dependent actions) and its visco-elastic properties (wall elasticity and viscosity). IMTc is increased in patients with type 2 DM and other independent risk factors, such as: age, hyperlipidemia and duration of DM. Subjects with DM have shown increased arterial stiffness. Type 2 DM is associated with reductions in FMD (endothelial dysfunction), which has already been reported to be inversely and strongly related to the extent of hyperglycemia. The underlying patho-physiological mechanisms are complex and remain to be fully elucidated. A complete understanding of the association between arterial alterations and early detection, and type 2 DM, may be critical for the primary prevention of DM-related macro-vascular disease.

The physiological impact of the nonlinearity of arterial elasticity in the ambulatory arterial stiffness index.

The ambulatory arterial stiffness index (AASI) is claimed to be a new estimator for arterial rigidity. It was recently defined as one minus the slope of the linear regression of systolic to diastolic ambulatory pressure during 24 h. Although several reports testify its clinical relevance, the explanation of how this new index is conceptually associated with arterial stiffness remains controversial. In this work we hypothesize that nonlinear arterial elasticity is behind AASI physiological principles. To that end, random number generators were used to emulate arterial cross-sectional area (CSA) during 24 h. Pressure values were calculated using linear and nonlinear elasticity models for rigid and compliant arteries. The AASI was calculated from simulated pressures and also analytically predicted for each model. Additionally, invasive aortic pressure and CSA were continuously measured in a conscious sheep during 24 h to test the nonlinear model. We found that analytical solutions agreed with simulation outcomes; for the nonlinear model, the AASI was higher in rigid arteries with respect to compliant arteries (0.51 versus 0.38) and the linear model systematically predicted AASI = 0. For in vivo pressure measurements, AASI was 0.31. Using the measured pulsatile CSA and an estimation of the elastic constant for the nonlinear model, the AASI was accurately predicted with errors below 5%. We conclude that the AASI is higher in stiffer arteries due to the nonlinear behavior of the arterial wall. With a nonlinear arterial function, the slope of the linear regression of diastolic to systolic pressures during 24 h depends on the product of an elastic constant by the pulsatile CSA. As the elastic constant dominates the product, the reported associations between the AASI and arterial stiffness indices now have a consistent explanation.

Simulación de la influencia de la elasticidad parietal sobre el índice ambulatorio de rigidez arterial AASI / Simulation of the arterial elasticity influence on the ambulatory arterial stiffness index AASI

Recientemente se propuso un índice de rigidez arterial denominado AASI (Ambulatory Arterial StiffnessIndex) derivado de mediciones ambulatorias de presión arterial durante 24 horas. Su asociación como índice de rigidez y lainfl uencia estadística de la dispersión en los valores presivos continúa bajo discusión. Proponemos estudiar estas controversias en el contexto de un modelo estadístico. Se realizó una simulación con valores similares a los de pacientes de arterias normales,rígidas y compliantes, utilizando 3 curvas exponenciales presión-diámetro. Se generaron diámetros pulsátiles aleatorios siguiendo distribuciones normales y se obtuvieron presiones sistólicas y diastólicas en tiempos paramétricos equivalentes a 24 horas. Se calculó el AASI como uno menos la pendiente de la regresión de presión arterial sistólica y diastólica. El AASI del grupo normal resultó 0,42, aumentó a 0,50 en el rígido y disminuyó a 0,34 en el compliante (siempre con r2>0,9). Disminuir la dispersión del rango de presiones provocó una disminución de r2 en la regresión de la nube de puntos de presión sistólica y diastólica, aumentando artificialmente el AASI. Por primera vez la elasticidad no-lineal de la pared arterial ayuda a explicar la asociación del AASI como índice de rigidez arterial. La simulación corrobora que la dispersión de los valores presivos condicionan el cálculo del AASI debido a su naturaleza estadística

Recently, an arterial stiffness index called AASI (Ambulatory Arterial Stiffness Index) calculated from ambulatory blood pressure measurements during 24 hours was proposed. The associations with arterial stiffness and the pressure dispersion dependence remain under discussion. We propose to study these controversies in a statistical model framework. A simulation was performed including values similar to the ones in patients with normal, rigid and compliant arteries. Three exponential curves ofpressure-diameter were simulated. Based on diameters randomly generated following normal distributions, systolic and diastolic pressures were calculated in a 24h parametric time. AASI was calculated as one minus the slope of the regression of systolic to diastolic pressure. The AASI for the normal group was 0,42, increased to 0,50 in the rigid group and decreased to 0,34 in thecompliant case (always r2>0,9). A dispersion decrease in the pressure values was followed by an r2 decrease in the diastolic vssystolic pressure regression, artificially increasing AASI. For the first time the non-linearity of the arterial wall helps to explain the association of AASI with a stiffness index. The simulation corroborates that 24 h pressure variability conditions AASI values dueto its statistical nature

Coronary arteries simplified with 3D cylinders to assess true bifurcation angles in atherosclerotic patients.

The geometry of coronary arteries affects regional atherogenic processes. Accurate images can be assessed using multislice computer tomography (MSCT) to estimate bifurcations angles. We propose a three-dimensional (3D) method to measure true bifurcation angles of coronary arteries and to determine possible correlations between plaque presence and angulations. The left main (LM) coronary artery, left anterior descendent (LAD) and left circumflex artery (LCX) were imaged in 40 atherosclerotic and 35 healthy patients, using 64-rows MSCT. This Y-junction was simplified fitting a 3D cylinder to each vessel to estimate true bifurcation angles and diameters. The method was tested in phantoms and interobserver variability was assessed. Geometrical results were compared between groups using an unpaired t-test. The cylinders fitted reasonably well with mean distances to measured points below 0.4 mm. LAD-LCX bifurcation angles were wider in the atherosclerotic group (p < 0.01). LAD (p < 0.01) and LCX (p < 0.05) diameters were also larger. In phantoms mean absolute difference between true and estimated angles (N = 27) was 0.44 +/- 0.54 degrees . Interobserver mean difference (N = 135) was 1.8 +/- 5.8 degrees . Simplifying coronary bifurcation with cylinders results in a reliable technique to assess coronary artery geometry in 3D, avoiding planar projections and decreasing interobserver variability. Geometrical risk factors should be incorporated to properly predict atherosclerosis processes.

Atheromatous plaque: quantitative analysis of the echogenicity of different layers.

INTRODUCTION AND OBJECTIVES: Echographic studies of the composition of atheromatous plaque make use of the median gray level, which provides an overall measure of echogenicity. We propose adding an additional dimension to this approach by dividing the lesion into layers and generating a curve that shows the variation in echolucency with depth. METHODS: Femoral and carotid plaque in asymptomatic patients was investigated using both the median gray level and new layer METHODS: Interobserver variability was assessed for both METHODS: Three risk factors were studied: age, gender and smoking status. Differences in echogenicity-depth curves between different groups were assessed using two-way ANOVA. RESULTS: The two methods gave similar results for the mean echogenicity of carotid and femoral plaque. Echogenicity increased as a function of depth (r=0.96; P< .001). With the median gray level method, none of the risk factors produced a change in echogenicity. However, with the layer method, the echogenicity of femoral plaque was found to increase with age (P< .001), though gender had no effect. Moreover, the echogenicity of superficial layers was less in smokers than nonsmokers (P< .01). In carotid plaque, echogenicity increased with age (P< .01) and was higher in men (P< .01). The echogenicity of deep plaque was greater in smokers than nonsmokers (P< .05). The reproducibility of the two methods was similar. CONCLUSIONS: The layer method was more effective than the median gray level method for identifying the effect of age, sex and smoking status on the echogenicity of atheromatous plaque.

Vascular access localization determines regional changes in arterial stiffness.

BACKGROUND: Vascular access (VA) dysfunction is a common cause of hospitalization in chronically hemodialyzed patients (CHP) limiting the improvement in health and has been largely studied in order to decrease the morbidity events that involves both the artery and the vein used in the construction of the fistula. In parallel, patients in end-stage renal failure show an increase in arterial stiffness. AIM: The aims of this work were: (a) to evaluate arterial stiffness through pulse wave velocity (PWV) measurements in the carotid-brachial pathway where the arteriovenous fistulae (AVF) was constructed, and (b) to determine possible differences in arterial stiffness between the carotid-brachial pathway with and without VA. METHODS: PWV, clinical and biochemical parameters were measured in 38 CHP. PWV was obtained in the carotid-femoral, and in the left and right carotid-brachial pathway. RESULTS: Carotid-brachial PWV determination in upper limbs with AVF (10.07 +/- ;2.43 m/s) showed significantly lower values than those observed in the contra-lateral arm without VA (11.55 +/- ;2.27 m/s). Curiously, the PWV value observed in arms with an AVF was significantly lower in diabetic than in non-diabetic hemodialyzed patients (NDHP) (8.00 +/- ;2.86 m/s and 10.38 +/- ;2.33 m/s; respectively). Measurements of PWV in the carotid-femoral pathway in CHP showed a mean value of 14.09 +/- ;3.12 m/s. Carotid-femoral PWV in NDHP (14.06 +/- ;2.44 m/s) was significantly lower than that observed in the diabetic patients (16.87 +/- ;3.42 m/s). CONCLUSIONS: Carotid-brachial PWV values obtained in the upper limbs, in which VAs were constructed, were significantly lower than that measured in intact arteries in the contra-lateral pathway in CHP.

Determinación no invasiva de aterosclerosis subclínica y estratificación del riesgo cardiovascular / Non invasive assessment of subclinical atherosclerosis and stratification of cardiovascular risk

At present, cardiovascular diseases are the most frequent cause of morbidity and mortality in the world. Atherosclerosis has an important roll in the pathophysiology of cardiovascular diseases, mainly on the ischemic cardiopathy...The incorporation of ultrasonic screening for non invasive detection of subclinical atherosclerosis would allow the identification of a higher numbe of patients at high risk for coronary event and recommended for primary prevention

Aterosclerosis subclínica y estimación de riesgo coronario: comparación de tablas de riesgo / Subclinical atherosclerosis and coronary risk assessment: comparing risk tables

Para guiar el tratamiento preventivo se utilizan distintas tablas de estimación de riesgo coronario. Por otro lado, las alteraciones de la pared arterial son una manifestación de aterosclerosis subclínica y su detección mediante ecografía puede emplearse para predecir eventos coronarios. Objetivo: Comparar la prevalencia de aterosclerosis subclínica evaluada mediante ecografía carótidofemoral entre grupos de bajo riesgo definidos por diferentes tablas. Material y métodos: Se estudiaron 151 pacientes dislipidémicos con edad de 53 ± 12 años (rango: 20-82 años; 45 por ciento varones), índice de masa corporal: 26 ± 3 kg/m2, 42 por ciento hipertensos, 17 por ciento tabaquistas y3 por ciento diabéticos a los que se les realizaron ecografías carótido-femorales y que calificaron paraevaluación de riesgo. Se calculó el riesgo individual mediante diferentes tablas de estimación de riesgo y se incluyeron los individuos con riesgo coronario estimado menor del 10 por ciento a diez años. Se excluyeron del análisis los pacientes con riesgo moderado y alto. Se definió aterosclerosis subclínica a la presencia de placas ateroscleróticas en la ecografía arterial. Secomparó la prevalencia de aterosclerosis subclínica entre los grupos de bajo riesgo. Resultados: Uno de cada dos pacientes considerados de bajo riesgo presentó aterosclerosis subclínica, independientemente de la tabla utilizada. No hubo diferencias significativas en la prevalencia de aterosclerosis subclínica entre subgrupos. El 73 por ciento de los pacientes fueron categorizados de bajo riesgo por ATP III y el 78 por ciento por AHA/ACC, en comparación con el 45 por ciento calculado por Europea II (p < 0,001). Conclusiones: La ecografía carótido-femoral complementa la evaluación realizada mediante tablas de riesgo en la toma de decisiones terapéuticas en prevención primaria.(AU)

Aterosclerosis subclínica y estimación de riesgo coronario: comparación de tablas de riesgo / Subclinical atherosclerosis and coronary risk assessment: comparing risk tables

Para guiar el tratamiento preventivo se utilizan distintas tablas de estimación de riesgo coronario. Por otro lado, las alteraciones de la pared arterial son una manifestación de aterosclerosis subclínica y su detección mediante ecografía puede emplearse para predecir eventos coronarios. Objetivo: Comparar la prevalencia de aterosclerosis subclínica evaluada mediante ecografía carótidofemoral entre grupos de bajo riesgo definidos por diferentes tablas. Material y métodos: Se estudiaron 151 pacientes dislipidémicos con edad de 53 ± 12 años (rango: 20-82 años; 45 por ciento varones), índice de masa corporal: 26 ± 3 kg/m2, 42 por ciento hipertensos, 17 por ciento tabaquistas y3 por ciento diabéticos a los que se les realizaron ecografías carótido-femorales y que calificaron paraevaluación de riesgo. Se calculó el riesgo individual mediante diferentes tablas de estimación de riesgo y se incluyeron los individuos con riesgo coronario estimado menor del 10 por ciento a diez años. Se excluyeron del análisis los pacientes con riesgo moderado y alto. Se definió aterosclerosis subclínica a la presencia de placas ateroscleróticas en la ecografía arterial. Secomparó la prevalencia de aterosclerosis subclínica entre los grupos de bajo riesgo. Resultados: Uno de cada dos pacientes considerados de bajo riesgo presentó aterosclerosis subclínica, independientemente de la tabla utilizada. No hubo diferencias significativas en la prevalencia de aterosclerosis subclínica entre subgrupos. El 73 por ciento de los pacientes fueron categorizados de bajo riesgo por ATP III y el 78 por ciento por AHA/ACC, en comparación con el 45 por ciento calculado por Europea II (p < 0,001). Conclusiones: La ecografía carótido-femoral complementa la evaluación realizada mediante tablas de riesgo en la toma de decisiones terapéuticas en prevención primaria.

Cryopreservation procedure does not modify human carotid homografts mechanical properties: an isobaric and dynamic analysis.

The viscoelastic and inertial properties of the arterial wall are responsible for the arterial functional role in the cardiovascular system. Cryopreservation is widely used to preserve blood vessels for vascular reconstruction but it is controversially suspected to affect the dynamic behaviour of these allografts. The aim of this work was to assess the cryopreservation's effects on human arteries mechanical properties. Common carotid artery (CCA) segments harvested from donors were divided into two groups: Fresh (n = 18), tested for 24-48 h after harvesting, and Cryopreserved (n = 18) for an average time of 30 days in gas-nitrogen phase, and finally defrosted. Each segment was tested in a circulation mock, and its pressure and diameter were registered at similar pump frequency, pulse and mean pressure levels, including those of normotensive and hypertensive conditions. A compliance transfer function (diameter/pressure) derived from a mathematical adaptive modelling was designed for the on line assessment of the arterial wall dynamics and its frequency response. Assessment of arterial wall dynamics was made by measuring its viscous (eta), inertial (M) and elastic (E) properties, and creep and stress relaxation time constant (tauC and tauSR, respectively). The frequency response characterization allowed to evaluate the arterial wall filter or buffer function. Results showed that non-significant differences exist between wall dynamics and buffer function of fresh and cryopreserved segments of human CCA. In conclusion, our cryopreservation method maintains arterial wall functional properties, close to their fresh values.

Smart damping modulation of carotid wall energetics in human hypertension: effects of angiotensin-converting enzyme inhibition.

Damping is the conversion of mechanical energy of a structure into thermal energy, and it is related to the material viscous behavior. To evaluate the role of damping in the common carotid artery (CCA) wall in human hypertension and the possible improvement of angiotensin-converting enzyme (ACE) inhibition, we used noninvasive CCA pressure (tonometry) and diameter (B-mode echography) waveforms in normotensive subjects (NT group; n=12) and in hypertensive patients (HT group; n=22) single-blind randomized into HT-placebo (n=10) or HT-treated (ramipril, 5 to 10 mg/d during 3 months; n=12). Vascular smooth muscle (VSM) null tonus condition was achieved from in vitro pressure and diameter waveforms (Konigsberg microtransducer and sonomicrometry) measured in explanted human CCA (n=14). Arterial wall dynamics was described by viscous (eta), inertial (M), and compliance (C) parameters, mean circumferential wall stress, viscous energy dissipation (WD), peak strain energy (WSt), damping ratio (xi=WD/WSt), and modeling isobaric indexes CIso and WSt(Iso). The lack of VSM tonus isobarically increased wall stress and reduced eta, CIso, and damping (P<0.01). Wall stress, eta, and WD were greater in HT than in NT (P<0.015) and arrived near normal in HT-treated (P<0.032 respect to HT), with no changes in HT-placebo. Whereas CIso increased in HT-treated (P<0.01) approaching the NT level, xi did not vary among groups. During hypertension, because of the WSt increase, the arterial wall reacts increasing WD to maintain xi. ACE inhibition modulates VSM activation and vessel wall remodeling, significantly improving wall energetics and wall stress. This protective vascular action reduces extra load to the heart and maintains enhanced arterial wall damping.

An in vitro study of cryopreserved and fresh human arteries: a comparison with ePTFE prostheses and human arteries studied non-invasively in vivo.

The surgical options in arterial reconstruction are: the use of autologous arteries; autologous veins; or expanded polytetrafluoroethylene (ePTFE) grafts. However, the development of intimal hyperplasia when using veins or ePTFE grafts has been associated with graft failure. Since autologous arteries are not always available, the use of cryopreserved arteries has to be considered. The aims of this study were: (a) to compare the viscoelastic properties of stored cryopreserved arteries and fresh arteries by in vitro analysis; and (b) to compare the viscoelastic properties of arteries measured non-invasively in normotensive patients, with fresh arteries, cryopreserved arteries, and ePTFE segments. The viscoelastic studies were performed in normotensive patients using stress-strain analysis with non-invasive measurement of pressure and diameter in the common carotid artery, and in vitro measurements of pressure and diameter in arteries and prostheses. The in vitro studies showed that the elastic modulus (E), viscous modulus (eta), Stiffness Index (SI), Peterson modulus (Ep), and the pulse wave velocity (PWV) values for human cryopreserved carotid arteries were similar to the values obtained non-invasively in normotensive subjects (P>0.05) and to human fresh vessels (P>0.05). In vitro, the SI, Ep, PWV, and E values of ePTFE were significantly higher than the observed values in subjects and with fresh and cryopreserved arteries (P<0.05); on the other hand the ePTFE eta values were the lowest (P<0.05). We concluded that cryopreserved arteries have similar viscoelastic properties to those obtained in vivo in the arteries of normotensive subjects and in vitro in fresh arteries. Consequently, we conclude that the cryopreservation procedure does not modify the mechanical properties of the arterial wall.

Evaluación de la función arterial mediante estudios in vivo e in vitro: validación de homoinjertos arteriales criopreservados / Evaluation of arterial function by means of studies in vivo and in vitro: validation of cryopreserved arterial homografts

Introducción: buscando reducir las diferencias entre la función de condución (FC) y amortiguamiento (FA) de las prótesis vasculares y las arterias nativas, la utilización de homoinjertos criopreservados es una alternativa creciente interés. El Instituto Nacional de Donación y Trasplante de Organos, Tejidos y Células ha utilizado técnicas de criopreservación de vasos sanguíneos para ser utilizados como sustitutos vasculares. Objetivos: 1) Evaluar la capacidad de la metodología de criopreservación utilizada para mantener la capacidad funcional de homoinjertos vasculares cripreservados/descongelados (C/D). 2) Evaluar la similitud funcional de los homoinjertos C/D y otros sustitutos actualmente utilizados (venas safenas y politetrafluoretileno expandido (ePTFE)), con las arterias de potenciales receptores. Método: se midieron de forma no invasiva presión (tonometría), espesor parietal (ecografía)en carótidas de pacientes normotensos, se midió presión, diámetro y espesor en segmentos arteriales carotídeos frescos y criopreservados, y venas safenas de donantes multiorgánicos, y en prótesis de ePTFE. Se calculó la FC como 1/Zc (Zc: impedancia característica), y FA como n/E (E, n: módulo elástico y viscoso). Resultados: en ambas condiciones hemodinámicas, los homoinjertos frescos y criopreservados no mostraron diferencias biomecánicas ni funcionales. En condiciones de normotensión e hipertensión los homoinjertos C/D presentaron la mayor similitud biomecánica y funcional con las arterias de pacientes. Conclusión: la criopreservación permitió mantener la capacidad funcional de homoinjertos vasculares. Los homoinjertos C/D mostraron la mayor similitud funcional con arterias de potenciales receptores. (AU)

Disipación energética y protección vascular durante la hipertensión arterial sistémica: rol del músculo liso / Energetic dissipation and vascular protection during the systemic arterial hypertension: rol of the smooth muscle

Introducción: las arterias amortiguan las oscilaciones de alta frecuencia de las ondas de presión y flujo disipando energía. El amortiguamiento protege la pared arterial de daños relacionados con dichas oscilaciones. Objetivo: analizar el rol del músculo liso vascular (MLV) en la protección parietal y disipación energética de arterias carótidas (ACC) de sujetos normotensos, hipertensos e hipertensos tratados con inhibidores de la enzima conversora de angiotensina (ECA). Métodos: presión (tonometría) y diámetro (ecografía) carotídeos se registraron en sujetos normotensos (n=12) e hipertensos (n=22) asignados aleatoriamente al tratamiento placebo (n=10) o inhibidores de ECA (ramipril 5-10 mg/día n=12). Se midió in vitro, presión, diámetro en ACC de donantes (n=4; tono vascular nulo), en condiciones hemodinámicas similares a las de los sujetos. Se calculó para cada latido, usando modelización adaptativa, el índice viscoso, elástico e inercial, la energía disipada (Wn) fue mayor (p<0,05) que en los normotensos, mientras que la protección parietal fue similar. Solo en los hipertensos tratados, la Wn se acercó a los valores de los normotensos, sin cambiar la protección parietal. En situación de tono nulo (in vitro) la Wn y la protección parietal fueron menores que en los normotensos (p<0,01), evidenciando la dependencia de estos parámetros con el tono muscular. Conclusión: el sistema arterial mantiene la protección parietal. El MLV protege la pared disipando energía. En hipertensos, la disipación energética aumenta, y se mantiene amortiguamiento y la protección parietal. La disipación energética puede reducirse (tratamiento), disminuyendo la poscarga ventricular y manteniendo la protección arterial. (AU)